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r
IE HEART
TEM
. lATION OF UDENTS INE
D.
r<ddam and Stir Tlioiiy
7^
DISEASES OF THE HEART
AND
ARTERIAL SYSTEM
DESIGNED TO BE A PRACTICAL PRESENTATION OF
THE SUBJECT FOR THE USE OF STUDENTS
AND PRACTITIONERS OF MEDICINE
BY
ROBERT H. BABCOCK, A. M., M. D.
Professor of Clinical Medidne and Diseases of the Chest, College of Physicians and Sur- geons (Medical Department of the Illinois Sute University), Chicago; Attending Physidan to Cook County Hospital and Cook County Hospital for Consumptives; Consulting: Physician to Mary Thompson Hospital, Hospiti. of St. Anthony de Padua, and of Marion-Sims Sanitarnim ; Fellow and former President of the American Climatolqgfical Association ; Member of the American Medical Association, etc.
v^ITH THREE COLOURED PLATES AND ONE HUNDRED AND THIRTY-NINE ILLUSTRATIONS
s/:coxn edition, revised
NEW YORK AND LONDON
D. APPLETON AND COMPANY
1907
• .•••••• • ••••• •
•• z • • • • * ••••••
• • *«••••« • •••••••
• •• ••!•• • •••••••
CoPYUioiiT, 1008, 1905 By I). APriiKTON AND COMPANY
I'fflMKIi \l IIIK Alll.KlON I KF.SS, \K\V %(»•<>>:, r. s. A.
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PREFACE TO THE SECOND EDITION
The changes made in this second edition while not numerous and not affecting the work as a whole are yet important. In the main they concern that form of insufficiency of the auriclo-ven- tricular valves which depends not upon endocarditis but upon alterations of the myocardium, and in the former edition was regarded as always relative. In this one the author believes he has given due recognition to that variety of mitral and tricuspid incompetence termed muscular. Hence a portion of Chapter XXTT has been entirely rewritten, while allusions to muscular insufficiency have been introduced here and there in other chap- ters. The work has been enhanced in value thereby and has been brought strictly up to date.
R H. B.
PREFACE
In the preparation of tliis work the author has endeavoured to present the siibjeet in a simple, practical fash ion that would suit the needs of the student and practitioner of raedicine. The- ories and s}>eeiilation3 have been omitted or given but scanty consideration, in the belief that thev tend to confuse the student. The anatomy and physiology of the circulatory organs have re- ceived only such notice as was thought necessary to a better un- derstanding of the matter in liand, since an extended consideration of them was believed out of place in a work devoted to diseased conditions. Although aware that physical signs are properly a part of the symptomatology of disease and should be considered under that head, still the author has thought it best to consider them separately, for the sake of facilitating the knowledge of that most difficult subject, the diagnosis of cardiac disease. S|>ecial attention has been paid to treatment, and this part of the subject will be found far more detailed than is tbc case in most books dealing with diseases cf the heart. It was hoped that by so doing the work might be given a more practical value to the general practitioner, although of course the author realized that he would lay himself open to adverse criticism, and could do but little more than lay dowTi principles for management. The phraseology has been kept simple and free from needless technicalities, while in the terminology an attempt has been made to employ the terms which are in most familiar use among American and English physicians. Xo claim is laid to originality, as is apparent from
in
IV DISEASES OF THE HEART
the numerous references to authors from whose works valuable suggestions and information have been derived. To all such authors, grateful acknowledgment is made.
In conclusion the writer desires to express particular thanks to the following gentlemen : Drs. O. L. Schmidt, for the article on Gaertner's Tonometer ; Edward F. Wells, for that on the Sphyg- mograph; Gustav Fiitterer, for anatomical specimens and photo- graphs; W. A. Evans, for post-mortem examinations and other aid ; and Milton W. Hall, for preparing the illustrations. Finally, the author wishes to publicly express his indebtedness to his wife, for her encouragement to undertake this work, for her perusal of his manuscript, and suggestions, without which many passages might have been obscure, and for her invaluable aid in the revi- sion of proof.
BOBERT H. BaBCOCK. 103 State Street, Chicago, III.
CONTENTS
GENERAL CONSIDERATIONS PERTAINING TO THE ANAT- OMY, PHYSIOLOGY. AND EXAMINATION OF THE HEART
PAOB
Introductory 1
Location of the heart 1
The relations of the heart to the anterior thoracic wall 2
Position of the great vessels and yalves 8
Cardiac percussion 5
Atueuliatary or stethoscopic percussion 8
Palpatory percussion 10
Auscultation of the heart 12
Normal heart-sounds 18
RedupliccUion of the heart-sounds 16
RedupliecUion of the first sound 18
OaUop or canter rhythm 18
Murmurs 21
EndocardicU murmurs of organic origin 21
Cardi<ic areas 25
Accidental murmurs 26
Mtmcdl mt^rmurs 29
Accidental musical murmurs 82
The di£Ferential diagnosis of accidental heart murmur 84
ExocardicU murmurs 86
SECTION I
DISEASES OF THE PERICARDIUM
CHAPTER I
ACUTE PERICARDITIS
Morbid anatomy 87
Etiologj 41
DET PEEICARDinS
Symptoms ^
Course and termination • , 56
T
vi DISEASES OP THE HEART
PAOB
Physical signs, Inapeeiion 56
Palpation 57
Pdreuwion 57
Aii^cuttatwn 57
Lucaiion of ih€ pericarduU friciion-sound 58
Ehtfihrn of ihe fnefi&fi-sQuud 58
Jni€nBityQfthefnciion*$OHnd 59
Quality of tht ffit^tifm-souud 59
£Se«t of pressure ozi the pericardi&l mormur 59
Diagnosis 60
Differential diagnosis 60
Prognosis 61
PERICARDITIS WITH EFFUSION
Symptoms 65
Course and termination 78
Physical signs. Inspection 74
Palpation 75
Ptrcuseion 76
Auscultation 79
Secondary physical signs referable to the lungs 80
Diagnosis * . 81
Differential diagnosis 82
Prognosis 84
Treatment 86
Treatment in the stage of effusion 90
CHAPTER n
CHRONIC PERICARDITIS
Morbid anatomy 100
Etiology 103
Symptoms 104
Course and termination 117
Physical signs. Inspection 118
Palpation 120
Percussion 121
Auscultation 121
Diagnosis 122
Prognosis 123
Treatment 124
CHAPTER III
L HTDROPEEICARDIUM
Morbid anatomy 127
Etiology 128
Symptoms 128
Physical signs. Inspection .128
Palpation 128
CONTENTS vil
PAGB
PBTcusaion • • • • . 129
Auscultation 129
Diagnosis 129
Prognosis 129
Treatment .• 180
n. OSMOPEBICAKDIUM
Morbid anatomy 130
Etiology 130
Symptoms 131
Physical signs 131
Diagnosis 181
Prognosis 181
Treatment 181
III. PNEUMOPERICARDIUM
Morbid anatomy 132
Etiology 132
Symptoms 188
Physical signs. Inspection 184
PtrcuBsion 184
Auscultation 184
Diagnosis 185
Prognosis 185
Treatment 185
IV. TUBERCULOSIS OF THE PERICARDIUM
Morbid anatomy 186
Etiology 187
Symptoms 188
Physical signs 188
Diagnosis 188
Prognosis 138
Treatment 188
v. SYPHILIS OF THE PERICARDIUM
Morbid anatomy 189
Etiology 140
Symptoms 140
Physical signs 140
Diagnosis 141
Prognosis 141
Treatment 141
YI. CARCINOMA AND SARCOMA OF THE PERICARDIUM
Morbid anatomy 141
Etiology 142
Symptoms 142
Physical signs 142
Diagnosis 142
Prognosis and treatment 142
vm DISEASES OF THE HEART
SECTION II
DISEASES OF THE ENDOCARDIUM
CHAPTER IV
▲CUTB ENDOCARDITIS paqb
Morbid anatomj 144
Etiology 15()
simplk endocarditis 152
Ulcerative ebokx^arditis 155
Symptoms 157
Acute simple endocarditis 157
Diagnosis 163
Course and termination 163
Ulcerative endocarditis 163
Course and termination 172
Physical signs. Inspection 176
Palpation 176
Ptrcussion 177
Auscultation 177
Diagnosis 178
Diagnosis of ulcerative endocarditis 179
Prognosis 188
Treatment 187
Treatment of acute ulcerative endocarditis 191
CHAPTER V
CHRONIC ENDOCARDITIS
Morbid anatomj 199
Etiology 201
Symptoms 205
CHAPTER VI
MITRAL REGUROrTATION
Morbid anatomj 216
Etiology 221
Symptoms 228
Physical signs. Inspection 239
Palpation 289
Percttssion 240
Ausctdtation 242
Diagnosis 245
Prognosis 246
Mode and causes of death 247
CHAPTER VII
MITRAL STENOSIS •
Morbid anatomy 249
Etiology 252
CONTENTS IX
PAOB
Symptoms 255
Physical signs. Inspection 258
Palpation 259
Ptrcuation 260
AttseuUcUion 261
Diagnosis 268
Prognosis 269
Mode and causes of death 270
CHAPTER VIII
AORTIC REOUROITATION
Morbid anatomy 278
Etiology 280
Symptoms 282
Physical signs. Inspection 297
Palpation 298
Percussion 801
Diagnosis 805
Prognosis 806
Mode and causes of death 807
CHAPTER IX
AORTIC STENOSIS
Morbid anatomy 819
Etiology 822
Symptoms 828
Physical signs. Inspection 885
Ptilpation 885
Percussion 880
Auscultation 887
Diagnosis 888
Prognosis 889
Mode and causes of death 840
CHAPTER X
TRICUSPID REGCJROITATIOM
Morbid anatomy 844
Etiology 845
Sjrmptoros 847
Physical signs. Inspection 849
Palpation 850
Percussion 851
Diagnosis 858
Prognosis 854
Mode and causes of death 854
CHAPTER XI
TRICUSPID STENOSIS
Mofbid anatomy 855
Etiology 856
X DISEASES OF THE HEART
Symptoms 867
Physical sigus. Inspeeiion . 861
Fisreusaion 862
AuseiUtation 862
Diagnosis 868
Prognosis 864
Mode and causes of death 864
CHAPTER XII
PULMONAAT KSOURGITATION
Morbid anatomy 866
Etiology 866
Symptoms 867
Physical signs 870
Inspection 871
FkUpation 871
FRretusian 871
AuscuUcUion 872
Diagnosis 873
Prognosis 874
Mode and causes of death . 874
CHAPTER Xin
PULMONARY STENOSIS
Morbid anatomy 876
Etiology 380
Symptoms 880
Ph sical signs. Inspection 886
Palpation 886
Percussion 886
Auscultatiofi 386
Diagnosis 887
Prognosis 887
Mode and causes of death 888
Summary of physical signs of yalve lesions of the right heart .... 889
CHAPTER XIV
COMBINED VALVULAR LESIONS
Combined mitral stenosis and regurgitation 890
Symptoms. 891
Diagnosis ... . . 891
Prognosis 892
Mitral stenosis and aortic stenosis 892
Symptoms 892
Diagnosis 892
Prognosis 898
CONTENTS xi
PAOB
Mitral stenosis and aortio aEou&orrATioN 893
Symptoms 893
Diagnosis 894
Inspection 895
Palpation 895
PtrcusHon 895
AuaciUtatian 895
Prognosis 896
Mitral rkouroitation and aortic stenosis 896
Symptoms 896
Diagnosis 896
Prognosis 896
Aortic regurgitation and mitral regurgitation 897
Symptoms 897
Diagnosis 897
Prognosis 898
Aortic stenosis and aortic regurgitation 898
Symptoms 898
Physical signs 899
Diagnosis 899
Prognosis . 400
CHAPTER XV
THE PROGNOSIS OF YALTULAR HEART-DISEASE IN GENERAL
Complications 405
Rheumatic diathesis 406
Digestive and bronchial disorders 407
Age 407
Temperament 406
Sex 409
Occupation 409
Habits 410
Home surrotindinp 410
The probable effect on the patient of the knowledge of his lesion . . . 411
TLd effect of digitalis on the patient 411
The relation of prognosis to life insurance 412
CHAPTER XVI
THE TREATMENT OF TALTULAR HEART-DISEASE
I. Compensation being still perfect 414
Exercise 414
Occupation 419
Habits 420
Marriage 422
Clothing 425
Baths 427
Pood 428
lUnesses 429
Use of drugs . 480
Change of climate, with special reference to high altitude .... 482
ZU DISEASES OP THE HEART
CHAPTER XVll
THE TRBATMUIT OF YALYULAR BKART-DISEA8B (continued) ^^^
II. Compensation being imperfect 485
Medicinal agents 444
Rest 448
Exercise « . 454
Resistance exercise 455
Nauheim baths 464
Diet 470
Clothing, habits, occupation 476
CHAPTER XVIII
THE TREATMENT OF YALYULAR HEART-DISEASE (eoncluded)
III. Compensation lost 478
The treatment of dropsy 489
Cathartics 492
The use of digitalis 494
Accessory heart tonics 499
Hypnotics 500
Rest 508
Exercise 502
Baths 503
Receiving Yisitors *. 503
Diet 503
SECTION III
DISEASES OF THE MYOCARDIUM
CHAPTER XIX
ACUTE MYOCARDITIS
Morbid anatomy 606
Etiology 508
Symptoms 510
Physical signs. Inspection 514
Palpation 514
Ptreueeion • • • • • 514
Auactdtation .•••••••••••• 514
Diagnosis • • • • 514
Prognosis 515
Treatment 615
CHAPTER XX
CHROinC MYOCARDITIS
Morbid anatomy 519
Btiolo^ 522
CONTENTS xiii
PAOK
Symptoms 526
Physical signs. In^peetion 543
Palpation 543
PtreuBsion 544
A%k9eiilt€U%<m 545
Diagnosis 547
Prognosis 549
Treatment 551
Commencing loss of heart-power 553
Cardiac incompetency pronminced 555
CHAPTER XXI
HTPERTBOPHT OF THE HEART
Morbid anatomy 565
Etiology 568
Symptoms 570
Physical signs. Inspection 571
Palpation 571
Percussion 571
Auscultation 572
Diagnosis 572
Prognosis 574
Treatment 575
CHAPTER XXII
DILATATIOH OF THE HEART — RELATITE AND MUSCULAR MITRAL IN8UFFICIENCT L DILATATION OF THE HEART
Morbid anatomy 576
Etiology 577
Symptoms 580
Physical signs. Inspection 585
Palpation . 585
Percussion 585
Auscultation 586
Diagnosis 586
Prognosis 587
Treatment 590
(1) BhodUtting 591
(2) Ifauheim baths 592
(8) Reeietance exercises 592
n. RELATITE AND MUSCULAR MITRAL INSUFFICIENCT
Pathology 595
Etiology 596
Symptoms • • • • 597
Physical signs 597
Diagnosis 597
Prognosis 598
Treatment 698
xiv DISEASES OF THE HEART
CHAPTEE XXIII
FATTT HEART— <;AU>IAG INADEQUACY OF THE COKPULEMT ^^^^
Morbid anatomy 599
Pathology 599
Etiology 600
Symptoms . 602
Physical signs. Inspection 604
Palpation 604
Ptreus9ion 604
Auscultation 606
Diagnosis 605
Prognosis 606
Treatment 606
CHAPTER XXIV
CARDIAC ASTHMA — CHETNE-STOKES RESPIRATION — ^BRADYCARDIA — 8T0KB8-ADAM8
STKDROm
I. Cardiac asthma 618
II. Cheyne-Stokes respiration 615
Disccuch in which Chcyne-Stokea breathing is ohaerved • • • . 617
Theories to explain Cheyne-Stokes respiration 617
Prognosis 622
Treatment 628
III. Bradycardia 624
IV. Stokes- Adams syndrome 627
Etiology and pathology 627
Symptoms .....•••...•. 629
Prognosis * • . . . 635
Treatment 635
CHAPTER XXV
ANGINA PECTORIS
Definition 637
History 637
Pathology and etiology 640
Clinical history and features of an attack 649
Diagnosis 654
Prognosis 657
Treatment 658
CHAPTER XXVI
SYPHILIS OP THE MYOCARDIUM — ^NEW GROWTHS IN THE MYOCARDIUM— ATROPHY OF THE HEART — SEGMENTATION AND FRAGMENTATION OF THE MYOCARDIUM
I. Syphilis of the myocardium 663
Morbid anatomy •••••. 663
Etiology 663
Symptoms 664
Diagnosis . . • • 664
CONTENTS XV
PAGK
PrognoeiB 665
Treatment 665
II. New growths in the myocardium 666
III. Atrophy of the heart 667
Morbid anatomy 667
Etiology 667
Symptoms 666
Diagnosis 668
Prognosis 668
Treatment 668
IV. Segmentation and fragmentation of the myocardium . . . • 668
CHAPTER XXVII
PEDUNCULATED AND BALL TH&OMBI OF THE HEABT
Pathogenesis and etiology : . . • . 674
Symptoms 675
Diagnosis 677
Prognosis 678
Treatment 678
Bibliography of cases of ball thrombi 680
CHAPTER XXVIII
DEXTBOCARDLA
Congenital dextrocardia 681
Symptoms 681
Diagnosis 682
Acquired dextrocardia 682
Morbid anatomy 682
Etiology 688
Symptoms 684
Diagnosis 684
Inspection and palpation 684
Psreusaion 684
Atucultation 684
Prognosis 685
Treatment 685
CHAPTER XXIX
CONGENITAL DISEASES OF THE HEART
Morbid anatomy 686
Etiology 689
Symptoms 690
Physical signs. Inspection 695
Palpation 696
Percussion 697
Diagnosis 701
Prognosis 701
Treatment 702
B
xvi DISEASES OF THE HEART
SECTION IV
CARDIAC NEUROSES Syn. : Functional Didordera of the Heart
CHAPTER XXX
PALPITATION, TACHYCARDIA, CARDIAC PAIN, PSEUDO-ANOINA PKCTORIS
PAOB
Pathology 703
Symptoms 704
Palpitation 704
Tachycardia 715
Cardiac pain 718
Pseudo-angina pectoris 719
Etiology 722
Diagnosis 724
Prognosis 726
Treatment 727
Treatment of the attack 727
Palpitation 727
The attack of pain 728
CHAPTER XXXI
ESSENTIAL PAROXYSMAL TACHYCARDIA
Pathology 781
Etiology 782
Features of the paroxysm 782
Diagnosis 784
Prognosis 785
Treatment 785
SECTION V DISEASES OF THE ARTERIAL SYSTEM
CHAPTER XXXII
Arteriosclerosis 788
Morbid anatomy 780
Etiology 741
Symptoms 745
Physical signs 750
Diagnosis 751
Prognosis 754
Treatment 754
CONTENTS xvii
CHAPTER XXXIII
ACUTE AORTITIS — ACUTE ARTERITIS — SYPHILITIC ARTERITIS — Ein>ARTERITIS OBLITERANS — PERIARTERITIS NODOSA— STENOSIS OF THE AORTA AND PULMONARY ARTERY — CONGENITAL SMALLNESS OF THE ARTERIES
I. ACUTE AORTITIS ^^^^
Morbid anatomy 759
Etiology 760
Symptoms 760
Physical signs 761
Inspection 761
Palpation 76i
Ptrcussion 761
Auscultation 762
Diagnosis 762
Prognosis , 762
Treatment 762
n. ACUTE ARTERITIS
Morbid anatomy 762
Symptoms 763
Physical signs. Inspection— PialpcU ion 763
Diagnosis 763
Prognosis 763
Treatment 764
III. SYPHILITIC ARTERITIS
Morbid anatomy 764
Etiology 765
Symptoms . . , , , 765
Diagnosis 766
Prognosis . . . 766
Treatment 766
lY. ENDARTERITIS OBLITERANS
Morbid anatomy 766
Etiology 767
Symptoms 767
Diagnosis 768
Prognosis and treatment 769
Y. PERIARTERITIS NODOSA
Syn. : Congenital Aneurysm
Morbid anatomy 769
Etiology 769
Symptoms 769
Diagnosis 77O
Prognosis and treatment 77O
XVIU DISEASES OF THE HEART
Yl. STENOSIS OF THE AORTA AND PULMONAKT AKTBET ^^^^
Stenosis of the aorta, congeiiital and acquired 770
Symptoms 771
Diagnosis • . 771
Prognosis and treatment 772
Stenosis of the pulmonary artery 772
Symptoms 772
Diagnosis 772
Prognosis and treatment 773
TIL CONOENFTAL SMALLXESS OF THE ARTERIES
Symptoms 778
Diagnosis 774
Prognosis and treatment 774
CHAPTER XXXIV
ANEURYSM OF THE THORACIC AORTA
Morbid anatomy 775
Etiology 777
Symptoms 781
Plain 782
DyapncM 783
Cough 784
ExpectorcUion 784
Physical signs. Jt^speeiion 800
Palpation 801
Percussion 802
Auscultation 802
Diagnosis 804
Prognosis 808
Modes and causes of death 808
Treatment 809
APPENDIX
Mechanical devices as aids to determining cardiac disease . • . 815
The X-ray 815
The sphygmograph 818
Gaertner's tonometer 826
LIST OF PLATES AND ILLUSTRATIONS
^
rACIKG PIATS HAOB
I, A natonncal relations of thoracic' and abdominal vb<3«r^, , . . 1 II. Anrtif rt-gurgi tat loll with, ertlcified vug-etation that swung In Wood cur- rent, causing atheron.a of endocardium and of intinm of aorta , , 278 III. Exterior of heart of Fig, 42» showing JijiHjrtrophy and diktation of
both ventricles , . . 576
PAa« Cardiac valve areas, skomng where gaunde are moat diet met 1 1/ heard , 4
Normal deep-seated cardiac dulness .6
Auscultatory percussion 8, ft
Hein*» palpatory percusaiou . , 10,11
Ebstein*s palpatory percussion , .11
M^uirc^s pal^iatory percussion , . , . . , . . , .12
Normal cardiac- cycle 14
Cardiac valve areas, indicating munds produced at varioue vaivee ... 25 Interior of left ventricle, showing fibrous bmid connecting aortic cuepe and
reaponeible for mueicul murntur , .31
Ueart of a buffalo calf, showing abtrrant ehordee tendinm in left ventricle , 33
Cor viJlfisum of acute pla^ittc |*ericarditis . , 30
Usual location of iiericardial friction sound and fremitus .... 58
Absolute diilness in case of acutf pericarditis ...... ^ 63
Case of pericarditis in whicb the sac contained 3^ pounds of fluid (B ram well) 65 Absolute dulness in case of pericardii^ with effusion ..... 71
Rotch'fl sign of l>eginning effusion 78
|fins and E wart's signs of pericardial effusion . 80
Apex-beAt and area of cardiac dulness in case of pericarditis with effusion . 93 The various sites for puncture in paracentesis pericardii , . . , , 04 Cardiac dulness and location of border of liver in special cases . . 108, 115
Vemicose endocarditis of aortic and mitral valves 145
Verruco»e endocarditis . , , 146
Malignant verrucose endocarditis of mitral valve , . » . . .147 Kalignant verrucose endocarditis of aortic valve, with perforation of a ensp . 149 Apex-beat and relative dulness in ease of acute endoi-arditis , , , . 159
A p#?x-beat and absolute dulness later in same case 161
A pex*b<^at and relative cardiac dulness; i»pfr I a/raae 165
Area of maximum audibility and transmission of murmur; epeeial caee , 165
Chart I. Temperature in cas^e of acute endoc^arditis 167
Chart II. Temperature in case of acut« endocarditis . . - , . 173 Diminution of relative cardiac dulness in one week under treatment . . 186
Bel atire dulness in case of chronic endocarditis 20fl
CooditioD of mitral valve causing regurgitation and obstruction . . .017
ZZ DISEASES OF THE HEART
PAOB
Diagram showing effects of a mitral leak on the circulation .... 220
Relatiye dulneas in case of mitral insufficiencj 227
Apex-beat and relative dulness in mitral regurgitation 230
Sphygtnogram, showing irregular pulse in case of mitral regurgitation . . 240
Relative dulness in a typical case of mitral regurgitation .... 241 Point of maximum audibility and area of transmission of mitral regurgitant
murmur 242
Time of mitral regurgitant murmur 248
Interior of left ventricle, showing buttonhole slit 250
Case of mitral stenosis, showing ascites and clubbing of finger-tips . . 258
Sphygmograra, from case of mitral stenosis 260
Location of apex-beat and area of deep-seated dulness in mitral stenosis . 2G0 Rhythm of characteristic murmur of mitral stenosis, ** auricular systolic " . 261 Area of audibility of the presystolic murmur of mitral stenosis . . . 262 Rhythm of occasional variety of mitral stenotic murmur through entire ven- tricular diastole 264
** Interrupted modified presystolic " murmur of mitral stenosis . . . 265
Location of apex and relative dulness in case of mitral stenosis . . . 271 Ijocation of apex and relative dulness in case of mitral stenosis and regurgi-
Ution 273
Location of apex and relative dulness in case of mitral stenosis . . . 276
Location of apex and relative dulness in case of aortic regurgitation . . 285
Sphygmogram of aortic regurgitation 209
Sphygmogram of pulsus bisferiens 300
Type of relative dulness in well-compensated aortic regurgitation . . . 802
Type of relative dulness in poorly compensated aortic regurgitation . . 302 Spot of maximum intensity and area of transmission of typical aortic
regurgitant murmur 803
Rhythm of aortic regurgitant munnur 303
Relative dulness in case of aortic regurgitation 311
Skiagram of chest in case of aortic regurgitation 312
Relative dulness and lower border of liver shortly before death , , . 816
Heart of aortic stenosis with adherent cusps and also acute endocarditis . 820
Heart of aortic stenosis showing calcified vegetations in sinuses of Valsalva . 821
Sphygmogram from case of aortic stenosis 329
Sphygmogram of uncomplicated aortic stenosis 836
Typical relative dulness in case of well-compensated aortic stenosis . . 836
Rhythm of aortic obstructive murmur 837
Place of maximum intensity and propagation of aortic stenotic murmur . 837
Relative dulness in case of primary tricuspid regurgitation .... 351 Relative dulness in case of tricuspid regurgitation secondary to dilatation of
right ventricle 352
Place of maximum audibility and area of propagation of tricuspid regurgi- tant murmur 352
Location of thrill and murmur in a typical case of tricuspid stenosis . . 361 Relative cardiac dulness in typical case of tricuspid stenosis .... 362 Area of deep-seated cardiac dulness in case of pulmonary regurgitation . . 368 Area of maximum intensity and of propagation of murmur in case of pul- monary regurgitation 369
The rhythm of murmur in typical case of pulmonary regurgitation . . 373
Heart of a boy, showing congenital stenosis of the pulmonary orifice . • 879
LIST OP PLATES AND ILLUSTRATIONS xxi
PAOS
Belatiye cardiac dulness in case of pulmonary stenosis 381
Location of thrill and systolic murmur in case of pulmonary stenosis . . 381
Heart from case of pulmonary stenosis 383
Same hearty left auricle open, showing patent foramen ovale .... 384
Rhythm of typical pulmonary stenotic murmur 387
Resistance exercises 456, 457, 460-463
Shape of relative dulness in hypertrophy 543
Heart showing left ventricular hypertrophy 566
Perforate interventricular saeptum 687
Cut showing cyanosis of congenital heart-disease, drum-stick finger-tips,
bulging prsDcordia, etc 601
Heart showing concentric hypertrophy of left ventricle 609
Sphygmogram case of paroxysmal tachycardia 733
Skiagraph showing aneurysm of the aorta 778
Dilatation of superficial veins secondary to pressure by aneurysm on vense
cavaB 786
Photograph : aortic aneurysm, showing slight bulging of anterior chest-wall . 788
Cut showing dulness and liver outline in case of aneurysm .... 789
Two figures showing external tumour in case of aortic aneurysm . . . ' 790
Post-mortem specimen of heart and aneurysmal sac 791
Trachea, from case of ruptured aneurysm, showing point of rupture . , 797
Opposite side of same specimen, showing interior of sac 798
Skiagraph of chest, showing tuberculosis of right apex and tuberculous peri- carditis with effusion 817
Sphygmogram of h«>althy man 819
Sphygmogram of woman during an attack of paroxysmal tachycardia . . 819
From man with recurrent bradycardia 819
From man with acute general gonorrhceal infection 820
From man with declining typhoid fever 820
Hyperdicrotic pulse from woman after twelve hours recurring hemoptysis . 820
From w(»man with moderate aortic insufiiciency well compensated . . 821
Initial high-tension pulse from man with arteriosclerosis 821
Sustained high-tension pulse from woman with chronic interstitial nephritis . 821
From a man with chronic interstitial nephritis 822
From a woman with mild myxcsdema 822
Prom a man with well-compensated mitral insufficiency .... 822 From a woman with arteriosclerosis and fairly well-compensated mitral
incompetence 823
Prom a woman with arteriosclerosis and mitral insufiiciency fairly compen- sated 823
From a man with arteriosclerosis, chronic interstitial nephritis, and mitral
insufficiency, with failing compensation, Cheyne-Stokes respiration . . 824 From a woman with mitral obstruction and regurgitation with failing com- pensation 824
From a man with mitral regurgitation, lost compensation, relative tricuspid
insufficiency, ascites, etc 824
From a woman with mitral obstruction and insufficiency, lost compensation
and relative incompetence of the tricuspid. Delirium cordis . . . 824
From a boy with acute rheumatism on second day of endocarditis . . 825
From same patient, two years later, with developed aortic stenosis . . 825
Cardiogram from a girl with mitral insufficiency 826
PLATE l
ANATOMICAL RKLATIONS OF THORACIC AND ABDOMINAL ViSCKBA.
DISEASES OF THE HEART
GENERAL CONSIDERATIONS PERTAINING TO
THE ANATOMY, PHYSIOLOGY, AND
EXAMINATION OF THE HEART
INTRODUCTORY
In this chapter are presented certain facts which, because of their bearing on the examination and the diseases of the heart, should be well understood.
Location of the Heart. — This main organ of circulation is situ- ated in the central and lower part of the thoracic cavity, resting upon the upper convex surface of the diaphragm (see frontis- piece) in such a manner that its long axis forms an angle of sixty degrees with that of the body (Rosenstein). The base of the organ is directed upward, backward, and towards the right side, while its apex points downward, forward, and to the left, so as to strike against the chest-wall in the fifth left intercostal space an inch inside the nipple-line. The larger portion of the heart, therefore, lies to the left of the median line. It is attached at its base to the great vessels and is inclosed by the pericardial sac, which invests it loosely Inflow, being bound to the central tendon of the diaphragm beneath, to the sternum in front, to the medi- astinal pleura at each side, and behind to the anterior surface of the oesophagus, trachea, and large bronchi. In consequence of the oblique position of the heart, the pericardial sac forms a loose fold at the lower right-hand corner, so that when it becomes dis- tended by an eflFusion the earliest evidence of the fluid is obtained in the fifth right interspace in what is known as the cardio-hepatic angle. Further details on this matter are contained in the chapter on Acute Pericarditis.
1 1
2 DISEASES OF THE HEART
The Selations of the Heart to the Anterior Thorado Wall are
highly important, and have been the subject of numerous investi- gations. As it is difficult to fix the heart in position for the pur- pose of investigation, attempts have been made to accomplish this either by thrusting long needles through the organ immediately after death or by freezing the cadaver, and subsequently sawing it into sections. Consequently the statements of investigators differ somewhat as to the limits of the heart in health, especially the level of its upper border. I shall state the lower of the two levels usually given, therefore, as it seems to me to correspond with what is most often observed clinically.
The superior boundary of the heart lies on a level with the upper border of the third costal cartilages and extends trans- versely from the third left costo-chondral articulation across the sternum to a point about an inch to the right of the right sternal margin. The right border of the heart, formed by the slightly convex base of the right auricle, extends from the up|>er edge of the third right costal cartilage, at the point where the superior cardiac teundary ceases, downward in a slightly convex direction as far as the middle of the fifth right interspace, about an inch from the breastl)one. Here, curving sharply inward, the inferior border of the organ passes across the base of the xiphoid process on a level with the upper margin of the sixth left costal cartilage at its junction with the sternum and terminates in the fifth left interspace at the site of tlie apex-beat, an inch inside the nipple- line. The left cardiac border corresjxmds to a line drawn from the apex-beat upward and somewhat inward to the junction of the third left rib with its cartilage, about 2 inches from the left sternal margin. A diagonal line extending from the junction of the third costal cartilage with the left edge of the sternum do^\^l- ward to the seventh right chondro-sternal articulation, represents the usual ix)sition of the auriculo-ventricular sa?ptum (Broadbent). A line which passes from the inner side of the apex upward through the fifth and fourth to the third left costo-chondral articu- lation, corresponds as closely as can be with the interventricular sa'ptum. The somewhat triangular area thus inclosed represents the right ventricle Avith its broad base forming the lower boundary of the heart, which rests in the sulcus between the anterior chest- wall and the upper surface of the diajJiragm. The upper extrem-
INTRODUrTORY
3
ity of this triaugiikr area is filled hy the puhiionarj artery and the tip of the left auricular appendix as it curves around the outer border of the left ventricle to appear in front to and terminate near the trunk of the great artery. It is ohviousj therefore, that r»iily the ujijier third of the right auricle lies behind the sternum, while its lower two thirds are to the right of this hone* The left auricle is situated beliind, being completely invested by the left lung and entirely t^bseured frum view from the front. The same 18 the case also with the left ventricle, excepting a narrow strip which forms the left border of the heart and is visible anteriorly. It is the inft^rior extremity of this narrow strip which, propelled against the wall of the thorax, occasions the apex-beat, Conse* quently it is a portion of the right ventricle only which is exposed to view after removal of the breastbone and adjacent costal car- tilages. The remainder of the heart, even that which lies ante- riorly, 18 covered from view by the lungs.
The anterior lung borders are in apposition behind the middle of the sternum from the level of tlie sec^ond to that of the fourth costal cartilages. At this latter situation they diverge, the border of rhe right king passing on downward to the level of the fifth right costal cartilage, where it turns off to the right tn unite with the inferior margin of the same lung. The anterior nuirgin of the left lung diverges abruptly at tlie level of the fourth cartilage, passing outward along the lower edge of this cartilage as far as its tmion with its rib. It then turns downward, and, after curving slightly inward and then outward, unites with the inferior border at the level of the sixth costal cartilage near its point of articu- lation with its rib. In consequence of this peculiar arrangement of the left lung a portion of the anterior surface of the right ven- tricle comes into immediate contact with the chest-wall, and, being uncovered by lung, forms the area of siiper/irud eardim' ilulness. By many this area is considered of great importance in the deter- minatioD of the size of the heart by percussion, as will be shown in dealing with the snbjprt of cardiac percussion.
Position of the Great Vessels aad Valves.^-The pulmonary artery lies a^)out half an inch to the left of the breastbone and extends from the level of the ceiitre of the third left interspace upward to the level of the second costal cartilage, where it divides into its two main branches. The position and course of the as-
DISEASES OF THE HEART
cencling aorta may be represeiitetl by a line drawn from the third left eboijJr«i-.sterniil articulation upward across the breastbone to the junctifin of the riglit edge of that bone with the second right costal cartilage, which, therefore, is sometimes spoken of as the aortic cartilage, because at this point the aortic valve-sounds are most dibtinctly heard. The superior vena cava passes downward along the right cardiac border from the level of the second costal cartUage to a point opixjsite the middle of the third right inter- space.
Tlic four sets of valves are bunched closely together not far from the junction of the tliird left costal cartilage with the border
of the sternum* the pnbnonary \mng most supertieial, the mi- tral most internal, the tricuspid most inferior, and the aortic fhe most central. They cannot, nhei'efore, be auscultated in the ' region of their anatomic seatJ I if one is to differentiate their' individual sounds. For this rt^ason we take advantage of the laws governing the conduc- tion of their sounds and aus- cultate them in certain areas named after the resijective valves.
Tbus the mitral area is Sr>uiid»iprodiiw!nt variou* vftive» ioaiaitod: situated at the apex-beat and
^, PQlmoiiftry : ii,iortfc; C, tricuspid; w, • i j r -^ i i- ^ « .. ■
^ml includes a liimted district im-
mediately roundabout. The tricmpid arm includes the lejwer end of the sternnin and a portion of the surrounding region. The pulmonic area is located in the second left intercostal space close to the edge of the breastbone, while the aortic area lies in the corresponding sitiiaticm on the opposite side. It nmst not be supposed that the valve-sounds and murmurs are heard only in these situations — they are widely propagated and blend with one another, and in particular endo- cardial murmurs are often so widely conducted as to l>e distinctly' audible in other areas than tliose to which they properly belong.
Flu. l.—CAKDiJir Valve Ajieas.
INTRODUCTORY
iring farther consideration of this subject at this time^ we now on to the <Hsciission of the nietho<ls by which the size of the lieftrt is ascertained during life (Fig. 1).
Cardiac Percussion, — In employing this means of examination we aim to dererniine, tin^t, the Ixmndariei? of the area of superficial dutnei«T aJ^d t^econd, ihe limits of deep-seated dulness. To accom- plish the former^ percussion must be made lightly, whereas the liittcr n?4}uire8 a tifni, heavy percussion-stroke.
The area of superficial or absolute cardiac dulness correspond- ing with the p<jrtion of the right ventricle uncovered by lung during inspiration, extends vertically from the upper edge of the fattrth left costal cartilage to the sixth, and transversely from the left bonier of the sternum to a pcdnt mithvay Ijctween the pSTiiEternttl aiul mamillary lines. As its outer or left boundary ii irregiilart and, roughly speaking, passes obliquely downw^ard foWirdst the left, this area is broader at its lower than at it::^ upper margin^ Enlargement of the heart erowds the lun^-borders aside, and hence generally increases the dimensions of superficial dtihieeSy e8j>ecially to the right in cases of hypertrophy and dila- tation of the right ventricle. But a variety of conditions outside of the heart may increase or diminish the extent of suiierficial dnlm^^, and hence render tliis not always a trustworthy indication of the actual size of the heart. Thus the lung-borders may be re- tracted by pleuritic adhesions and exprtse an abnormally large jiortion of the right ventricle, or Iveing distended by pulmonary f!inpbysema« they may diminish or entirely obliterate this area.
<\ins4Hpiently it is preferable to rely upon deep rather than Fjmperficial percussion in endeavouring to ascertain the size of the irt, since when the limits of deei^seated or relative cardiac duljies9 are found increastHl we know it is due to increase in the aiie of the organ itself* Vierordt objects to this latter method beeattfe of its gn»ater ilitficulty and uncertainty, since pulmonary l«0oi|iance shades so gradually into the relative dulness overlying th* heart that two obser\'ers of apparently equal skill may not a^ree in their results. Doubtless iutlividual judgment depends very largely upcm pMctice and delicacy of hearing, and doubtless emphysema f intdj|$tieity of the ribs^ great thickness of the parietes, eie^f often make it im]io!isibIe to accurately determine deep cardiac limiti^ Xe%*erthelesfi the cases in which relative dulness is possi-
e
DISEASES OF THE flKART
ble of defection are so niimeruiii^ that 1 prefer to rely upon it rather than on siiperticiul diilncss, and always urge students to make ii^e of this method*
The Deep Boundaries of the Ueati (Fig. 2). — It is well kiio\^Ti that all hearts are not of the same size even in health, the male heart being larger than tlie female^ and that of a child relatively larger than that of an ailiilt. Moreover, the right auriele lueai^fures more during diastole than dnritig systole. Conaeiqnently measure- ments.cannot he given that are invariahle. Yet tlie following figures taken from Vii-mnlt may lie stated as the average. The
adult heart *" extends from about 8 or l» centimetres to the 1^'ft n{ the median line (apex of '\iv heart) to ahout 4 or 5 een- tiuK/trc's to the right of the same, i, e., altont one and a half tinger-hreadths to the right mC The right border of the ster- num (riglit auricle).'* Busse, wlui employed Ehstein's palpa- tory ]>erenssion, found the left hrirder of the heart in health never passed outside the mam- illary line, while llornkohl (h'tenuined the average in adults to he 7.3 centimetres from the left sternal margin. On the right side the heart ex- tended a variable distanre liovond the sternum, de]K'nding on the stature of the man, lieing 2.0 centimetres for one 130 centi- metres tall, and 3J> centimetres for a male of IW eentimefr€*s in height. In women theso tigures are slightly less, while in children the area of the ht-art measures relatively more than in adults. If the meilian line is taken as the landmark from which to measure, llurnkohrs tigures must be inereaseij by 1 to l..'^ centi- metre, which, aeeording to Ehstein, is half the width of the ster- num. Consequently it is found that Vierordt's and IIornkohFs estinuites are not so much at variance as they at first appear.
Three methods nf pi/rtMission are in use, and mentioned in the
PP. pftfMtttTDAl liDe; MM, inttnUikiT line.
INTRODUCTORY
order of their ix>pularity are: (1) plessimetric, (2) auscultatory, (3) palpatbry pereiissitm. I do not proiK3se to discuss the ad%'^an- tages or (lisadvautagei* of employing a pleximeter and hammer^ hut merely to express my very positive preferejiee for the use of the lingers, for the reason that thereby one is enabled to obtain valuable information from the sense of resistance.
In ascertaining the area of absolute dulness light strokes are eeeential, while the reverse is the case as regards deep-seated dul- ]ies8. Moreover, in outlining the area of rehitive dulness the pleximeter finger should be pressed firmly against the chest-wall, to exclude so far as possible tbe vibrations of the bony structures. This is the ** abgeddmpfte '' p>ereussion of the Germans. The finger is placed firmly at right angle to the ribs at a point well outside the cardiac areu, ami perciissiuti is nMnle with considerable force at ever decreasiug distanced from the sternum until a slight rise in pitch and increase of resistance indicate that the airless organ (the heart) has been reached.
In this manner one is to percuss from above downward along the left parasternal line, t^eginning in the first intercostal space and ceasing when the upper border of tlie liver is reached. At the sides, percussion is U.\ be perfonued first in an oblitpie diree* tion from above downward tnid itiward, and next on a transverse line from without towards the centre. If, wherever comparative dulness is perceived, a mark is made with a dermographic pencil^ these marks can subsequently lie united, and will then represent the firohnble limits and shape of deep-seated cardiac duiness. \i one prefers he can, instead of placing his finger across the ribs, press it strongly into the intercostal space parallel with the ribs, mnA if his finger is slender can thus conv€*y his percussion-strokes more direi'tly to the heart without eliciting so much vibration from the elastic structures intervening,
San»om makes usp of a narrow pleximeter, wliich is of such small size as to fit well «hjwn into the intercostal space, and claims remarkably accurate results, more precise indeed than in any other way.
It may l>e well to liere remark that, when in women accurate percitssi«m of the heart is impossilile on account of the large size of the mammas fairly trustworthy infnnuation concerning the fiize of the heart may be gained by carefttl palpation of the apex-
8
DISEASES OF THE HEART
beat Since tlif mamillary line is not a trustworthy guide in femalesi, it is better to measure the site of the apex impuW from the mid-srenial line or from the mid-clavicular line^ it being in the fifth interspace, an inch within the latter.
Two statements shouhl also be made regarding percussion of the heart in chiMren. In the tirst place, the area of su|x*rficial dulness is said by Ilornkohl to be somewhat more extensive than in adults, particularly above, where it is asserted to reach up into the third intercostal space, while its outer margin passes some- what further beyoml the left i>arasternal line, i* e,, to a point a lit- tle nearer the mamillary than the parasternal line. In the sec- ouil place, it is important to bear in mind tlie great elasticity of the chiUrs chest, and hence to |K*rcuss with far more delicacy than IS advisable in g^o^^^^ pcnnple* Otherwise the note of pulmonary resonance and the vibrations of underlying structures will assur- edly prevent acctirate and trustworthy rcsidts. For these rensons it is far preferable to rely on the other modes of percussion now to be described.
FlO. 3, — AutCITLTATOllT PBUCrWUnjf,
Auscultatory or $Steihoscopic Percussion. — Tliis is a combina- tion of auscultatifm and percussion^ and is based on the principle that %vhen the stroke is made over a solid organ its note is higher,
INTRODUCTORY
9
Flo. 4, — AcaCULTATOlKT PEBOVBBtOy.
sharper, and more clearly defined than when over an air-contain- ing organ. It is found, moreover, that there is a distinct differ- ence in the character of the note of two viscera of similar strne- ture. This is, of course, tlie same principle that underlies plessimetric percussion, but tlie auscultatory method enables one to appreciate more delicate shadings of tone and to define more precisely the deeply situ- ated bonlers of an organ or solid thoracic tumour. It even enables one to distinguish l>e' tween the duhiess of pleuritic or pericardial effusion ami I hut of a contiguous pulmonary con- solidation.
It is practised in either of two ways: The examiner nuiv with one hand hol<l the bell of his binaural stethoscope against the centre of the cardiac area, while with the tip of a finger of the disengaged hand he laps the chest-wall lightly from without inward and on a line with his stethoscope (Fig. 3), or he may have his instrument held by an assistant while he performs percussion in the ordi- nary manner (Fig, 4). The former mode is preferable, because more delicate. Such astonishing and incredil>le accuracy is clfliraed for atiscultatory percussion^ notably by Bezly Thorne, that Broadbent and others have lieen led to test it, and have come to the conclusion that it possesses no advantaires over plessinietric (>ercus8ion. I have employed it a great deal, and, although recog- nising its liability to error and its limitations, still I believe it is in certain cases with thin-wallcd elastic chests and when practised carefully a very accurate means of outlining the heart, I have repeatedly compared its findings with those of the two other meth- odii, especially plessimetric, and find it satisfactory and trust- worthy. One occasionally enconnters chests in which for one rea- iOn or another it is next to impossible to determine the deep limits of the heart in the ordinary fashion. It is well in such cases to
10
DISEASES OF THE HEART
try the uietlicwl undor distntssicm, siiieo it will often lif*lp one out
jf liis dik
1 should
uend
rt-*cuiiimena its einplovment to the exclusion of the plessiuietric niethcKl, but merely m an adjunct thereto.
Pafptttortf Ptrcuasiou. — By this term is meant a method of ue^ing Ijoth imlpation and i>en*ut^sioii at the same time. In other words, it is a method of ascertaining the heart's resistance, and therehy of ascertaining it& outline and dimensions. It makes use of tlie feeling of resistauee rather than of the auditory jH'reeption of ditTerent-€^s in sound. Aueidjrugger and Laennec [x^rcussed the chest'Widl immediately — that is, without the intervention of a pies- simeter ; tlie former, by striking with the tip of his finger, and the latter wifh the end of his Sitethoseujve, It is needless to say this mode of }ierforming percussion is mure or less painful to the pa- tient. In 1877 Ebstein [»ro|n>sed palpation of the heart and other solid viscera, as the liver, as a means of appreeinting their size by their resistance, and at the International iledical Congress at Kome in 181)4 he reatl an elaliorate pajM?r in which he discussed
and explained his method at considfn'ahle length. In this Jul per he called attention to a J net Ik h1 employed hy J, Ilein, which consists in ) ml pa ting the hrart with one finger while [ler- cussing with the other in the following manner: The palmar surfiiee of the terminal pluilanx of the outstretched middle fin- ger is placetl uj)on the chest, while a light tap is mad<' nu the chest with the tip of the bent f<>refinger (Figs. 5 and 0). Then while the extremity of the first finger rests against the wall of the thorax he gives a light blow to the chest with the jiad of the middle finger. In each instance the fingers are allowed to remain for an instant in contact wirli the part jiercussed, so as the better to perceive the sensation of resistance imparted. In this way, by alternately tapping with the
I
INTRODUCTORY
U
two fingers, the entire area is traversed. This is said to yield very
accurate resiiltSj hut is hy Ehstein considered inferior to his
method, because not altogether devoid of pain to tlie patient.
Ebslein, therefore, makes use of a small glass plexinieter, upon
which he givt^s a gentle pressing
stroke with the tip of one fin- ger^ which, flexed at its mefa-
carpal articnhitiun, is held
slightly and rigidly curved as
the stroke is given (Fig. 7).
The blow is not made with a
quick relwmnd (staccato)^ Imt
with a firm [jushing movement
(legato). The stroke is L^ivt ri
in a line perpendicular to the
surface thus percussed and tlie
plexinieter is held firmly in
position. Ebsteiu's pleximeter
of glass is i an inch ( 1.3 eenti-
melre) in width, If inch (4.0
centimetres) in length* and sur- mounted by a small handle i of an inch (1.5 centimetre) in height.
With such a pleximeter El>stein asserts the meth^id is not only
gi'atifyinglT precise, as lie has repeatedly lU'oveJ on the radaver
by means of needles, but is easily aetpiirefl, which is an opin- ion contrary to tliatexpressi^tlby Vierordt. ilore- ovi4\ it possesses the arid it ion al advantage of en- abling the ex- aminer to avail himself of his percept ion of the sound and pitch
Fio. 7.— t8»<TEiN'i» Palpatorv PisRcus»joif. ^f fj^^ Hotc UrO*
diiee<b HS wtdl as of the sense of resistance. In this way two unpre^fiiions are received simultaneously which serve to control
<j. — UErN''» PALJ'AtnjlV CeIU i;ft**|OK.
12
DISEASES OF THE HEART
Fia. 8.-
-MAaniRE'ti Methuu of Paljpxtubt
each other* Ebsteiii ikx*hires aho that hy his method one cm obtain satisfactory reJ^iiUs in eases of emphy5?emn and in iK^rsons witli a thick paiiniciilns of fat or large mammary ghmds, all of
which usually preehide accu- rate fvercussion after the ordi- nary method.
Robert Maguire, of Eng- land, advocates ]ialpatory j^er- eussiou by tapping lightly with the siift palmar cushion of the tenuinal phalanx of one iiiiger, and claims equally accurate re- sults (Fig. S). He expressly states that the stroke must be not short and quick, hut long and pressing, as if one were feeliug or palpating with the tinger. It is applicable, he says, not only to all soli<l or- gans, spleen and kidneys, as well as heart and liver, but also to collections of fluid in thoracic and }>eritoneal cavities.
In cases which are at all obscure it is well to verify the con- clusions derived by any one metliod — plessimetric, auscultat<»ry, or palpatory — by each of the others. For my }iart I value the aus- cultatory method the least highly, because so liable to error in exactly those castas which offer the greatest ditfieidty to ordinary percussion' — that is, emphysenmtous, fat, and rigid chests.
Aiiactiltation of the Heart is another and indis|>ensable means of Hjakiug eariliac examinations, and by the inexjK^rienced is apt to Ix^ relied upon, if not exclusively, at least to a degree out of pro- portion to its imiKirtance as compared with percussion. Xeither can be complete without the other. I desire also to emphasize the folly of atteinptiug to do accurate work without the use of a stethosc(»|>e. Whatever form or kind of instrument enables one to hear the most distinctly is, in my opinion, tlie best for him, re- gardless of the arguments advanced in favour of certain sorts, I make use of a simple binaxrral and of a monaural stethoscope, era- ploying the latter %vhen desiring such information as is sometimes
IiNTRODUCTORY
13
obtained from tbe impulse of the hypertroplueJ or dilated heart against the chest-wall* A stethoscope with a small eud-piece en- ables one to differentiate sounds and murmurs and to trace them to their source in a way that cannot be done by the ear placed against the ]invM:ordia.
Normal Heart-sounds. — The detection of luunnurs is not the only object of auscidtation. The heart-sounds themselves often affnrd as much, if indeed not more information than do bruits. TheretV»re, if one is to correctly interpret what he hears come from the heart, he must be familiar with the characters of the nor- mal sounds of this organ. To this end he must know how they are produced,* and keep in mind wliat is going on within^ during the portions of the cardiac cycle, at the time of the sounds and during the intervals of silence.
If one listens at any point upon the cardiac area he hears two distinct sounds, kuo\\'n as the first and second soimd resj>ectively. Over either of the ventricles, in the neighbourhood of the apex, the accent falls on the first, w^hich is longer, of a lower pitch, and more intense — that is, more booniiug thyn the yecond, which is, eonvTrsely, short, shar|*» antl eliekiug^ having a valvular quality we say. Moreover, the ear detects two intervals or periods of silence, of which the shorter occiirs during systole between the first and succeeding second sound. The longer, known as the pause, falls between the second and next ensuing first sound^ dur- ing diastole. This succession of sounds and silences gives to the heart-sounds their j>eculiar rhythm, likened to the ticking of a ehx^k. If now auscultation be made at the base of the organ, in the second interspace at eitlier side of the sternum, it is perceived that the accent falls on the second sound, since this is the louder and clearer and higher pitched of the two. Their rhythm is, how- ever^ the same as at the a|iex, Furthermore, it is generally per- ceived that the second sound is louder on one side of the sternum
• It i* common to speak of rounds, whether normal or abnormal as produced Within the heart or chest. Of course such phraseology is loose and not in accord- ance with the kpown laws of acousitics. Sounds are the auditorj perception of ^aves imparted to the air by the vibration of structures within the thorax, the tia*iie9 serving &» i?ood conduetors of these vibrations^. With this understanding of the mrH]e of production of Ihese acotiiitic phenomena, I shalt, for the sake of convfmicnce and the avoidance of circun[ilocution, 5pcak of sounds as generated in lUe heart or chest.
14
DISEASES OP THE HEART
than on the other, the position of greater intensity not always being uniform in different individuals, depending on various con- ditions, as age, etc.
What occasions this slight diversity between the sounds at the apex and base? Why do not the two sounds in all situa- tions have the same character? I will answer the latter query first. The first sound is synchronous with the apex-beat, and is therefore produced during ventricular systole. Physiology teaches us that the duration of this phase of the cardiac cycle is y^ of a second, subdivided as follows (Fig. 9): During the
Fio. 9. — Normal Cardiac Cycle. Phases of cycle above line ; sounds below.
first tenth of a second the ventricle is initiating its contraction and is silent ; during the following ^^^ of a second its contrac- tion readies its maximum energy, the auriculo-ventricular valves close, and the first lieart-sound is heard; the final tenth of the second, during which the ventricle still remains contracted, is again a period of silence and terminates the phase of ventricular systole.
During the stage of active contraction blood is being forced from the ventricles into the aorta and pulmonary artery. With the completion of this propulsive stage the ventricles relax; arte- rial walls recoil, forcing the mass of blood against the sigmoid valves, which, thus thrown into tension and closed, give forth a tone, the second sound, which signals the closure of the valve and
INTRODUCTORY
15
the coinmen cement of diastole. TLis ^sonnd is, therefore, diastolic, and, ushering in tlie stage of cardiac repose, is succeeded by the period of silence or long pause*
This brief statement uf what takes place dnring the different phases of tlie cardiac cycle will lieljj lis to nnderstaud the mode of production of the two sounds. During the middle portion of systide, when the first >iound is audible, the ventricle is actively contracting and the auriculo-veutricular valves are closed and hidd closely in contact through the contraction of the papillary muscles. Experiments have shown that if cither participant in this stage can \)e made to act without tlie other a stiund is still andilde, but it has lost its normal character. If in the bl(»odless heart the ven- tricles are made to contract while the aurieulo-ventricular valves are hooked back, the sound is low in pitch, prolonged, and boom- ing, while if the ventricle be opened and the valves closed without contraction of the muscular walls, the sound produced is higher pitched, shorter, and less intense. It is thus apparent that the first cardiac sound is a composite one made up of two elements, a muscular and a valvular.
On the other hand, the second sound is due solely to the vibrations generated in the semilunar valves at the instant of their closure and pi»ssesses no mnsctilar element. It is conse- quently of higher pitch, shorter dnrution, and less intensity than the first sound. Inasmuch as the first is a roiaposite sound, it is obvious that its two elements must synchronize exactly if the sound is to be pure and nurmal. Furthermore, there are two ventricles and two sets of aurieulo-ventricular valves. Consequently each half of the heart is responsible for its own first sound. Ausculta- tion at the apex, however, reveals but one first stmnd, which is the result largely of the blending of the two sounds generated in the two halves of the organ, but conducted to this point. That this is the case is proved by the clinical experience that occasionally over one or the other ventricle the systolic sound is heard to be of altered quality or divided into its two elements, while over the opposite half of the organ it retains its normal characters.
Inasmuch as there are two sets of semilunar valves, there are ^o separately produced yet svnchronmis spcofid sonmh. Of these, the aortic is heard most distinctly »t the right edge of the sternum in the second interspace, while the area of greatest audibility for
16 DISEASES OP THE HEART
the pulmonic is in the corresponding interspace at the left border of the sternum. In the early years of life, by some said to be up to the thirtieth, the pubnonic second sound is the louder of the two, while at and after middle age the reverse obtains.
Conditions which raise blood-pressure in either the lesser or greater system will correspondingly alter the intensity of these soimds. The more feeble first sound heard at the base at either sternal margin is probably transmitted thither from the respective ventricle. Tiegerstedt says it is not impossible that vibrations caused by the opening of the semilunar valves play a certain role in the production of the first heart-sound. If this be the case, then the systolic tone audible at the base of the heart in the aortic and pulmonary areas respectively, is not to be regarded merely as a conducted sound transmitted thither with less intensity than to the apex.
Reduplication of the Heart'Soinids. — Either the first or second sound may under certain conditions be doubled — that is, divided into two parts or split, as is sometimes said. This occurs most fre- quently with the second sound, and is best heard over the base of the heart. It may be perceived if the breath is held at the close of a deep inspiration, and under these circumstances is spoken of as physiological. Pathologically such a reduplication is appar- ent when in consequence of disease there is an alteration of blood- pressure in either the pulmonic or aortic system. It is most fre- quently observed in mitral or jnilmonary diseases which augment blood-pressure in the vessels of the lesser circulation. It has been contended that in such a condition the valves at the pulmonic ori- fice close slightly earlier than do the aortic curtains, and emit their sound an appreciable interval of time in advance. Oppo- nents of this theory admit the lack of synchronism in the closure of the two sets of sigmoid valves, but maintain that the increase in blood-pressure causes a delay, not a premature occurrence of the soimd, since to overcome the unnatural resistance in the pulmonary artery the ventricle is compelled to contract more slowly (Barr). In other words, the ventricle, whether right or left, dejx?nding on the system in which blood-pressure is raised, completes its systole perceptibly later than does its 'fellow. Guttmann's theory of the doubling of the sound being due to asynchronous closure of the
INTRODUCTORY
17
iBflivitlual leaflets of a valve i;^ rcganled as fiiUacioiis. RetJnpHca- tion of tbe seecmd soimd, therefore, is an iiidieation of some alter- ation of blood*pres.s\ire in one or the other system.
There is another form of doubling of the second sound which, among English writers, who appear to have paid particular atten- tion to this anomaly of the heart-sounds, is distinguished from the foregoing as apparent or simulated doublintj. This variety, if I may so term it, is lioard only at or near the ajK^x, and appears to be cuntined to eases of mitral disease with predominating stenosis. The phenomenon is believed to be due to the addition or inter- polation of a fhird sound ehjsely following the physiological seconds The only theory regarding its mode of i>roduetion that appears tenable is, so far as I am able to learn, that advanced by Sansom* He believes it to be a sound of tension in the altered segments of the mitral valve* Upon tlie (rf?eurrence of ventricular diastole the mass of bloud held back during syst<de in the left auricle and pulmonary veins rushes forcibly into the rapidly relaxed ventricle, and, streaming in the direction of least resistance, fills the space behind the thickened and disjdaced mitral cusps, '* bellying them out/* after the manner of sails tilled In- the wind. This sudden bulging of the diseased curtains produces a soimd of tension which is audible in the fore part of diastole soon after the normal second sound, which in mitral stenosis, in Sansoni's opinion, is the pul- monic second, transmitted to the apex. The aortic second is, he thinks, too feeble to be heard at the apex. That this third ele- nient of sound is produced at the mitral orifice seems sujiported by the oliservation that it occasionally beconjcs transformed into a diastolic murmur occupying the same pf)sition in diastole — i. e., following the normal second sound. The diagnostic value of this seeming doubling of the second sound at the apex will be discussed in the chapter on ilitral Stenosis.
Bewail likewise attributes this reduplication of the second flound to the tone of valve-tension, but explains it on the hypothesis that the irritable papillary ninscles, stinudated by the inrush of blood from the overdistendcd auricle, contract too soon — i, e., in the fore jmrt of diastole. Thi^ explanation may hold for those eases in which doubling of the sixxjnd sotind is a transient phe- nomenon, as heard sometimes during states of great cardiac ex- citement, but not for cases of mitral stenosis.
18 DISEASES OP THE HEART
Reduplication of the First Sound. — Under certain conditions, as that of abnormal blood-pressure within one or the other ventricle, there is heard not a single first sound, but a reduplication or split- ting of this sound. This abnormality is less frequently j)erceived than is doubling of the second sound, and is equally difficult of satisfactory explanation. Two main theories are advanced to ac- count for it. One of these finds its causation in a hemisystole, by which is meant the separate and indej>endent contraction of the two ventricles. Although there have been recorded a few cases in which highly comi)etent and careful observers believed they de- tected such hemisystole, still it is so at variance with the physiol- ogy' of the cardiac action to suppose the ventricles can fail to snti- chronize in their systoles that many authors are not willing to accept this explanation. The other theory assumes that the two components of the first sound in one or the other side of the heart do not fall together, but are sei)arated by a brief yet distinct in- terval of time, so that to the ear the first sound over that ventricle gives the imj)ression of splitting or reduplication. One or the other constituent of the so\md is generated either too soon or too late to synchronize with the other. As the j)henomenon occurs when blood-pressure in one of the ventricles is too high, and as under these conditions the cardiac wall has lost its normal tonicity, it seems reasonable that the tension into which the valves are thrown and the contraction of the heart-wall should not be per- fectly simultaneous. Sewall argues that the cause of the redupli- cation lies in the failure of the papillary muscles to contract at their proper time, their contraction, and hence the note of valve- tension, occurring either before or after that of the ventricular wall. Whatever be the true ex])lanation of this phenomenon, its occurrence betokens excessive, and it may be dangerous, increase of pressure in that ventricle, to which the reduplication can be traced. It may be audible over either half, and I recall a case of mitral regurgitation in which this doubling appeared in the right ventricle only when the patient assume<l the recumbent j)osture. It is not seldom present over the left ventricle in cases of chronic nephritis, and then betokens dangerous excess of blood-i)ressure in the arterial system, and, secondarily, within the left ventricle.
Gallop or Canter Rhythm, — A phenomenon, sometimes ob- served and due to the interpolation of a third sound (which, ac-
INTRODUCTORY
19
cording to its position in the diastole, produces an apparent redu- plication of either the first or second sound), resembles so closely the hoof-beats of a galloping horse that it has been termed the canter-rbvthiM or bruit de (jnlop. The merit of having first de- scribed it is accorded by the French to rjoiiillaud; yet to Potain, but to Barie in particularj belongs the credit of having first brought it to the notice of the profcssiMU. Fracntzcl Itas also given a most clear and discerning descriptirm of the phenomenon based on accu- rate scientific observation. When the peenliarity nnder considera- tion is present J the auscultator bears nut merely two sounds of normal relati^^e strength and rhythm, but three, of which the last IS an accidental or inter])olated sound occurring in the long pause. Fran^ois*Franck, according to Sewall, is authority for the state- ment that this third sound may occur in any one of three posi- tions: Immediately after the normal second, in the middle of the diastolic interval, or at the end of the long silence shortly before the first sound. When it falls directly after the normal second sound, it must not be confounded with the apparent doubling of the sei*onJ sound already described. It is distingiiishalde from this latter by its peculiar tempo. Its canter rhythm is imparted to it by the shortening up of the long interval and by the accent fall- ing on the middle one of the three sounds — i, e., the normal second (Fraentzel), If one will imitate the sound of a slow canter by striking his hands on his knees, he will at once appreciate the cor- rectne^ of Fraentzel's statement.
Any one, however, who has studied tliis rliythm of the hoart- donnds in a large numlK'r of cases will have appreciated the fact tliat it not infrequently possesses the characters of a rapid gallop rather than a slow canter. When such is the case, Fraentzel's description does not flpply. Ttie tempo and accent are now clianged, as may be proved by again imitating the sound by the hftods. It will now be observed that the interval separating the from the second sound is shorter than that separating the ond from the third or interpolated sound, while the accent falls }n\*^i sharply sometimes on the first, sometimes on the third, but in every case least strongly on the middle one of the three sounds. In still other instances the rhythm described by Fraentzel is main- tainedf but the accent is on the first sound, thus prodncing a not quite t>T)ical can ter-rhyt lira. It ia this lack of uniformity in
20 DISEASES OF THE HEART
rhythm and accent, which, as it seems to me, explains the diversity of opinion expressed by diiferent writers.
Potain's explanation of the phenomenon is that it is due to an increase in the elastic resistance of the ventricular wall over its muscular tonicity, in consequence of which the inrush of blood from the auricle causes it to generate a sound of tension. Sewall, on the other hand, attributes it to the contraction of the papillary muscles taking place prematurely — i. e., during diastole. What- ever be its mode of production, this rhythm is an evidence of abnormal blood-pressure within the ventricle, and hence of dan- gerous tension of its wall. Its occurrence is most commonly ob- served over the left ventricle in cases of chronic nephritis, par- ticularlv the interstitial varietv, and w^hen thus observed it is to be regarded as an evil prognostic omen. It indicates a giving way of the ventricle, which is no longer able to cope successfully with the resistance in the arterial system.
I agree fully with those who look upon it as a sign of the end being not far distant in cases of chronic nephritis, since I have never known an individual to recover in whom this rhythm was detected. In the spring of 1900 I had under treatment a com- paratively young man, with stiffened arteries and interstitial nephritis, who presented this phenomenon at different times in its most tyi)ical form. Several times, under the influence of nitro- glycerin and cathartics, his gallop-rhythm disappeared entirely, becoming replaced by two heart-sounds of normal rhythm. Yet so soon as pulse-tension was increased, either through lessened vigour of this medication or the administration of digitalis, the ominous disturbance of rhythm reappeared. This patient suc- cumbed after about two months.
This interesting canter-rhythm is never heard at the base of the heart, but always over one or the other ventricle, and conse- quently in either the mitral or tricuspid area. It may be of tran- sient duration, yet is often persistent. It may be heard in hyper- trophy alone or combined with dilatation, it may occur in dilata- tion alone, in acute infectious diseases, such as typhoid fever and diphtheria, croupous pneumonia, scarlatina, acute articular rheu- matism, and acute miliary tuberculosis (Fraentzel), all of which lead to myocarditis or to simple weakness of the heart-walls. And lastly, it may be heard in pernicious anaemia, leneoemia, and grave
INTRODUCTORY
SI
eacfaexife, which induce profound cardiac asthenia and ccmseqiient want af tonicity.
According to French authors, it sometimes occurs over the right ventricle in cases of gastric disease, and Johnson savs it may he produced hy jndnionary emphysema, Fraentzcl mentions it as occurring in other lung affections, leading to dihitation and hyper- trophy of this right cliamher, with marked cachexia. I once ob- served a true galloivrliythm in the fourth and fifth right inter- ppaces close to the sternnni, for a hrief time, during which there was very obvious overdistention of the right cavities secondary to a rhenmatic mitral regurgitatioiK The very mnisua! situation of the rhythm in this instance is only explicable hy the sujiposi- tion that in consequence of the enormous distention of the right ventricle the anricukwentricnlar sa^ptum had become pushed so far towards the right that the wall of the ventricle extended to the fourth and fifth right interspaees. It disappeared so soon as treatment had unloaded the cardiac chambers.
Murmurs. — This is a conjprehensi%'e term, which includes all those adventitious acoustic phenomena connc*ctcd in some w*ay with the hearths acth>u and not resembling in tone the nonnal car- diac Bounds. They may be primarily divided into endocardial and exocardktL The endocnrdui} are svdidivide*! into organic or struc- tural and inorganic or accidental, callecj also functional, amemic, hipmic, and dynamic. Exocardial are divisible into i>ericanliah pleuropericardial, and cardio-pulmonary»
By organic murmurs are meant such as owe their origin for the mo8t part to stnu'tural defect or alteration of the cardiac ori- fices or valves — in other w(ir*ls, tit detinite patliological changers of the stnicturea recognisable after death, Accidenfa} iruirmurs can- not, on the other haml, be ascril»ed to detinite patholngieal lesions, and therefore have received a variety of a|jpellations in accord- ance with the various theories offered in explanation of the phe- nomena.
Endocardial Murmurs of Onjanic Orifjitu — These were once thought to be caused by friction of the blood in its passage over the roughened inner surface of the heart. This theory was shown to \)C untenable as long ago as l?*i4T, when it was replaced by the one now generally ftccei»tcd — namolyj that currents or edilies are produced in the stream of blood, the same as in any other flnid.
22 DISEASES OF THE HEART
whenever it passes a point of constriction in its channel or flows suddenly into a portion of the containing-tiibe, which is wider than that directly above. These eddies and currents in their turn generate vibrations which are audible. These secondary currents are the fluid veins first demonstrated by Savart, but applied by Chauveau to the explanation of vascular and cardiac murmurs.
Some of the conditions governing their production in the vas- cular system are the following : Constriction of the coats of a ves- sel by external pressure; projection into its lumen of calcareous plates or masses capable of turning the blood-stream from its direct course ; aneurysmal sacs or vascular dilatations into which the blood-stream may swirl ; and in the heart itself, all pathological changes by which orifices are narrowed and valves rendered in- competent. In addition, murmurs can be produced by vibration of thin membranes and bands as the blood-current sweeps over them.
In Virehow's Archives, Band cxl, is one of a series of sug- gestive papers, by Richard Geigel, wherein he takes exception to the prevailing notion concerning the causation of endocardial and vascular bruits. Bv a series of mathematical formula^ Geiffel en- deavours to prove that if murmurs of the pitch of those usually heard were produced by vibrations in the blood-stream these would have to be of a length that would be physically impossible within the cardiac cavities. lie therefore states that the origin of bruits in eddies and currents is utterly im|X)ssible, and declares them due to transverse vibrations of the walls of the structures inclosing the blood-stream. Ilis line of reasoning is ingenious, and to my mind has much to commend it, since the generally accepted theory is not altogether satisfactory.
It is this consideration which makes me venture to dwell for a few moments on the explanation of murmurs offered by David- son, of Edinburgh. According to his theory, murmurs are due to vibrations set up in the valves by the impact of the blood-stream at an oblique angle. By numerous experiments he claims to have demonstrated that when a stream of fluid was injected into a rubber balloon or a portion of the small intestine, one end of which was tied securely about the nozzle of the syringe while the other was tightly ligatured, the fluid veins and eddies thus generated at the end of the nozzle within the elastic receptacle did not pro-
INTRODUCTORY
98
duce more than a very faint miirinur, audible by means of a binau- ral sterhoscope. When, however, the lluid was made to strike the inner s^urface obliquely a distinct olear sound was generated^ the intensity of which depended u|H>n the force of impact. By re- ducing the rapidity and force of the stream Davidson was able to produce murmurs of varying loudness aud roughness. By another set of exi>erinient9 he was able in the same manner to generate an aortic systolic bruit.
The conditions which favour the generation of organic vas- cular aud cardiac murmurs are multiform, and hence such adven* titious sounds vary in respect to intensity, pitch, quality, and duration. They also oliey the laws of conduction and are propa- gated in different directions, according to the seat and time of their production. Moreover, twij murmurs of indeiieudent rhythm may be generated at the same orifice, or two or more may be pro- duced simultaneously at different locations. So that if one is to differentiate endocardial murmurs, and correctly interpret their signilicance, he must be familiar with these various character- bties.
The inienmly of a murmur l>ears a direct ratio to the ampli- tude of vibrations in the blood-stream, and therefore to the force of cardiac contractions, and 'is not at all a critenon of the gravity of a lesion. The forcible escape of blood through a small fenes- tration in a valve-segment, in itself a comparatively trifling regur- gitatiou, may be declared by a very loud murmur that is audible to the pat lent J or even to a bystander a number of feet distant. Thus Miller and Gibbs narrate the instance of a girl w4io pre- sented a murmur of such intensity that it could be plainly heard li feet away when tlie listener was in the same room and patient fully dressed, and 3 f«*et distant when separated from the patient bjr a dosed door. On tlie other hand, a very grave vah'ular affection may, if cardiac power is feeble, occasion a scarcely audi* ble murmur or even none at all It is well known, for example, that a presystolic murmur of mitral stenosis, intense while the heart is strong, may fade away to complete inaudibility wlien the heart becomes feelde.
Conversely, a murmur scarcely audible during a period of car- diac asthenia may grow in intensity as heart-power is regained. This is the case particularly in aortic regurgitation. Tn the ex-
24 DISEASES OP THE HEART
amination of a patient we therefore avail ourselves of the knowl- edge that forcible cardiac action intensifies a murmur by having him jump about or otherwise excite his heart to bring out an otherwise faint or inaudible murmur.
Posture also influences the loudness of these sounds, some being more plainly, others less distinctly, heard in the recumbent position. Those of stenosis are more intense in the erect posture, while those of regurgitation are so in the recumbent. The reasons for such variations in intensity are based on the influence of the force of gravity, which is greater in some than in other positions (Gibson). Mitral systolic murmurs are nevertheless often louder in the upright than the supine posture, an effect to be attributed to the greater vigour of ventricular contraction when the patient stands. There are so many exceptions to the effect ordinarily exerted by position that a patient should always be examined sitting, standing, and reclining.
The pitch depends upon the rapidity of the vibrations pro- ducing the munnur. Therefore, some murmurs are low-pitched, while others are high. The imion of overtones with the funda- mental tone determines qualityy and as pitch and quality go hand in hand, low-pitched murmurs are a|)t to be rumbling, growling, rasping, etc., while shrill ones are often musical, whistling, filing, sawing, twanging, and the like.
Finally, the duration of murnnirs is variable, depending on the length of time the vibrations endure. Other things being equal, it requireii* more time for the blood-stream to pass through a nar- rowed orifice than it docs for it to regurgitate through wider os- tium whose valve is defective, and therefore direct murmurs, as those of stenosis are called, are generally of greater duration than are the indirect ones of valvular insufliciency. It may be stated as a general proposition, therefore, that the murmurs of ob- struction are less intense, lower in pitch, less musical in quality, and of longer duration than are those of regurgitation, which, for the sake of emphasis, may be conversely stated to be higher, louder, more musical, and shorter. There are, however, excep- tions to this law. Fortimately, murmurs generated s^Tichronously yet at different ostia are never identical in these four character- istics, and hence are usually distinguishable from each other.
It is also of the utmost importance to note the rhythm of mur-
INTKODUCTURY
25
niiirs, since in this way alone oan be detenniiied in what period of the cardiac cycle they are produced. They are either systolic or diastolic. Even the nninmiv of mitral and tricuspid stenosis is diastcflie, sincv it occurs durintr the pause; yet» as it is generated at the time of auricular contract ii>n — that is, immediately prior to ventrienlar systole — it is commonly designated as presystolic, or, as propo.sed by Gairdner, as auricular systolic.
The Iransmiss-ion of a murmur is along the surrounding solid media, and in the general direction iu which the stream ]U'<>ducmg it flows. It is also governed hirgxly hy the intensity of the nuir- mur. Fortunately for diagnosis, it is this law of conduction which aids in the tracing of a murmur to its seat of prodtietion. As already stated, the anatomical locations of the four orifices with their valves are so closely related within a circnniscrihed area that if the sounds, of whatever nature, were not pn*j>agated to certain regions where they can \*e heard with maximnm intensity, tlieir correct interpretation wouhl be vastly more difficult. Every exam- iner of exjierience has realized the truth of this in the not very infre<juent cases in which nuir- murs are widely conducted and yet not most distinct in their own areas.
Cardiac Areas, — These are four in number, correspond iug to the ostia, and are detinitcly located in eireiimscriberl regions on the chest- wall, where the re- spective valve-sounds and mnr- nnirs are lieard most clearly (Fig. 10). Tims the aortic arr is located at the junction of the second right interspace and cor-
Fift. hi — Cardiac Valvk Ajif^i*.
responding costal cartilage with Soundji produced at vnriow^ valve* iiidicAtod: .t • J _t ^t ^ T^i P» p'tlinoniiry: «, aortie; I, tricuspid; m,
the brirder of the Stern unu The ^.j^^^ *->■-«
sounds, whether normal or
adventitious, which are here the loudest, are generated at the flOrtte opening. The pnlmonary area lies in the corresponding situation at the opposite or left edge of the hreasthone. The
26 DISEASES OP THE HEART
pulmonic sounds and murmurs are heard with maximum intensity in this area, although other bruits may be transmitted thither more often i)erhaps than to the aortic. The tricuspid area is located at the lower end of the sternum and corresponds quite accurately to the anatomic seat of the right auriculo-ventricular orifice — i. e., between the fourth left chondro-sternal articulation and the junc- tion of the fifth right costal cartilage with the sternum. Aortic, diastolic, and mitral systolic murmurs are frequently very distinct in this area, while tricuspid bruits may often have their greatest intensity at a short distance therefrom, at either side or below. The mitral area is located at the situation of the apex-beat, but is not confined to this! Aortic regurgitant bruits are often trans- mitted, though feebly, into this region, and mitral systolic mur- murs are sometimes even more audible at some point above and to the inner or outer side of the nipple than directly at the apex. Details regarding the conduction of the various mur- murs may be found in the respective chapters on valvular affec- tions.
Before leaving the subject of organic murmurs, although still more applicable to accidental ones about to be considered, I wish to caution against the error of relying upon these abnormal sounds in the diagnosis of heart-disease to the exclusion or subordination of other physical signs. In a sense, murmurs are only guide- posts which point out the way one is to look. They are highly valuable signs, but the information they furnish should be con- firmed by secondary physical signs, if it is to l>e taken to indicate valvular disease. A murmur may mislead one because accidental, and the failure to hear a bruit mav do the same, but secondarv signs will not, because they are founded on changes in the heart and circulation brought about by the valvular defect. The reader will find more on this topic in the section devoted to valvular lesions.
Accidental Murinurs. — These are adventitious sounds heard in cardiac neuroses and certain blood-states, as chlorosis and various forms of anaemia.
Numerous terms are employed to designate this class of mur- murs, as functional, inorganic, ha^mic, ana?mic, spana?mic, and dynamic. The first two imply that there is no structural cardiac affection, and that the murmurs are in some way dependent upon
IXTBODUGTORY
37
perversion of the heart's function, JLi?niie, ami*mic, and spana^ mic commit one to the proposition of an altered blood-state being responsible for the murmurs^ The appellation dynamic carries with it the assimiption that the acoustic phenomena depend upon vibrations set np by powerful, perhaps irregular and fanltj, action of the heart -muscle. The term accidental sufficiently declares its own meaning, and implies nothing more than that the murmur is a chance result of cardiac action*
Theories to account for these murmurs are many and various, and so long as the condition or conditions governing their produc- tion are not definitely ascertained there can Ije no term that is not oj>en to objection. These abnormal sounds may be heard in any situation over the organ, but are most frequent in the pul- monic and mitral areas. They are systolic and have a blowing or be]li>wsdikc eliaraeter. Such competent and intelligent observers have advanced diverse theories in explanatiun of these murmurs that it seems to me the part of wisdom to assume that no one hj^pothesis is appliealde to all cases, ilay they not have their origin in a variety of conditions, some within and some without the heart 'i I shall descril>e briefly only the more important theories,
Xauuyn explained the systolic murmur heard in the pulmo- nary area in cases of chlorosis and other deprave<l blood-states as being in reality due to mitral regurgitation, and assumed that, instead of obeying the law usually governing its propagation^f it is conducted along the left auricular ap|tcnilix to the tip, which^ as we have st^en, lies directly l>encath the chest-wall in front, some- timed overlapping the base of the pulmonary artery. This theory was warmly supjiorted by Balfour, but api>ears now to meet with general disapproval. Russell proposed two theories, of which one attribute^l the murmur to narrowing of the pulmonary artery by pressure ui>on it of the dilated left auricle. In other cases he be- lieved a murmur of tricuspid insufficiency was transmitted into the conus arteriosus, which, in consequence of dilatation of the right ventricle, became displaced outward in the second left inter- space. Ilanford claims that the phenomenon, which is either heard only or intensified in the dorsal decidtitus, results from the pressure upon the artery of a flabby and dilated heart* Foxwell agrees with Russell as regards pressure in some cases of the dilated
28 DISEASES OP THE HEART
left auricle upon the artery, but explains other cases as due to a displacement upward of the pulmonary artery and a change in its axis and that of the right ventricle, in consequence of which its normal curve is increased and it is flattened somewhat against the wall of the chest. Bramwell attributes the murmur to the sudden discharge of a large wave of blood of abnormal composi- tion into the probably dilated artery. Sansom thinks that in a condition of right-ventricle weakness toiling to overcome increased resistance in the pulmonic system fibrillar tremors can be initi- ated at the overstrained portion of the right ventricle — i. e., the conus just below the valves — and in this way the murmur in ques- tion can be induced. Gibson holds that auricular or cardiac dila- tation cannot be assumed in these cases because the murmur oc- curs long before such dilatation takes place; also that the experi- ments on which Foxwell's view is based were f aultv ; also that if Sansom's theory is correct, then the murmur ought to exist more often than it does, and therefore advocates the view that it is the murmur of tricuspid insufliciency propagated into the pulmonary area. Quincke, cited by Balfour, concluded, as a result of obser- vations in 6 cases of healthy hearts and arteries, but with retrac- tion of the lung-borders, that a systolic basic murmur can be pro- duced by pressure by the heart of the pulmonary artery against the chest-wall.
Vierordt agrees with Sahli that in many cases venous mur- murs are transmitted from the great intrathoracic veins to the heart. Potain urges the cardio-pulmonary origin of accidental murmurs, maintaining they are generated by the impulse of the heart's apex against the lung, an hypothesis that appears sui>- ported by an observation of Franc^ois-Franek's, who, during an operation upon a dog, detected a systolic murmur in the region of the apex which disai)peare(l so soon as the ])rocessus lingualis was lifted away from contact with the heart, and returned when this portion of jmlmonary tissue was allowed to again rest against the surface of the organ. Such cardio-puhnonary origin is especially claimed for the murmurs of anji'uiia. Winckler, on the other hand, believes he has discovered the origin of accidental apex- bruits in a defective action of the papillary muscles or a faulty insertion of the valve-muscles, which i)ermits of regurgitation.
Finally, it has been urged that these murmurs may have a
INTRODUCTORY
89
h?pmic origin in eases of periiieioiis and other grave secondary ana*riiia^, while opponents of this view urge the elinieal observation that ill such blood-states niurimirs are nut always present, and, on the other hand, occur when anteULia does not exist. Bearing on this objection are the experiments of Thalma, who found that par* tial exsanguiuation of dogs did not give rise to accidental niiir- imirs. A condition of overfulness of the vessels caused by the injection of a warm saline solution into the femoral vein was followed by their appearance.
The number and diversity of the foregoing theories serve but to emphasize the sad fact that in medicine there are still many phenomena which have to hv accepted as facts, without a satisfac- tory explanation. In resjiect to the origin of accidental murmurs, therefore, we can but place ourselves in a judicial attitude and await further proofs.
Musical Murmurs.— Thei^e are here introduced because I pro- pose to classify them, not according to their acoustic characters or rhythju, but as organic and accidental, depending upon the ana- tomical conditions underlying tliem. First, organic musical mur- murs are those nut infrequently lieard in clearly demonstrable cardiac affections, usually valvular. In iheir time they may be systolic or diastolic, and in patch and tindire diey are variable. Thus they are describcil as sawing, filing, buzzing, whistling, etc. Their intensity may be such that the patient is annoyed by the niurmnr, and it is audilde several feet distant, or it may rei|uire ch>se attention for its detection. Regurgitant musical murmurs are, as a rule, Uiore intense than direct ones. Yet I recall an elderly gentleman who presented a systolic aortic bruit of a strik- ingly sawing ^juality so loud as to be almost painful to the ear. In the case of a negro i»bscrved in my dispensary service some years ago there was an aortic diastolic murmur which was audible a short, distance from the chest and had aroused the wonder of its possessor* It was not constant, and when present wholly obscured a soft diastolic murmur that was appreciable when the musical one was silent. Each time the sawing sound was present it was accompanied by a thrill in the third left interspace near the stemum of such intensity that it tickled the palm of the palpating hand. This bruit disappeared! some weeks prior to death, and at the autopsy no cause for its peculiar quality could be discovered
30 DISEASES OF THE HEART
Other than the sclerotic and incompetent semilunar valves. In another man, with a bruit of almost identical characters, except- ing that it was constant, the necropsy revealed sclerotic aortic valves, one of the cusps being fenestrated, and there being two thin fibrous bands stretched between the edges of two of the curtains. This patient was a pauper at the Cook County Poorhouse, and before the autopsy could be made his body was confided to the tender mercies of one of the medical colleges. It was there found, and the heart secured after a lapse of three weeks. The heart was injured by the preserving fluid, pale and softened, so that during the examination of the delicate fibrous bands they were ruptured. Before the photograph was taken two threads of sew- ing cotton were passed through the edges of the valves in rep- resentation of the bands. The examination and preparation of this heart, shown in Fig. 11, were made by Dr. AV. A. Evans. In this instance the fenestration permitted reflux of the blood-stream and the regurgitant wave set the bands to vibrating, and thus occa- sioned tlie murmur and accompanying thrill over the body of the heart. Engel has reported a similar case, in which a fibrous band was stretched across the aortic orifice to a pocket of one of the cusps.
The Russian, who under the name of Lewis travels from one medical school to another to exhibit himself to the students, is the proud possessor of a *^ musical heart." In his case the singing bruit is systolic and of maximum intensity over the right ventri- cle, and by some observers has been thought to indicate tricuspid insufficiency and to be generated in the right ventricle at the auriculo-ventricular orifice during the reflux.
In addition to fibrous bands or cords, some of the conditions causing a murmur to have a musical quality are said to be vibra- tions imparted to the thin, stiffened edge of a cusp or fenestra- tion, or to a delicate atheromatous plaque by the blood-stream as it passes over them. In a case of aortic stenosis with a loud systolic musical murmur reported by INfayne, two fibrous bands were found stretched across the cavity of the ventricle just below the greatly narrowed orifice. In another case of mitral insuffi- ciency, which during life had exhibited a musical murmur at the base and a systolic murmur at the apex, Potain discovered post mortem a cord which passed to the wall of the ventricle from the
IXTRODUCTORY
81
edge of tlie anterior mitral \'alve just below the aortic orifice, Deoiange reported a case of tricuspid regurgitation in which the muisica] uiurmur was evidently due to a fibrous band stretched across the interior of the ventricle close to the tricuspid ring. Schroetter has suggested that a musieul murmur may be generated
>^Av
Fn>, n,— LVTKIIIUR MF LtrT VE!rmiCLE,
Sliowirjg flhrotif band ijomivctiiig uortic cii#«ps and re>i>oiiJ^itjIe for rou^icfll murmur,
by the vibration of a tendinous ctjrd swinging free in the ventricle, or by one that, as a result of eiubx^arditis, had been ru]>tured and sul>de<iuently attached in an abnormal situation. It is nee<lless to remark that the musical quality of these nuirniurs possesses a pathological interest, but scarcely a diagnostic significance* At the most we cannot do more than conjecture their mode of
32
DISEASES OF THE HEART
cairs^tion during life until the true condition is revealed by the autopsy.
Accidenlal musical murmurs are rare, and yet that thev do occur 18 attested by the fullowing case: Mibs V. was referred to uie Ijv Dn Charles True, €>f Kankakee, in the spring of 1897, be- cause of attacks of intense nervousness and agitation accompanied by palpitation and pnecordial ]jain, for which no adequate cause in the heart had been discovered. The patient was a farmer's daughter, nineteen years of age, tall and slender, and gave no his- tory of articular rheumatism or any other infection that would have led to inflamuiation of the cardiac structures. Family his- tory was also negative. The girl was extremely excitable and unable to give a very lucid or intelligent description of her s^Tnp- toms further than that she nfteti l>c*came frightened, at what was not at all clear, ai>iirL"hended some imaginary danger to herself or family, and bad rapid lieating of the heart. During my ex- amination she was much agitated, and tlie heart action was greatly accelerated, about 12(^ but perfectly regular. The area of cardiac dulness, Ixjtii su|:K:*rficial and deep, was not increased, but there wa8 a blowing systolic murmur at the a|>ex, the heart-sounds l>eiDg sharp and ringing. She was moderately ana*niic, and there was a slight ei»teroi*t<»sis, A^^ide from a not very troublesome fermenta- tive indigestion and constipation, her functions appeared to be normal an<l the urine was negative. The ease was considered one of cardiac neurosis, the murnnir accidental, and treatment con- sisted of hanuatics, laxatives, and remedies designed to lessen the indigestion. The patient was seen by me at rather infrequent intervals, anxl each time appeared to be somewhat improving, Re- jMi^ated examinations of the heart failed to elicit anything more than at her first visit, and the murmur subsequently disappeared. On one occasion, however, siie seeme<l more than ordinarily per- turbed, and her pulse was more rapid than I bad ever seen it. During my exanjination of tbr heart, which was always made as a matter of routine, I was asTrmished to hc»ar over the body of the right ventricle a distinct, short, exquisitely twanging murmur of very high pitch ami pleasing i|uality. It seemed, as well as the tachycardia won hi allow me to judge, of a systolic rhythm. The actiim of the heart at the time was extremely rapid and violent. This interesting, and to me exceptional, phenomenon lasted for
■
IN'TRODITTORV
33
ral tninutefs in»IcH^l 8o lunj^ as the rapiiHty of eardiac action twItirtnL \Vhei) att Ieii|::tb \u*t pulse ^cw moro (juictt. the musical lurttiur became inauilible and did not reai>ix*ar. Tliis patient i Been by me in Sc^ptenilier, IIHJO, after a lapse of more than a If frtitn her last visit, and although I diligently sought for the ;ing 8ound and any signi? of cardiac disease, I failed to detect any abnomialify. The patient reported herself as in much better bfalih and h\ss excitable, being but rarely annoyed by her former iptoniB, and indeed appeared nc^t the least distiir[K?d by the li oat ion.
A
^
Fi«. l± — HtAKr uf A BitrAUo C'ALr. ^hoivinir aljvmuit rhonLr UMKiiniv In UiX vciitriete.
The only explanation that has seemed to account for this re- markable phenomenon t»« that the musical murmur was due to the iribnifioli of one of the so^alleJ nhnnmi rordtt (Fig. 12) or tnod-
34 DISEASES OF THE HEART
eralor bandsy of which so admirable an account has been given by H. F. Lewis. These aberrant cords are thin Hbrous bands which, most often discovered in the left ventricle, are seen running along the inner aspect of the wall, or stretched across the upper part of the cavity from one side to the other, or from a papillary muscle to the sspptum. They have nothing whatever to do with t he chordju tendinejv, and unless sought for are likely to be severed in the opening of the ventricle and thus escape detection. Al- though without question most frequent in the left, they have yet been found in the right ventricle, and there are rare instances of such a band passing from the valve of the foramen ovale into the cavity of the left ventricle and attached to a leaf of the mitral valve. It is supiK)sed that the function of these moderator bands is to strengthen the cardiac walls in times of overstrain. In the case just narrated it is assumable that in conscijuence of the tachy- cardia the cardiac chambers became overfilled and an aberrant cord was thus put on the stretch. In this state of tension it was set to vibrating by the energetic and rapid cardiac contractions, and thus generated the twanging murmur in the same manner as in the case of a violin-string twitched by the finger of the musi- cian. Lewis says it is these aberrant cords w^hich are resi>onsible for tlie systolic, and sometimes diastolic, musical nmrmur heard before death. As we have seen, several of the musical murmurs observed in connection with valvular defects have apparently been due to aberrant fibrous bands, so situated as to have been throwTi into vibration by the blood-stream.
The Differential Diagnosis of Accidental Heart Murmurs. — Under some circumstances it may be a matter of no small difficulty to differentiate these from organic murmurs. The patient's anam- nesis is to be carefully considered, since, if painstaking inquiry fails to elicit a history of articular rheumatism or any infectious disease likely to have set up an endocarditis, it furnishes some evi- dence in favour of the non-organic nature of the murmur. This is strengthened if the patient is manifestly neurotic, anaemic, or chlorotic, if there are digestive or pelvic disorders that are likely to produce disturbance by way of the sympathetic nervous system, if by reason of the patient's excitability the heart's action is easily perturbed, or if there is a history of cardiac overstrain. If the individual is given to vicious habits, as sexual excesses of one kind
I XTHU DOCTOR Y
35
or another, particularly mnjjrurbutiuii, ur indulges U.hj freely in tobaceo, tea, or coffee, the presuuiption is strengthened that the murinnr is aceidentah Of ef>ursL*, the»e and numerous other fac* tors that are said to aflford prima facie evidence of the malady being not organic may exist in a given ca&e with an endocardial murmur of valvular disea^. There must, therefore, be made a careful examination uf the heart ami other viriceru.
It may be stated as a general proposition that accidental mur- murs are not accompanied by secontlary changes in the size of the heart or by circulatory disturbances, such as generally attend and dejjend upon vjilvnlur affections. Tlie discovery of hypertrophy or dilatation of the heart nuikes strungly for the organic and I against the accidental origin of a nuirnnu". Snialluess, feebleness, and intermittence of the pulse, cyanosis, dyspntra of effort, hepatic and other visc-erul engorgement, etc, are not usual accompaui- ments of acci<lental juuruiurs. Such signs of seriuus endiarrass- ment of the circulation failing, information may be sought for in the rhythm and other characters of the murmur itself. Accidental bruits of cardiac origin are rarely if ever diastolic, whereas or- ganic ones may occur during any or all phases of the cardiac cycle, I-*eul>e has never heard such a fliastolie accidental murmur, ami doubts it^ occurrence. Although tliese murniurs may exist in any [mrtion of the pricconlia, they are most f re<pient over the base, in or near the pulmonary area, and next in frequency at the apex in the mitral region. In transmission they are usually rather limited, and such an a^H^x4iruit is not propagated to the angle of the left scapula. Organic murmurs, on the contrary, occur with frequeucy in all areas, and often have a wide extent of audibility besides beiog propagated in definite directions and to considerable distances. In the matter of intensity, murmurs of both organic and accidental origin are variable. Leube is of the opinion that, as a ride, the latter are the less loud of the two, but the reverse occasionally obtains* The munnur of cldorosis and ana*uua, so often sjioken of as ha*mic, which is heard eliiefly in the pulmonic area, is gen- erally intensified in the dorsal decubitus, wdule Drummond states correctly, I believe, that the ** neurotypic " (cardio-inuscular) bccoinos less pronounced after rest in the recumbent posture has flowed the heart. This latter type is most intense during ex- citement and in the standing position. The same is true of the
36 DISEASES OP THE HEART
cardio-pulmoiiary murmur. These last two diminish or di8ai>- poar in the lateral decubitus, particularly when the patient lies on his right side. Organic bruits never wholly cease in the re- cumbent or lateral position. Respiratory movements also affect the intensity of accidental, but not the organic murmurs. The basic chlorotic bruit is loudest at the end of forced expiratioriy and at the close of deep inspiration may cease entirely. A neuro- typic (cardio-muscular) murmur is also intensified at the end of forced expiration, and less or absent at the close of a deep inspira- tory effort. The cardio-pulmonary or cardio-respiratory murmur, on the other hand, is influenced conversely, being loudest at end of forced inspiration and weakest at end of deep expiration, or ceases when the patient holds his breath.
The pitch of accidental murmurs is usually higher than that of the organic, yet is rarely musical, and may occasionally be lower. In quality the former is apt to be softer, yet may be harsh, even grating, and the a])ex-bruit in neurotic individuals is not in- frecjuently vibrant or *^ whizzing" (Drummond), and may be ac- companied by a systolic thrill in the upright position or when the murmur is the loudest during excitement. Finally, the pulmonic second sound is not so accentuated, as a rule, in accidental mur- murs as in mitral systolic bruits of organic origin. The reason is obvious; in the former there is not the same likelihood of sec- ondary pulmonary hypeni^mia. This lessened intensity of the pulmonary second sound goes hand in hand with the absence of appreciable enlargement of the right ventricle.
In a considerable proportion of cases a definite opinion cannot be expressed at the first sitting, and must be reserved until the pa- tient has become accustomed to an examination or has grown less nervous, or until after the results of treatment have been observed.
Exocardial Murmurs, — The pericardial friction-sounds that come under this head will be found fully considered in the appro- priate chapter. Pleuro-pericardial murmurs may result from the friction of the heart on the roughened surface of the pleura, where it comes in contact with the former. Their differentiation from pericardial or endocardial murmurs, which they may at times simulate because of the rhythm, is usually accomplished by having the patient hold his breath, when the friction-soimd disappears. A deep inspiration often increases its intensity.
SECTION I DISEASES OF THE PERICAEDIUM
CHAPTER I
ACUTE PERICARDITIS Morbid Anatomy. — The perictirdiiim is a dosed sac lined with serous menibraiie whit-h surrounds the heart, a visceral layer of the serosii (the epieardinni) ]>eing reflected over the surface of that organ, and for a short distaiiee ah>ng the roots of the great blood-vessels. The parietal layer of endothelium is re-enforced by a strong tibrons lamina, extending from the diaphragm below, to be eontinnons with the tibrons shealhs of the great vessels above. The pericardial sae usually contains after death a few drachms (10 to 15 cubic centimetres) of a clear straw-coloured fluid.
An inflammatory process of the pericardium may involve only the serosa, or may penetrate into the myrjcardinni or into the fibrous tissue of the parietal layer. It may involve tlie entire sur- face nr it may confine itself to limited areas, single or multiple, thus giving rise to the circumscril>ed form of the disease. The morbid anatomical condition is the same in the two forms except in the extent of involvement, and the same description applies to both.
The first evidence of inflaniuuftiim is the injection of the blood-
^vesscds lying beneath the transparent serous membrane, the process
usually beginning in the parts of the sac surrounding the great
vessels. This is associated with considerable desquamation of the
rendothelimn, which gives an appearance that is described as of
kliaving been breathed upon* As the endothelial cells are those
which lubricate the surfaces, this desquamation oecasious friction
iBetween the two layers of the sac, giving rise to the sounds that
"are heard during life. This is the simplest form of pericarditis,
a?
38 DISKASKS OF THE HKAUT
and the disease may proceed no farther. Usually, however, exuda- tion (K*curs, and the formation of the exudate is in nuiny cases tlie prominent feature of the disease. The character of the exudate varies extremely. It may he librinous, serous, purulent, or ha»m- orrhagic, sero-fibrinous, or tibrino- purulent. In fact, almost any combination nuiy oc»cur.
In the fibrinous, dry, or plastic form the exudate appears at first as a thin smooth pellicle, of a grayish-white or yellowish- white cohiur, easily detached from the injected surface beneath. Later the exudate becomes thicker, and is of a pasty consistence, and not so easily detached from the underlying surface. The incessant motion of the heart causes the plastic exudate to assume forms that have bt^en variously describe<l by diflferent authors. A common condition is one resembling the appearance produced by tearing apart two pieces of thickly buttered bread. At other times fine threa<ls <*f fibrin attached all over the surface of the pericardium give to the heart the shaggy or hairy api)earance that has received the names of cor hirsutum, cor villosumy and cor tonientosufii (Fig. KJ). In still other instances the fibrin is ar- ranged in coarser nuisses of the characteristic grayish-yellow col- our. Such an exudate, being in contact with both layers of the pericardial sac, forms between them adhesions of the kind de- scribed as recent or fibrinous, in contra<listinction to the old or fibrous adhesions found i!i the chronic form. The appearances d(»scril)ed are to some (extent the result of the tearing apart of the two layers of the sac, thus loosely bound together. The pr(x?esses leading to the repair of this lesion are those eventuating in chronic pericarditis, and are considered in that connection. Ac- cording to Osier, plastic pericarditis is freipiently tuberculous, but the tubercles nre very easily overl(M>ked in the presence of the fibrinous (»xudate.
When the exu<late into the cavity is of a fluid nature the con- dition is known as iK'ricanlitis with effusion. The effusion may be serous, purulent, or ha'morrhagic in character, but the most commonly occurring con<lition is that in which the effusion shows mixed or int(»rmediate characters. In the serous form there is an effusion of serum from the inflamed surface, which may be ]x;r- fectly clear, but more commonly contains fibrin in the form of shreds, flakes, or larger masses, which nuiy float in the fluid, or
FhoCogiupb
40 DISEASES OP THE HEART
may be deposited on the walls of the sac as a creamy layer. This is the form of the disease known as sero- fibrinous pericarditisy and is the one most commonly met with. It usually begins as a dry l^ericarditis, the effusion developing later, and indeed in the dry form there is aways some transudation of fluid, although its amount is insignificant compared to that of the fibrin. The fluid is often slightly turbid from the presence of leucocytes, but in insufficient number to entitle the eflfusion to be called purulent, or a small proportion of blood may give to the fluid a reddish or brownish tinge. The amount of fluid varies from a few ounces to several pints.
In the purulent form the effusion is rich in cells, and of a thick, creamy consistence, but all degrees of variation exist be- tween this form and that presenting a serous exudate with slight turbidity from the presence of pus-cells, so that a sharp line can- not always be drawn between the two conditions. When the effu- sion is truly purulent the condition is practically an abscess, and the pus may burrow and rupture externally, as, for instance, in the first right interspace, or in the neck above the clavicle. The condition is a serious one, and shows but little tendency to resorj)- tion, and yet the pus may become inspissated and calcified.
In the hcrmorrhagic form tlie effusion contains a large propor- tion of blood, or even, as in scurvy, may seem to be composed of pure blood. In cases of long standing the decomposition of the haemoglobin gives the fluid a brownish rather than a red colour. Aside from the scorbutic form, luvmorrhagic pericarditis occurs most often associated with tuberculosis of the pericardium and with malignant disease. The effusion is usually very large, and may take place so suddenly as to produce the symptoms of acute secondary anivmia.
Various bacteria have been found in the exudates of acute pericarditis, including the various pyogenic organisms, the diplo- coccus pneumonia^, and the bacillus tuberculosis, but it is not always possible to demonstrate bacteria. The presence of organ- isms causing putrefaction may give to the effusion a foul odour. The Bacillus aerogenes capsulatus may produce gas in the peri- cardium. This production of gas is probably a post-mortem change (Osier), but according to Coplin (1899) occurs during life.
ACUTE PERICARDITIS
41
Secondary changes arc found mainly in the myocardium, which may show iiiflamniatory intiltratiun, or a fatty or albumi' nous degeneration of its muscle-fibres, leading, after the acute stage has passed, to an iiisterstUia! myocarditis. There may be c%'idence of recent disease of the endocanlinnij usually due to the same morbific agency as the pericarditis. Associated disease of the lungs or plouni^ usually hears an etiologic relation to the dis- ease of the pericardiuuT. If there has hoen high fever, the vari- ous parenehyniatous organs show elondy swelling.
Etiology* — If nue tMjHii>are the statements of older authors with those of mt»dern writers concerning the causation of acute peri- carditis^ the chief difference tlnit will impress him will l)e found in the change of views regarding the freipiency of the primary as opposed to the secondary form of this affection. The term pri* miiry was made to iucbide those cases regarded as idiopathic or of s}H»ntaiitMjus origin. A better knowledge of pnthology and etiol- ogy, founded tni the results nf bacteriological investigation, has taiigbt us the fallacy of a belief in spontaneous cjevelopment of disease. Authors now restrict primary inllamnuition of tlie peri- cardium to those* cases originating in trauma, and inchide among the stTonthiry all itthcr cases once cotisidered primary or idio- pathic. This is nnt!oultte<lly due in i^nrt to a more accurate knowl- edge, and therefore more frequent recognition, of the rheumatic nature of many disorders wIkjsc pathology was formerly but indis- tinctly understood — as, for instance, certain rheumatic nodules occurring in chihlhoofh The chief reasfiu, however, is to he found in the renuirkable additions made to our knowledge dnring the past twenty years or so regarding the pathology ami hMctrriology of disease, above referred to. At present tlie pliysician would be far iH^hind the times who failcnl to recognise inllanunation of the f>ericardium as a local manifestation of a general constitutional disiease or as a secondary int\t*ti<m in the course of some disease having pathogenic ortrnnisms as an etinlngical factor. For in- stance, the primary iicricarditi;* that was formerly thought to fol- low exrKisurc or chill was probably due to a rheumatic attack, the true nature of which escape<l recognition.
Furthermore, some of the cases nf f>eriearditis, formerly re- garded a^i idiopathic, were uhserved in imlividnaU whose general esistance had been greatly reduced by privation or chronic aico-
42 DISEASES OF THE HEART
holism. In such the pericardial inflammation was, properly speak- ing, due to infection. The sero-fibrinous pericarditis arising in the course of articular rheumatism is a local expression of the rheumatism, and the suppurative pericarditis sometimes seen in puerperal septicaunia is due to the primary infection. Roberts goes so far as to say: " In my own experience I have never met with an instance of acute pericarditis which, when carefully inves- tigated, could not be included as a secondary event in one or other of the etiological groups now to be discussed." Among these, he includes pericarditis from extension or irritation, from trauma and perforation, from cardiac and aortic disease, and those associated with new growths, general miscellaneous diseases, and blood- states.
In his investigations regarding '* terminal infections " in chronic disease, Flexner has made some highly interesting and important observations with reference to the etiology and bac- teriology of acute pericarditis. I cannot do better than to repro- duce (me of his tables, which gives the fre(|uencv with which cer- tain bacteria were found and their point of entrance:
BacU»ria. FYequency
MifrocMH'Cus lanceolatus 11
Streptococcus 4
Stapliylocoocus aureus 1
Hacillus pyocvancus 1
Micrococcus la nceolat us and Bacillus coli. . 1
Hacillus influenzae 1
Streptococcus, Staphyloc(K-cus aureus, and i .
Bacillus coli * (
Staphylococcus an<l Hacillus coli 2
Unnle'ntificd bacilli 1
Infection Atrium.
Pneumonia. H times. Bronchitis. 2 times. ErysijMjlas, 1 time. Leg ulcer. 1 time. Peritonanim. 1 time. Tonsils, 1 time.
Cancer, stomach, 1 time.
Sloughing mvoma, 1 time. Doubtful.
Tubercle bacilli should be added to this list. From the fore- going it is plain that acute pericarditis may be a secondary infec- tion following a great variety of l(X*al infectious processes, or it may arise in the course of an infectious disease, and be due to the pathogenic organism of that disease.
Rheumatism. — All observers agree in placing articular rheu- matism first in the list of those affections which give rise to acute pericarditis. The certainty of this connection was established by Pitcairn in 1788, although his views were first widely published in 1795. Writers have been in accord concerning their causative
ACUTE PKRICARDITIS
43
connection^ yet there bus been great diversity of opinion regard ing the frequency with wliioh i>eric'arditis oeeurs in the course of rheumatism ; whetlicr it r»eeurs most frecpiently in the first or sub- secjuent attacks; whether it h most likely to be associated with intlamniation of one or Sicveral j^iints, or any particular joint; whether with chronic as well as acute articular inflammation; and whether or not it precedei* or follows or develops coincidently with the joint affection, iVmeerniog the first of these questions, it is generally held that pcriearditis occurs less frequently than endocarditis, yet there is a wi<le divergence in the figures given by authors regarding its uuuicrical rehiti(»n to attacks of rheuma- tism. Chambers gave it as occurring in J?j jK^r cent, Ormerod in 71-7 per cent, Bamberger in 80 per cent, while BaueFj although believing exact figures cannot be stated, considered from 16 to 20 per cent not far from the truth. Of Poynton's 150 fatal cases of rheumatic heart disease in children^ be found evidence of pericar- ditis in 113 eases (75 per cent). PersonaUy, I regard such statis- tics as of but small value, and consider it sutficicnt to state in gen- eral terms that rheumatism is so fr€?quently complicated by acute pericarditis that in every case of the former affection the medical attendant sbnuld keep a sbarji hfukont tV»r the development r»f pericardial iuflauinuition. Alost authors agree, I tbink^ in the opinion that pericarditis is more apt to occur in the first and endocarditis in the subsequent attacks of articular rheumatism* Bauer asserts that it bears no dep'nite relation to the number of joints affected nor to [he involrement of any parlicular joint. It certainly dm^s not ixTUr uuire frequcutly in rbeurnatism of the upper than of the hnver extremities. The last-named author states emphatically, also, tluit it dues not occur in the course of chronic rheumatism, nor when but a single joint is affected. The devel- opnirmt of acute pericarditis is by others thought more likely in the severe forma of the rheunuitic affection, and therefore when a number of joints becouie attacked.
Although such a relationshi|> between acute pericarditis and f severe rheumatism was noticed by Sibson, it w^as not constant. In chihlren rheumatic manifestations are often mild, and yet the little ones do not escape pericardial inflammation. In one case coming under my notice the pericarditis followed no other evi- dences of rheumatism than vague pains in the knees, with ery-
44 DISEASES OF THE HEART
thcnia accompanied by mild fever, these symptoms having been preceded by follicular tonsillitis.
There are no constant time relations, moreover, between an attack of rheumatism and inflammation of the pericardium. The latter may even precede the former, although it most commonly develops during or after the rheumatism. It generally makes its appearance from the fourth to the sixth day of the rheumatic dis- order, sometimes not before the tenth or fifteenth day, and has even been knowTi by Sibson to be postponed as long as the sixty- third day. Rheumatic pericarditis may exceptionally attack in- dividuals of all ages, but is imdeniably most frequent in young adults who have been rendered susceptible to it by hard work or exposure. In England it appears to be particularly prevalent among young servant-girls below the age of twenty-one (Sibson), and among i)ersons of both sexes thus afflicted at a later age, the majority were found by the same author to follow more or less laborious outdoor occupations.
Its prevalence among children is shown by statistics gathered from children's hospitals by Sturges and Poynton. Yet Roberts states that, according to his experience, jx^ricarditis is very much less frequent in children of the better classes, a fact which, he be- lieves, shows the predis|>osing influence of hardship, not alone in the i)roduction of rheumatism, but also in the development of peri- carditis.
Satisfactory evidence of the infectious nature of the rheumatic poison has not yet been adduced, although many observers have expressed the belief that the pathogenic organism will yet lx» dis- covered. If such an organism should one day be identified, then pericarditis would no longer be considered a complication, but a natural though not a necessary j)art of the pathological process of inflammatory rheunuitisni.
Nephritis. — The im])ortance attached to renal disease in the production of acute pericarditis is scarcely a])preciated, I think, by the majority of ])hysicians. A few writers of wide clinical experience place nephritis as only second in this regard to inflam- matory rheunuitisni. It should, however, yield place to acute pneumonia in this regard. The pericardial inflammation is not limited to acute nephritis, as might be supposed, from the fact that the latter is so frequently observed in the course of acute infec-
ACUTE PERICARDITIS
45
tiuus diseases, IjiU mny a[>[>ear during the jirogress of any one of the ehroiiie forms i»f kidney disease. Indeed, it is said to be a speeially fret|nent eoinplieatir>H c*f the small red kidney, Unemia seems to jmrtieidiirly preiHsiHjse to acute perieanlitis, while the supervention of the latter eiuitrihutes largely to the fatal termina- tion of the primary ailcction. Most authors content themselves with a statement of the fact and make no attempt to explain the well-known etiological connection between acute or chronic in- Hainmatiun (»f the kitlney ancl inllnmiiiation of the pericardiunj. Two explanations may be given, however. By some the blood of nephritic patients is thought to C4)ntain souu^ noxious substance, possildy of eheiuical nature, possildy of (*atabolie origin, which results from renal disease, and w^hich in consequence of renal inadequacy is not excreted.'*^ This noxa is an irritant^ and gain- ing access to the ]>ericarflial cavity, there sets up an irritative in- flanmiatirm. Givaditiovitch expresses the opinion that acute peri- carditis in Bright's disease is of true toxic nature. It is mostly fibrinous, but nmy Ijc hicmorrbagie and very rarely sero-fibrin- ous, and always cjccurs in an advanced stage of the renal dis- ease. According to the other less conservative explanation, peri- carditis is a true secomlary infeetiim, causenl by the conveyance to the pericardium nf genus eirculating in the bUxxl, and re- sponsible for the acute or chronic pericanlitis. In cases of the small red ki^luey, it is assumed that invasion of the perieardivun by bacteria takes place either berausc the renal disease has im- paired the germicidal action of the blood, or because it interferes ^nth the proper elimination of the niicrrMirganisma,
Apropos of the statement that infection frequently occurs in Bright*s disease, Flexner s observations may again be quoted. Of ??2 cases of chronic nephritis occurring alone, in which there was general infection, micro-organisms were positively identified in
• Chntin has reported four cases of porit'nrditif> in [mtient.s sulTcnii^ from OephrtiiB, In thr^e eta^Qs with effusitm hactiTioln^ic fxnininntjon sliowfil lie fluid to Iw frterile, la these thn»e cjipcs the st-riim wa.^ tiyf>erto\ic. The toxic elements »nppt>?*»ci to be re^jKmsihle for the inflammrttion of the perieardiuin have been fauml ndthcr in the eirrulatin^ hlowl m^r in the efftision ; and the existence >f aseptic and Hrnicroliic pericarditis in eerOiin eases of Bright's disease is well iblished. The penonrditis of nephritis may siiometimes develop as a compliea- r<||»»n of an orrtinary infection, and i^ iiaually aseptic or sterile. — Revue de m^ecine, Julf lU. 19U0.
46 DISEASES OP THE HEART
29. It is worthy of note, however, that in none of these eases was pericarditis present. On the other hand, pericarditis was found 23 times in cases of chronic nephritis in which there was local infection, whether the nephritis existed alone or in combina- tion with some other chronic disease, as of the heart or liver. It would seem, therefore, that although a general infection may occur in the course of chronic nephritis, pericarditis does not take place unless there be some other local infection. In the majority of cases of pericarditis in the course of chronic nephritis there was pneumonia, either croupous or lobular. It may be queried, there- fore, whether the pericardial inflammation is not secondary to the local infection rather than to the nephritis itself.
Acute Pneumonia. — This infection should certainly be given a place only subordinate to articular rheumatism in the etiology of acute pericarditis. The frequency of this association has been recognised by authors, but has been brought out with special clear- ness by Preble, who found pericarditis in 92.4 per cent of 79 cases of fatal pneumonia collected from the post-mortem records of Cook County Hospital. Preble came to the conclusion that the danger of pericarditis bears a direct relation to the extent of lung involvement, and is also relatively more frequent in left-sided than right-sided pneumonias. The inflammation of the pericar- dimn may result from direct extension through the lymphatics or may occur independently, and is due to the pneumococcus, which has been frequently identified in the exudate.
Scarlatina. — This is sometimes complicated by the occurrence of acute pericarditis, and in some cases this has taken place dur- ing the stage of desquamation. As the scarlatinal organism has not been identified in the i)ericardial effusions, this latter is prob- ably to be regarded as a mixed infection due to streptococci or staphylococci. Bauer observed a post-scarlatinal pericarditis co- incident with rheumatic manifestations, and was therefore inclined to attribute it to the affection of the joints; but inasmuch as pus germs are often responsible for the rheumatic affection, the peri- carditis, as w^ell as the rheumatism in that case, may very well have been an instance of mixed infection following the scarlatina.
Other Infections. — Other diseases in the course of which acute pericarditis has occasionally been observed are erysipelas, small- pox, typhoid fever, measles, cholera, and even diphtheria. It
ACUTK PERICAIIDITIS
47
muat also be reiueiiil>ered that Floxiier IVhiikI as fwi of infection bronchitLs, leg iileer, sloughing luyoma, eancGr of the stomach, and even tonsillitis and disease of the peritonanniL In some it was probalilv a seeoiidary event, in others a trne mixed infeetion. When pericarditis couiplicates acute pleuritis it is generally stated to be by extension. It is, in fact, either a secondary event due to the one and the same cause, or it is a mixed in feet ion.
Acute inflammation of the pericardium has been associated with varying diseases of neighbouring parts — e. g., enlarged
■glands or tumours in the mediastinuiu, abscess, or caries of a rib, and has resulted from a rnpture into the sac of an empyema, from perforation from an ulcer of the (cso])hagus or stomach, and even from intra f>eritoneal abscess. When caused by such conditions the pericarditis is usually jnirulont. One very renuirkable case has been narrated of [>t*rforation and iidlammation of the pericar- dium by a set of false teeth whicli had l>een accidentally swal- lowed and had lodged in the oesopliagus, where it caused ulceration. Acute jK^ricarditis is sometimes «x*easioned by aneurysm of the aorta and liy new growths in the ]>€ricardial sac — e. g., tul>ercles. These are capable of setting up an acute inflammatory process of the |>ericardium, but as a rule the inflammation is subacute or chronic, which probably exjdains why it m frequently esca{:)es clinical observation. It is doubtful whether giunnuita ever in- duce acute pericarditis.
Iltemorrhagic pericarditis oecurs as a secondary infection in the course of scurvy, purpura hiiiuorrliagica, and hivnioidiilia, Some writers also assert that cjincer and tuberculosis induce the hiem- orrhagic variety. Ebstein Inis rej>orte<l two cases of hiemorrhagic pericarditis, and stated that periciirditis was specially likely to be haemorrhagic in the chronic or recurring form, and also in the aged and in the ba^morrhagic diathesis. In this condition, he thinkii^ there is a toxic or infectious cause that creates a tendency to ha*morrliagic exudates. Such changes are at least as important
ias the mechanical ones. The pericarditis secondary to scorbutus may be regarded as a tyjie of this class. It may also occur in
^ alcohol ism, which induces tlie ha*morrhagic diathesis. In most
^ eases of traumatic pericarditis the blood found in the sac comes from the bleeding wound. Cases of traumatic origin in which the pericardium is not perforated are harder to understand.
48 DISEASES OP THE HEART
Valvular Defects, — Chronic valvular disease seems undoubt- edly to predispose to pericardial inflannnation ; this is said to be particularly the case with aortic insufficiency. Why valvular le- sions should thus tend to the production of pericarditis is a mat- ter for conjecture. By the advocates of the doctrine of the infec- tious origin of all inflammations, it would probably be explained as an instance of secondary or mixed infection, in consequence of the very close anatomical and physiological connection existing between the endocardium and pericardium.
Trauma. — Finally, acute pericarditis is sometimes the result of direct injury, as gunshot or stab wounds, blows uix)n the chest- wall and laceration by fractured ribs. Under such circumstances micro-organisms are usually introduced into the i^ericardium, and there set up an acute inflammatory process which, if the cocci be pyogenic, will prove to be suppurative.
DRY PERICARDITIS
Syn. : Fibrinous, Plastic, Adhtsive Pericarditis
The pathology and etiology of this form have already been considered, and therefore I shall j)ass at once to
Sjnnptoins. — This disease usually arises during the course of some already existing infectious j)ro(*ess, and therefore its inva- sion, and even its subsequent ])rogress, are likely to be masked for a time by the clinical phenomena of the j)rimary affection. In- deed, some authors go so far as to state that there are so few subjective symptoms attending dry pericarditis that it may be said to be a latent affection. In many instances this is probably correct, but I believe the existence or absence of subjective phe- nomena is determined by the degree of intensity and extent of the pericardial inflammation.
If in the course of acute articular rheumatism there is a sud- den elevation of temperature which cannot be explained by the fresh involvement of other joints, or if delirium or pronounced disturbance of the nervous system suddenly takes place, especially in children, it is suspicious of some of the heart-structures having become invaded by the inflammatory process. This organ, there- fore, should at once be carefully examined, and if necessary re- |)eatedly examined, for, according to the figures already quoted
DRY PERICARDITIS
49
from PovBton, the pericardium in eliildren 18 a specially frequent seat of inflammatiou. If, as thought bv Kolierts, the opinion api>ears to be quite prevalent among general practitioners that acute fibrinous pericarditis is not very frequent antong children, and not apt to leave serious contiequenccs behind^ it certainly would seem to be in place to again call attention to Ponton's figures. Out of 150 fatal cases of rheumatic heart-disease in chil- dren, there was evidence of more or less acute plastic ijcricanlitis in all but 9. In 113 the pericardium was more or less adherenti while in 77 the adhesion was complete, iloreovefy the iiericarditis appeared to contribute more to the fatal issue than did the endo- carditis, for the reason that the iiitlammatory [jrwcss extended from the jyericardium to the myocardium and led to dangerous dilatation,
Paiu. — This is an early and fairly constant symptom, although in some cases it appears to be more like a vague sense of distress than actual pain. It is generally felt in the cardiac region, but may l>e hx^ated in the epigastriiun, while in some cases it radiates over the front or side of the chest, even along the course of the brachial plexus into the arm. In a case of this kind described by Sib^n there was also endocarditis. Occasionally it is experienced between the shoulders, and is then held to indicate inflammation of the posterior jMirtion of the sac. Bauinlcr has described pain and sensitiveness on the side of the larynx. In some instances there is associated with tlie pain such a hypern^sthesia of the skin of the pnecordia as to make percussion of the heart almost im|Kj8* Bible* Painful deglutition has lK*en frequently reported, and is not difficult to luiderstand when we remember that the pericar- dium is attached to the a-sophagus and would l>e pressed upon by the ingesta in their passage down the gullet. Patients have also been kno\\Ti to complain of the heart hurting them with each contraction, and it may well be that when the covering of the heart is inflamed pain can l>e felt every time the organ changes in fnrm during systole.
In character and severity this s^miptom differs much in differ- ent cases. It may lie sharp and cutting or dull and heavy. In a cast* observed recently the |>atient was only able to describe his pain as a steady dull ache over the heart. Usually the anguish is continuous, although in some cases it is intenuittent, coming and
50 DISEASES OP THE HEART
going like a veritable neuralgia. In others again it assumes a paroxysmal character. The countenance generally betrays suffer- ing by an expression of pain or distress, and the patient not infre- quently keeps his hand upon his heart. Although this symptom, pain, is doubtless due, in large part at least, to the friction pro- duced by the rubbing together of the inflamed pericardial sur- faces, still its intensity depends also upon the sensitiveness of the patient, it being well known that some persons never feel pain so acutely as do others of a less phlegmatic temperament. The pain of pericarditis persists so long as the inflamed surfaces continue to rub against each other, and hence when these become separated by eifused fluid this sjanptom abates or disappears. Therefore, if pain suddenly ceases while the continuance of pyrexia points to continuance of the active inflammation, it may be taken to indi- cate beginning effusion into the sac.
Cough may or may not be present, but when present is usually dry and frequent, and when conjoined with pain may give rise to the suspicion of pleurisy. In a fourteen-year-old girl seen not long ago and in whom the inflamed pericardium had led to great car- diac dilatation, with consequent pressure on the left lung, the attending physician at first mistook the case for one of pneu- monia. This case is so instructive that I will briefly report its salient features. On a certain Friday this girl complained of slight pain and stiffness of one of her legs, but was not prevented thereby from going to school as usual. The following Monday she felt several slight chills, which were attributed to the coldness of the room in which she w^as at the time. For several days follow- ing she showed signs of malaise, and in other respects did not seem well, yet did not give up and go to bed. Friday night, a whole week from her initial rheumatic attack^ she spent at a friend's house, but when the next morning came was unmistakably ill, and the family doctor was sent for. He found her with a dry cough, hurried respirations, rapid pulse, considerable fever, and a sharp pain in the left side above the heart. Examining the lungs, and discovering some dulness and bronchial breathing at the left posterior base, he pronounced the case pneumonia — an error that could have been avoided by a proper examination of the heart. Three days later another physician saw the patient, and at once recognised the true character of the disease. When on the ensu-
DRY PERICARDITIS
51
ing afternooii I was called in consultation^ the cardiac dulnes3 prciieiited the characteristic triangular outline and a systolic apex- mui-mur was audible, but the friction-sound had disappeared. The eaee was one of acute pericarditis, as shown a few days subse- (juently by the results of aspiration. The amount of effusion was small, however^ and the marked increase in the area of cardiac (lulness was due chiefly to the dilatation the heart had undergone. It was impossible to say whether the mitral systolic murmur indi- cated a valvular lesion or was relative in consequence of the dila- tation. But as there was a history of some sort of illness three years before, at which time she had '* heart troulde," it was feared that the valves were defective and were perhaps sharing in the present inflanitmition. In this case the pericarditis had probably egun almost a week before she w^as obliged to give up, so that it is not strange tliat the process should have induced signs of pres- sure by the end of the first week* This patient ultimately made a good recovery.
The pulse in these cases is accelerated, running sometimes as high as 130y or even 140 to the minute, and is usualy compres- sible and regidar in the early stage before the myocardium has come much affected.
The trspirafions are usually rapid and often shallow, either because the patient shrinks from tiiking a deep breath, lest the pain be intensified, or because an actual sense of dyspna?a is ex- j:)erienced-
Temperature, — An elevation of body-temperature probably at- tends most cases of acute pericarditis, but is often masked or modi- fied by ilie fever due to the primary affection. As a rule, the degree of pyrexia is not great, averaging perhaps 102^ to 103*^ F., and being generally continuous or mildly remittent. When it rKX*urs in the course of chronic nephritis, or when it is associated with chronic myocardial or endocardial lesions and independent of rheumatism, the pericarditis frecjuently runs its course with- out fe%^er, or at all events with so slight a pyrexia as to be over- looke<h The duration of the temperature is somew^hat variable, depending on the intensity of the infection, Init may be said to average two to three weeks.
Loss of appetite and other derangements of the digestive tract, as flatulence and constipation, are usually present, the same as in
52 DISEASES OF THE HEART
other febrile and acute infectious processes, while the urine is scanty and high-coloured. If it contains albumin, this is due to an associated nephritis or depends either upon a primary affection or upon a long-standing visceral engorgement resulting from ante- cedent cardiac disease and is not due to the pericarditis itself.
Sleep is disturbed or prevented altogether by the pain and nerv^ousness caused by the inflammation. Children are often fret- ful and restless. The countenance is pale and anxious or expres- sive of suffering. In the spring of 1J>01 I treated a gentleman of fifty-five for sjTuptoms of failing heart, the result of chronic myo- carditis and associated vascular and renal changes. He was tak- ing a course of Xauheim baths and seemed to be getting on very well, when I left town for a few days. Upon my return I re- ceived word that he was very ill and in much pain. I found Mr. H. sitting in a chair looking pale and drawn, and when he spoke it was with a hollow, feeble tone of voice. This was Thursday afternoon. He stated that on the Tuesday morning preceding he had been seized with a dull, heavy pain over the heart, which had not left him for a moment since. He had not slept for two nights, and could not lie down on account of his great shortness of breath. The pulse was 106, weak, inclined to be thready, yet regular. His breathing was not noticeably disturbed so long as he was quiet, but his temperature in the mouth was 101.2° F. Suspect- ing pericarditis, I yet purposely reserved my investigation of the heart for the last and went over the lungs carefully, finding noth- ing more than rales of hypostatic congestion at the posterior bases. Coming to the heart I could detect no change over what had been discovered at my last visit, the Saturday previous, excepting that the tones were much more feeble. The area of dulness did not appear increased.
I was about to give up, in doubt of the nature of the trouble, when I chanced to catch in a circumscribed location over the roots of the great vessels at the left of the sternum a soft brush- ing murmur that had not been there at any of my examinations before. This murmur was systolic and short, not at all like a pericardial rub in rhythm, but upon pressing firmly with the stethoscope I discovered that the murmur entirely disap])earod. This convinced me that the case was one of acute pericarditis, and, knowing the feebleness of the degenerated heart, I believed
DRY PERICARDITIS
58
the attack would prove speedilv fatal. A mustard-plaster, fol- lowed l>v hot fomentations, was ordered, and a nurse was at once secured. At my next visit, four hours later, the pain was miti- gated somewhat, but the patient's condition was manifestly worse. Strychnine^ -^^ was ordered hypodermieally every two hours, and in addition | of morphine with atropine was injected. I left him, feeling that the night was to prove a critical one, and at mid- night I received a telephone message that ilr. II. waf< failing rai> idly, his breathing being very laboured, and his pulse at the wrist too rapid and thready to be counted. A physician living close by the patient was sent at once and began the administration of stimulants, but with no apparent effect, as the patient died two hours later. It was subsequently stated to me that as his condi- tion grew worse tie pain became less. Consciousness was re- tained to tite last. Xo autopsy was held, but I believe that effu- sion l^egan to take place, which relieved the pain by separating the inflamed surfaces, and at the same time overpowered by its pressure the degenerated myocardium, which led to rapid asystolism.
The insidiousness of onset yet intensity of subsequent symp- toms are well shown by the cat^e of Jlrs. B., a Xorwegian, aged twenty-eight, who consulted me in April, 1887, '* for heart trou- ble." Her mother had died of rheumatic heart-disease under my care, and her younger sister had mitral regurgitation, also of rheu- matic origin. Six years previously, after the birth of her only child, the patient had articular rheumatism and was ailing for a year, yet had not ha<l symptoms of heart-disease afterward. In December, 1886, she had rheumatism in right knee, lioth eliM»ws, and left shoulder. Three weeks before coming to me she had begim to suffer from pniXNirdial pains, dyspnma, and jvalpitation, each heart-beat aeeompanicfl by pain, which was increased by deep breathing and lying down.
Percussion occasioned pain, the pain being most marked over the stemiun and adjacent left intercostal s]>aces, from the second to the sixth, particularly in the third and fourth. The patient's face was dusky, the eyes dull, and a systolic pulsation was visible and palpal)le in the pulmonic area. There was slight epigastric pulsation, and the pidse was regular and feeble. The a|)ex'beat was in the fifth left interspace, somewhat too far to the left, quick,
54 DISEASES OF TOE HEART
and accompanied by a feeble thrill. Cardiac dulness was in- creased in all directions, and in the mitral area there was a loud, harsh systolic murmur transmitted to the back. All the sounds, especially the pulmonic second, were sharply accentuated, and over the base of the heart was a triple murmur that by its rhythm and other characters was plainly a pericardial friction-rub.
Excepting retraction of their anterior margins the lungs were negative. Her temperature and urine were normal. The diagno- sis was mitral insufficiency of rheumatic origin, and acute peri- carditis, probably plastic, and also rheumatic.
Patient was sent home to bed and a blister was applied to the pnccordium. At first, after rest in bed, local applications and salicylate of soda, the patient's condition improved, and she was allowed to get up at the end of ten days. In a few days, however, she again took to her bed, and from this time forward her symp- toms steadily grew worse. Cough became very troublesome, with difficult mucous or muco-sanguineous expectoration, and there were anorexia and constipation. The pulse always remained at 120, and as it failed to be slowed by digitalis, the drug was discontin- ued. June 2d there was a sudden attack of acute rheumatism in the left hand and wrist with substernal pain, and temi)erature rose to 102° F. Salicylate of soda gave prompt relief to pain, and as the urine was scanty and acid, the salicylate was discontinued for the bicarbonate of potash, which was administered until the urine became alkaline. June Gth, at 2 a. m., there was a sudden exacer- bation of substernal pain and distress. A pericardial friction- sound now develoi>ed over the body of the right ventricle, chiefly below and to the left of the ensiform appendix. There was great epigastric tenderness and interscapular pain. The anterior mar- gin of the left lung became somewhat more retracted, and the apex- beat now moved nearer to the left anterior axillary line. The patient complained much of i)ain across the front of the chest, along the lines of the diaphragm, from the right inframamillary to the left infra-axillary region. She complained bitterly of pain in the pit of the stomach, and suffered with nausea and vomiting. Jime 8th found patient much distressed for breath and unable to retain food. Epigastric pain diminished, but condition of the heart very much as before. Fever was 102° F. at 8 p. m. Stimu- lants and food in small amounts were ordered. At 11 p. m. there
DRY PERICARDITIS
5fi
were sudden dt^fervescence, and profuse perspiration for the rest of the nigbt. Jnne tUh patient orthopuadc, pnke 138, unetjual, and weak; pain abated; Init patient restless. Examination re- vealed dullness of left base, as high as lower angle of scapula. Ex- pectoration scanty; eongh ahnoi^^t impossible; passed a very bad night; opiates given freely. Jnne 10th, summoned hastily at noon to see patient. Abdomen very distended with gas; breath very short; heart very feeble; carminatives, stimulants, and enemata ordered, but very little relief obtained. Death at 1J}0 i\ M. Treatment throughout tonic, supporting, sedative, and anti- rheumatic.
Autopsy by Dr. EllK^rt Wing nineteen hours after death. The inner surface of the perieardinui was covered here and there with loose tibrous threads, which presented the appearance of tor vlHo- sum, while U[H>n both the anterior and posterior surfaces of the heart Mas an area of recent pericarditis. The sac contained a small amount of serous effusion. The myocardium showed changes of chronic myocarditis, probably dating from the time of the previous attack of pericarditis. The mitral valves gave evi- dence (►f chronic endocarditis that had led to their insufficiency, and showed also the effects of recent endocarditis. There w^as acute circumscribed pleuritis of the left side with about S ounces of sero-fibrinous effusion. In the right pleural cavity were old pleuritic adhesions. The lungs were hypenemic and redema- tons. There was subacute diaphragmatic [icritonitis, also sub- acute splenitis, and passive cougestion of the Hver. Ki<]neys and other organs were negative.
In S4:>rae patients, particvdarly children suffering from acute articular rheimiatisni, there may be marked symptoms pointing to profound disturbance of the nervous system. These are jactita- tions, subsultus tendimmi, cerebral excitement and restleasness, and low muttering delirium.
It must not be suj)posed that all the foregoing symptoms are of a necessity present in any one case of acute fibrinous pericar- ditis, or that they always have the gravity just described. In one patient pain is the chief complaint, another may be annoyed by |>ersistent palidtations, others may manifest no particular disturbance either of tlie heart or nervous system. Unless the pericarditis is associated with inflammation of the endocardium,
56 DISEASES OP THE HEART
dyspnoea is not likely to be marked until the acute inflammatory process gives place to extensive effusion. Respiration may be accelerated, but there is not actual air-hunger.
In many instances, as previously stated, this affection remains so latent that if the physican were to rely for its detection upon subjective manifestations, the disease would surely be overlooked. For this reason the medical attendant should make daily examina- tions of the heart as a matter of routine practice, in all cases of rheumatic fever or other infectious diseases capable of lighting up pericardial inflammation.
CSourae and Termination. — If an acute dry pericarditis is circumscribed, the plastic exudate not involving the whole sac, the activity of the process may speedily subside, and all evidence of its existence disappear in the course of a few days or a week. If, on the other hand, the inflammation is intense, and involves the myocardium, or if the plastic exudate is poured out over the entire organ, the course of the disease may extend over several weeks. In such cases, particularly in children with already existing valvu- lar disease, death is nqt unlikely, or if the patient recovers, he is likely to be left with a damaged heart.
Acute cardiac dilatation is not infrequent, as shoA\Ti by Poyn- ton's statistics. Indeed, all clinical observers of much experience with pericarditis in children have come to look upon dilatation of the heart as a quite general result, and to regard its occurrence with considerable apprehension. The extension of the inflamma- tion to the myocardium is a matter of grave danger, and one that is likely to result fatally. If fibrin be deposited in a thick layer over the entire surface of the dilated organ, it may act as a me- chanical hindrance to the subsequent return of the heart to normal size. This extensive fibrinous exudation results, furthermore, in an adherent pericardium, which will be described in a subsequent chapter.
Physical Signs. — Inspection. — From the very nature of acute fibrinous pericarditis it is evident that no information of more than a merely negative kind can be derived from an ocular examination of the patient. The countenance may express anxiety or suffering, and inspection of the chest may note some disturb- ance of respiration or an exaggerated and rapid heart-beat; but if there be evidence of deranged circulation this will probably
DRY PERICARDITIS
67
be found due to associated cardiac disease, as acute endocarditis, myocarditis, cardiac dilatation, or a chronic valvular defect.
Palpation, — In some eases the hand, or, as preferred bv Rob- erts, the tips of the finders, laid gently on the pra^cordiunij detects a vibration or fremitus, which is the tactile impression proihiced by those conditions that give rise to the pericardial friction-sonnds subsequently to be described. If felt at all, this fremitus is de- tect e<l over the body of the heart, usually in the second or third intercostal space, not far from the left sternal margin. It may, however, in rare instances be detected at different points through- out th«* y>ni*cordium. Unfortunately this sign is not often present, but when it exists, it conveys the impression of ii rubbing or grat- ing of two rough surfaces, a sort of " to-and-fro " or back-and-forth rub, which is not strietls^ synchronous with cardiac systole and diastole. It is this peculiar gliding character of the friction- fremitus which readily enables one to distinguish it from an endo- cardial thrilL Pressure may modify the intensity of this fremi- tus: moderate pressure increasing, forcible pressure diminishing or obliterating it altogether.
Percussion. — In tliis form of pericardial inflammation the out- line of cardiac dulness may only be affected in so far as this dis- ease leads to dilatation of the heart; in other words, percussion reveals nothing characteristic of plastic pericarditis, or that will be of material ser%^iee in arriving at a diagnosis.
AuscuUalion. — In the early stage of acute pericarditis of whatever form, and it may be throughout the entire course of dry pericarditis, auscultation furnishes for the most part our only means of diagnosis. Xornially, the two pericardial surfaces glide over each other without friction and noiselessly. But when one or both of them have become roughened by fibrinous exudation more or less friction of movement is occasioned, and this is de- clared by the so-called pericardial friction -sound.
Before describing this in detail, it may Ije well to state that a pericardial friction-sound has also been detected indepeiideutly of pericarditis. It may be produced by the milk-spots usually found on the inferior surface of the right ventricle, also by con- cretions (Bauer); by dr^Tiess of the serous surfaces (Ct>llin and Walsh); and by viscosity of the pericanlium during an at- tack of cholera fPleischl)* Nevertheless, such facts do not viti-
58
DISEASES OF THE HEART
ate the truth of the sJtatenient tliat in the recognition of the peri- cardial frietion-soimd lies our best and usually our only reliable means of arriving at a diagnosis.
Location of the Pericardial Friclion-munnar, — As this exo- cardial niiirtnurj as it is called in oantradistinction to end<jcarJiul
nuirmurs of valvular disease, is often very circumscribed, it is important to know where it is most frequently and best Iieard. This is generally over the hody of the heart at the origin of the great arteries ujKin which the i)eri- canlium is reflected, or in <*mie cases upon the anterior surface of the right ventricle, very rarely at the apex of the heart. Conseipiently this frietion-snund is audible at the U'ft of the sternum in the sec* ond, third* and fourth left in* tercostiil spaces in the same loi-ality as that in which friction-frcniitus is conmionly felt ( Fig, 14). In some instances of extensive |3ericarditis it is heard at scattered i>oints or throughout the pnecordiuni,
Rht/thm of the Fricfion-muud, — This is the most impirtant feature of the periearditie rub, and the one upon which depenJ- ence is chiefly placed in t!ie interpretation of its nature. It is very variable, but whatever its jx^cnliarity in any given case, it is as a rule not limited fo systole and diastole, as are endocardial murmurs. Instead of being syiiclin»nous with either the first or second heart-sound, or liearing a definite relation to these tones, the i>ericardial rub seems to overlap them or to occur at a time that is wholly independent of them. Thus, according to Skodt , it may accompany, precede, or follow the heart-sounds in what seems to be a sort of hit-or-miss fashion. The rbythni is very ditticult to describe, but when once heard in a tvjiical case is again easily recognised. In most instances the friction-murmur is composed of either two or three parts, and when of but tAvo, baa a to-and-f ro
Fm
14.— Usual Locatioju ur I'xuuakdul Friction Souwd and Fremiti,*,
I
^
DRY PERICARDITIS
or back-and-forth rbytlui), after the manner of a double aortic bruit, but distinguishable from this by its time and quality. The variability iu tlie rhythm of this sound is owing to the fact that the niuti:hened pericardial surfaees are iiKide to rub against each Other eitlier during contraction or relaxation of tlie auricles or during the corresponding phases of the ventricles. Therefore, wlien this friction-inurniur is made up of three parts, one is pre- systolic, produced by the systrde of the auricles, and the other two, of lunger duration, fall in the systole and diastole uf lite \'eutrick*s. Very infrequently, according to liaiier, each side of the heart can produce a systolic and a diastolic rub of different duration, so that each heart-beat may be accnmpanied by four murmurs. Very rarely also a friction-murmur is synchronous with either one or the other heart-sounds, and when this is the case its duration is greater tliaii that of the tone it acconipauies, a circumstance by which its true character can generally be recognised. If in such A case one is in doubt as to whether the nuirmur is exocardial or endocardial, he can generally ascertain its nature by noting the effect of pressure, since this exerts little if any influence upon valvular nmrmurs. Finally, it shoiila be reniemlxi'red that a fric- tion-sonnrt may disappear for hours together and then again be- come audible,
Intenrnty of ike Friction-sound, — This depends upon two con- ditions: (1) the nature of the exudate, (2) the force of cardiac contractions. If the deposit is fresh and semifluid and the car- diac action feeble, the sound of the rub is likely to be indistinct. If, on the other hand, the tibrin is dry and uneven and the lieart is beating forcibly, the friction-sound is likely to be loud.
Qunliiy of the Friction-sound. — This differs in different cases, depending probably ujkui the dryness and viscosity of the fibrin. It may be grating, creaking like leather, crackling like parchment or like the crunching of dry snow beneath the heel, etc*, but in my exf>erience is most often of a soft brushing quality, very dis- similar to the timbre of valvular bruits.
The Effect o' Pressure on (he Pericardial Murmur, — It is usually found that pressure with the stethoscope modifies this friction-sound in its inttmsity if not its quality. Gentle pressure by bringing the r^jughencil surfaces closer together intensifies it, while firm pressure diminishes or obliterates it entirely* It is
60 DISEASES OP THE HEART
sometimes found also that the intensity of the murmur is affected in one way or another by the patient's position, being louder in the erect, weaker in the recumbent posture or the reverse. In some cases also the intensity is affected by respiration, being louder when by forced inspiration the pericardial layers are brought into firmer apposition, and contrariwise enfeebled when separated by expiration. The reverse of this has been observed, however.
There is nothing in acute pericarditis per se to cause abnor- mal alteration of the heart-sounds. As stated by Roberts, either tone may be obscured by an unusually loud and harsh friction- murmur, but in general they are heard through the murmur in those cases in which they happen to be synchronous. When the inflammatory process has invaded the myocardium or has weak- ened it through dangerous dilatation, the cardiac sounds are likely to become feeble, and the first at the apex may be more or less toneless, but there is nothing in this peculiar to pericarditis. Stasis in the pulmonary system is evinced among other things by undue accentuation of the pulmonic second tone, while in conse- quence of the feeble discharging power of the left ventricle the aortic second sound becomes enfeebled.
Diagnosis. — The diagnosis of dry pericarditis is not as a rule attended with insuperable difticulty. In cases in which it is latent or its symptoms are masked by those of the primary affection it may be easily overlooked. In most instances its presence is declared by the history of an antecedent or associated rheumatism, by prax^ordial pain, etc., and by the character- istic rubbing thrill and murmur. When the anamnesis and symp- tomatology are negative, reliance must be placed upon the auscul- tatory phenomena, and these failing, a correct diagnosis is hardly possible.
Differential Diagnosis. — This concerns acute endocarditis, pleurisy, and pneumonia. The diagnosis of acute endocarditis is hardly possible unless valvular murmurs and other definite changes in the sounds and shape of the heart and embolic phenom- ena are detected. The differentiation of endocardia] from exocar- diai murmurs is based on the laws concerning the latter just de- scribed, and as a rule is not particularly difficult if due attention is paid to their rhythm.
DRY PERICARDITIS
61
In acute pleurisy reliance must be placed upon the detection of the characteristic pleuritic rub, and the possible development of pleuritic effusion, since the history and symptoms of a left- sided pleuritis may he very like those of pericarditis. A point of priuie impjrtance is that the pleuritic rub ceases when the breath is held, while that of pericarditis does not.
In pneumonia there are the initial chill, the higher continu- ous fever, painful difficult cough, tenacious rusty sputum, loss of normal pulse-respiration ratio, dulness of one or more lobes, crepi- tant rales, and bronchial breathing, and, lastly^ the termination by crisis after five to seven days.
One would scarcely think that aortic aneurysm would be mis- taken for pericarditis, and yet I recall two instances in which such was the case. A middle-aged gentleman once consulted me because of pain in the upper front chest The only abnormal sign was a faint scratc^iing sonnd in the region of the great vessels not Jaynchronous with either heart-sound. In the absence of other find- ings, I pronounced in favour of hx^alized pericarditis, and yet four months later I discovered in the same situation a well- marktnl aneurysm. The second instance was that of a man in Cook County Hospital who presented a to-and-fro rubbing mur- mur over the base of tlie heart, also not synchronizing with either cardiac tone, no dulness, no pressure-symptoms » and the necropsy disclosed three small aneurysmal sacs surrounding the base of the aorta. They were of about the size of English walnuts, and the swish of the blood as it entered and left the sacs had evidently occasirmed the psend4>»pericardial rub.
Prognosis* — This is always grave, but depends upon the se- verity and duration of the attack. In children with articular rheumatism an acute attack of i>eriearditis, even without effusion, is so likely to set up dangerous <]ilatation of all the cardiac cavi- ties that if the disease is protracted there is imminent danger of a fatal issue. Dangerous weakness on the part of the myocardium is shown by feebleness and muffling of the first sound at the apex, diminution of the aortic second sound, and by a thready and in- termittent pulse. Great derangement on the part of the nervous fivstem is also a sign of danger, even though the life of the patient be not immediately threatened. The remote prognosis is unfa- Tourable, since acute plastic pericarditis may be followed by
62 DISEASES OF THE HEART
effects that will greatly hamper the heart in the future. Firm adhesions at different points may unite the two layers of the pericardium, which, if they do not become stretched, may ulti- mately lead to weakness and dilatation of the right ventricle (Broadbent), or the sac may be boimd down to the heart through- out, forming what is known as synechia pericardii^ the baneful effects of which will be described in a subsequent chapter. Broad- bent has related a case in which the anlema and other signs of persistent venous engorgement throughout the body were found due to fibrous bands which had partly constricted the right auri- cle and led to total obliteration of the inferior vena cava.
Although it is stated that the plastic exudate may sometimes be absorbed, this is a very remote contingency, and should never be reckoned upon as at all likely. WTien the disease is complicated with endocarditis, pleurisy, or pneumonia, or when it occurs in the course of chronic Bright's disease, the prognosis is usually more unfavourable than when it occurs independently or in the course of rheumatic fever.
The mortality of fibrinous pericarditis is not generally con- sidered very great, and yet a study of the 150 fatal cases of rheu- matic heart-disease collected by Poynton shows the erroneousness of this opinion. In 34 of his cases myocarditis was present as secondary to pericarditis and death seemed due to the effect upon the myocardium. Even when the inflammation does not extend to the heart-muscle the heart of a child is very likely to undergo a serious degree of dilatation, and when both these conditions are combined with endocarditis recovery is very improbable. This was well shown in the case of the ten-year-old coloured boy, from whom was obtained the specimen shown in Fig. 18. When seen for the first and only time a few days prior to death, this boy was sitting up in bed on account of diflficulty of respiration and of pain in the heart-region. His illness had begim with rhoumatisni and lasted ten weeks, and he had become strikingly emaciated and his countenance showed marks of patient suffering. The thorax and abdomen were distended from just below the clavicles to the um- bilicus, were unnaturally broad across the loins, and thus filled out presented a striking contrast to the thinness and smallness of the neck and extremities. Breathing was extremely rapid and shallow, and as evinced by the pulse the heart's action was also
DRY PERICARDITIS
63
rapid and feeble. The skiu was dry aud sealj and felt hot, although as a niatter of fact there was but slight fever.
The cardiac iiiiput^se was very feeble, and the apex*beat could not be clearly tJetint^d. Absolute dulness was eiionuouHly in- creased in all diaineters, reach- ing a3 high as the second cosial cartilages, and transversely friiiu at least 2 inches to the righr of the sternnm far be- yond the left nipple almost to the anterior axillary line (Fig. ir»). This gave to the dulnegs a pyramidal shape closely resemlding the outline of the pericanliiTUi distended with rtiiid, but differing from it in the circumstance that the left border of d illness did not pass outside the limits of cardiac impulse. The heart- fiouuds were feeble, and all over the prtecurdium was a hnid, harsh systolic niunuiir, having its greatest intensity in the mitral area and aiulible thrnnghout the back of the chest. No pericardial friction-rul) couhl l>e dis- tinguished, but there was one sound that at first was quite mis- leading.
Beneath the right claviele» and therefore in proximity to the aortic area, was a double blowing sound, having a to-and-fro rhythm of a qnah'ty very like a harsh double endocardial murmur. It was so loud as to obscure the heart-tones, yet, although very rapid, not fast enougli to be generated in the heart, and moreover was audible over the back. So soon as these differential points had been noted it was conchided to he respiratory, and accordingly was found to cease so sixai as the little patient held his breath. The lung-niargins in front were retracted by the pressure of the largf* heart; pulmonary resonance was impaired to right and left of the heart, as well as at the i>osterior base of tlie left lung. There was manifest engorgement of the liver and other abdominal vificera, but there was no ofdema.
64 DISEASES OP THE HEART
In the matter of diagnosis it was not so easy to determine whether effusion was present or whether the enormous area of dulness was due to dilatation, as it might at first seem to be. However, by carefully comparing the left lateral limit of dulness with the feeble cardiac impulse and finding that they pretty closely agreed, it was concluded that the condition was mainly dilatation, secondary to acute pericarditis, and probably also endocarditis, with perhaps a small amount of effusion, but certainly not enough to warrant tapping in the hope of relieving the child's dyspnoea. The hopelessness of the prognosis in such a state of affairs was justified by the fatal issue about a week subsequently.
The autopsy disclosed acute plastic pericarditis, without effu- sion, acute endocarditis, and fatty degeneration of the myocar- dium, and death was probably to be attributed to the state of the heart-muscle.
PERICARDITIS WITH EFFUSION
SerO' fibrinous. — As already stated, a sharp dividing line be- tween fibrinous and sero-fibrinous pericarditis cannot always be drawn pathologically, because, although a pericarditis may remain dry throughout its course, the fibrinous exudate is generally united with an effusion of serum, so that a process which was plastic at first may afterward be characterized by an effusion of a large quantity of serum within the pericardial sac. The two elements of fibrin and serum may be mixed in varying proportions ; in one case the former being abundant, while in another the fluid may contain but an insignificant proportion of plastic material. The amount of effusion in any given case varies within wide limits; there may be 1 or 2 ounces, or the sac may be enormously distended by 1, 2, or more pints (Fig. 16). The effusion generally takei* place gradually, but in some instances occurs with such rapidity that the sac becomes entirely filled in twenty-four hours from the onset of the affection.
Purulent, — In this variety the effused fluid is composed chiefly of pus with but little fibrin, and contains pyogenic bacteria. In rare instances the micro-organisms may be of such a nature that the purulent fluid becomes fa?tid, and the disease assumes a very grave aspect from the onset.
PERICARDITIS WITH EFFUSION
es
Hwmorrhagic, — This form is characterized bv the effusion of Wood into the pericardial sac as a result of the intensity of the process, which iinderiuines the integrity of the pericardial blcK)d* vessels. Or a sero*tibrinoiis effu- sion may lK*eouje deeply blood- stained through hiemorrhages from juinute vessels.
These three varieties of effu- sion may be looked upon as differ- ent iiuuilfestations of one nnd the sanio procesSy having tlie same pathology, and differing only in the etiology and intensity of the inflammation*
Symptoms. — These are to be diviiled, according to the stage of the process, into ( 1 ) those that at* tend the onset, and which are chiefly inflammatory in their na- ture; and (2) those that result from mechanical distention of the sac, which are, therefore, symp tonis of pressure on the heart and neighWmring viscera. Further- more* the three kinds of effu- sion !>h<jnld lie tlieoretically distin- guished one from the other by the severity of their symptoms — that is, of their constitutional effects; as a matter of fact, however, there is often nothing in the symp- tomatology that declares the nature of the exudate.
The phenomena attending the early or ijtflammatory stage have been described under Dry Pericarditis, and therefore we may pass at once to the consideration of the symptoms due to fluid aeeumulation in the sac.
As effusion takes place it gradually distends the sac from below upward, and, separating the roughened and inflamed peri- cardial surfaces, causes a cessation of the ]*ain attending the onset of the affection. The fever of the inflammatory stage still per- sista, however, as may also the cough. With distention of the
Fio. 16. — Capk Mr i^£iticAllDlTtii tlf WHICH TfiE Sac goktaiked S|^ Poinds of Fluid. (Bramwell.)
66 DISEASES OF THE HEART
sac, the symptoms due to active inflammation gradually merge into and are subordinated to those occasioned by pressure. When the amount of exudation is small, symptoms of active inflamma- tion may still predominate, but when it completely fills the sac, reaching, it may be, one or more pints, pressure-effects assert them- selves, and may even become dangerous.
Children impress me as complaining less of these effects than do adults, yet, of course, individual peculiarity largely determines the amount of complaint upon the part of the patient. I have seen children with an enormously distended sac who yet uttered no word of complaint and whose silent suffering was truly pa- thetic. They are usually restless, however, and display fretful- ness when disturbed. In many cases their patient fortitude as regards subjective symptoms presents striking contrast to the objective evidence of circulatory and respiratory embarrass- ment.
The face is pale and anxious, or there is congestion of the cutaneous vessels, producing a blue-white appearance, and the veins of the neck are turgid. The pulse is small, rapid, and of low tension, which gives it a degree of abruptness that may make it somewhat resemble the sudden pulse of aortic incompetence. Some writers describe the jnilse in the stage of effusion as larger and fuller than would be expected from the feebleness of the heart- sounds. Marked irregularity, and even intermittence, are some- times observed, particularly after the effusion has persisted for a considerable time. Such arrhythmia coming on late is a sign of danger, since it i)oints probably to failure of the heart-muscle. It should not be forgotten, however, that irregularity and inter- mittence of the pulse may be present from the beginning of the pericarditis, when this latter is associated with a valvular defect, in which ease it is not to be attributed to the pericardial effusion or inflammation.
The disturbance of the circulation everywhere evinced is a direct result of pressure on the heart by the abundant effusion. Not only does the heart have to sustain the weight of the super- imposed fluid, but when the effusion is great enough to distend the sac, it is confined under high tension and forced, therefore, to press inward on the heart. According to Sibson, the thick- walled and powerful ventricles are better able to withstand such
PERICARDITIS WITH EFFUSION
67
pressure than are ilie thiii-wallt?d auricles and veins, which con- sequently have their enpaeity tliniinished. There is actual me* ehanical impediment to the inflow of blood into the right heart, and likewis^^e to passage of the stream out of the pulmonary veins into the left auricle. Thus are produced the smallness and weak- ness of the radial pulse with fulness of the systemic veins.
This is not all of the presaure-effectiij however. The distended pericardial sac take^ up more room than it did prior to the ctTu- sitm, and cousetpiently it exerts pressure on the adjacent viscera. It pushes aside the elastic lung-borders ; and as the heart lies more to the left than to the right of the median line, it is the left lung that feeis the greater pressure. The lower lobe^ therefore, ia shoved backward to make room for the distended perieardiunij consequently the patient suffers froui respiratory embarrassment more or less iiranoiince^L Xt*t only are the respimiions acceler- ated and shallow, but the i>atient is compelled to sit up in bed to breathe (orthopua*a)» or in some instances to lean forward with his elbows on his knees, so as to allow of as much gravitation of the sac away from the lungs as is |)ossible under tlie circumstances* No doubt that carl)onie-aeid intoxication resulting from the me- chanical im|iedimeut to respiration also plays a part in the pro- duction of dyspmva*
Insmnf}ia is often a very troublesouie symptouj, and seems to be due not only to passive cerebral congestion, but also to the patient's dyflpntea, which renders it impossible for him to lie down, or speedily arouses him when so fortunate as to fall into even an uneasy sleep.
There is usually anorexia ; not only has the patient no appe- tite, hut the tlyspncea and dysphatjia render the taking of food difficult, and children often turn away from it when proffered*
The urine is scanty, the abdomen is distended both from re- tention of gas in the bowels and from congestion in the portal system. The liver is turgid in consequence of meelumteal inter- ference with circulation through the lungs, and is more or less tenfler; there may he constipation or small frequent watery stools, because of serous transudation into the intestines from the en- gorged vessels within their walls. T have always lo<:»ked upon this fliJirrhtea as Xatnre's effort to unload the di^rended vessels, and therefore as a very valuable therapeutic hint* If the disease be
68 DISEASES OP THE HEART
protracted, and venous congestion very marked, there may even be some oedema of the lower extremities.
Fever is of variable intensity and character; it is likely to abate somewhat as the active inflammatory stage passes into that of effusion, and if this latter stage persists for some weeks the temperature usually returns to normal, or nearly so.
The symptoms of pressure as above described usually manifest themselves gradually, but appear suddenly in those cases in which the sac becomes rapidly filled. The gravity of the symptoms usu- ally bears a direct relation to the amount of effusion. WTien this is small, but 2 or 3 ounces, or when it takes place insidiously in the course of cachectic diseases, symptoms may be entirely latent.
When the i)ericardial effusion is purulent^ the gravity of the symptoms depends both upon the amount of the exudation and the kind of micro-organisms concerned in the process. It is in this form that the sac often reaches its greatest degree of disten- tion, and since the degree of mechanical interference with both circulation and respiration accords with the amount of effusion it requires no further comment.
Scarcely had the foregoing been penned when I was asked to see 2 cases of acute rheumatic pericarditis in children, which illus- trated so well certain features of similarity, and yet of contrast, that I have decided to narrate them here. A girl of twelve years, seen with Dr. F. S. Johnson, gave the history of a severe attack of inflammatory rheumatism five years previously involving several joints, but the heart was said not to have been affected. She after- ward had two mild, rheumatic attacks, of which the last was a year ago. During the past summer and fall the patient was thought by her parents to have been remarkably well. About four weeks ago she had an attack characterized by mild fever, coated tongue, and slight jaundice, but no distinct rheumatic symp- toms. Ten days ago she was allowed to attend the opera and eat freely of candy, after which the symptoms of two weeks earlier returned with greater intensity.
When Dr. Johnson assumed charge of her case he found the patient with mild intennittent pyrexia, ankles and knees painful, but not red or puffy, slight prjecordial pain, great nervousness, restlessness, and so much cutaneous hypenesthesia, as well as pain, that a very thorough examination of the chest was not possible.
PERICARDITIS WITH EFFUSION
69
He found weak, rapid, but regular pulse, 120 to 130, and respira- tions of 60; great increase of both absolute and relative cardiac dulnesSj particularlv upward and to the left; a loud systolic mur- mur throitghout pra^Hirdiuni, but most intense at apex, together with a shtjrt presystolic murmur limited to a small area within and above the a|)ex-beat.
The upex-beat was in fifth space outside left nipple, heart- sounds were everywhere audible, pulmonic second banging and split. A pericardial friction-sound existed at the base, over right auricle. Left lung was compressed and the liver palpable just abcjve the level of the nmbilicns. There was no dropsy, and the urine was negative.
The case was regarded as one of acute rheumatic pericarditis supervening upon a combined mitral lesion, and having led to great general dilatation of the heart Three days later tempera- ture was 102^ F., pnlse 120 to 130, but regnlary and respira- tions 60 to 80. Patient was in evident distress, complaining of pain in the heart abo%*e the left nipple, She also had great diffi* cnlty in swallowing. A -^ grain of morphine gave her a fairly csomfortable night, and the morning when I saw her the condition was as follows: Patient lay nearly flat in bed, several joints of botli lower and upper extremities anointed with a liniment con- taining oil of wintergreen and swathed in bandages. She was excitable, fretful, and inclined to cry out when touched. There was no cyanosis, but respirations were shallow and rapid, flO or 80 to the minute, the pulse of fair volume, but dicrotic, was about 120, perfectly regular. The abdomen was distended and tym- panitic, tense and painful in the region of the liver, which could be made out extending nearly to the level of the nmbilicns. The heart's apex was visible and palpable, though rather weak and diffus^ed, in the fifth left interspace outside the nipple-line. There was no pericardial fremitus, hut the cardiac impulse was diffused from apex to base and froni left mamillary line to tlie sternum.
Cardiac dulness, both superficial and deep, was increased transversely, but clu'efly to the left, the deep limit reacliing nearly to the anterior axillary line, but not extending outside of or be- low the palpable impulse of the apex. A harsh mitral systolic murmur was everywhere audible, as were also both sounds, the pulmonic second being greatly intensified and split. Over the
70 DISEASES OF THE HEART
body of the sternum pressure with the stethoscope brought out a soft rubbing murmur, which, from its quality and rhythm, was easily recognisable as pericardial. The inferior boundary of car- diac dulness was not depressed ; indeed the abdominal distention occasioned an elevation of the heart.
This high position of the liver caused the upper margin of hepatic dulness to reach the level of the fifth right costal cartilage and interfered with the determination of the presence or absence of Rotch's sign. It seemed to me, however, that the outer border of the right auricle lacked its natural cur\'e do\vnward and inward, and that the line of dulness joined that of the liver at nearly a right angle. The pain which change of position caused the little patient, rendered examination of the back of the chest inadvisable. The doctor stated, however, that the day before he had found dul- ness with corresponding alteration in the breath-sounds at the left posterior base.
The diagnosis was acute rheumatic pericarditis with great cardiac dilatation and possible acute myocarditis supervening upon a previously existing endocarditis that had led to mitral in- sufficiency. Distinct signs of effusion were not obtainable, and hence it was concluded that the exudate was fibrinous, or if united with serum, the proportion of the latter was not large. The ex- tensive dilatation present was attributed in part to the mitral lesion, and in part to the dilating influence of the pericarditis, whether associated with acute myocarditis or not.
The symptoms in this case were not distinctly those of pres- sure; respiration was greatly accelerated, to be sure, but there was no cyanosis, no downward displacement of the liver, and no orthopnoea; in short, the symptoms pointed more to disturbance of the nervous system, with consequent rapidity of breathing, than to circulatory embarrassment. The very considerable hepatic en- gorgement could be very reasonably referred to the free mitral leak and the greatly overstrained right ventricle. This patient ultimately made a good recovery.
On the same day on which I saw the preceding patient. Dr. Jo- sephson asked me to visit a little girl of six, who was also suffer- ing from acute pericarditis. She had passed through an attack of scarlatina in the July preceding, and for the past three or four weeks had been suffering from acute articular rheumatism, which
PEEICARDITIS WITH EFFUSION
n
was still present wlien she eanie nntier the doctor's charge eight days before my visit. He had at once recognised an acute inflam- matory affection of the heart. Her somewhat fluctuating tempera- ture had averaged ahout 102^ F,
The child's condition when I sa^v her was as follows: She was sitting in hed, not even venturing to rest against the pillows, breathing 0<> or more times to the minute, and during the forenoon of that day her respirations had actually been iH} to the minute* The pulse was very rapid, small, and tlicrotic, but perfectly regu- lar. The expression one of patient suffering. Upon removal of the clothing the skin was found hot, dry, and scaly, yet broke out into a perspiration a few minutes afterward upon the child making a little exertion. There was every evidence of capillary and venous congestion. The abdomen was distended and hard, particnhirly about the waist-line; the thorax was evi- dently distended to its utmost capacity, the entire front of the chest bulging, and the in- tercostal spaces more or less smixjthed out. The apex-beat was feebly palpable below and a little to the left cif the nip- ple, and there w*as diffused systolic shock over the body of the organ. Absolute cardiac flatness (Fig. 17) began at the right nipple, passed upward to the lirst interspace, then downward and outward into the left axillary region, well outside of the visible an<l palpable apex-beat. Its lower boundary reached at least to the eighth eustal cartilage^ and the distended sac could be felt in the ei>igastrium. A rough, blowing systolic munnur was %'ery loud in the mitral area to the left, w^hile the heart-sounds were loud over the base of the organ, the pulmonic second being very banging and slightly split. From the middle of the sternum down- ward to the ensiform was a grating pericardial friction-sound, which had a simple t<>and-fro rhytlmi not synchronous with either
Fio. 17,— AuffoLiTS Dt'LNBM, Ca»k or Perk^ariktis with Erfvstoiv,
72 DISEASES OP THE HEART
systole or diastole. At the left base, posteriorly, was a dull patch corresponding with Ewart's dull patch in outline, but the harsh, very hurried breath-sounds were everywhere audible. In front, resonance was impaired beneath both clavicles, and the sense of resistance imparted to the finger upon percussion of the praecor- dium was remarkably intense.
In this case the diagnosis was also acute pericarditis, but, unlike the foregoing, there was a massive exudate, occasioning very grave pressure-signs. There was also present the same valvu- lar lesion, mitral regurgitation, but there was very strong suspi- cion of the existence of acute endocarditis, since from the history of scarlet fever in Julv, with more or less rheumatism subse- quently, with no other previous etiological factor, it was not likely that the mitral disease dated back more than six months.
Deglutition gave this little sufferer so much distress that she would hesitate for minutes together before making up her mind to take the proffered medicine or nourishment. In this case the urgency of the s\Tnptoms arose from pressure. Dyspnoea was so great that the little thing begged to be allowed to stand up, evi- dently to relieve the thoracic organs, already much compressed, from still greater pressure by the abdominal viscera forced upward against the diaphragm in the sitting position.
The contrast presented by these two cases was most instructive. In this latter case paracentesis pericardii was advised without delay. It would have been cruel, if not useless, to postpone the operation imtil trial had been made of cathartics and diuretics. Far better tap first, and administer these afterward.
Suppurative perkarditis generally occasions phenomena of sepsis, but chills, fever, and sweating are sometimes said to be absent (Roberts). When present they are an indication of sepsis, and as such may be a part of the symptomatology^ of the primary affection as well as of the pericarditis. When the effusion is foetid, as rarely happens, septic symptoms are most marked, and pros- tration comes on early and is extreme. In some cases there is nothing in the nature of the s\Tnptonis whereby one may deter- mine the purulent character of the exudate.
The symptomatolog;v of hcvmorrhagic pericarditis depends upon the rapidity with which the effusion takes place, rather than upon its nature. A ha?morrhagic effusion into the pericardial sac
PERICARDITIS WITH EFFUSION
during the course of scorbiitiis, for example, may take place so suddenly that s^Tuptoms of pressure and of antpmia rapidly de- velop. In other cases the effusion is slowly produced, and syiup- toms manifest themselves gradually or are entirely absent.
In Ebsteiu's two cases the symptoms were those of pressure, cyanosis, dyspna*a, cough, and pain, hnt in one the condition was thought to be extreme cardiac dilatation, and its true nature was not recognised until at the autopsy. Although in the secotnl ease pericardial etfusiun Avas recognised during life, there was nothing in the symptoms to point to the hiemorrhagic character of the exudate.
Course and Termiiiation. — There is no uniformity in the clinical history of pericarditis with ctfusion. Cases vary ^videly from each other in the mode of onset, in the course they pursue, and in their mode of termination. An ordinary case occurring during a rheumatic attack may be expected to terminate by absorp- tion in two to four wrecks; this happy event may very rarely take place within a few days, the disease having passed through the suc- cessive stages of inflammation, effusion, and absorption in less than a week. In other instances the affection manifests a strong tendency to become either subacute or chronic. While in others, again, the disease is characterized by phases of partial absorption and improvement, which are each in turn followed by a recurrence of inriamr.iation and increased effusion (Bauer), until at length the patient is worn out by the persistent and obstinate nature of the disease. These varintifins depend, no doubt, upon the activity of the etiological agent, and are not at all surprising, for, as every one knows, no disease presents uniformity in its clinical phenomena.
Other conditions besides the activity of the pathogenic agent lalso detennine the course and severity of an acute pericarditis. Its occurrence with or as a sequel to pleurisy or pneumonia is also likely to influence its course and termination, in accordance with the intensity of these latter processes and the degree to which they have undermined the patient's resistance. When pericarditis is the result of chronic nephritis it is very likely to nm a slow and latent course.
In children with inflammatory rheumatism the disease is apt to prove itersi stent, and if it does not destroy life by invading the myocardium, terminates in complete or partial synechia pericardii-
74 DISEASES OF THE HEART
Suppurative pericarditis is a very serious affection, manifest- ing but little tendency to spontaneous recovery. It is stated, how- ever, that if the pyogenic bacteria be not very virulent, and if life be prolonged for a considerable time beyond the stage of active inflammation, absorption of the more liquid portion of the exu- date may take place, the residue becoming cheesy and in time in- filtrated with lime-salts. They are eventually transformed into calcareous plates, which may even be so extensive as to inclose the heart in a case of bone-like hardness. I have observed two such cases; in one a calcareous plate the size of a silver dollar was found on the anterior surface of the left ventricle, while in the other, masses of lime completely surrounded the organ. This latter case will be described in the article on Adherent Pericar- dium. Most cases of purulent pericarditis, unless relieved by sur- gical interference, pursue a rapid course, and patients succumb more or less speedily to the effects of py»emia, resulting either from the pericardial or primary affection.
In the form of hsemorrhagic pericarditis, which occurs in the course of scurvy and is observed in the maritime provinces of Russia, the effusion often takes place with great rapidity and destroys life in one or two days. In these cases death seems due in no small measure to the rapidly induced ana?mia.
Finally, the course of acute pericarditis with effusion is deter- mined not alone by the intensity of the inflammation, but by the amount of the exudation. If this is sufficient to greatly distend the sac, its absorption is hindered by the tension thus occasioned. In some instances, no doubt, a pericardial exudation is absorbed, and no permanent ill effects remain.
Physical Sig^ns. — Inspection. — The degree of information afforded by inspection dei)ends uix)n the amount of effusion and the conditions residing in the chest-walls. In a child of tender age or a person with a yielding chest-wall a comparatively small pericardial effusion may occasion perceptible prominence of the pra^ordium, while if the thorax is voluminous, and the costal car- tilages have become hard and inelastic from age, it is possible for even an enormously distended sac to produce no visible bulging of the cardiac area. As a rule, however, more or less prominence in this region is observed, while the intercostal spaces look filled out, and the skin covering them appears tense and shiny. The apex-
PERICARDITIS WITH EFFUSIOX
75
beat is not visible, or but faintly so> and cardiac impulse is feeblj diffused or wanting. The aiM?x-beat, luoreover, if visible, may be situated lower tlian normal %vlien the liver is depressed by a mas- sive effusion, and in sueh a case there nniv be bulging of the epi- strium.
\ Cyanosis and distended veins give evidence of circulatory dis- turbaneej while respiratory embarrassment is evinced by hurried breathing and restricted movements of the chest. If copious effu- sion occasions great pressure, and j>artieularly if tliis has formed rapidly, the attitude of the patient and the expression of his coun- tenance betray suffering and it may be oppression.
Inspection is an aid to diagnosis, but cannot solely be relied upon, since pra'cordial bulging in children may be the result of cardiac enlargement without pericarditis.
Palpation. — In great effusion the roughened pericardial sur- faces are removed from each other, and hence rhe hand no longer detects the peculiar fremitus present in the beginning of the pro- |>oe68, when the exudate is fibrinous and not serous.
Otherwise pal]>ation serves chiefly to corroborate the result of lnsp€M:tion. The |>ni'cordial area may impart a sense of increased 'resistance from internal pressure, and the normal intercostal de- pressions are found obliterated. Rarely there is fluctuation. In- creased resistance and tension may also be detected in the epigas- trium. Older writers w^ere acctistomed to attach great importance to an elevation of the apex-beat, which they explained by lifting of the ai>ex of the lieart by the effused liquid. Roberts, Ewart, and others regard this as erronc^ous, believing that what was thought to be the apex-beat is, in fact, the iminilse of the body of the heart as it is thrown against the anterior chest-wall by the collection of fluid belli nd, the apex of the organ being at the same time moved backward and to the left. In cases of extreme effu- sion the depression of the diaphragm, occasioned by the heavy sac, lea*ls to an actual lowering of the apex-beat (Bauer). The peri- cardial fremitus present during the inflammatory stage disappears w^ilh the occurrence of effusion. In sonie cases the head of the left clavicle is said by Ewart to be elevated so that the first rib can lie felt all the way to the sternum (*' first-rib sign '*).
The most striking character of tlie ptdse is its want of tension. It is rapid and may be regular or irregular, even intermittent. In
76 DISEASES OP THE HEART
some instances pulsus paradoxus is present. This is an inversion of what is usually observed during the two acts of inspiration and expiration. Instead of becoming stronger and fuller at the end of inspiration and the beginning of expiration the pulse becomes small and weak, or may even disappear during deep inspiration, becoming again stronger and fuller toward the end of expiration and the beginning of the next ensuing inspiration. Pulsus para- doxus is inconstant and is not pathognomonic w^hen present, and possesses therefore only a negative value.
Percussion. — This method of investigation furnishes the only reliable sign of pericardial eifusion, since by this means one is often able to determine the presence of so small an amount as 100 cubic centimetres (Bauer), 150 to 200 cubic centimetres (Aparti and Figaroli). That one may understand why so much reliance is to be placed upon percussion, I will consider for a few moments in what way pericardial effusion alters the normal relation of the parts and modifies the area of cardiac dulness.
The pericardium is a closed sac, which is thrown around the heart, being wrapped about the origin of the great vessels above, and attached to the central tendon of the diaphragm below. \Mien fluid is eflFused into this closed cavity it sinks to the most depend- ent part, and then creeping upward distends the sac in all direc- tions, pushing aside the anterior borders of the overlapping lungs. The area of absolute cardiac dulness now becomes altered in a striking manner (Fig. 17), and to an extent commensurate with the amount of effusion. Some authorities consider that this alter- ation of cardiac dulness corresponds in shape with that of the dis- tended sac (Bauer, Sibson), while others attribute it chiefly to the crowding aside of the lung-margins (Duchex, Rotch). My own opinion is that the configuration of this area depends largely upon the anatomical arrangement of the hmg-borders overlapping the heart, since when thev become retracted by adhesions and in cardiac dilatation, the shape of the resulting dulness is essentially the same, though less extensive, as in pericarditis with effusion. Probably both factors, the shaj>e of the sac and the arrangement of the lung-borders, are responsible for the peculiar outline of the area of dulness observed. This area of absolute dulness or flat- ness is variously described as triangular, pyramidal, pear-shaped, or pyrifomi, that of a truncated cone, or " that of a bag of fluid
PERICARDITIS WITB EFFUSION
77
spreading out at the base " (Ewait). Its broad base rests upon the diaphragm, while its rounded apex occupies the tipper sternal ^region, A glance at Fig. 17 shows that the direction of the two gide-lines is not the same, heiiig rather more vertical at the right Tlie right arm of this irregular triangle is shorter and straighter, while the upper or left boimdary presents an indentation or con- cavity soon after leaving the apex, and, sloping gradually down- ward, joins the base-line at a rounded somewhat obtnse angle.
The shape of this area is by most authors considered very char- acteristic, although Shattnck is of the opinion that the peculiar feature is not the form, but the fact that the dulness spreadia out in all directions. Kosenbuch lays stress on the increase or movabil- ity of dnlness to the right when the patient lies on his right side.
Although Bauer agrees in the statement that the flat area of pctricardial effusion may be recognised by its characteristic pear- shaped ouUinCj he nevertheless expresses the opinion that more importance should be attached to the surrounding zone of relative dulness^ " since, indexed » the absolute cardiac dnlness not uncom- monly in cases of well-nuirked effusion shows little or no altera- tion."
In cases of extreme pericardial effusion the base of this fiat area may extend nearly across the anterior surface of the chest, from within, or in some cases even outside the right mamillary line, to a variable distance outride the left mamillary or to the left anterior axillary line* In consequence of the depression of the left IoIk} of the liver caused by the weight of the distended sac, the inferior margin of this area may reach as low as the sixth, or in extreme cases even the seventh left intercostal space, while its broad conical apex may extend as high as the level of the second costal cartilage or the first interspace.
WTien this flat area has attained such proportions it is usually not diflicult to determine the nature of the case. Yet, since a greatly dilated heart may also crowd aside the lungs and occasion a similar extension of the area of cardiac dnlness, error can only be avoided by attention to the following points: (1) \\nien the y>ericardial sac is distended by fluid its left latero-inferior bound- ary extends beyond the situation of the apex-beat, and hence this latter, as determined by auscultation, is found situated within and above the extreme left lower angle of cardiac dnlness. In dilata-
78
DISEASES OP THE HEART
tion of the heart, on the other hand, it is the organ itself which determines the diilnes^, ami therefore the apex-beat corresponds with the outer and lower limit of cardiac dnlness* Leube lays great stress on this point in the differential diagiiosis of these two conditions, (2) In cases of pericardial effusion the line of de- marcation between the arr^a of Hatnet^s and snrronnding pulmo- nary resonance is verv abrupt, while in cardiac dihitation the transition froin tiatness to resonance is much less prononnced. Bauer and Sansom both attach great importance to the abruptness of this transition in cases of pericardial effusion. At the same time one should not forget the fact that oeeasionally the distended sac may be overhq>i>tHi Ijy the kings, and Tlieref*tre absolute dnlnesa may shade off rhrough a surrounding ;:one of comparative diilnesa into full jKilnionary resonance.
When perieardial etTnsiun takes place the first change notice- alfle upon percussion is the development of a small triangular area
of <lnlness in the fifth right in- tereartilaginous space, or, as the (iennaus term it, in the ranlio'kepaiie angh (Fig. 18), 111 is sign, first described by Rntrb, and sometimes called Iiolrh\s sltjn, is due to the fact tliat when effnsiun collects it tirst distends the sac at its knrer right corner^ occupying The space between the curved inferior margin of \W heart and the upper line of hepatic dnhiesH immrdiately to the right of the lower end of the sternum. Ewart and Ebstein have also directed attention to the occurrenee of this small triangular dull patelu
Xornuilly, the outer bound- ary of cardiac dulness over the right auricle presents a curved line, passing from the level of the third costal cartilage downward and outward, and, after crossing the fourth cartilage, passes in-
Fio. 16. — EoTcn^i Siosr of Beoittxitco F*KRtcARxiUL ErrisioK.
Dq1u«m in sbaeieti urea or cnrdlo-heptttic ang te r c. d,, cunlJAC dulnens ; h. d,^ hopfttio
k
PERICARDITIS WITH EFFUSION
ward as well m downwanl to join the inferior margin of ttie right ventricle. (See Fig. 2.) In the formative stage of pericardial effusion, on the contrary, the right border of heart-dulness is no longer curved, but pas.ses directly downward, joining liver-dulness at an abrupt angle. Rotch's sign is therefore of great value in determining the beginning of pericardial effusion.
One occasionally sees statements to the effect that an altera- tion in the extent of cardiac dulness depending up>n the patient's position makes strongly for pericarditis with effusion. This is nevertheless a very untrustworthy sign, since, if the heart is greatly enlarged, it may fall away from the anterior chest-wall in the dorsal decubitus with consequent diminution of cardiac dul- ness, and in the erect posture again approach the anterior parietes and occasion a corresponding increase in the heart's area» No inconsiderable danger of fatal syncope sometimes attaches to the patient's change of jwsition from tlie rt^umbent to the erect, and since the sign just allnded to is of but slight value, one is hardly justified in thus subjecting a patient with jiericarditis to the risk of sudden death.
AuscuUatmn. — As a rule, the jvericardial friction-sound of the first stage disappears with the occurrence of effusion, to reappear after absorption has again allowed the roughened pericardial sur- faces to come in contact. Xevertheless all writers agree in stat- ing that the persistence of the frictinn-suuud is not incompatible with a considerable amount of fluid, even as much as a quart (Cejka)^ in the pericardial sac. The explanation of the non- disapi>earance ui the friction-sound in such cases is found in the presence of adhesions over the IkkIv of the heart, which prevent the separation of the epicardium from tho pericartliura, and force the fluid to ihe de|>endent |iarts surrounding, or in failure of the sac to be completely filled. In other instances the friction-sound becomes faint when not %vholly inaudible.
Any alteratirm that takes place in the heart-sounds affects their intensity rather than their quality, since they have to Ive trans- mitted to the ear from a distance proportionate to the recession of the heart from the chest-wall and through a layer of fluid. If the effusion is mass:ve and fills the sac to its utmost capacity the cardiac tones may l>e inaudible, but this is so rare that I have never observed a case in which they were wholly absent. In most
eo
DISEASES OP THE HEART
cases the eounds at the apex are feeble, but not wanting, while at the base they are heard more clearly. The pulmonic second sound is accentuated and the aortic sound is diminished.
In a recently observed ease of extensive pericardial effusion in a ebild tlie cardiac impulse, the sounds, and a previously ex- isting endocardial murmur all remained distinct over the lx)dy of the organ, and were attributed to t!ie presence of adhesions that had forced the tluid to the side of the sac.
Secondary Physical JSigns lie fe table to the Lungs. — ^ Valuable information of the existence of pericardial effusion may also he obtained by exainiuation of the lungs. The retraction and com- pression of pulmonary tissue iKx^asions a loss of normal pulmonary resonance in the neighbourhood of the sac. In the left infra- clavieidar region percussion elicits Sk<Mlaic resonance^ or if the compression be very great, impairment of the note. Both Pins and
Ewart have called attention to certain changes discoverable by ]>ercussion and nuseultation at the posterior base of the left lung. The " Pins' sign " is dulness and bronchial breath- ing in the left infrascapular region^ which, upon the pa- tient leaning forward, give way to t'vmpanitic resonance, crepitant rales, and finally vesicular breathing. This dul- ness and bronchial breathing can bardly be attributed to ]iteuritie effusion, if one bears in mind the curved npjier line of the dulness in this latter affc*ction.
Ewart has described a pos- terior patch of dulness in eases of extensive pericardial effusion situated at the base, and which, extending from the spinal column outward nearly or quite to a line corresponding with the internal border of the scapula, turns abruptly upward at a right angle, and, after reaching the level of the ninth or tenth dorsal spine, agaiu
Fit*, n^. — Location or Piliionaby Changes iif Pisfs^ (P) AKii EwAKT^ {Ef Signs
OF PlXlGAHtltAL EfruSlOX
PERICARDITIS WITH EFFUSION
81
turns sharply inward to reach the side of the vertebral column (Fig. lU ), Over this patch breath-sounds are wanting and voice- sounds are feeble. Occasionally a similar dull area may be found to the right of the spine. Ewart attributes this sign to *' altered dorsal relation of the liver/' Immediately below and to the left of the tip of the left aeapula, especially in children (Sansoui), is a dull patch of about 2 inches diiuneter, in which are bronchial breathing and bronchophony or iegophony. Ewart haa
i also directed attention to a somewhat inconstant sign consisting of a small area of bronchial breathing in the right mamillary line, between the right nipple and the upper surface of hepatic dnl- ness.
Diagnosis* — As a rule it is not difficult to determine the ex- istence of pericardial exudation when this is abundant, but it is not easy nor always possible to determine its nature. If the peri- carditis arises in the course of articular rheumatism, and signs of distention of the sac present themselves, the exudation is probably sen>-tibrinoiis. Of 324 cases of fatal ]ieriearditis occurring at the Berlin C'harite between 1806 and 1^70, and which were analyzed by Breitung (Eielihorst), serofibrinous was fotmd 108 times, as against 24 of purulent and 30 of ha^morrhagic exudation. Fur- thennnre, the nature of the primary affection to which the peri-
'carditis is attributable is of diagnostic sig-nifieance, since it is likely to detenu itie the nature of the exudate. If the inflamma- tion occurs in the course of septicirmia, or results from extension of empyema, or from the perforation of a gastric ulcer, from a perforating wound, etc., it is likely to be purulent. The appear- aiice of distinct septic phenomena, rigors, and an irregular inter- mittent fever, profuse jierspirntions, great and rapidly increasing prostration, a dry, coated tongue, diarrha'a, etc, warrants the diagnosis of pyopericardium.
If signs of fluid distention of the sac develop rapidly in the course of scorbutus or purpura ha^Diorrhagica or some other dys- crasia, as cancer, and particularly if accompanied by pronouncrd and rapidly increasing anaemia, the probability is in favour of a ha^morrhagic pericarditis* Inasmuch, however, as such theoretical distinctions in the svTuptomatology of the three varieties are not ttlwavB elearly defined, a differential diagnosis is often only possi- ble by means of exploratory puncture.
Mm
82 DISEASES OF THE HEART
Differential Diagnosis. — Before considering the differentia- tion of fluid-collection within the pericardium from certain other conditions with which it may be confounded, it is well to speak of the difliculty of diagnosis arising from pulmonary emphysema and old adhesions that date from a previous attack of pericarditis. Emphysema may prevent the lung-margins from being crowded aside, and hence the characteristic area of cardiac flatness may not exist. In such an event reliance must be placed on the outline of deep-seated dulness, and this failing, absolute diagnosis is hardly possible. When old adhesions exist over the front of the heart they force the exudate to accumulate at the sides and bot- tom of the sac or to be pent up posteriorly. Accumulation of fluid along the lateral and inferior margins causes increase of dulness in these situations, its triangular outline being fairly well main- tained. In addition, the cardiac impulse and tones, together with the friction-rub, remain both palpable and audible over the body of the organ.
When effusion is confined to the posterior aspect of the sac its recognition is most diflicult, if not impossible. In such a case one must rely mainly on the symptoms of (1) inflammation, as pain and fever, and (2) of a deeply situated collection of fluid and pressure on the (esophagus and bronchi, dysphagia, and dyspna?a. The last two symptoms are very suggestive of exudation into the posterior portion of the sac. !Massip calls this an Encysted Peri- carditis with retrocardiac effusion, and says its s\Tnptoms are so obscure that one can do no more than diagnose the pericarditis without being able to decide whether effusion is present or not. He thinks that dulness at the left posterior base with muffling or absence of heart-tones in this region, together wuth signs of pres- sure on the a^sophagus and of active pericardial inflammation, are strongly suggestive of a posterior effusion.
Dilatation of the heart is the condition which most often has to be differentiated from pericardial effusion. The enlargement of the organ causes retraction of the lung-borders and an area of dulness very like that of effuiriion, and if the heart-tones and im- pulse are very feeble, from fatty degeneration, a precise diagnosis may under certain circumstances be extremely difficult. The main point on which reliance is placed is not, as sometimes stated, greater distinctness of heart-shock and sounds in dilatation as
PERICARDITIS WITH EFFUSION
83
with effiisioHj biU is the position of the aiiex-beat wiib relation to the outer and inferior margin of dnlness (see page 77). Theoretieallv this is very tine, h\it every experienced clini- cian knows that in many cases it is impossible t^ say definitely whether they correspond or not on account of the indistinctness and difFnseness of the cardiac iiupiilse, I once saw the late dis- tinguished von Ziemssen, one of Germany's most skilful clinical teachers, make a loistake in just such a case. The patientj who ivas in extremis, was presented to tlie class as an instance of massive pericardial exudation. There was a large triangular area of absolute cardiac dulness over which impulse was wanting, and f heart-sounds were scarcely audible, iloreover, rales of acute pul- monary oedema rendered auscultation highly uesatisfactory. The autopsy, next day, disclosed a fatty and extremely dilated heart, hut no eifusitm, and von Ziemssen took the occasion to teach a most instructive lesson on the difficulties of differential diagnosis. Should it prove impossible to locate the apex-impulse in the I recumbent posture, the patient may be slowly and cautiously lifted [into the erect position in the hope uf the heart gravitating for- l"ward, and thus declaring the situation of its apex. If this not entirely safe procedure fails, then aid nuiy sometimes he derived from careful study of the pulse, which in pericar<lial effusion is aaid to occasionally be relatively stronger than the feebleness of the heart-sounds would lead one to expect.
This is also a theoretical |>oiut which I have never found to stand the test of practical experience. When a pericardial exu- dation is massive, as well as when extreme dilatation simulates effusion, the equilibrium of circulation is lost, the veins are over- filled, and the arterial system is empty, so that, as a matter of fact, the pulse of extensive effusion is small, weak, and rapid. Should all attempts to arrive at a differential diagnosis fail, then, as sug- gested by Leube, we may have recourse to digitalis and other therapeutic measures in the hope of clearing up the condition. In dilatjition proper treatment may revive the flagging heart and restore the apex-heat and heart-sounds, while in pericarditis it may keause absorption of fluid and a reappearance of pericardial I friction.
Pleurisy mith effusion may be mistaken for pericarditis, or rather a pericardial may be considered a pleuritic effusion. There
84 DISEASES OP THE HEART
is much similarity in the pain, fever, and dyspnoea, as well as cer- tain pressure-effects, but error is avoidable by attention to the fol- lowing points: (1) In pleuritic effusion there is a curved line of flatness which extends from the back around the side to the front, which line usually shifts with change in the patient's position. (2) A left-side effusion (the only one likely to lead to error) pushes the heart over to the right of the median line. (3) Breath- sounds at the left base are diminished or absent, instead of exag- gerated or bronchial, as in pericardial effusion. (4) Dysphagia is very rarely if ever present in pleurisy. (5) In pericarditis there is usually a history of rheumatism or other acute infectious process to lead to cardiac involvement. In an adult a differential diagnosis between these two affections is seldom difficult, but I have seen young children in whom it was at first not at all easy to say which was the process, owing to the great compression of the left lung and consequent extent of dulness laterally and behind.
The foregoing are the only two affections likely to mislead; yet the careless, and still more the inexperienced, may mistake for pericarditis a number of conditions that occasion increase in cardiac dulness upward and to the left. These are mediastinal tumours, which crowd the lung-margins aside and displace the heart, and jmlmonary tuberculosis or old pleuritic adhesions, which cause permanent retraction and fixation of the anterior bor- der of the left lung. Error ought to be avoided, however, by due attention to history, symptoms, and physical findings. The history is that of insidious commencement and slow course — s\anptoms are those of a chronic process without fever, except, of course, in the case of pulmonary tuberculosis, when there is characteristic sputum to act as a guide — and as regards clinical findings, the dulness lacks the distinctively triangular shape of pericarditis with effusion. Time settles the diagnosis l)eyond question.
Prognosis. — This depends upon the nature of the exudate, the rapidity of its formation, its amount, the effect, both of in- flammation and resulting effusion upon the myocardium, the ex- istence of comj)lications, as acute or chronic endocarditis, Briglit's disease, tuberculosis, etc., and finally, the age and vitality of the patient.
Suppurative pericarditis, unless recognised and treated surgi- cally, is very likely to prove fatal, and yet, as previously stated,
PERICAEDITIS WITH EFFUSION
85
if of rather a benign type the flnid portion of the exudate maj ultimately la^come absorbed, lea%'ing a cheesy, and at times a cal- careous, mass behincL
Pericarditis hwmorrkagica ocula may destroy life within a few days. When the malady is eh runic, its prognosis is essentially that of the seorlnitus or other primary affection.
An effusion of whatever nature that fonns rapidly and to a large amount is always serious, because time is not allowed for the system to adjust itself to the altered conditions. Such a case may speedily prove fatal If the inflammation extends to the myo- cardium, or if this latter has undergone previous degeneration, the heart-muscle will be ill prepared to sustain the pressure ex- erted by the fluid confined within the tense and resisting sac. Serious circulatory and respiratory embarrassment, or the possibil- ity of fatal syncope, renders tlie immediate prognosis nmst grave.
Acute endocarditis is a serious complication, and the existence of a chronic valvular lesion occasions a degree of gravity which might not l^e the case if the pericarditis existed ulnnc. If the dis- ease occurs in a ^►erson with acute or chronic nephritis, or if pul- monary tiibercub>sis coexists, the patient is hardly in condition to successfully copo with the occurrence and long duration of an exu- dative ]_>ericarditis. Moreover^ coming on as it does toward the end of chronic nephritis^ the |K^ricarditis contributes largely to the fatal result.
Finally, emphasis has been repeatedly laid on the serious na- ture of pericarditis in cljildreii, owing to the frequeuey with which it implicates the heart-muscle and the strong likelihood of ita leading to cardiac dilatation. In children, therefore^ the imme- diate, as well as the ultimate prognosis, is serious. In old people and those enfeebled by some chronic malady that has brought them to a state of cachexia there is small likelihood of the patient sur- viinng until time can bring about absorption of the effusion.
In all cases, even when death does not result directly from the acute inflammatory or exudative process, there is a possibility of the heart being crippled by inflammatory damage to the myocar- dium, or by partial or total obliteration of the sac. Of the 324 cases analyzed by Breitung, there were circumscribed adhesions in 111, and complete adhesion of the pericardium in 23. Tlie remote prognosis depends upon the richness of the exudate in fibrin; in
86 DISEASES OF THE HEART
such the likelihood of adhesions is the greater. Pericardial in- flammation, therefore, of whatever nature, should never be looked upon as a trivial complaint.
Treatment. — We possess no means of arresting an attack of pericarditis, and therefore we must content ourselves with en- deavouring to combat the rheumatism or other affection in the course of which pericardial inflammation occurs, in the hope of preventing the latter. If, nevertheless, the sac becomes involved, we must strive to lessen the severity of the process, and this fail- ing, to relieve s^^nptoms and sustain the powers of life until the disease comes to a natural termination.
Inasmuch as we are powerless to abruptly terminate pericar- ditis, and it occurs most often in the course of articular rheuma- tism, every possible effort should be made to cut short or mitigate the intensity of the rheumatic attack. This is no place to discuss the treatment of the latter affection, yet I wish to record my con- fidence in the salicylic-acid treatment, especially in methylsalicyl- ate, both locally and internally. If this is not a specific, we at all events possess nothing better, and must await the time when defi- nite knowledge of its nature may supply us with an efficient weapon against rheumatism.
The importance of physical rest cannot be too strongly in- sisted upon whenever fever or other rheumatic symptoms make their appearance. This is particularly wise in the case of children who have an old-standing valvular lesion. Such children ought to be seen by the family doctor whenever sore throat or other sus- picious symptoms arise. Physical exertion by increasing the force and frequency of cardiac contractions, tends not only to intensify pericarditis when it is already present, but may even determine its develojmient in the same way that use of a rheumatic joint may aggravate the arthritis. If an adult is unwilling to submit to rest, he should be informed of the possibility of endocardial or pericardial inflammation, and thus perhaps be induced to take proper care of himself.
When pericarditis once sets in, measures are indicated to lessen its intensity. Vesication of the pra?cordia was once extensively used for this purpose, and there are still many physicians who believe in the efficacy of this treatment in the initial stage. Per- sonally, I am sceptical of the influence of blisters in this regard.
PEBICARDITIS WITH EFFL'SIOX
87
and believe that milder measures will do ju?t as much good, while at the same time saving the patient from the pain and diseomfort of a large hliater. The real benefit of vesication, in my opinion, is fonnd in the relief of pain, and therefore I think it is prefer- able to adopt small blisters, a fresh one being applied so soon as the previous one has filled. This is the plan advueated bv Caton, because of the ease to pain thus afforded, 1 have had no great experience with this mode of treatment, because I prefer the application uf cold to the cardiac area. I know that connter- irritatinii often eases the snffering occasioned by inflammation of serous membranes, and therefore advise that if cold is not well borne and the intensity of the initial ]>ain seems to call for some measure of the kind, that this be a sinapisiu nmde of English mus- tard by tlie nurse, and that it be left on until the skin becomes thoroughly reddened. When the mnstard-clranght is removed, its place may be supplied by a poultice or by hot fomentations. Moist heat to the j>nccordium givrs great relief in some eases, and is much extolled. Roberts applies 2 or *3 leeches over the heart in suitable cases, but as a rule finds ponltieing in the early stage gives positive relief to pain.
I-ees is a strong advocate of the continuous use of the ice-bag, and asserts that it not only gives comfort by alleviating pain and palpitation, but tends to mitigate the severity of ihe inflammatory prtjcess. This mcxle of treatment has always appealed to me as rational, and in all cases in which I have seen its use faithfully tried it has appeared to be very comforting and agreeable. The iee- bag must be light, so as not to oppress tlie patient by its weight, and should 1m? held in place by a cord passing around the neck. As the sufferer is usually in a semi-recumbent posture, the bag, thus susjx^udpd* rests lightly on the prtwordia without danger of slipping off. Furthermore, the ice-bag must not Ix- allow^ed to rest against the bare skin, as it is apt to wcasion irritation, but a small piece of dry, thin cloth is to be interposed between the surface of the chest and the l)ag. In this manner the bag is generally well borne, when before it couhl not be endured. Children are some- times uneasy at first, yet if the application of cold is firmly in- sisted upon, they not only learn to tolerate it, but actually find it soothing. Should idiosyncrasy render an individual absolutely intolerant of cold, then it may lie replaced by jxiultices. Hot fo-
88 DISEASES OP THE HEART
mentations are objectionable on account of the liability of their wetting the clothing, and of a chill when the cloths are changed. In the emplojTnent of the poultice due attention should be paid to the principle that to be efficacious it must be hot, not merely warm, and must be replaced by a fresh one so soon as it grows cool. When at length poultices are discontinued the surface of the chest must be covered by a layer of cotton or flannel.
Treatment in the inflammatory stage is largely symptomatic, and in most cases something more than either heat or cold is re- quired to allay pain and restlessness. In mild cases an anodyne liniment, as belladonna, chloroform, or one containing morphine, may suffice, and should be tried before recourse is had to internal medication.
When pain and restlessness are severe nothing is so 8er\^iceable as opium in some form. In the case of adults a hypodermic of morphine is the best ; to children it is far better to give the remedy by the mouth. Their well-knowTi susceptibility to the drug makes it advisable to try the effect of codeine before resorting to opium or morphine. In some cases it will be found that a combination of codeine and sodium bromide will act efficiently and render more powerful remedies unnecessary — a consideration to be al- ways borne in mind with children.
Besides allaying pain and quieting the little sufferers, thes^e agents tend to lessen the violence of heart-action — a desideratum of importance — and to promote sleep. Insomnia is often very trou- blesome, and when not overcome it contributes greatly to the pa- tient's ner\'ousness and inability to bear well the strain of a pro- tracted illness, which, like pericarditis, makes great demands on the patient's powers of endurance. An opiate steadies the nerves, and if it does not too greatly disturb digestion and secretion I believe it cruel to withhold it in cases characterized by the fore- going symptoms.
Cough is an annoying feature in some cases, and when this is so it affords an additional reason for the administration of codeine or morphine. A preferable remedy, however, is heroin, which to an adult may be given in the dose of ^ grain, and to children in proportionately smaller amoimts. It not only allays cough efficiently, but is devoid of the unpleasant after-effects of morphine.
PERICARDITIS WITH EFFUSION
89
Nausea and vomiting may in some cases tax medical skill to the utmost J and, as in a recently observed instance, defy all at- tempts to allay them. In such an event it becomes necessary to stop oral administration of food and medicines, and to rely on enemata in the hope of the stomach becoming quiet.
Fever drtes not always require antiinTCtic treatineiit, bnt should it persist at 102*^ F. or higher it may be reduced by sponging.
In this early stage rapid^ violent action of the heart is often present, and seems to call for quieting measures. Digitalis does not appear to me to Im? indicated^ for tachycardia is now not a manifestation of weakness, bnt of irritation, and in my experi- ence the heart does not bear kiudly attempts to slow it by digitalis. Xeither should aconite or veratrum be prescribed for this purpose, since they are too depressing, and the heart is likely to need all its reserve force before the struggle is over. I believe no therapeu- tic measure is more efficient in quieting the organ than an ice-bag worn continuously*
The routine administration of digiialis is objectionable in any form of cardiac disease, and in pericarditis is especially so. The real indication for its use in this affection is not merely rapidity of the pulse, but feebleness* together with rapidity. Therefore, should the unchecked tachycardia begin at length to tell on the heart, or should the organ furnish signs of dangerous dilatation with scantiness of urine and otber evidence's of visceral conges- tion, then it is well to prescribe digitalis. The hypodermic ad- ministration of digifalin does not seem to me so reliable or effec- tive as the internal use of a fat-free tincture, or of the infusion in moderate doses, 10 drops of the former and a tablespoonful of the latter to an adult, and to a child a proportionately smaller amount every four to six hours.
Sinjchnine is a heart-trmic whicb cannot be dispensed with in this stage. Its dose does not need to be large at first, perhaps ^ if the patient is grown, 3 or 4 times a day. It may be given by the mouth, but under the skin is preferable, since its action is more direct and powerful.
There is always a more or less pronounced tendency to con- gestion in pericanlitis, the liver feeling the bnmt of the attack, and hence Ix^ing usually palpable. Consecpiently it is well to re- lieve visceral and portal congestion by a mild daily laxative, calo-
1 3
90 DISEASES OP THE HEART
mel or a saline aperient water. Vigorous depleting measures in the inflammatory stage are harmful, however, rather than bene- ficial, and should be reserved against the time when fluid accumu- lation occasions distress.
Food must be light and nutritious, consisting largely of milk and nourishing soups and broths, into which a raw egg has been dropped. If fever is not high, and the patient's condition de- mands heartier food, this may be given in the form of chicken, raw oysters, a bird, or a small piece of carefully broiled beefsteak, with toast or light biscuit. An occasional eggnog is also excellent. It is better to feed these patients often and in small amounts than to supply them with a hearty meal only 3 times a day. Pure or slightly acidulated water should be given freely so long as fever and thirst are present. It also promotes excretion and pro- tects the kidneys from the injurious effects of toxins. In most cases skilful nursing is far more necessary and beneficial than medication.
Treatment in the Stage of Effusion. — ^With the appearance of exudation and abatement of active inflammation, symptoms of pressure super\'ene and demand attention. The object of man- agement is now threefold : ( 1 ) to restrict the rapidity and amount of effusion, (2) to aid the heart in its attempt to maintain circula- tion, (3) to promote removal of the exudate by absorption or other- wise.
In my opinion, it is very doubtful if we possess any means of limiting the amount of effusion, since we have no criterion by which to estimate the efficiency of measures employed in any given case. A single large blister or a succession of smaller ones over the pra^cordia is recommended by some authors; but what assur- ance have we that the withdrawal of serum in anywise diminishes the amount pourecl out in the sac ? As a matter of fact, the quan- tity of the exudate, and the rapidity of its formation, are deter- mined by the intensity of the inflammation. If, therefore, we are to lessen the amount of effusion, we must restrain the activity of the inflammatory process. Measures to this end have already been discussed, and although undoubtedly they should be employed, their utility is open to doubt. I pass, therefore, to the considera- tion of the second object of treatment.
In some cases effusion takes place w4th such rapidity and in-
PEttlCARDITIS WITH EFFUSION
91
duces such urgent pressiire-symptoms that surgical interference has to be resorted to without delay, More often, however, indi* cations of pressure appear slowly, and time is afiForded for a trial of medicinal treatment.
Absolute rest is now imperative, and the patient, if old enough, must be advised of the necessity of refraining from any sudden movement, lest it oceaHion fatal sylieofje. He should be supported in a semi-recumbent posture by a bed-rest or pillows, and he must not be allowed to sit up to take nouriijihuient or medicine. He bIiouKI be disturbed as little as possible for the purpose of examin- ing the heart.
The state of the circulation, as shown bv pulse and venous engorgement, is to be carefully watched, and so long as the quality and rate of the pulse remain good, strychnine may be the only heart-tonic required. So soon, however, as the pulse shows diero- tism or irregularity in force, size, and frequency, tincture of fat- free digitalis must be ordered in doses suitable to the age of the patient — to an adult 10 drops every four to six hours.
The daily quantity of urine should l>e accurately noted, and in these cases a pronounced falling off uf its amount is an indication for digitalis, even though tlie pulse reuutins fairly good.
Careful examination of the Vixer will always detect more or less engorgement of tliis organ. Palpation of the liver is often painful or unsatisfactory by reason of abdominal tlistention, but we know by experience and deduction that stasis within the por- tal system is taking place, and hence hydragogue cathartics form , an im{>ortant, nay an indispensalde, part of our therapeutic meas- ures in this stage. By depleting tlie portal systein catliarsis aids in maintaining the venous circulation. Instead of weakening the patient, it adds materially to his comfort by lessening epigastric pain and relieving abdominal pressure.
Sleep should be induced by a hypnotic, for nothing will more Burely tend to exhaust the nervous system than insomnia. X have sometimes found that the additioTi of a | or i grain of codeine to a sulphonal powder insures the action of the latter. At this stage morphine or a preparation of opium is to be given with very great caution. It may be indicatcn^^l by dyspntea or restlessness, but actual danger attends the administration of the drug, through its I depression of the respiratory centres. If it be given to allay the
92 DISEASES OP THE HEART
dyspnoea, atropia should always be added to the morphine, because of its well-known effect in deepening respiration.
The passive congestion within the abdominal cavity impairs digestion and lessens absorption, yet nourishment is imperatively demanded, both by the nerve-centres and heart-muscle. Only such food should be given as can be easily assimilated, and as but a small amoimt should be taken at a time, it should be concentrated and highly nutritious. Some of the prepared foods will now be found to be of great service.
When by the subsidence of the pyrexia, if that has existed, it is judged that the active inflammatory process has ceased, or when repeated examinations of the heart indicate that the amount of effusion is stationary, the query naturally arises. What means are to be employed for its removal? Shall an attempt be made to promote this by absorption, or shall paracentesis pericardii be per- formed? This brings up the question, is absorption of the effu- sion possible ? Clinical experience certainly gives an afiirmative answer. Theoretically, absorption of the exudation may be hin- dered or prevented by an abundant coating of fibrin over the surface of the pericardiimi whereby the fluid cannot reach the lymphatic spaces, or in consequence of great venous stasis the hTuphatic vessels may be surcharged, and the flow in them be too sluggish to promote active absorption. Nevertheless, particu- larly in rheumatic cases, experience affords abundant proof of the frequent, even rapid, absorption of extensive pericardial effusion.
Therefore, I believe the physician is culpable who refuses to make the attempt at least to carry off the fluid by a resort to diuretic and cathartic remedies. A great degree of venous stasis often neutralizes the effect of diuretics until congestion within the renal veins has been relieved by resort to hydragogue cathartics. The two classes of remedies should be conjoined therefore. In my opinion, the infusion of digitalis affords the best means of estab- lishing free diuresis. A tables})oonful to begin with may be ad- ministered to an adult every four hours, while the patient also receives daily some unirritating cathartic, capable of inducing a number of copious watery stools. I have seen truly astonishing results follow such a plan of treatment. This is well illustrated by the case of a boy of seven years with mitral regurgitation of
PERICARDITIS WITH EFFUSION
93
rheumatic origin^ in a state of perfect compensation, who had been under occasional observation for a year.
On May 9, 18DU, Le developed what appeared to be a mild ease of follicular tonsillitis, for which he received appropriate treat- ment. Three days later he was reported not so well, and at my visit that same day he was found to have a temperature of 101° F* He complained of vague jmins in die knees, which were not red- dened or swollen, but ?^howed an erythema. As the attack was un- doubtedly rheumatic, salicylate of soda was ordered, and as the l>oy lived in a suburb he was put in charge of a local physician. May 2Sth I was asked to see him again, when a pni'cordial fremitus, which disappeared upon pressure, and a soft to-and-fro murmur, quite different from his endocardial one, with which I was so familiar, left no doubt of the existence of an acute pericarditis. The attending physician stated that these friction-murmurs had developed a few days previ- ously. By Jime 5th the actual increase in the area of cardiac duhiess gave evidence of the occurrence of effusion, though the cardiac impulse and fric- tion-si»unds still persisted over the body of the organ. Py- rexia was moderate, pulse 120, of good quality, and respira- tions were accelerated* An ice-bag had been ^vorn most of the time since May 2Hth, althfiugh pain had at no time been a very marked feature. From now on the exudation increased steadily in amount until, by pJune 2ftth, the ex- treme limits of cardiac dulness reached from just within the right nipple, qnite to the left axillary line, far outside the easily located apex-beat (see Fig. 20).
Tlie persistence of the pericardial rub, somewhat less intense, to be sure, together with palpable cardiac impulse over the body of the heart, and the distinctness of the heart-sounds and of the
FUr. L'M. — Al'E^-BtAT AM» ArI:A Ot t'ARinAC
DLLNsaa IN Cask up PSRicARUtTiti with
u
DISEASES OF THE HEART
uiitral regurgitant murmur, were thouglit to indicate the existence of adhesions on the anterior surface of tiie organ and U} have prevented the effused fluid from covering over the heart. That the etfusioti was considerable wa^ evinced bv the great distcution of the sac laterally and downward, by great pressure upon the lungs, and pronounced circulatory einbarratisment. There were marked cyanosis, distention of the superficial veins, great enlarge- ment and tenderness of thi* liver, and slight ankle anJeina. Respi- rations were 48, jndse 140, small^ and dicrotic, hut still reguhir. Salicylate of soda had been diseontinued upon appearance of the effxisioTi, lest it niiglit too greatly depress the heart, and as the scanty urine was highly at-id, hicarbuuate of soda and citrate of potash had been substituted. As digitalis and mild cathartics had failed to appreciably diminish the amount of effusion, surgical interference was decided up^in.
The selection of the site of puncture was left to nie, ami, be- lieving that in eonsc*qnenee of adhesions over the fnmt of the heart tlie exudation could he most surely reached at iiouie lateral
point, I selected the tifth left interspace, between the apex- impulse and the outer margin <»f flatness (Fig. 21). Accord- ingly the surgeon introduced his trocar in that situation and obtained tiuid. This was cHs- tinctly bluody in a ]i pea ranee and so surprised the L*[>erator that after permitting an ounce or two to flow he withdrew Ins cannula for the purpose of dis- cussing the significance of the hlood. We concluded it was a Inemorrhagic effusion, and ad- vised a fresh tapping. This was now objected to by the parents on the ground that once at a time was enough, and a repetition of the procedure w*as deferred. It w^as never repeated, however, and hecause of the following considerations:
¥u... L'l— The V*ARiors StTEt ron Pfxcrt re
IX Pa»AO£17T1BIS PSRICAKDII
Dotted line iudicatea conr^e of inteiutt) rTiam m&nr urtery.
I
PEKICARDITIS WITH EFFUSION
95
The great obstacle to absorption \vas believed to lie in the enor- mous congestion within the portal system, and the boy's dis* tress was due not so niiieh to jiressiire from the effusion as to the extreme stasis %vithin the abdomen. Tapping the pericar- dium might relieve the heart, but with all the conditions pres- ent in the mitral regurgitation for the raaiiitenanee of hepatic engorgement it eonld not materially improve the state of things in the portal system. Consequently, with the heart-muscle show- ing no very threatening signs of failure, it was thought best to make one last vigorous onslaught on the stasis within the hepatic vessels. Accordingly a drachm of the saturated solution of Epsom salts was ordered hourly until it l:H?gan to exert effect. At the same time a drachm of the fresh infusions of digitalis made from English leaves was prescrilied every four hours. The results were astonishing. Several doses of the magnesia sul- phate were taken next morning without any very marked effects upon the bowels, but instead the kidneys began to act^ and in the next twenty-four hours diuresis amounted to something like 8 quarts* Not only did the patient's dyspmea lessen, lait the area of cardiac dulness began promptly to diminish in size, the liver became softer and less tender^ and the patient's improvement was clearly noticeable even to his parents. The salts were con- tinued daily, though with gradually diminishing amounts. After two or three days sirup of squills was added to the infusion of digitalis, and the progress towards recovery continued without in- terruption. This little patient lived nearly three years, and then died from a fresh pericarditis, with signs of dilatation, but not effusion.
Some are sceptical concerning the efficacy of medicinal treat- ment in promoting absorption, basing their objections on the fact that absorption sometimes sets in spontaneously, even after the pericardial effusion has remained stationary for some time. Nevertheless, in this ease, the change for the better began so soon after the administration of the magnesium-salt that I believe it can be justly regarded as an instance of propter hoCj not post hoc. Unfortunately, the result of thern pontic measures is not always so brilliant as was this. The effusion persists in spite of hydragogue cathartics and diuretics, or the exudation takes place so rapidly and copiously that it threatens to overpower the heart before time
96 DISEASES OF THE HEART
is allowed for remedies to exert their eflFect. In either event the pericardium ought to be tapped, and it is best not to delay. It seems to me there can be no question concerning the indication for paracentesis in such cases, but early in the disease I see no call for surgical interference so long as alarming pressure-symp- toms do not supervene.
Sites for Puncture, — Properly performed, this operation is safe, and as it is likely to afford prompt relief, one should always stand ready to tap whenever such intervention is indicated. The indications are not always found in dyspnoea, cyanosis, and rapid- ity of the pulse; these symptoms are present in all cases of peri- cardial effusion of considerable amount, but indications are present whenever the heart shows evidence of dangerous weakness by syn- copal attacks and intermittence, or when sufficient time having been given for spontaneous recovery, or for absorption through medicinal treatment, these do not take place. Paracentesis being decided on, it only remains to select a suitable point for punc- ture. Various sites (see Fig. 21) are recommended, and all aim at reaching the fluid most readily without fear of wounding the heart, internal mammary artery, or other structures.
The point most usually recommended is in the fifth left inter- costal s])ace at a safe distance from the internal mammary artery. As this passes downward from \ to ^ inch from the edge of the stornuni, the needle may be introduced either very close to the sternal border, so as to be between it and the vessel, or at the outer side of the artery 1 inch or more from the bone. Rotch pre- fers the fifth right interspace close to the sternum, since at this point the sac is sure to be distended, even should the amount of fluid prove smaller than is anticipated. Shattuck has punctured in the fifth left space, 1 to 2 inches outside the nipple-line, just within the left lateral border of cardiac dulness, where, as a mat- ter of fact, I advised tapping in the case narrated, although at the time I was not aware of Shattuck's recommendation. The objec- tion urged against this site is the possibility of wounding the pleura at this point. This is^ of course, a cogent reason, yet if the sac is greatly distended it will have pushed the border of the left hmg well aside, and the pericardium will occupy the region normally filled by the lung. In my case fluid was readily reached, and the surgeon was confident he did not touch the pleura. An-
PERICARDITIS WITH EFFUSION
0T
other jioiiit at which the sac can often he safely pierced in cases of extetir>ive effutiiou is in the angle between the left margin of the xiphoid cartilage and the adjaeeiit costal cartilages. The fluid tends to gravitate to the hottoni of the sac, and consequently weighs down the diajihnisrui and left lobe of The liver, so that if the needle is thrust upward and backward there is very little danger of wounding the diaphragm. For additional particulars concerning paracentesis., as well as incision of the jjericardium, the rea<]er is referred to works on surgery.
Whetlier all the effusion jxyssible is to be withdrawn, or whether only a portion, sutiieient to lessen the pressure and favour subsequent absorption of the remainder, is a matter that must be left to the judgment of the operator. Personally, I advocate the removal of the whole or of as nnieh as can be taken without danger of the heart coming in contact with the point of the needle.
Theoretical considerations suggest the expediency of following the oi)eration by the administration of diuretics and heart-tonics. The latter include digitalis and its congeners, which sustain and strengthen the heart-muscle while at the same time they increase pressure in the renal artery, and thus re-enforce any other diu- retic remedies. The employment of such agents serves to deplete visceral congestion and to thus enhance the benefit derived from the withdrawal of the tluid which is the original cause of the stasis.
The treatment of purulent effusion should be surgical. Should the nature of the primary infection and svTuptoms of more or less pronounced septi(*a*mia suggest that the pericarditis is suppura- tive, the character of the exudate should be determined by explora- tory puncture, and if this prove to l>e pus, it should l>e evacuted witiiout delay in accordance with proper surgical methods. Lil- ifnthal, of New York, reported before the Xew York Academy of Medicine a case of suppunitivx- pericarditis, occurring in a lad who was recovering from |)neunu>nia» affecting three lobes. Eight- een ounces of pus were withdraxvn at the time of the exploratory puncture, and 40 more at the time the sac was cut down upon and opened. The pus contained numerous pneumococci. The tem- perature had been irregidarly intermittent. Complete recovery followed the operation. Eucaine w^as used as a local anaesthetic.
Ifopmorrhagic effysion is to be managed according to the prin- ciples governing the treatment of the sero-fibrinous form, no spe- 7
Mtti
98 DISEASES OF THE HEART
cial indication for treatment being presented by the bloody charac- ter of the eflFusion. !Xo great effect is to be expected, however, from either medical or surgical treatment in those cases in which the affection is associated with a serious blood-state or dyscrasia, and measures should be directed to the removal of these latter.
The subsequent management of a patient convalescing from acute pericarditis consists in such measures as will rapidly restore the general health and heart-tone in the hope that the organ may not be left seriously damaged. We [K)ssess no means of either preventing adhesions or i)romoting the absorption of fibrinous deposits.
CHAPTER II
CHRONIC PERICARDITIS
Syk. ; Adhtrenl Pericardium, S\/nechia Ptricardiif C(fn€retio Pierieardii Seu Concreiin Cordis
CitKoxic pericartlitis may l>e <livide<l into two groaf groups: (1) That in which it iiivolvt?^ onlv the two layers of the sac, peri- carditis interna chronica, and i2) that in which the process in- volves both the pericardium and mediastinum, pericarditis in- ienm et externa chronira. In both of these forniH; intliinmuition results in the formation of fibrous tissue, which binds the parts more or less closely and extensively together. There is still an- other niuch rarer form in %vhich the chronic inflammation is asso- ciated with serous distention ui the sac^ and is termed therefore chronic pencarditis with effttsion.
Adherent pericardium is the term most commonly applied by English wTiters to the first form, while the second is known as chronic adhesive (s. fibroufi, s. indHrative) mediasiinopericardUij^, Adherent fiericardimn has loug been recognised by pathologists, but, owing to the difficulty of its diagnosis, esca]^d clinical recog- nition, although it is a comparatively fre*pient post-mortem find- ing. Out of 8»> cases of heart-disease examined after death at St. Mary's Hospital frr^m lSf»0 ro 1^1)3^ there w^ere, according to John Broadbent, 31 instances of adherent pericardium.
Although, according fo Rolnprts, Sir Samuel Wilks had fre- quently called attention both pathologically anc! clinically to the existence of chronic fibrous tliickening within the mediastinum and involving the pericardium, phronic indurative mediastino- pericarditis was first systematically described by Kussmaul in 1873. In 1804 Harris, of Manchester, added another valuable contribution to the subject and collected all the published cases. For much of what will be said in the following pages I wish to
90
U>0 DISEASES OF TOE HEART
express aeknowledj^^ment to Harris's monof:^raph» and to thank- fully acknowle<]ge the stiniuhis deriveil therefroiiL It Ims ea- abled nie to give more intelligent and discriminating study to the cases which have eome to my notice* I now systematically look for indications of chronic niedia!>finopericarditis, and discover them many times when otherwise I should probably have over- looked them* UnfortuTiatelVj ante-mortem observations of several pronounced cases have l)een made in w4iich post-mortem corrobora- tion of the diagnosis has been denied. Several instruct ive and typical instances will be narrated in these pages, I wi^-h also to express my indebtedness to John Broadbent's mon<>gra|»h on this subject, as well as to Friedel Pick\s pajn^r, Fericarditic Pseudu- cirrhosis of the Liver, in which ih particularly discussed the effects on the liver and the production of ascites.
Morbid Anatomy.— The morhid anatomical chaiig«?s found in clirunic pericarditis are almost always the result of previous acute intlammation. The more common form is the result of the organization of the fibrinous exudate of an ordinary plastic peri* carditis. This prf>cess may tn^gin as early as the third or fourth day of the acute inflammation. It is essentially a conservative proeeas, ten<iing to make gtxMl the damage wrought by the inflam* mation. This is brought alx>ut by the conversion of the iDflam- matory exudate into a granulation-tissue, and finitlly into fibrous cicatrical tissue.
The dei*j>er layers of the exudate are first invaded by newly forming blombvessels and connective-tissue cells with many leuco- cyte^, which form the granulation-tissue. This gnidiially grows into and noplaces the entire exudate, and in the course of time the development .of intercellular substance converts it into the glisten- ing, white cicatrix. If during this pn>eess the two layers of the I>ericardiuin are in contact, union takc»s place and the cicatriza- tion produces firm adhesion between the opposing surfaces. These hesions may be general or local, varying with the extent of the iginal process, and with the condirlno* obtaining at the time of organization of the exudate.
WTien the adhesion is cinnmiscrilKMl it is most frequently found in the parts of the sac w^here the motion is the leasts most frequently, then, at the base of the lieart, ab*>ut the great vessels, less often at the apex or at the borders of the organ. When adhe-
CHRONIC PEEICARDITIS
101
«oi^o^^otocctir, the formation of scar-tissue produces glisten- ing white areas on the surface of the heart, which show where the previous inflaiujjiatioii existed. These are the so-called roilk- «pota or macule tetvdinifp.
An intenne<liate condition l»etween this and the synechia peri- cardii, or completely adherent pericardium, is that shown when filight cireimiscribed adhesions have been partially or completely torn apart by the motion of the heart* prcMlncing string-like pro- cesses of fibrous tissue that may connect the two surfaces, or may, in rare cases, hang loose in the pericardial sac. When the layers are not adherent, in rare cases fluid is found in the sac.
The layers of the pericardium may be a<lhcrent with but slight Uiickening, but it is the rule to lind considerable increase in fibrous tissue, especially in the chronic tuberculous form, where it may ln*come extreme.
Calcification may occur, especially following a purulent peri- carditis, the i»U8 becoming first inspissated, and then impregnated with lime-salts. Such calcareous plates may be isolated, or may form a complete investment for the heart, resembling a coat of mail (Ziegler). In this case the motion of the heart is iK?rmitted by cracks and fissures in the calcareous mass.
Chronic periciirditis is often associate<l with chronic endocar- ditU, for the reason that they both often have the same rheumatic origin* Moreover, chronic valvular disease seems to predispose la pericarilial inflammation.
Secondary to the pericarditis are usually found more or less hypertrophy and dilatation of the heart, with degeneration of the myocardium, which [probably are the result of the mechanical hin- dranct* to the hearths action, and also of the visceral changes that are always the result of long-standing circulatory disturbance.
Also associated with the chronic j>ericarditis may be an indura- tive mediai^tinitis. It may exist alone, but its more frequent oc- currence in combination with indurative pericarditis renders it appriipriate to consider it here. It consists of a more or less ex- Imsive h^-perida^ia of the conne<*tive tissue of the mediastinum, wbteb binds together the structures contained therein, and is often associated with adhesion of the two layers of the pericardium. This development of fibrous tissue results either from an extension of a chronic pericarditis through the parietal layer of the peri-
100
DISEASES OF THE HEART
express acknowledgment to Harris's monograph, and to thank- fully acknowledge the stimulus derived therefrom. It has en- abled me to give more intelligent and discriminating study to the cases which have come to ray notice. I now systematically look for indications of chronic mediastinojK^riearditis, and discover them many times when otherwise I should jirobably have over- looked them. Unfortunately, ante-mortem observiitions of several pronounced cases have been ma<le in which post-mortem corrobora- tion of the diagnosis has been denied* Several instructive and typical instances will he narrated in these pages. I wish also to express my indebtedness to John Broadbent^s monograph ou this subject, as well as to Friedel Pick's pafjer, Perioarditic Pseudo- cirrhosis of the Liver, in which is particularly discussed the effects on the liver anil the production of ascites.
Morbid Anatomy. — The morbifl anatomical changes found in chronic pericarditis are almost always the result of previous acute inflammation. The more common fonn is the result of the organization of the fibrinous exudate of an ordinary plastic jieri- carditis. This process may l>egin as early as the third or fourth day of the acute inflammation. It is essentially a conservative process, tending to make good the damage wrought by the inflam- mation. This is l>rought about by the conversion of tlie inflam- matory exudate into a granulation-tissue, and finally into fibrou&_ cicatrical tissue.
The deeper layers of the exudate are first invadetl by newl^ forming blood-vessels and connective-tissue cells with many leuco- cytes, which form the granulation-tissue. This gradually grows into and replaces the entire exudate, and in the course of time the develo]mient,of intercellular substance converts it into the glisten- ing, white cicatrix. If during this process the two layers of the pericardium are in contact, union takes place and the cicatriza- tion produces firm adliesion bi^tweeu the opposing surfaces. These adhesions may 1m* general or local, varying with the extent of the original process, and with the conditions obtaining at the time of [>rganization of the exudate.
When the adhesion is circumscribed it is most frequently found in the parts of the sac where the motion is the least, most frequently, then, at the base of the heart, about the great vessels,
often at the apex or at the borders of the organ. When adhe-
CHRONIC PERICARDITIS
101
, do69 BOt occiir^ the formation of sear-tissne produces glisten- 1^^ white areas on the surface of the heart, which show where the pre%*ious inflarniiiation existed. These are the so-called milk- or maculw lend into*. An lOtcmitHliate condition between this and the synechia peri- irdiip or coniideiely adherent ix^ricardium, is that shown when lit circumscribed adhesions have been partially or completely torn apart by the motion of the heart, producing string-like pro- cesses of tibrons tissue that may connect the two surfaces^, or may, IB rare cases, hang loose in the pericardial sac. When the layers are not adherent, in rare cases fluid is found in the sac.
The layers of the ijericardium may he adherent with but slight thiekening, but it is the rule to find considerable increase in fibrous tissue, eispecially in the chronic tuberculous form, where it may become extreme.
Calcifleation may occur, espc*eiaHy following a purulent peri-
< carditis, the pus becoming first insjussated, and then impregnated
irith lime-saltd. Such calciireous plates may be isolated, or may
liorm a complete investment for the heart, resembling a coat of
tiail (Ziegler). In this ease the motion of the heart is i>ermitted
Ihy cracks and tissures in the calcareous mass.
Chronic pericarditis is often associated w*ith chronic endocar* for the reason that they UaIi often have the same rheumatic 3Joreover, chronic valvuhir disease seems to predispose to pericardial inflammation*
Secondary to the pericarditis are usually found more or less ^h>Tiertrophy and dilatation of the heart, with tlegeneratiou of the lyoeardium, which probably are the result of the mechanical hin- drance to the hearths action, and also of the visceral changes that are always the result of long-standing circulatory disturbance.
Also «ss4^ioiated with the chronic pericarditis may be an indura- tive med last in it is. It may exist alone, but its more frequent oc- eurrrnctj in combination with indurative pericarditis renders it i|ipri*priate to consider it here. It consists of a more or less ex* sive hyjierplasia of the connective tissue of the mediastinum, which binds together the structures contained therein, and is often iriated with adhesion of the tw*o layers of the pericardium* bia developnjent of fibrous tissue results either from an extension a chronic pericarditis through the parietal layer of the peri-
100 DISEASES OF THE HEART
express acknowledgment to Harris's monograph, and to thank- fully acknowledge the stimulus derived therefrom. It has en- abled me to give more intelligent and discriminating study to the cases which have come to my notice. I now systematically look for indications of chronic mediastinopericarditis, and discover them many times when otherwise I should probably have over- looked them. Unfortunately, ante-mortem observations of several pronounced cases have been made in which post-mortem corrobora- tion of the diagnosis has been denied. Several instructive and typical instances will be narrated in these pages. I wish also to express my indebtedness to John Broadbent's monograph on this subject, as well as to Friedel Pick's paper, Pericarditic Pseudo- cirrhosis of the Liver, in which is particularly discussed the effects on the liver and the production of ascites.
Morbid Anatomy. — The morbid anatomical changes found in chronic pericarditis are almost always the result of previous acute inflammation. The more common form is the result of the organization of the fibrinous exudate of an ordinary plastic peri- carditis. This process may begin as early as the third or fourth day of the acute inflammation. It is essentially a conservative process, tending to make good the damage wrought by the inflam- mation. This is brought about by the conversion of the inflam- matory exudate into a granulation-tissue, and finally into fibrous cicatrical tissue.
The deeper layers of the exudate are first invaded by newly forming blood-vessels and connective-tissue cells with many leuco- cytes, which form the granulation-tissue. This gradually grows into and replaces the entire exudate, and in the course of time the development .of intercellular substance converts it into the glisten- ing, wliite cicatrix. If during this process the two layers of the pericardium are in contact, union takes place and the cicatriza- tion produces firm adhesion between the opposing surfaces. These adhesions may be general or local, varying with the extent of the original process, and with the conditions obtaining at the time of organization of the exudate.
When the adhesion is circumscribed it is most frequently found in the parts of the sac where the motion is the least, most frequently, then, at the base of the heart, about the great vessels, less often at the apex or at the borders of the organ. When adhe-
CHRONIC PERICARDITIS
101
sion does not oociir^ the formation of scar-tissne prodiiees glisten- ing white areas on the surfaee of the hearty which show where the previous inflamniation existed. These are the so-called milk- apots or macitlw iemUnur\
An intermediate condition between this and the synechia peri- cardii, or completely adherent perieardimn, is that shown when alight circnnisoril>ed adhesions have heen partially or completely torn apart by the motion uf the heart, prodneing string-like pro- cesses of tibrouii tisssue that may connect the two surfaces, or may, in rare cases, hang loose in the pericardial sac. When the layers are not adherent, in rare cases fluid is fonnd in the sac.
The layers of the pericardinm may he adherent with but slight thickening, but it is the rule to find considerable increase in fibroiis tissue, es^iecially in the chronic tuberculous form, where it may l)e<x>me extreme.
Calcification may occur^ especially following a purulent peri- carditis, the pus becoming first inspissatetl, and then impregnated with lime-salts. Such calcareous plates may he isolated, or may form a couiplete investment for the heart, resemlding a coat of mail (Ziegler). In this case the motion of the heart is permitted by cracks and fissures in the calcareous mass.
Chronic pericarditis is often associated with chronic endomr- diti^^ for the reason that they both often have the same rheumatic origin, ^loreover, chronic vah^ilar disease seems to predispose to pericardial inflammation.
Secondary to the jnzTicarditis are usually ffiund more or less hypertrophy and dihitation of the heart, with degeneration of the myocardium, wln'ch probably are the result of the mechanical hin- drance to the hearths action, and also of the visceral changes that are always the result of long-standing circidatory disturbance.
Also asscK?iated witli the chronic j>ericarrlitis may be an indura- tive mediastinitis. It may exist alonp, but its more frequent oc- currence in combination with indurative pericarditis renders it apjiropriate to consider it here. It consists of a more or less ex- tensive hyperplasia of the connective tissue of the mediastinum, which binds together the structures contained therein, and is often associated with adhesion of the t\vo layers of the pericardium. This deveIo]jment of fibrous tissue results either from an extension of a chronic pericarditis through the parietal layer of the peri-
102 DISEASES OF THE HEART
cardium, or from a chronic proliferative inflammation of the me- diastinum itself, either alone or associated with pericarditis. Ex- tensive fibrous adhesions may bind the heart-sac inseparably to the diaphragm, or the sac may be united to the anterior chest-wall, to the pleura*, (esophagus, spinal column, or to all these structures. In some instances the contents of the mediastinum are so matted together by dense fibrous tissue that they cannot be separated without laceration of the organs.
When such extensive adhesions exist they may be found to form but a part of a chronic inflammatory or proliferative process which has led to extensive or general adhesions between the two layers of the pleura, or between the lungs and the diaphragm.
In excei)tional cases fibrous adhesions have formed only at the rcx)t8 of the ^reat vessels, and have led to partial or complete oblit- eration of the superior vena cava, either alone (Roberts), or in combination with involvement of the main trunk of the pulmo- nary artery, or the ascending aorta (Kussmaul). At the present writing I have under observation a female patient, in whom, to jn<l^e from physical signs, chronic mediastinopericardial adhe- sions have led to such retraction of the borders of the lungs that the entire anterior surface of the heart is imcovered. The apex- beat is held immovably fixed in the seventh intercostal space, anterior axillary line. The normal excursion movements of the diaphragm in front are entirely abolished, and the respiration is of purely costal type.
The secondary effects of this form of the disease are not lim- ited to the heart, as in the simple adherent pericardium. As the disease is usually combined with chronic valvular disease, it is difficult to say how much importance is to be attached to this, and how much to the fixation of the pericardium in the production of the great hypertrophy and dilatation found in these cases. The changes in the lungs of chronic bronchitis and brown induration are due partly to the passive hypenemia secondary to the cardiac disease, and partly to the retraction and immobility of the lungs incident to the pleuro-pericardial or associated pleuritic adhesions.
Cirrhosis of the liver is generally present, and is largely re- sponsible for the ascites so frequently observed as a terminal event. There may be also thickening and contraction of the capsule of the liver and spleen, and more or less evidence within the abdom-
CHRONIC PERICARDITIS
103
inal cavity of what appi^ars to hiivo been a general serositis or pro- liferative intlamruatioii of the serous membranes.
Chronic Pericarditis with Effusion, — This form of pericardial disease is but rarely eneo^nitered ; vvbeii, however, it does exists it mav be considered to have originated in one of two ways: (1) It may start as an acute attack, which, instead of undergoing complete subsidence, suffers repeated exacerbations, and finally merges into a chronic inflammatory process. (2) In consequence of the mildness of tlie infection the pericarditis assumes a slowly progressive character from the beginliing, at no time manifesting a tendency to undergo arrest. In the former class tlie exudation fluctuates in amount from time to time, according as the intensity of the inflammation al>ates, and partial absorption occurs, or ac- cording as fresh infection occurs the inflammatory process again rekindles. In the second class, chronic from the outset, effusion acciunulates slowly^ and either remains stationary, after having reached a certain degree, or tends to gradually increase. This form of chronic pericarditis is said to be observed chiefly in elderly or aged individuals, and to be associated with chronic nephritis. Ivoberts expresses the opinion that such cases can lie differentiated only with great difficulty from instances of hyilro* pericardium, and that it is *juite possible, indeed, that ibe chronic pericarditis originated in a simple serous transudation. This, it seems to me, is quite unlikely unless the originally serous effusion becomes infected by pus-cocci^ in which event it would likely be transfonued into pyoperieardium.
Etiology, — (1i runic |jericarditis is in most instances of either rheumatic or tu!>erculous origin, the inflammation having been slowly progressive fntm the start. In other cases an acute process passes into a chronic one, which exhibits no tendency to abate- ment, hut persists for years with repeated exacerbations of the inflammation. This is the case particularly with the form which, starting in tlie sac, s]>reads to the mediastinum, and ultimately becomes a chronic fibrous mediastinojiericarditis.
In some cases a mediastinitis is first set up and subsequently invades the pericardium. This last form may originate as either a chronic or acute mediastinitis, which is set up by disease of the bronchial or mediastinal glands, malignant tumours, tuberculosis of the lungs, pleura or glands, pneumonia, or by trauma,
104 DISEASES OP THE HEART
The disease is most frequently obsen-ed in young adults and in children. Of 22 cases collected by Harris in which autopsy was held, only 2 occurred in persons past thirty, while 9 were under eighteen years of age. Several instances have been re- ported of its post-mortem discovery in infants. According to Har- ris, chronic indurative mediastinopericarditis is much more fre- quent in males than females, 20 out of 25 cases having belonged to the former sex.
Symptoms. — Many cases of adherent pericardium run an absolutely latent course, and are only discovered on the autopsy table. In other cases the symptoms are those of circulatory and respiratory embarrassment, and are attributed to dilatation or to an associated valvular disease. In a third series of cases the synechia |x^rieardii is overlooked owing to the development of ascites and other symptoms of hepatic cirrhosis. For the most part the last-mentioned class of cases belongs to what has been described as chronic adhesive mediastinojiericarditis.
The explanation of these clinical differences is not always clear, but probably dej)ends upon several factors. If the pericar- dial adhesions are of limited extent they may produce no appre- ciable secondary effects on the heart or circulation, but if they lead to total obliteration of the sac, and particularly if this latter is also bound to some of the surrounding structures, cardiac hyper- troj>liy is likely to result, which, if slight, is not recognised clinic- ally and dr>es not occasion symptoms of embarrassed circula- tion. If, however, the heart is dilated as well as hypertrophied, it is very apt to be more or less inadequate with resulting respira- tory and circulatory symptoms. The enlargement of the organ may be recognised, but not its cause, and the condition is perhaps considered canliac myasthenia or even chronic myocarditis.
Sir William Broadbent is of the opinion that pericardial adhe- sions lead most frequently to enlargement of the right heart in consequence of the relative thinness of its wall, while others main- tain that the entire heart is hypertrophied. The mode of produc- tion of hypertrophy in cases of adherent pericardium is difficult of satisfactory explanation, but is due in some way to the hampering of the heart's work.
In most instances conditions are present which easily account for the cardiac hypertrophy. Chronic valvular disease and adher-
CHRONIC PERICARDITIS
105
ent pericardium coexist, or the lieart is restricted in its function by adliesions between it and surrounding parts (elironic adhesive mediaatinoperiearditisj. In still other instances the effects of a valve lesion are intensified bv mediastinojK'ricardial adhesions. In anv case the pericarditis either prevents the establishment of adequate comijcnsation or occasions premature loss of such com- pensation as mav have been attained.
When symptoms eventually a|ipear they may Iw? such as are seen in uncomidicated hut uneomiiensated valvular defects; ve- nous stasis, hepatic and other vis<^eral engorgement^ ledema, as- cites, dyspniea, and cough with or without expectoration, which may be simply catarrhal or blmxly, according to the degree of pub mo n a ry eo nges t i o n .
In some cases without coexisting valvular disease the earli- est symptoms are paljiitatiou, either with or without dysjmtTBa, caDed forth by effort or excitement, and cK'casion much discom- fort and alarm. In such the pulse is apt to be habitually rapid, while cardiac impulse is exaggerated in force and extent. In other cases, again, circulatory disturbance is shown by digestive disorders, lasting for many years and attribute*! to simple dys- pepsia or chronic gastritis, but never traced to their proper source because of its obscurity or impossible diagnosis of the peri- cardial adhesions. In all such cases there is nothing to distin- guish them from ordinary instances of cardiac incompetence due to dilatation or mitral disease.
Physical examination usually discloses hepatic enlargement, and if signs of heart-disease are not apparent the condition is thought to l>e cirrhosis of the liver, either hypertrophic or atro- phic, according to the degree of enlargement and density or smoothness of the organ.
In cases of adherent pericardium displaying pronounced en- gorgement *'f the liver, T have been impressed by its peculiar ob- stinacy to treatment. The hepatic congestion is most difficult of reduction by ordinary methods, and displays a striking tc^ndency to recur so soon as treatment is abandoned.
For several years I have had in charge a patient whose mitral valve leaks and whose enornionsly enlarged heart is apparently completely incased in fibrous tissue that binds down the organ on all sides, so that no amount of rest in bed or digitalis seeras to
106 DISEASES OP THE HEART
reduce its size in the least. The liver has always been greatly engorged, extending for a long time nearly to the crest of the ileum, and requiring the daily use of saline laxatives to relieve the patient from pain and discomfort. For the past year the organ has been gradually diminishing somewhat in size and in- creasing in thinness and hardness. The patient has experienced remarkably little dyspnira on effort, but is greatly annoyed by the pounding and tumultuous action of the heart, this sensation being specially noticeable in the epigastrium. Of late, she has had a great deal of cough, difficult mucous expectoration, and upon several occasions slight haemoptysis. She has to be extremely careful in her diet, and her urine and menses have become scanty.
Another female patient with pronounced mitral insufficiency has i)ericardial adhesions that bind down the left side and base of the heart, fixing the apex-beat immovably in place, far to the left and downward, but the border of the right heart is apparently free from adhesions. Whereas the left ventricle never varies in size under any conditions, the right heart, as shown by the area of cardiac dulness, becomes dilatetl with the greatest ease and rapidity. The liver, which is ])ersistontly enlarired, fluctuates somewhat in size in accordance with the state of the right heart, but even when at its smallest always extends from 2 to 3 inches below the inferior costal margin, no matter how vigorous may be the onslaughts u\Km it by means of Epsom salts. This patient's symptoms are not of the digestive organs, but are those of short- ness of breath and a rapid pounding action of the heart and gen- eral weakness. The urine remains fairly abundant, and the menses are too profuse and protracted. She is always promptly benefited by absolute rest in bed, a milk diet, cathartics, and digi- talis, although this last-named agent never materially slows the heart.
The most interesting class of cases are those whose clinical fea- tures closely resemble a case of atrophic cirrhosis of the liver. These cases, usually of chronic fibrous mediastinopericarditis, generally pursue a latent course for many years, and often, even after symptoms have set in, are not recognised as adherent peri- cardium until they come to autopsy. Not only is there a chronic engorgement of the liver, but there is a perihepatitis with increase
CHRONIC PERICARDITIS
107
of the interistitiiil eouneetive ti-ssue. In time this fibrous tissue, undergoing contraction, causes a reduction in size and marked increase in the hardness of tlie liver, which, extending below the costal arch to a variable distance, feels thin, dense, and regular, the notch being iutensitied, and often one lobe disproportionately larger than the other. It is now, when the organ has shrunken and gro%vn dense, that symptoms begin. The patient*s attention is first attracted by an increase in the size and firmness of his abdomen. In some instances ictL*rus iiecompanies or even pre- cedes this increase of girth.
At length driven to seek medical advice, he is discovered to have slight icterus and ascites, usually wit hunt a'dema of the lower extremities. The physican examines the heart and urine^ detects no heart-disease and discovers no album in, but j>erhaps some bile. The ciise is jmt down as one of hepatic cirrbosis. The following is an illustrative case:
A man of fifty-five, who had been intensely jaundie€*d for near- ly two years, and in August, IDOO, was tai>i)ed for ascites, called me in consultation a short time ago. The ascites^ which had for a time been reduced by apocynum caunubinum, only to sjieedily recur, had been again drauTi off the morning of the day I saw him. Tie had had articular rheumatism eighteen years before, but had suffered no shortness of breath or other discomfort since. The thin-bordered, dense, slightly granulnr-feeliiig liver extended in the median line nearly to tbo umbilicus and from one costal arch to the other, being lost beneath tlie right ribs, just outside the right nuiuiillary line. Owing to the recent paracentesis, the peri- toneal cavity was free from fluid, and there was no cedema, The c^ardiac area was somewhat increased to the right and downward, the sounds were clear and strong and free from murmurs. The rather tapping apex-beat was in the fifth left interspace inside the vertical nipple-line, and there was a distinct though feeble pulsa- tion in the epigastriiun. In the fifth and sixth interspaces, be- tween the apexdieat and sternum^ and nlso in the sulcus between the ensiform ap];)endix and adjacent costal cartilages, a systolic re- traction could be perceived both by palpation and inspection. Furthennore, when tbe patient was instructed to take a slow, deep breath, the right external jugular could be seen to bulge out during the inspiratory effort. This distention was also palpable. Pulsus
108
DI8BA8ES OF THE HEART
paradoxiis could not be iletermined. I had no hesitation in mak- ing a diagnosis of pseudo-atrophic cirrhosis of the liver seeondary to an adherent pericardium. This patient died a few weeks later.
One of the most typical cases, and hy the way the first of the kind I ever saw, was seen in 1891 with Dr. Christophe. The patient was a male, aged fifty-two, had always enjoyed good health until an attack of the grip in FebniarVy l.^SD, after which his health failed progressively. Six weeks prior to my visit he took to the house with ilropsy and ascites. The former yielded to caf- feine and digitalis, but the latter jiersisted until drawn off by tap- ping the day before I saw him. The patient was in Ited, of medi- um height, eonsideralfly emaciated, and complained of dyspncea,
dry CHiigh, anorexia^ tlatu- lence.cimsitipation, scanty non- albuuiinous nrioe, pain in the hepatic region, and insomnia. The lungs were nt^gative, but on examining the heart the a]iex-l>eat was found to be a weak tap in the fifth left in- terspace on the nipple-line and fi^ ]h' followed by a distinct - 1 1 iM » 1 1 ]i- rebound or shock, while there was in addition an unmistakable systolic rcces* si<ju o{ the fifth interspace, from the border of the ster- num to a point outside of the a j>cx-i u I pu Ise. Ca rd iac dul- ness extended from the right sternal kirder to ^ an inch outside the left nipple, and in the mitral area was a harsh systolic mur- mur that was transmitted to mid-axillary line (Fig. 22). Both heart-sounds were audible, and the second at the apex was followed by a short diastolic murmur. The inferior hepatic border was palpable 2 inches below the costal arch, and was thin, hard, and somewhat irregular. The pulse was slow, tense, and regular, and there was no icterus.
The diagnosis was plainly that of mitral regurgitation and
Ft a. 22. — 8iffjiws Cardiao Pi lnicj«» ani»
L<»CATlON or BoKUfiC OF LiVER,
CeRO?^iC PERICARDITIS
109
adhereDt pericardiimi with soeondary cirrhosis of the liver and ascites.
The chronicity of isuch a ease is attested by the fact that after repeated tappings and prolonged eoiifineiiient to the house this patient again appeared in public, and was accidentally encoun- tered by me in the fall of 1S95. He admitted that he was not very well, and that he still had his ascites. He died a few months sub- sequently. In this interesting case cardiac sj-mptonis did not as- sert themselves, and the clinical history was essentially tliat of atrophic cirrhosis of the liver, and would ordinarily pass for such.
The following case is narrated because of its interesting clini- cal course and instructive pathological findings: Mrs. M., aged forty-five, consulted me in Febriuu-y, 1893, because of an obsti- nate cough which had developed tlie November previous and re- sisted treatment. She gave a history of scarlatina at the age of seven, and of a pain, probably rlienniatic, in the right hip almost eontinuallv between her tenth and thirteenth years. She stated, also, that at that time she suffered from shortness of breath upon attempting to run or go upstairs, and at such times had an inclina- tion to faint. She thought her pulse had always been irregular, since whenever she had had cccasion to require the services of a physican comment was made upon its irregularity. She was mar- ried at the age of twenty-one, and two years later gave birth to her only child, both the pregnancy and hibour having been uneventful, excepting for a mild '" milk leg/' Fourteen years subsequently she became a widow. She had considered herself well except for nen-ousness and attacks of neuralgia. In the fall of l-*^92 was treated for pain and swelling of right leg, between ankle and knee, and for *' fulness and tightness ^' about the waist. In No- vember had contracted a bronchitis^ and since then had not been free from cough, although under treatment for same.
Her only symptoms at the time she consulted me ivere fre- quent paroxysmal cough, with scanty mucous expectoration, pain across the chest, in consequence of the cough, and moderate short- ness of breath on exertion. Digestion, bowel movements, and mic- turition seemed normal. She had passed the menopause several months before.
She was 5 feet 1 inch in height and weighed 145 pounds. The pulse was 103, somewhat irregular, not intermittent, small,
110 DISEASES OF THE HEART
and weak. The lungs were resonant throughout, and the breath- sounds vesicular; no rales except fine inspiratory crepitus at the extreme right base, close to the spinal column, and at the extreme lower limit of the left lung, from the anterior axillary to the pos- terior scapular line. These rales were thought to indicate old pleuritic adhesions. The apex-beat was in the fifth left space 2 inches from the sternum, broad, strong, and at times thumping. There was slight epigastric pulsation, and cardiac dulness was increased somewhat to the right.
The pulmonic second sound was accentuated, while the first at the apex was at times split and thumping, at times preceded by a short, rough presystolic murmur. A systolic apex-murmur was not very distinct. Xo signs of adherent pericardium were noted at that time either because overlooked, or because the chronic me- diastinitis did not develop until a year or two subsequently. The lower border of the liver, firm and rounded, was palpable nearly at the level of the umbilicus. There was no (xnlema.
The diagnosis was made of mitral stenosis in a fair state of compensation, secondary hepatic engorgement, and chronic bron- chitis, probably secondary also to the mitral disease.
Under appropriate treatment, directed mainly to relieving stasis in the pulmonic and general venous systems, cough gradu- ally <lisap|>eared, and the patient considered herself in fair health during the summer. In IMay it was noted that the pulse was 100, not intermittent, but slightly irregular in force. The following October, after I had returned from Bad Xauheim, and instituted the balneological treatment of heart-disease in my practice, the patient decided to try a course of baths. For a time they seemed to benefit her, but after about three weeks she said she began to notice increase in the size of her abdomen at its lowest part. I at once examined her, and to my surprise detected unmistakable signs of moderate ascites. The baths were discontinued in the belief that inasmuch as they had not prevented the development of ascites, they would not cause its removal.
From that time onward ascites gradually increased until in June, 1894, paracentesis was performed for the first time. From this time to the date of her death, a period of three years, the fluid was drawn off 32 times, the longest interval between the tap- pings being seven weeks and the shortest six days. In addition
CHRONIC PEftlCARDITIS
111
she took elaterin in large doses and various diuretic remedies. Palpation of the liver now showed that it had heconie thin, very hard J and deeplv notcdxed.
About two years before her death she began to suffer from what appeared to be attacks of subaente bronchitis. At sneh times there was mild continuous pyrexia an<l the cough was most harassing, often eifeetually pre vo^n ting sleep and requiring large doses of codeine phosphate. All known expectorants in various eomlnnations were tried with ajijiarently mi more effect than to facilitate expectoration. The only treatment that seemed of ma- terial benefit was truly heroic catharsis, since the withdrawal of the ascites seemed only to remove pressure on the diaphragm, but not to lessen the great venous engorgement.
These attacks grew Uiore frecpient^ the intervals between them shorter, luitil at last cough became chronic and jiersisted to tlie end. During these months I saw her but rarely, as her son, who was a physician, devoted himself to her care. At one of my visits, a year or more before her death, I discovered fine crackling rales all around the base of the right lung, particularly in front, which were brought out distinctly by deep inspiration, and were un- changed l\y cough. These rales eventually spread so as to be heard nearly to the clavicle, while as time went on similar crepitant sounds became audible more or less extensively at the base of the left lung. They did not st^m to have the characters of pleuritic friction, and I was at a loss to explain them. It may here be stated, however, that the autopsy subsBpiently showed them to have been due to wide-spread pleuritic adhesions.
A year before her death her son first detected systolic reces- sion of the intercostal space, close to the site of the apex-beat, and pulsus paradoxus. Bacilli w^ere never discovered in the spu- turn, and repeated examinations of the urine showed nothing more than tite usual changes due to passive congestion. The last months of life were spent in a continual struggle to keep within reasonable limits the ever-present and never-conquerable venous engorgement. Oedema of the lower extremities supervened many weeks Ijefnre the end, which finally took place in May, 1S97, with aynaptoms closely resembling but not identical with Tirfpmia.
Thanks to the intelligent study of the case by her son, the ante-
112 DISEASES OP THE HEART
mortem diagnosis was made of chronic indurative mediastino- pericarditis. Xo other signs ever developed than the few men- tioned above, pulsus paradoxus and a visible systolic recession in immediate proximity to the apex.
The autopsy was made by Dr. W. A. Evans twenty-seven hours after death, and was briefly as follows : The abdomen contained a small amount of fluid, and the omentum was adherent to the ab- dominal wall above the umbilicus and along the linea alba, adhe- sions being so firm that they could not be separated without tear- ing the omentum. The uterus was larger than normal, the right tube very firmly adherent to rectum and jwsterior part of the uterus, right ovary being normal; left tube also firmly adher- ent to the left side of the rectum and side of pelvis and posterior wall of the uterus, completely covering the left ovary, which was also normal. There was an exudate upon the anterior surface of the left broad ligament. The liver was adherent to the abdominal wall over both right and left lobes, the ])arietal layer of the peri- tomeum being thickened and its visceral layer showing evidence of old inflammation. The organ measured 9 by 5 inches, its right lobe 4 inches vertically, and its left lobe 2 inches in its antero- posterior diameter. The surface of the liver was markedly irregu- lar and divided by scars into large areas, its lower border being so notched that it was practically im])OSsible to make out the lobes. Its capsule was irregularly thickened, presenting the ap- pearance of lace-work. The substance of the organ was firm, cut- ting with resistance, and the lobules, very irregular in size, stood out prominently, and the connective tissue of the capsule could be traced into the underlying liver substance — in short, it was in a state of advanced Glissonian cirrhosis.
The right kidney, 5:J: inches long and 2^ wide and 2 thick, showed increase in the thickness of its capsule, some parencluTii- atous degeneration and interstitial overgrowth. The left kid- ney, 5 by 3 by If inches, with capsule firmly adherent in places and thickened, showed other changes the same as in right kidney.
The spleen showed marked thickening and some interstitial splenitis.
The gastro-intestinal tract showed no especial changes, except that the peritoneal covering was thickened.
The appendix was firmly bound down to the right iliac fossa
CBRONir PERICARDITIS
118
by a solid mass of adhesions behind the ca^cimij and was less than 1 inch in length.
The right pleural cavity was the seat of very extensive adhe- gions, which were most firm anteriorly and more abundant at the apex than at the base. There was considerable fluid in this cavity, and the lung was firmly attached to the diaphragm. The pulmo- nary pleura was thickened, and on section the surface of the lung showed considerable anaemia, no tuberculous nodules, and no in- flammation.
The left lung was adherent at base anteriorly and also poste- riorly, adhesions to diaphragm being very solid. At apex was a superficial calcareous mass attached to the visceral pleura, and in other respects the left lung was of the same appearance and con- dition as the right lung.
The pericardium was attached to the pleura? and chest-wall, and in situ felt like a solid bony shield, reaching to the sixth rib and i an inch within the left mammary line. Upon removal of the heart it was found that the organ was completely incased by se%*eral calcareous platens, which were closely in apposition with yet separated from each other, so that the lines of separation had allowed the heart to undergo contraction and relaxation. These plates of lime united the two pericardial layers firmly. The walls of the several cha miters were hy pert ro phi ed, ]iarticuhirly the left auricle and right ventricle. With exception of the left ventricle the cavities were all moderately dilated. The heart-muscle had the appearance of brown atrophy. All valves excepting the mitral were healthy, these being thickened, stiffened, adherent along their edges, and projected into the cavity of the ventricle like a cone or funnel. The mitral orifice was moderately thickened with old sclerotic tissue and admitted one finger.
To me it is very interesting and quite remarkable that the pa- tient was never able to give any history of an attack of pericar- ditis, which the necropsy showed must have been very extensive* It probably occurred at so early a period in childhood, perhaps subsequent to the scarlatina, that it failed to be impressed on her memory, or was not discovered at the time. If it was secondary to the scarlet fever, forty-one years elapsed before it finally led to the patient's denth. The post-mortem findings, furthermore, revealed in a striking manner the extent to which chronic pro* 8
114 DISEASES OP THE HEART
liferative inflammation may involve other structures, notably the liver, and may lead ultimately to the clinical features of hepatic cirrhosis with ascites. The adhesive inflammation of the pleurae probably occurred at the time when the patient manifested a low grade of fever with cough, and fine, dry crepitus over the front and base of the right lung, and subsequently also of the left. This case also illustrates the chronicity of some of these cases, and the fact that death is the result not so much of cardiac asthenia as of the effect on the system of the associated conditions. That etio- logical data in such cases are frequently wanting, and that there- fore the primary cause of the symptoms may be unsuspected to the end, is shown by the following case :
Mrs. D., a physician's wife, aged forty-six, was first seen by me December 24, 1S94, because of increasing sj-mptoms of cardiac disease. Her statements were positive that with the exception of measles and whooping-cough in childhood she had never been ill before the onset of her present trouble. She had been a school- teacher up to her marriage three years before. Her husband stated that he at first noticed tachycardia shortly after marriage, but no other symptoms had been observed until ilay, 1S94. She then developed dyspna*a on exertion, and occasionally oedema of the lower extremities and face. During the summer of 1894 she took sulphate of strychnine, digitalis, strophanthus " off and on " without a]>j)arent benefit, but had recently shown some im- provement on iodide of potash and belladonna. Her menses were absent since July ; the only symptoms complained of were slight, dry cough, a not very marked breathlessness on exertion, a feeling of weakness, and occasional pufliness of the lower extremities.
She was of medium height and well nourished. Examination discovered signs of fluid in the right pleural cavity, reaching to the lower angle of the scapula, and some fine crackling rales at the extreme posterior left base that grew more abundant after cough.
Otherwise the lungs were negative. The pulse was small, weak, regular, and moderately accelerated. The apex-beat was in the fifth left interspace, just outside the nipple-line, diffused and weak. There was no epigastric pulsation, but at the level of the fourth costal cartilage deep-seated cardiac dulness reached from 1
CHRONIC PERICARDITIS
U5
inch to the riglit of the sternum to fully midway between the left nipple and the anterior axillary line (Fig. 23), There were no mnrmurs, but the first sound at the apex was weak and the second at the base rediiplieatedy the pulmonic second being accentuated. No signs of adherent pericarditis w^ere noticed. The lower hepatic border was palpable at the level of the unibilicus, and was thin and hard. The spleen was not enlarged, mid there was no ascites.
The ease was considered one of general cardiac dilata- tion supervening upon a previ- ous hypertrophy of the left ventricle and upon the in* creased pubnonary blood-pres- sure occasioned by the fluid in the right pleural cavity. How much of the increase in heart's dulness to the left was attributable to dibitation. and how nnieli to traiispi^-i tion of the organ from [un- sure by the intrapleural fluid, was left an o|*en question. In the absence of a definite his- tory of pleurisy and of other signs of drox)sy, the nature of the liquid in the pleural cavity, whether an exudate or transudate, was a matter of doubt. The liver was evidently cirrhotic. Exam- ination of the urine was negative.
In spite of physical rest, digitalis^ diuretics, and cathartics, the amount of intrapleural fluid remained stationary fur the next three weeks. Paraeentesis was then performed, and the fluid rap- idly reaccumulating, the operation was repeated within a week. After the second aspiration the fluid mounted to the upper level of the third rib and symptoms of pressure increased. It was then decided to try the efficacy of t)iUhs (Bad Nauheini). These were endured so badly, however, that they were discontinued after four days. By Febrmiry Hth the actual embarrassment had become so pronounced that this fact, together with the failure of paracen- tesis to permanently reduce the amount of pleural effusion, led the
Dil:*ic.*», AMU Ljv»u Borukh m Ca»k (p. 114).
116 DISEASES OP THE HEART
consulting surgeon to advise resection of a rib in the hope that permanent drainage would afford time and opportunity for the heart to regain its former vigour. The proposal having been laid before the patient and her husband, and their consent obtained, the operation was done the next day. Everything seemed to pro- gress favourably for a few days, when suddenly symptoms of pro- nounced fibrinous pleuritis developed in that side. Temperature rose to 102° F., strength waned rapidly, and the patient died ten days after the operation. I may say here that the infection was subsequently proved to be a pneumococcus one.
The autopsy was made by Dr. Hektoen twenty-four hours after death, and the findings may be briefly stated to have been a totally adherent pericardium, with several plates of lime-salts upon the surface of the ventricles, the largest lamina being about the size of a silver half dollar. The sac was also bound by adhesions to the left pulmonary pleura, but not to the chest-wall. The valves and myocardium seemed normal, there was evidence of recent right- sided pleurisy with collapse of the lung, and acute <pdema of the left lung with some fresh diaphragmatic pleurisy on that side.
The liver was cirrhotic, but not atrophied. Kidneys were healthy, and there were evidences of perihepatitis and peri- splenitis.
The necropsy seemed to make it evident that the condition within the right pleural cavity had been a hydrothorax, while the pericardial adherence explained why medical treatment had been unavailing. Had this patient lived, and time been afforded for shrinkage of the liver to take place, ascites would undoubtedly have developed, and the case have presented the clinical features of what Pick terms pericarditic pseudocirrhosis of the liver, the same as did the others.
In explanation of ascites in such cases Heideman lays dowTi the four following propositions: (1) In these cases there is chronic inflammation of all the serous membranes. (2) The stag- nation occasioned by degeneration of the cardiac muscle leads to ascites, because on account of the chronic peritonitis the peritoneal vessels offer a locu^ minorus resistentice, (3) The cirrhotic pro- cess in the liver so often observed under these circumstances is oc- casioned by extension of the inflammatory irritation from the capsule of the liver as well as by the chronic hyperiemia. (4)
CHRONIC PERICAKDITIS
117
By the growth and contraction of this connective tissue in and about the liver tlie stagnation and transudation in the abdominal cavity are increased.
Course and Termiiiatioii. — The course of chronic adhesive |,jerieanlitis varies much, depending upon the extent of the adhe* sions and the coexistence or not of other diseases, as chronic valvular lesions. If the process is confined to obliteration of the sac the condition may last for many years, and the patient subse- quently die fruni some independent a if eel ion. Usually, however^ the same as when mediastinopericiirditis leads to extensive union with the surrounding parts, the disease^ after having persisted for a long time without symptoms, is likely to bring about those cir- culatory and respiratory disturbances already Jeseribedj and so well illustrated by the foregoing cases. If adherent pericardium is associated with valvular disease it affects the latter injuriously^ and its more rapid course is inseparably connected Avith that of the endocardial lesion. In such a case cardiac breakdown is inevita- ble, and not likely to be long postponed, Nevertheless, even here much depends upon the treatment and upon the patient's intelli- gent appreciation of his condition* In the case of the young lady whose mitral insuificiency is sadly complicated hy adhesion of the left side of the heart and apex to the retracted lung-border and chest-wall, s\^nptonis of right ventricle failure came on only three years after her first attack of rheumatism, and were undoubtedly hastened by the pericardial adhesions (see page 100). It is now nearly eighteen months since her symptoms l>ecame alarming^ and the fact that her overburdened right ventricle is to-day actually doing better work than a year ago is due to the persistent use of appropriate remedies and to her having learned that so soon as the first signal of danger is perceived she must take to her bed until the right heart recovers its tone.
The manner in which many cases of this affection terminate has already been made apparent. Either the symptoms are those of atrophic cirrhosis of the liver or they are indicative of cardiac insufficiency of mitral disease. Either stasis in the systemic veins and viscera increases until the patient succumbs to general exhaus- tion, or in another set of cases he is worn out after months or years by the ever-rwurring ascites, the heart not evincing s^iecial weak- ness. According to Kussmaul, pulmonary infarcts are particu-
118 DISEASES OF THE HEART
larly frequent in cases of chronic mediastinopericarditis, and these may prove the cause of death.
PhyBical Signs. — Inspection. — The ease and certainty with which adherent pericardium can be recognised clinically depend upon the situation and extent of the adhesions. If the sac is bound down to the heart, but not to surrounding parts, the condi- tion does not of a necessity produce recognisable physical signs, and this fact explains why sinechia pericardii is so often first de- tected on the post-mortem table. In the cases in which an adher- ent pericardium is diagnosed there are generally adhesions be- tween the sac and some of the surrounding structures, as the ante- rior thoracic wall, the pulmonary pleura on either side, and the diaphragm.
Accordingly, it is in cases of chronic indurative mediastinoj>eri- carditis that the diagnosis is most easily and frequently made. This is owing to the fact that the existence of adhesions interferes with the change in form and position of the heart normally occasioned by ventricular systole. During this phase in its contractions the heart becomes depressed at its base, and assuming a more rounded shape thrusts its point forward, upward, and towards the left, and thus produces the impulse against the chest-wall known as the apex-beat.
It is evident that if adhesions restrict these movements the heart will of a necessity jnill on the part to which it is bound. This pulling action is exerted during ventricular systole, and con- sequently the most obvious and the most frequently observed sign of adherent j^ericardium is a tumble sysfolic recession of the chest- wall. It may be perceived in various situations, but most com- monly in the neighbourhood of the apex-beat. Only a very lim- ited area may be thus drawn inward, but in most instances a systolic sinking takes place in several of the interspaces near the apex and even in the epi<rastrium, the extent and location of the adhesions determining the extent and position of this sign. It is best observed by placing the patient in a strong light, and then looking at the bared chest from above downward or from one side to the other.
It is well to have the patient suspend respiration for a mo- ment while inspection is being made, that the observer may not be deceived or confused by sinking of the soft parts incident to move-
CHROXIC PERICARDITIS
119
merits of the diaphragm. Ordinarily, there is but slight diffit-iilty in ileteeting this systolic indrawing in question. One should be careful, however, not to mistake for a sign of perieardial adhesions the systolic depression that sometimes takes place in the third and fourth interspaces close to the left border of the sternum iu cases of great cardiac hypertrupliy, and wliich is due to atmospheric pressure as the base and body of the heart recede from the chest- wall during systole.
As might be exj)eetedy it is the yielding soft parts that display systolic retraction most readily, and as it is possiltle that even near the aj)cx this may he o%ving to atmospheric pressure, this sign is not pathognomonic. The value of the sign is far greater, therefore, when the ril>s and end of the sternum are drawn inward together with tlie intcrsi)aces. 1 have not observed this, but it is said to sometimes occur.
Sir William TSrr>adl>eut first described a systolic retraction of the tenth and eltncntb interspaces below the inferior angle of the left scapula in cases of adherent pericardium, and hence it is often spoken of as Broadbenfs sign. It is occasionally |)erceived on the right side also. It is ascribed to tlie drawing on the diaphragm of a hyi>ertropbied antl powerfidly ci>ntracting heart, and when pres- ent is considered indicative of extensive adhesions between the sac and the diaphragm.
Gibson very justly attaches great importance to fixation or im- mobilily of the apex. Normally the heart, and hence its apex, gravitates towards the dependent side whenever the patient as- simies either lateral de<'!d>itus. 'When he lies on the left side the point of the heart strikes the chest-wall a couple of inches farther to the left than when he is on his back, while in the right lateral position the impulse is nearly or quite behind the sternum, and henre imperceptible. Cousei^uf^ntly in any ease in ^vhich this mo- bility of the apex is not observed, it is suggestive, nay indicative, of its fixation by external adhesions. The position of the heart's apex should also become lowered during the inspiratory descent of the rliaphragm, striking behind the sixth costal cartilage, or even the sixth interspace. The existence of adhesions may pre- vent this, and accordingly fixation of the apex during the two res- piratory acts is likewise a sign of adherent pericardium.
The other phenomena i)erceived by inspection in some cases
120 DISEASES OF THE HEAKT
are connected with the external jugular veins, and are (1) in- spiratory swelling of the veins, knowTi as KussmauVs sign^ and (2) diastolic collapse of the veins, known as Friedreich's sign. In my experience these signs are not as frequently met with as is the drawing inward of the interspaces, and I do not recall an in- stance of diastolic collapse of the veins. Kussmaul's sign is pres- ent when pericardial adhesions prevent the dilatation of the right auricle that normally takes place during inspiration. Instead of the inspiratory act exerting an aspirating effect upon the contents of the veins, and thus collapsing them, the opposite effect is pro- duced, and the jugulars become visibly distended. Diastolic col- lapse does not ap{>ear to be limited necessarily to the jugulars, since Broadbent has observed it in the superficial veins on the front of the chest, and says it was due to traction of fibrous bands on the coats of the internal mammary vein uniting this vessel to the peri- cardium, and causing its sudden dilatation during ventricular re- laxation. In the case of the cervical veins their diastolic collapse is probably to be explained by the aspiratory force exerted by the sudden diastolic rebound of the right auricle, pulled upon as it is by adhesions between it and surrounding parts. Two other physi- cal signs that remain to be considered are best perceived by the hand, and are therefore described under palpation.
Palpation. — In some exceptional instances the hand laid over the apex perceives a distinct sudden shock not synchronous with systole, but with diastole. It is spoken of, therefore, as the dias- tolic shock or rebound. It is caused by the pulling of fibrous adhe- sions which, put on the stretch during systole, pull the heart sud- denly back against the chest-wall after systole has ended. Such a rebound can scarcely be occasioned by any other condition than ex- ternal pericardial adhesions, and therefore by some is considered pathognomonic of the disease under discussion. I have observed it but twice, once in the patient whose case I have reported, and the other time in a man at Cook County Hospital who had, in addition, aortic insufficiency.
The second phenomenon observ^able by palpation is the pulfnis paradoxus. Xormally the pulse becomes fuller and stronger to- wards the end of inspiration, smaller and weaker towards the end of expiration. In the paradoxic pulse, on the contrary, the re- verse obtains, strong inspiration causing a diminution in the force
CBROXIC PERICARDITIS
121
and volume, it may be even an intermission of the pulse, while towards the close of expiration the pulse regains its usual strength and fulness. This peculiarity may sometimes be perceived in pericarditis with effusion, and therefore, while its presence serves to corrubonite other signs of adherent jKnica rdium, it in nowise can Ix? kxjked upon as pathognonnjiiic. Aside from enabling one to appreciate the two signs just mentioned* palpation is of service in determining the mobility or fixation of the apex and the degree of enlargement and den?^ity of the liver— conditions I deem of con* siderable importance in doubtful cases.
Percussion, — This is of great value in all cases of suspected or known heart-disease. In adherent pericardium cardiac h\"]>er- trophy or dilatation is very apt to exist, and hence one should in every suspected ease attempt by percussion to ascertain the limits of deep-seated dulness, since in the absence of any other etiological factor to account for enlargement, this condition would point to the likelihood of adhesions.
It is not unc*nnmon in cases of suspected adhesions for the area of absolute cardiac dulness to be increased in all directions^ particularly upward and to the left. This may be due to a simple crowding aside of the anterior lung-margins b\' a hypertrophied heart, yet the borders may be retracted and fixed by pleuropericar- dial adhesions. In this latter condition the line of demarcation between pulmonary resonance and cardiac dulness is unaffected by respiratory movements. Thereforej percussion is of service in enabling one to determine whether or not the lung-borders are bound down by adhesions.
Auscullafiotu — For the most part this is of negative value, particularly if the synechia pericardii is not associated with me- diastinopericarditis. In the latter condition auscultation some- times detects fine friction -rales alrmg the margins of the lungs where they join the area of superficial cardiac dulness; and if such parchment-like crackling sounds persist during the cessation of respiratory movements, they furnish strong proof of the existence of pleuropc*ricardial adhesions.
Roberts quotes Perez as authority for the statement that in Bome instances of chronic mediastino|>ericarditis a creaking sound upon the body of (he sternum is audible during up and down movements of the arms, I have tested this in several of my pa-
122 DISEASES OF THE HEART
tients, and in two I detected this creaking friction-sound described by Perez. As in these cases other positive signs of adherent peri- cardium were present, this sign of Perez possessed considerable interest, if not material importance.
Diagnosis. — From the foregoing description of the physi- cal signs it is apparent that in some cases the diagnosis of peri- cardial adhesions can be made almost at a glance, while in others the most skilful diagnostician may not be able to decide whether the pericardium is adherent or not. The difficulty is found in cases in which the two layers of the sac are united without adhesions to the surroimding parts. In such, one must observe critically the jugular veins and the radial pulse in the hope of detecting some of the anomalies that have been described. The size of the heart should also be mapped out by percussion, and the liver should be examined as to its size, density, and outline, since synechia pericardii may declare itself by no other signs than by its effect on these organs.
In cases of chronic indurative mediastinopericarditis the mat- ter of diagnosis is usually far less difficult. Indeed there may be a conjunction of several physical signs. Thus in one of my pa- tients the apex is firmly fixed far below and to the left of the nipple. There is systolic retraction of the soft parts between the apex and the epigastrium, and of the intercostal spaces below the left scapula. The anterior margins of both lungs are drawTi aside and immovable, causing nearly the whole heart to be uncovered, as shown by the great area of sujx^rficial dulness. The liver ex- tends nearly to the iliac crest and is hard and deeply notched, while owing to the enormous size of the heart and liver the front of the chest looks distended and smooth, and when the patient stands the abdomen ap])ears disproportionately large and pendu- lous. Pulsus paradoxus and inspiratory swelling of the cervical veins are also present.
Lastly, one should always be suspicious of an adherent peri- cardium in every case of rheumatic valvular disease, and if in such a case the liver resembles in thickness and density the organ in atrophic cirrhosis, yet is not so contracted, if ascites develops without apparent cause, or takes place prior to or out of propor- tion to anasarca, there is good reason to suspect the complication of an adherent pericardium.
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The differential diaynosis between Laennee's atrophic cirrhosis of the liver and the periciirditie pseudoeirrhosis just ecmsidcred is often the most ditlieult. Aid may he ohtttined hv attention to the following points: (1 ) In Laennec's cirrhosis there is often a history of aleohulisin, inahiria, or syphilis, while in the other form there may be a history of previous periearditis, a rheumatic at- tack in childhood^ or of some acute illness with pnecordial pain and other symptoms suspicions of pericarditis. (2 ) In Laennec*s cirrhosis ascites develops jvrior to anasarca, wherejis in rhe variety nuw Considered it may sometimes tVdlow nitjre or less oedema of the lower extremities (Pick). (:3) In the former there are no signs of heart-disease, while in the latter careful examination usually detects enlargement of the heart either alone or in combination with valvular disease* (4) In the |*seudo-ii trophic forui there may be some of the signs of adherent pericardium.
Finally, before leaving ttie subject of diagnosis of chronic peri- carditis, it is necessary to say a few words concern ing the recogni- tion of that rare form in which the chronic inflaitnmition is shown by fluid distention of the sac. In this variety there are apt to be pressure-effects, but if the effusion takes place insidiously such effects may not declare themselves. In such an event the effusion is usually detected accidentally, or if discovered its true nature may not l>e suspected* Roberts cites a ease reported by Samuel West of the existence of a supposed cyst which was rei>eatedly tapped during life» yet which after cleath was found to Iw^ a chronic peri- cardial effusion. Unless this condition is observed to have origi- nated acutely its diagnosis must depend njxm percussion and aus- cultation evidences of distention of the sac in accordance with the rules Uiid down for the diagnosis of acute pericarditis with effusion.
Prognosis.— If pericardial adhesions occur independently of other disease, and if not so firm or extensive as to materially ham- per the heart's action, they may in nowise affect life prospects. If, on the contrary, pericardial s\Tiechia is complicated by a chnmic vnlvc-lesion, the prognosis is unfavourable as to great length of life. If the heart is U^und down more or less completely to the surrounding parts, it is only a question of time when serious inadc<]nacy will develo|). In some cases the adhesive process is stationary, while in chronic indurative mediastinopericarditis the
124 DISEASES OF THE HEART
tendency to subsequent adhesive inflammation of other serous membranes and to the spreading of the adhesive process within the mediastinum furnishes an exceedingly grave outlook for the future. When ascites, anasarca, and other symptoms of the final breakdown appear there is small prospect of a restoration of compensation. Under such conditions the duration of life is likely to be bounded by a few months or even a few weeks. Although, as in the cases narrated, the struggle may be extended over a number of years, the patient is a chronic invalid at the best, and can only with great difficulty postpone the fatal event. The absence of all subjective and objective symptoms furnishes presumptive evi- dence that the adhesions are not extensive. If, on the contrary, symptoms of engorgement within the lesser and greater circula- tion are never wholly absent, they afford the basis for unfavourable prognosis. The greater the secondary cardiac hypertrophy and dilatation, particularly in children, in whom chest capacity is small, the slighter the prospect of the long retention of adequate compensation. When the last stage of the journey is reached it is likely to be a short one.
The prognosis of chronic pericardial effusion depends upon its etiology and the length of time during which it has existed. It also depends upon its association or not with some other disease, as chronic nephritis, and upon its amenability to treatment.
Treatment. — It goes without saying that we possess no means of breaking up the pericardial adhesions; at the most we can only strive to lessen their ill effects and to prevent an exten- sion of the process. In our endeavour to accomplish the latter, any rheumatic attack or acute illness, no matter how trifling, should be promptly and energetically combated by appropriate means. The patient should be at once confined to the house, and if possi- ble to the bed, in order to relieve the heart of any unnecessary work, and thereby if possible prevent fresh pericardial inflamma- tion or restrain the activity of the process, sliould the pericardium again become attacked. Salicylates, counter-irritants, or other mild antiphlogistic measures are in order.
The chief aim of management should be to preserve compen- satory hypertrophy, and so far as possible to minimize the ill ef- fects produced by the cardiac disorder. In my opinion, the first essential is that the patient be not left in absolute ignorance of
CHRONIC PERICARDITIS
125
liis eonflition, le^^t he fail to grasp the full importance of the rules laid down for his guidauce. Most individuals are greatly alarmed by being told they have heart-disea&e, and therefore great judg- ment and tact are required in imparting such information. If the patient has no suspicion of anything being wrong with his heart, and is of a nervous, excitable temperament, he would better be uAd only a imrt of the truth. It may be stated that his heart is not strong, and that if he will prevent the development of serious trou* ble he must obey certain injunctions, the careful observance of which will preserve his health. In other instances the whole truth may be told plainlyj but in a manner not calculated to create alami. Only in this way can we exj>ect our patient.^, ignorant of physiol- ogy' and pathology, to avoid harmful efforts^ and to correct injuri- ous habits.
In a word, a heart handieap|ied by extensive adhesions, and perhaps also by serious valvodisease^ must not be given more work to perform than it is capable of without strain. Inasmueli as what will be said on this subject in the chapters devoted to the treat- ment of Valvular Disease in General is applicable to the affection now under consideratioUj the reader is referred to those chapters for the details of this part of the managemeot.
The injurious secondary effects of adherent pericardium are not limited to the heart, but are also felt by the organs of diges- tion and elimination. Congestion witliiu the portal system nuist be diminished from time to time by the administration of a brisk cathartic. The patient, and even the physician, often rest con- tent with the fact tliat the bowels move regidarly every day, and lose sight of the benefit derived in these cases from penodifafff/ unloading the liver* Xothing is better to this end than a blue pill or a grain or two of calomel, followed the next morning by a glass of some saline aperient water. The patient should remain under the regular, though perhaps not very frequent, supennsion of a physician, who, detecting early indications of cardiac strain, may promptly meet the danger by onlering an appropriate beart-tonic. Digitalis and strychnine should not l>e given as a routine practice, but should be reserved for times of emergency.
As a rule the sjvmptoms pointing to overstrain on the part of the heart can be allayed by regulation of the diet, restricting the amount of work or exercise, and it may be by insisting upon rest
126 DISEASES OP THE HEART
in the house for a time. The food should be relatively rich in proteids, moderate in quantity, and taken at regular inten'als. If the individual is inclined to corpulence, or suffers from fermenta- tive indigestion, carbohydrates and fats should be allowed spar- ingly. Unrestrained consumption of fluids is objectionable, since it is a very easy matter for the intake of liquids to greatly exceed the needs of the system and the eliminating power of the excretory organs.
When the breakdown of compensation at length comes, with all its attendant manifestations, the case is to be managed in ac- cordance with the principles governing the treatment of the same condition in any other form of cardiac disease. It has been my experience that one cannot exixK*t or achieve as brilliant results from the emplojTiient of digitalis in these cases as in vahnilar affections unfettered by adhesions. It is not so much a question of whipping on the jaded heart as it is of relieving it of as much of its load as possible. Physical rest must be strictly enforced therefore, and catharsis must be brisk. Digitalis must be given for the purpose of invigorating rather than greatly slowing the heart, and with a view of obtaining its diuretic effect. Diuretin and other diuretic remedies are also in order. It is now that strychnine is of particular service, and to produce its most bene- ficial eflFects it should be administered hypodermically. Pain, cough, insomnia, and other distressing sjTnptoms are to be relieved as they arise. One should not hesitate to remove ascites by aspi- ration whenever it accumulates to the extent of seriously embar- rassing the heart and respiratory organs. If the anasarca does not yield to appropriate remedies, it may be drained off by the use of Southey's tubes or by incising the ankles, always under strict aseptic precautions.
CHAPTER III
HYDROPERICARDIUM - HiCMOPERICARDlUM - PNEU- MOPERICARDIUM-TUBERCULOSIS OF THE PERI- CARDIUM-SYPHILIS OF THE PERICARDIUM-CAR- CINOMA AND SARCOMA OF THE PERICARDIUM
L nYDRoPEBICAHDIUM
By tliis term 18 meant a transudation of senim into the peri- irdial sac. It h a noii-inflauiiiiatorv pnxiess, and the analogue of what takes place under similar conditions in other serous cavi- ties. The presence in the periearflium of 1 or 2 drachms of serum may be regard€?d as phy.siological ; the condition is patholugieal only when the transudate reaches such an amount as to constitute a veritable dropsy (hydrops pericardii). Although the condition is the counterpart of transudation into other serous cavitieSj it does not occur with anything like so great frequency as hydro- thorax and ascites.
Morbid Anatomy. — Upon the chest heing open the pericar- dial sac is found more or less distended and iliictuating, the same as in pericarditis %vith eif nsion ; a great difference is tliscovT^recJ^ however, when the sac is opened. Instead of fibrin-masses and other evidences of inflaiiunation, together with a serous exudate, the sac contains a clear, straw-cohmred fluids poor in albumin, and containing very little if any fibrin. Because of its relative defi- ciency in albumin the specific gravity of the transudate is lower than that of a sero-fibrinous effusion, ranging from LOOS to 1.015. The pericardial tissues may look more or less oedematousj but aside from this appearance and being filled with serum, the sac presents nothing worthy of note. In addition, there are assoeiated changes in other tissues and organs^-snch as redema, depending upon the same cause as the hydropericardium; as chronic diseaees of the heart or kidneys, or both, which have served to bring about
127
128 DISEASES OF THE HEART
the serous transudation into the sac. The transudation into the pericardium varies in amount from a few ounces to several pints.
Etiology. — Hydropericardium is a dropsy, and therefore is produced in the same manner and depends upon the same variety of causes as dropsical fluid in other situations. The causes may be divided therefore into general and local. The general include chronic cardiac disease, nephritis, both acute and chronic, and ca- chexias. By local causes are meant those diseases, such as tumours, which, situated within the thorax, exert pressure on neighbouring blood-vessels, and thus bring about stasis in the veins and capil- laries of the pericardium. Chronic heart-disease leads to dropsy in the same way, but the stasis within the pericardial vessels is only a part of a general condition.
Symptoms. — These are likely to be overshadowed by those of dropsical accumulation in the pleural cavity and general venous congestion. If by chance hydropericardium exists alone, a very rare event, or forms the leading pathological condition, the s^Tiip- toms are those resulting from pressure, and consist of the same phenomena of circulatory and respiratory embarrassment as are observed in cases of extensive sero-fibrinous pericarditis. Dysp- na*a is more or less marked, and may even amount to orthopnoea ; cyanosis and venous congestion are also present, and the pulse is small, feeble, rapid, and it may be irregular. The more rapidly the hydropericardium supervenes the more pronounced the symp- toms. As dropsical distention of the sac, when it develops in the course of chronic cardiac or renal disease, is one of the terminal events, it develops so slowly that symptoms are likely to l)e hitent, and therefore escape notice.
Physical Signs. — Inspection. — This affords but little if any information, owing to the fact that in most cases distention of the chest has already been produced by associated hydrothorax or the heart and lungs have been crowded upward by ascites. Shoul<l some local disease have occasioned the hydropericardium, and the thoracic parietes be sufficiently yielding, there will bo more or less pnecordial bulging, together with absence of cardiac impulse.
Palpation, — What has l)een said regarding inspection applies also to palpation. The chief, and perhaps the only thing noted, is absence of cardiac impulse, and possibly a sense of increased prse-
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cordial resishiiifo, The {nihe presents nntliing characteristic, since tlie fhangcs ubserved in it arc ali^o produced hy the primary cardiac affection.
Percussion, — This affords us our chief means of diagnosis, the same as in pericardial effusion; for jiarticolars tiie reader is re- ferred to what has aln^ady heea said nmler that head. Owing to the prohable association of hydroi>ericardium with hydrothorax^ the characteristic shape of pnccurdial dulness is likely to be modi- fied by and merge into that of the latter affection* Under such cireumstanees, it would onlj Vm* at the upper part of the sternum that percussion might Ik* of any sfiecial vnhw as regards the detect tion of the hydropt^ricardiuuL If the area of cardiac flatness exicuds high np towards tiie suprasternal notch, with a bluntly rounded a|>eXj well above ihe area of dulness due to the hydro- tharax^ this fact mightj theoretically at least, be of aid in deter- ntining the existence of transudation into the pericardium,
AuscuKadon.- — Owing to the intervention of Huid between the heart and the chest- wall, cardiac ^o//m/.s' are feeble and didanl^ and they may indeed be almost inaudible. If murmurs, due to some pre-existing valvular disease, are also present, these are likewise enfeebled.
Diagnosis. — ^From the foregoing considerations it is evident that the diagnosis of hydro{>ericardinm is not oidy difficult, but may be actually impossible.
In those extremely rare cases of pericardial dropsy due to local causes the diagnosis is go%'erned by the same principles as in mass- ive pericardial exudation.
Tlie difjerenfial diagnosis between these two conditions is to lie made by the history, syiuptoms, associated diseases, and pres- ence or absence of pericardial friction. In effusion there is his- tory of rheumatism or some acute infectious disease, of pyrexia, pneeordial pain, palpitatiiUi, etc. Even in distention of the sac pericardial friction-sounds may be retained. In hydropericar- diuni, nn the other baud, tliere is history or evidence of some chronic vaK^ular or rcmil disease, and all symptoms of acute in- flammation are wanting, and there is no pericardial rub.
Prognosis, — This is nnfavrairable, both Iwcause of the natui*e of the primary disorder to wliich the hydropericardinm is secoTuT- ary, and because the distention of the sac is likely to hasten car-
130 DISEASES OP THE HEART
diac failure. The prognosis is also influenced by the amenability to treatment of the cause of the dropsy.
Treatment. — This resolves itself essentially into the treat- ment of the primary disorder, since with the removal of the gen- eral dropsy the fluid within the pericardium is absorbed. Unless the symptoms be exceedingly threatening, surgical treatment, if not actually unwise, affords only a very temporary relief. In other words, the treatment of hydropericardium is unavailing un- less its cause can be removed. The management of dropsy when associated with chronic cardiac disease, will be found fully nar- rated in subsequent chapters.
II. HiEMOPERICARDIUM
By this term is not meant hsemorrhagic pericarditis, but an extravasation of blood into the pericardium independent of any inflammatory process. It is fortunately a rather rare condition, and yet occurs many more times than it is recognised. It requires but very brief consideration.
Morbid Anatomy. — As with serous transudation or effu- sion, the escape of blood into the pericardium causes a distention of the sac proportionate to the amount of the extravasated blood. If the haemorrhage takes place rapidly the amount discovered post mortem is usually not large, because it has speedily occasioned the death of the patient. If, on the other hand, it takes place slowly, the sac may be greatly distended. The blood may be wholly fluid or have undergone more or less coagulation. After the evacuation of the i)ericar(lial contents, careful scrutiny discovers evidence of some one of the causes of the haemorrhage.
Etiology. — Blood may be effused into the pericardium in consequence of external injury, as by gimshot or stab wounds, laceration of the sac by the sharp edge of a fractured rib, etc. It also follows rupture of the heart-muscle, the bursting of an aortic aneurysm, or in rare instances, of one of the coronary arteries. It is stated that sacculated aneurysms of the ascending arch fro quently rupture into the pericardium. Of 953 cases of aortic aneurysm analyzed by Hare and Holder, death took place from rupture 289 times, and of these, 75 cases ruptured into the peri- cardium. Rupture of the heart occurs from degeneration of the myocardium, and is fortunately a comparatively infrequent event.
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181
Laceration of tlie heart-wHll bus cKrcasionally been observed to fol- low a enisiiiiig injury to tlie ehest
Symptoms. — As would natiirally be expected, hieniorrliage into the pvericardial sac occasions the very gravest symptoms. If this takes place slowly through a minute slip in the wall of the heart or aurta, Hymptoms vjiuw cm gradually, and are thuse of acute anaemia, together with slowly induced and progressive heart-fail- ure. These are a sense of priveordiul tlistres?^, anxiety, wcniktiess and prostration, dyspnoea, pallor with cyanosis, a weak, rapid, perhaps irregular, pulse, coldness of the extremities, and clammy perspiration. Death takes place within a few hours, or perhaps a day or two.
Should the hsemorrhage lie free, and the sac become rapidly distended, the symptoms are those of sudden and profound shock, the patient passing quickly into a state of collapse, and dying in a few minutes. If the rupture does not occasion appreciable pain there may be nothing in the symptoms to direct attention to the pericardium. In most instances the course is rapid, leading to a S{)eedily fatal termination.
Physical S%iib. — These are the signs of fluid distention of the sac, and hence do not require repetition. In the majority of instances death is too rapidly induced or the distention of the pericardium too small to occasion appreciable physical signs.
Diagnosis. — If the life of the patient is sufficiently prolonged, and if the sac is sufficiently fille<l, it is i)08sible for the tnie nature of the difficulty to be recognised by exatuination of the priccor- diuni. If the presence of fluid in the ]iericardium is made outj the history of its sudden apjfrearance and the symptoms of shock and collapse will probably enable one to surmise at least the true na- ture of the malady and to difl^erentiate it from liydropericardium. Diagnosis may also be facilitated by history of some antecedent affection as aneurysm, likely to lead to haemorrhage.
Prc^nosis,^ — If h<Tmopericardium results from trauma, the prognosis dt-pends ujK)n whether or not the injury is amenable to surgical treat nient. In cases due to aortic or cardiac rupture the prognosis is absolutely unfavourable, and death is the inevitable^ it may bc^ the immediate, result.
Treatment. — This in traumatic cases is surgical, and is best left to text-books on surgery. In the other class of cases there
132 DISEASES OF THE HEART
is no treatment, except possibly in those rare instances of trau- matic laceration of the heart, when the surgeon should promptly lay open the sac, evacute the blood, in the hope of discovering the source of the luumorrhage, and of being able to repair the injury by suturing the heart-muscle.
Medicinal treatment is limited to stimulation of the heart and an attempt to support the powers of life. In most instances the physician arrives on the scene too late to do more than witness the death-struggle or sign the death-certificate.
III. PNEUMOPERICARDIUM
This is so extremely rare an affection that but few have been so fortunate as to observe an instance of the kind. By this term is meant a collection of air or gas within the pericardial sac, and hence it is the counterpart of the condition known as pneumo- thorax.
Morbid Anatomy. — Pneumopericardium is usually associ- ated with collection of fluid, most commonly of pus, within the sac. The amount of contained air or gas is variable, but is suffi- cient, together with the exudation, to occasion great distention. If the gas is not absorbed, and the pericardium be opened post mortem, the gas escapes with a hissing noise and often possesses a fditid odour. In some instances its avenue of entrance can be easily ascertained, while in others there is no discoverable 0}x*n- ing into the pericardium, either because, if such have existed, it has become closed, or because the gas has been generated in loco. There are usually present also evidences of acute i)eri- carditis.
Etiology, — Pneumopericardium may be produced in any one of three ways: (1) Perforation of the sac from without may allow of the entrance of atmospheric air; (2) communication may be established between the sac and some portion of the digest- ive tract, thus permitting the ingress of the gases normally exist- ing in the latter; or (3) gas may be generated within the peri- cardium without solution of its continuity. The entrance of atmospheric air into the sac usually takes place through a perfo- rating wound, as from a bullet or some stabbing instrument. In rare instances air may enter the pericardium through the lung in consequence of laceration by the sharp edge of the fractured ster-
PNEUMOPERICARDIUM
133
num or rib, or by rupture of a pulmonary cavity situated in im- mediate contiguity to the sac.
When a communication is established between die jTerieardium and a-sophagus, air is forced into the former with eaeh act of swal- lowing. Walshe has narrated an interesting ease of perforation of the pericardium J and resulting pneumo]K*ricardiumj during an attt'inpt by a juggler to swallow a i^hort sword.
When gas is admitted to the sac from some one of the lioUow viscera it is usual Iv in consequence of the extensi(m of a previ- ously existing ulcerative process. The most frequent communi- cation formed in this way is with the stomach, by reason of an ulcer, w^hen situated on its posterior walL Of 28 cases of [perfora- tion of the diaphragm by gastric ulcers collected by Liidwig Pick, only 10 were cases in which the uleeration had perforated the pericardium. Colling wood Fen wick records a very interesting case which t>eeurred in his practice^ in which a gastric ulcer had perforated the pc*ricardium with an immediately fatal result, and yet no previous symptoms had tH^curred to point to the presence of the gastric idcer. In 4 of tlie 10 cases collected by Pick the tw^o surfaces n{ the pericardium hiid hecome adherent hefore the ulceration had perforated, so that the ulcerative process involved the substance of the heart itself. Ulceration into the sac may also take place from the cpsophagus, but, as already stated, atmos- pheric air is then admitted, instead of stomach or intestinal gases.
In the min<ls of some, f he spontaneous development of pneumo- pericardium is a matter of douht. Gibson is of the opinion that in some of the cases supposed to be of this origin the pneumoperi- cardium was in reality the result of an opening into the sac, which, however, l>ecame so quickly and perfectly ctoseil that no trace of such opening could Ik? discovered. Nevertheless, the disc*overv of gas-forming Imcilli ronders intelligible and possible the spontaneous development of pnenniopericardinm, and may ex- plain some cases that w^onld be difficult or impossible to account for on any other hypothesis. This mode of production is exceed- ingly infrequent, to say the least. Such a pneumopericardium is preceded or accompanied by acute suppurative or ha^niorrhagic pericarditis.
Symptoms. — Suhjeetive manifestations are essentially those of sudden distention of the sac from any other cause. They are
134 DISEASES OF THE HEART
symptoms of pressure ; but inasmuch as the entrance of gas takes place suddenly, symptoms develop rapidly and are extreme. In some instances there are symptoms of shock; a weak, irregular pulse, a pale, anxious countenance, the skin covered with cold sweat, which, together with orthopnoea, produces a picture of mor- tal agony. The physician's attention is at once directed to the heart, the examination of which reveals a most singular group of objective symptoms.
Physical Signs. — Inspection and Palpation. — These afford evidence of pericardial distention but not of the nature of the dis- ease, and are of minor importance since the diagnosis is readily established by other means of exploration at our disposal.
Percussion. — The phenomena perceived by percussion are unique; instead of cardiac dulness, encroached upon and sur- rounded by pulmonary resonance, the pra»cordium is found to be tympanitic, either throughout or at its upper portion. If the peri- cardium contains fluid, as well as air or gas, there is dulness over the dependent part and high-pitched tympany above. Gas being lighter than the exudate, change in the patient's position from the recumbent to the upright, and from side to side, causes the gas to move about, so as to be always above the level of the fluid; hence there is change in the location of dulness and tympany ac- cording to the posture of the patient. In the erect position dul- ness occupies the bottom and tympany the apex of the sac. If the patient lies on his left side the fluid gravitates in that direction, with corrcvsponding dulness sunnounted by tympany ; and, on the other hand, the assumption of the right lateral decubitus causes a corresponding alteration in the relative }>osition of the gas and liquid, with resulting transposition of tympany and dulness. Moreover, the larger the amount of exudate the smaller the space allotted to the gas, and hence the higher the pitch of the tym- panitic note. Stokes claimed in one case to have detected " cracked-pot " resonance.
Auscultation. — Perhaps the most striking features are the peculiar sounds obser\^ed on auscultation. The movements of the heart cause an agitation of the gas and liquid contents of the sac, and hence a true succussion-sound or splnshing. This is variously described as churning, splashing, or like that produced by a water- wheel. These are sometimes accompanied by that musical sound
PNEUMOPERICARDIUM
13S
knoM^ as tlie metallic tinkle, likened to the dropping of water* This pericardiiti spbiihing is of preeiiseK' the same character aa the hypQcratic succuss ion-sound elicited hv shaking « patient with pneiimohydrothorax. In some instances these metallic sounds are aiidihle at a distance from the patient's chest.
Diagnosis, — This combination of a clear ringing tympanitic percussion-note with i^plashing in the cardiac area is so unique that an erroneous diagnosis can scarcely he made. It seems to me, therefore, far aticld to discuss the ditferential diagnosis between this affection and dihUation of the stomach or puhnonary vomica in immediate proximity to the heart, which are conditions said by some authors to render a mistake in diagnosis possible. Finally, the confuiniiliiig of tJiis disease with the presence of air and fluid within the pleural cavity is scarcely likely, if one will War in mind that in pneumotliorax the snccnssion-sound is only obtaine<l when the patient's Wly is agitated, w^hile in the affection under discission the peculiar sound is present even when the patient is at rest.
Prognosis. — This is always serious, yet in traumatic cases there is hope of cure through surgical iuterfereuce, while the same may be said regarding eases associated with purulent jieriearditifl. Should gas gain entrance to the pericardium, and l>e not followed by infection of the sac and inttammatiou, there is a possibility of its nhimate absorption. Moreover, the jmignosis dej>t*n<ls uixjn the suddenness of the formation of pneumopericardium. If this is sufficiently rapid to CH'casion symptoms of shock, there is strong likelihrxKl tliat the patient will succumb. If, on the other hand, the cfmdition dcvehi|)s slowly, symptoms may not be very urgent, and time nuiy l>e allowed for surgical inten^ention.
Treatment.— It jj^ix^s without saying, that in most cases if sur- gical skiil cininot remrne the cause, ottier treatment^ no matter how energetic, will be found unavailing. The same principles govern the therapieutic uuinagement as in other forms of pericardial dis- ease. Supporting and stimulating measures are aways indicated, and may eveu enal>le the patient to rally from the initial shock. Pain and distress should l>e relieved by a dose of morphine admin- istered hypulermically. Heat should be applied to the extremi- ties. Camphor, ammonia, ether, and brandy are useful stimu- lants, and should be given freely. The physician should not for-
136 DISEASES OP THE HEART
get the great value of strychnine and digitalis in supporting the heart; the former should be administered under the skin.
IV. TUBERCULOSIS OP THE PERICARDIUM
Morbid Anatomy. — Tuberculosis produces in the pericar- dium all of the characteristic lesions to which it may give rise in other regions of the body. The process may be acute or chronic in course, and either exudative, productive, or destructive in nature.
The acute process is not often to be distinguished from an ordinary acute pericarditis except by microscopic and bacterio- logical methods. The exudate may be fibrinous, scro-fibrinous, or purulent, but tuberculous pericarditis shares with the inflamma- tion of malignant disease the distinction of being the most fre- quent cause of hemorrhagic exudation in the pericardium. Tuber- cles may not be demonstrable post mortem, and when found are often exceedingly small, even microscopic. They are usually found on the parietal layer of the sac, owing to the frequency with which the infection extends from neighbouring viscera. The mil- iary tubercles may be covered by the fibrinous exudate, and are then to be discovered by detaching the fibrin. They may, however, be easily seen, and when collected in groups give rise to areas of caseation. These caseous areas may invade the myocardium, and in one instance a cheesy mass had perforated the wall of an auri- cle and projected into its cavity, being covered by a thrombus where it was in contact with the blood.
Again, when the production of granulation tissue is the pre- dominating feature of the process, the two layers of the pericar- dium are bound together by a bluish translucent mass of new- formed tissue. This of course becomes white as it grows older, and the condition of adherent pericardium is produced. Only rarely is the caseous mass calcified after the cessation of the active process — calcification being more common in the inspissated re- mains of jnirulent exudates.
Acute pericarditis is probably tuberculous in a larger propor- tion of cases than has been supposed, and indeed cannot be con- sidered a rare condition. Of 1,048 autospies on adults dead from all causes. Wells found this condition in 10 cases, or nearly 1 per cent; and since in 128 cases the pericardium was actively involved.
TUBERCULOSIS OF THE PERICARDIUM
137
the 10 case?a antoiiiit to alxmt 8 per cent. Osier reports 7 per cent fmni his serit^s of eiises,
Cliruiiic tul>erciikni8 perkanHtis iimy follow an acute attack, aiul in diis ease tlie post-niorteiu findings are those of an ordinary ehroiiit* pericanliti^, with the addition at times of gravish tiiher- ek*s, or of areas uii<lergoiiig caseous degeneration. It is the excep- tion, however, rather than the rule, to iintl distinct evidences of tiil>ereulons origin, even in cases in which the clinical history almost eonetnsivelv ji roves this. Indeed, in spite of the large nnnd^^r of cases of acnte pericarditis that are tnherenlar, and which pass on into the chrt^nic ft^rm, it is very exceptional to dis- cover any eonehisive jKist-mortem evidence of tnberenlosis in cases of chronic jK^ricardilis. The findings include thickening of the nn'nd.irane and more or less complete a<lhesions of the two layers, the translucent bluish grannlation tissue of flie acute stage having been replaced by firm, white eicatrieia! tissue,
Pericanlial tuberculosis may be chronic from the outset, in which event the lesions are more apt to be of a distinctly tuber- ciihms nature, tubercles and easeating areas being common.
Etiology •^ — Authors distingnish a primary as well as a sec- ondary furm of pericanlial ttdpereulosis. According to Osier, the primary form may be ** associated imly with caseation of the bron- chial or, particularly, the anterior nu;^diastinal glands,'' In other cases there are no such assrK?iated lesions, and in these the tuber- culous afTcction of the perieardiuiii is un possible to exphiin.
The secondary form is the one generally encounteredj and de- pen<ls upon previously existing tulierculouy disease elsewhere in the bixly. This may l>e caries of a vertebra^ a rib, or the sternum, caseous bronchial or mediastinal glands, tubcrcub^sis of the hing, pleura, or retroperitoneal lymph-glands, or tuberculous peritonitis. Occasionally miliary tubercles within tlie pericardium are a part of a general miliary infection.
This form of pericardial disease is nmst common between the ages of fifteen and thirty, yet has tieen seen in individuals at either extreme of life. Osier met with a case in a child of five, Duck- worth in an infant of only five months, and Lajard in a woman of eighty-eight. A jiatient of mine who died of pulmonary con- sumption, witli ac<|uired dextrneardia, and in whose adherent pericardiuni tubercles existed, was a young man of eighteen. The
138 DISEASES OF THE HEART
disease affects both sexes, but for some strange reason appears to be rather more common in males. Other predisposing causes are all those conditions that render an individual susceptible to this form of infection.
Symptoms. — In most cases the disease is wholly latent, and is only discovered on the autopsy table. This is due to the fact that the disease is generally subacute or chronic, and arises insidiously. If it gives rise to acute inflammation with effusion the sjniptoms are those of acute pericarditis from other causes — pain, palpita- tion, fever, friction-sounds, and, upon distention of the sac, the pressure-effects already considered. Even an exudative pericar- ditis of this origin may in some instances pursue a chronic course.
Physical Signs. — Objective manifestations of the disease are wanting unless the affection is declared as an acute process. When such is the case there are the fremitus, pericardial friction- sound, and, with filling of the sac by exudation, the evidence of fluid distention — i. e., triangular area of dulness and disappear- ance of the cardiac impulse, etc. ; in short, the signs already de- scribed in the chapter on Acute Pericarditis.
Diagnosis. — Owing to the insidious onset and latent nature of this disease it is rarely diagnosticated during life. If in the course of pulmonary tuberculosis or of pleuritis in a tuberculous subject the physical signs of pericardial involvement should make their appearance, one might with confidence make the diagnosis of pericardial tuberculosis ; but without such favouring conditions it is not at all likely that the disease would be discovered.
Prognosis. — This is not always serious so far as it affects the duration of life, yet it undoubtedly contributes its share to the unfavourable termination of the general tuberculous disease. Its remote effects are an adherent pericardium and cardiac insufii- ciency. The appearance of a tuberculous pericardial effusion in the late stages of pulmonary tuberculosis, the patient being al- ready cachectic, would undoubtedly hasten the fatal issue.
Treatment. — This is to be conducted on the lines already laid down for the management of other forms of acute pericarditis.
V. SYPHILIS OF THE PERICARDIUM
Invasion of the pericardium by syphilis is so rare an affection that most text-books on diseases of the heart either do not con-
SYPHILIS OF THE rERlCARDIUM
139
sider it at all or give it the very briefest possible mention, Eich- horst, for example, simply states that gummata in this situation have been described by Lanceroaiix ami Orth. In Allbntt's Sys- tem of Medicine I fail to find any mention of syphilis under dis- eases of the perieardiiim, and the same may be said of Hay den and Walshe in thc^ir classical works on the heart. Gibson^ whose remarks on this subject are more voluminous, devotes but a single page to it, and would seem to have been largely indebted to Mra- cek's paper, which has likewise furnished the inspiration for the following brief roiLsideration;
Morbid Anatomy, — Syphilis of the pericardiimi is always a very rare atfection, and is almost never met with unaasoeiated with syphilitic changes in the heart-muscle. When present, the disease is limited to the visceral layer and manifests itself either as gummata or circumscribed thickenings. Although cases have been described as syivhilitic jM^ricarditis with sero-fibrinous exu- dation, Mraeek is of the opinion that their syphilitic nature is open to doubt. Of the Uvo forms in ^vhich pericardial syphilis declares itself, fibrinous thickening is much the more common. At the time ilracek's monograph appeared only 3 authenticated
fcases of guuunii within the pericardiunj had been described — one each by Lancereaux, Orth, and Mraeek.
The portions of the epicardium that appear thickened and fibrous are usually foimd to overlie and be intimately connected with areas of pronounced myocardial fibrosis or a gumma situated within the heart-muscle. The development of connective tissue
•usually l>egins in the immediate neighl>ourhoinJ of the blood^ves- Bels, and then extends more or less widely into the surrounding parts.
In the second case of Mracek's series, in which the epicardium was thickened an<l elevated in a circumscribed zonCj immediately overlying a stoail ginnuia, the microscoix? revealed signs of recent
Knflanmiation of the adipose tissue. This tiasue was thickly infil- trated with cells, particularly in those parts next to the nmscle- snijstance and around the borders of the gummy tumour. Imme- diately above the gimmia there was, in addition to cellular infiltra- tion, a pronounced hyperamiia of the veins and capillaries. On the overlying surface of the epicardium the fibrous tiasue was old and finn.
140 DISEASES OP THE HEART
In the course of time the blood-vessels supplying the newly formed connective tissue undergo obliteration, and the latter be- comes transformed into firm cicatricial tissue. Thickening of the serous membrane is not necessarily associated with a deposit of fibrin, and consequently pericardial adhesions are not always ob- served. In some instances, however, the two layers are found loosely imited in the areas in which the connective tissue has undergone hyperplasia. Total obliteration of the sac is almost never encountered.
Syphilitic pericarditis is a very chronic process, much more so than is tuberculous pericarditis; and Mracck affinns that in those cases in which it is difficult to determine whether the process is tuberculous or syphilitic, the presence of a sero-fibrinous or hannorrhagic exudation tells in favour of its tuberculous origin. In cases of exudative pericarditis syphilis is the last thing to be thought of. In some instances the sac may be found to contain a small amount of clear serum, but when present this is a transuda- tion due to compression of the blood-vessels by the products of syphilitic disease. Very rarely hiemopericardium may also be produced, as in one ease by a rupture of a small cardiac aneurysm, itself the result of syphilitic fibrous myocarditis.
Etiology. — Syphilitic disease in this situation is a late mani- festation of the infection. There arc no known factors which determine its invasion of the })ericardial sac, but, as it is a consti- tutional disease, it is only singular that it is not more frequently present in this location.
Symptoms, — Syphilis of the jwrieardium either occasions no sym})tonis, or these are obscured by those of syphilitic disease in other j)arts of the body or in the heart-muscle. Inasmuch as pericardial changes of this nature are almost always found in con- nection with luetic disease of the mvocardium or endocardium, it is impossible to say how much, if any, of the s^^nptolnatology is to be attributed to the pericardial disease. It is highly probable, however, that the chief role in this respect is played by the myo- cardial degeneration or the sclerotic endocarditis, as the case may be. The cardiac manifestations will be fully described in the chapter on Heart Syphilis.
Physical Signs. — Kxc(»])t in the rare cases in which the pericardial changes lead to the development of a friction-sound
CARCINOMA AND SARCOMA OP THE PERICARDICM 141
or to (Iropsit'til dislontioii of tlie sac, (here arc no distinctive ob- jective si*i;ihs 4>f the loeal discMsc.
Diagnosis. — Even in a liielic patient with distinct cardiac symptoms, they are far more likely to be due to syphilis of the iiiyoeardium than of the perieardiiini, and hence une ri^liould be very guarded in luakini^ the dia|j:iHisis of the latter cnnditioiK The intra-viiafti n ■cognition of pericardial syphilis is on the whole, theref«>r<% very nnlikely.
Prognosis. — 7Vr .se pericardial sy|>hilis cannot be regarded as a dangerous aiTeetion ; the adliesions it induces are nsnally so cireuniscrihed and loose that they probably exert little if any in- jurious influeiiee in tlie way of cardiac hypertrophy and dilata* tion* In general it may l)e stated thai the prognosis is that of syphilitic disease of the heart-muscle, which, as experience shows, is very amenable to proper management.
Treatment. — This consists of the vigorous employment of mercury and the iodisles, and need not here he discussed.
VI, CARCINOMA AND SARrOMA up TUK PERICARDIUM
Malignant disease, like sy|>hilis, attacks the pericardinui with such infreqnency as to merit but brief consideration.
Morbid Anatomy. — Owing to the extreme rarity of pri- nuiry tmnours of tiie sac, but little can be said concerning them. Williams and Miller have reported a case of sarcoma of the peri- cardium in a boy of thirteen. The tumour was a diifuse, small- celled sarcoma of the parietal layer, which had produced uniform thickenings but had nut invaderl the e|neardiunL Tliere was no dis* eoverable involvement of the lyniph-nndes in any other part of the body, and for this and nther reasons the authors concluded that the [growth had originated in the lymphatic structures of the sac itself.
Of secondary tunmurs, those most commonly invading the sac are lymphosarcoma from the inetliastinal nudes, and carcinoma from the stomach ur (esophagus. The new growth may uniformly infiltrate the parietal layer of the sac, or single nodules may pro- ject into its interior. There is always more or less fluid in the sac, either of inflanmiatory or of dropsical nature. The inflam- mation due to cancerous disease of the pericardium is particularly apt to pr<Hluce a ha*niorrhagic exudate — being in this regard like the tuberculous disease.
142 DISEASES OP THE HEART
Etiology. — Primary malignant disease of the pericardimn is so rare that, according to Gibson, the only authentic case on record was the one observed by Koester. Sir William Broadbent has, however, reported an instance of sarcoma, which was thought to be primary, and I have mentioned above the case reported by Williams and Miller. In the vast majority of cases this affection of the sac is secondary to new growths in other situations, as in the oesophagus, lungs, pleura, mediastinal glands, liver, etc.
Symptoms. — As a rule this disease of the pericardiimi is latent or the clinical picture is that of the primary tumour.
Physical Signs. — So far as known, there are no distinctive physical signs of malignant invasion of the pericardium. If such are produced, they are those of secondary inflammation or of drop- sical distention of the sac, and require no repetition.
Diagnosis. — This is rarely if ever possible, and would natu- rally depend on objective manifestations of pericardial disease, which, as just stated, are very uncertain.
Prognosis and Treatment. — The former is hopeless, since the disease is not amenable to surgical interference, and the lat- ter must be confined to measures calculated to relieve suffering and promote euthanasia.
SECTION II DISEASES OF THE El^DOCARDIUM
CHAPTER TV
ACUTE ENDOCARDITIS
Tins is an intkiiiiiiation of tlie lining membrane of the heart, which it hits kjiig been customary to divide into two forms, for rea* sons apparent in tlie various adjectives applied to them. Thus one is called simple or benign, because it does not often destroy life directly, but permits the jKitient to recover, although with valvular lesion. The terms vegetative and verrueose are also ap plied to this variety, particularly by the Gennana, on account of the nature of the inflammatory changes induced. Simple and l»enign refer to its clinical manifestations, verrucosa and vegeta- tive to its aiuitomieal characters.
The other form, fortunately much less frequent than the pre- ceding, is spoken of as nmlignaut, to designate its usually fatal ending; and infectious or infect ivo, in allusion to certain etiological and clinical charaeteristies. Its anatomical features, on the other hand, are shown by its other names — ulcerative, diphtheritic, mycotic. Diphtheritic was applied to it by Virchow, and mycotic by Winge, who was the first to describe microbes in the valves.
In conformity with the plan of this work, which is to desig- nate diseases by their most familiar and generally employed names, these two affections will be spoken of as aeute simpte and aeufe vlremtive eu«hx'arditis. In accordance with custom, more- over, they will be considered as distinct clinical entities, although I am not mimindfnl of the fact that a sharp dividing line cannot always Ik* drawn between them either clinically or anatomically.
The endocardiimi nuiy liecome inflamed during firtal as well extra-uterine life; hnt the two halves of the heart are affected
143
144 DISEASES OP THE HEART
with different degrees of frequency during these two periods of existence. After birth it is the lining membrane of the left side that is generally attacked by inflammation, as is so well shown by Sperling's oft-cited statistics of 300 cases at the Berlin Pathologi- cal Institute. Of these, the left side alone was found affected 268 times, right heart alone 31 times, both together 29 times. Of the cases affecting the left side, the mitral valves were involved 255 times, the aortic but 129 times.
Morbid Anatomy. — The endocardium is the lining mem- brane of the heart, and is continuous with the intima of the blood- vessels through the various openings in the auricles and ventricles. It consists of two lamina} — a fibrous, very thin in most portions, and an endothelial, the latter consisting of a single layer of flat- tened cells, which are in contact with the blood.
The valves of the heart are folds of the endocardium, the fibrous layer being increased to give them greater strength. The valves contain no muscular tissue, and are avascular, with excep- tion of the attached margins of the mitral and tricuspid leaflets, which contain a few very small vessels. These are the only por- tions of the endocardium that contain blood-vessels, as the mural endocardium, as well as the remaining portions of the valves, de- rives its nutriment from the blood passing over it. Lymphatics are, however, numerous.
Anatomically, it is exceedingly difficult to draw any sharp dis- tinction between the benign and malignant forms, as all inter- mediate grades are found and the differences seem to be only those of intensity of the process. These differences are doubtless de- pendent on infection by different organisms, of which a large num- ber have been described by different investigators.
In the simple form tlie first change visible to the unaided eye is a cloudiness or 0})acity of the membrane. This is probably in all cases preceded by the lodgment of micro-organisms on the sur- face, which had been rendered v^ilnerable by some previous injury. Wyssokowitch, Prudden, and others have shown by animal experi- ments that cultures of i)athogenic bacteria, injected into the cir- culation, produce the lesions of endocarditis only when the endo- cardium has been previously injured, as by passing a probe down the carotid artery or jugular vein. This probably explains the fact that the lesions are most often found on the valvular endocar-
ACUTE ENDOCARDITIS
145
diiini, as tlie^e portioiii? art* most liable to injiirv. In intra-uterine life endocarditis h most common in tke right heart, and more often on the tricuspid than on the pnhaonary valves*
In extra-uterine life the lesions are most common on the mitral valve, next on the aortic, and only very rarely on the valves of the rijrht side. Furthermore, the lesions are usually found, not
Fi*i. 24.^ViiiKUOf>«K EirpooAKDtTiB «r Aortic ami IriiTRAL Valves. Spt>dmeii In collection of Dr. fiu»t«v Futtcren
an the free margins of the valve-cusps, but along a line correspond- ing to the point of maximum contact when the valves close (Fig, 24). In the caj^e of the aurieulO'Ventrieular valves this is on the auricular surface, while on the semilunar valves it is on the ven- tricular surface. From these facts it is evident that the work that the valve has to do and the strain to which it is subjected are fac^ tors in the determination of the location of the process* to
146
DISEASES OF THE HEART
FollowiDg fhe appearance of cloiuliness, the membrane becomes thit'kened and a-demataiis, while the straining and pounding to which the segiiients are subjected are very apt to produce erosions
1
Fio, a.'^, — VKRiirct>»« EsDocAnuiTift ttr MtTKAL V^alvr. Specimen in collection of 0r, Gu4«uv FuCUsrcr.
or lacerations. Tlie^^e naturally wcnr at the points weakened by the invasion of micro-organisms, and if the eroded surface is not at once covered by the deposit of fil»rin from the blood, a consid- erable loss of substance may take place. This is far more common, however, in the nuiliguant ff>rni, altbougli it has been oliserved in simple ein!<K'arditis couiplicatiiig rbeunnitism. Alore eoninionly the ororlcMJ surfacf^, necrotic from the action of bacteria, is at once centered by a deposit of fibrin from the IjhiiHL This fibrin forms a firm warty mass of a yellowish or reddish colour, which rises above the surface of the memlirane, and hence has received the name
ACUTE ENDOCARDITIS
147
of vegeiui'wn. The name is, howerer, not very itppropriote, ns the eo-ealled vegetation is in its furmation and eompositioii a throm- bus, and niay contain all tlie element?^ of a throinbnsj til)rin, red and white blood-eorpuscles, and blond-phitelets.
By the time that tlte vegetation has reached such a size as to be noticeable to the nnaided eye, the process of repair has begun at its base. This is accomplished by tlie ingroA^'th of ymino: pon-
M.V
m
\ *
FlO, 2<J. — MaUOXaNT VeuIHCopE EyiirHAllDITlK nr MiTRAtr VaLVK,
Spedmt;n in collectloii ol" Dn Guwlftv B'utierer,
nective-t issue cells and the formation of a irranidation tissne which finally replaces the entire mass of adherent tibrin, and in time becomes covered by the endothelium from the neighbouring
148 DISEASES OF THE HEART
membrane. The growth can now be more properly termed a vege- tation, as it is essentially an outgrowth from the subjacent tissue, and some authors limit the term to this form. The accumulation of fibrin over such an affected area may be very large, but the average vegetation is about 3 millimetres in length. When of the irregular form described, the endocarditis is spoken of as the warty or verrucose variety (Figs. 24-27).
The vegetation may be large and polypoid in shape or long and string-like, attached at one end so as to swing in the blood- stream. The disease is then spoken of as of the polyix)id or vil- lous variety respectively. The vegetation may be too large for complete organization, and may soften and redissolve in the blood-stream, or portions may break off and be carried in the blood until they reach a vessel of too small calibre to pennit their passage, when they plug the vessel and cut off the circulation of the parts supplied by it. The infarcts thus produced by the emboli of simple endocarditis are usually of a non-infective nature.
The further repair of these lesions and the changes in the valves consequent to them are dealt with under the head of Chronic Endocarditis.
The malujnant form of the disease is mainly characterized by the intensity of the infection, and the fact that embolic phenomena are more common than in the simple, and are almost always of a septic nature. The local lesions may be vegetative^ suppurative, or ulcerative, dejiending on the nature and violence of the infec- tion. In all eases the necrosis of the affected areas is more marked than in the simple form, and ultimately leads to loss of substance, the portions sloughed off passing into the circulation as septic emboli.
The valve-cusp thus ulcerated is naturally weakened, and fre- quently gives way before the pressure of the blood, forming small pouches in the valve, the so-called valvular aneurysms, or giving way completely perforate the valves. Acute valmlar insufficiency can thus be produced (Fig. 27). A valve-leaflet may become partially detached, and the free end swing in the blood-stream. Ulceration of the papillary muscles or the chordiv tendina? may produce stretching or rupture of the cords, or a thrombus covering the affected area may mat them closely together.
When the lesions are situated on the mural endocardium, per-
IM
DISEASES OF THE HEART
ease. It is very often a?sociated with the chronic form of endo- carditis.
The secondary i^-Langes in the simple form art* trifling, and as a rule produce no symptoms. It is only in the cntirse of time, when the dia^ease passers into the chronic form, that serious damage is done. Secondary to the fnalifjnant form, on the contrary, are circulatory distnrhances consei|iient on the ulceration or perfora- tion of the valves, and more imjiortant still, the metastatic foci of disease set up all over the body hy means of septic emboli. The splei^n and kidney are espeeially apt to snffer in this way. The infarcts so produced may he few, or innumerable minute foci of suppuration may be scattered over the whole body. It is to these seplie eml)oli that this form of the disease owes its malignant eha meter.
Etiology. — It may l>e stated as a general proposition, that the bacteriid origin of acute €*ndoearditis, both simple and idcerative, has lK*en established. IIeibc*rg's discovery in 1872 of mierocr»eci in the thrombotic masses of the malignant form has led to an unbroken series of researches and exj^erinients by the most bril- liant patliologi^ts in Europe and thi^ country, with the result that the cloud of doubt and speculation once envelojiing this sub- ject has at length Ijeen cleared away. Special activity in this work was displayed during the years immediately foIlo%ving 1885, and prominently figuring in this line of investigation are the names of Virchow, Ivlebs, nirch-llirschfeld, Koester, Weichseb banm, Fraenkel and Saenger, Rosenbach and Ketter in Germany; Gilbert and Lion, ( Virnil and Babes, Koux, Josseraut, and Dessy, in France; Dreschfeld, Cayley, Purser, in England; Osier, Flex- ner, and Priulden in this country. It is manifestly im]joa-iib!e within tlie limits of this work U* give a detailed account of the nature of the researches made liy these eminent workers, and it must suiK(*e to state the facts that have been ^established,
M icro-organi^ms have been quite generally found in eases of maliffiiani ertdorardifis^ some of them being the same as those found in other infectious diseases, a few being specific to endo- carditis. Occasionally two or more varieties have existed in the same case. The bacteria most usually discovered have been strep- tococcus pyogenes, |)articularly of erysipelas; stajdiylocoecus pyogenes, aureus, and allms, and the micrococcus hmeeolatus.
1
ACUTE ENDOCARDITIS
151
The gnnococous, the bacillus of typhoid fever, of diphtheria, of in- fluenza, and of tuhercidosis have also been found, although much less frequently.
Weichselbauni identified oertain bacteria, wliieh, Ix^eause they apjx^ar to occur only in endt»earditis, he named bacillus endoear* ditidis griseus and capsulatus and micrococcus endocarditidis rugatus. The bacillus imniobilis et frjctidus was also found by Fracnkel and Sacngcr. That these various bacteria are capable of inducing endocarditis has been shown by experimentation on ani- mals. A number of investigators injected pure cultures of micro- organisms obtained from infected valves into the jugular veins of dogs and rabbits, and afterward found these cijcci, often in masses, both on the surface and in tlie deeper layers of both aortic and mitral valves, the valves themselves showing characteristic inflam- matory changes. By some experimenters it was asserted that endocarditis could be only thus proiluced after the valves had suf- fered trauma by chemical or mechanical irritation. Others, on the contrary^ claimed to have produced endocarditis by injection of microbes into animals witliout previous injury of the endo- cardium.
In numerous instances the bacteria found on the affected valves have also l>een identified in the septic emboli thrown off during tlie course of the flisease, while in a few instances the blood of patients suffering from infective endocarditis has been found to contain septic organisms.
The bacteria found in the lesions of ulcerative endocarditis occurring as a complication of typhoid fever and diphtheria are usually pyogenic. This is also true of most cases of gonorrheal endocarditis, although the gonococeus has been definitely identi- fied in the endoc^arditic lesions. The pneumococcus of Fraenkel has been frequently found in endocarditis, both simple and ulcera- tive, but, according to Osier, more frequently in the latter variety- It appears well established that a primary endocarditis of bac- terial origin is occasionally, altluntgh rarely, met with. Most in- stances of endocarditis are secondary to some general or local in- fection.
There has lieen considerable speculation, and for a time there was a heated iliscussion, particularly between Klebs and Koester, over the route by which microbes are carried to the infected valves.
152 DISEASES OP THE HEART
Klebs and Virchow maintained they were deposited on the surface of the cusps out of the blood, while Koester declared they were carried thither in the minute capillaries situated in the deeper layers of the valves. He maintained that the masses of cocci caused embolic plugging of the vessels, which was followed by rup- ture, thus setting free the bacteria and allowing them to reach the surface. Against this explanation was urged the scarcity of blood- vessels in the valves, as well as the fact that the earliest evidence of inflammatory change is along the line of contact of the cusps. It is now held that both contentions are correct, but Virchow's view is accepted by the majority of observers. The adherents of Virchow's opinion believe that the pressure of the blood forces the micro-organisms between the endothelial cells of the endocardium — a theory that probably accounts for the development of endocar- ditis in the left heart after birth and in the right side during fa?tal existence. As is well known, blood-pressure is greater in the right ventricle before and in the left ventricle after birth.
Another explanation for the localization of endocarditis is that inasmuch as oxygen is necessary to the growth and activity of most bacteria, these organisms are most active in blood relatively rich in oxygen, a condition obtaining in the right cardiac chambers in the fcetus and in the left during extra-uterine existence.
A most interesting question relates to those conditions that de- termine whether the endocarditis is to be simple or ulcerative, since both forms are of microbie origin, and some of the same organisms have been found in the endocarditic vegetations of both varieties. What are the factors that determine the malignancy or benignity of the affection I It has been suggested that this de- pends upon the number of bacteria present. It is more probable, however, that when healthy valves are attacked the nature of the endocarditis depends upon the virulence of the infecting organ- isms. Other factors are of influence, however, aside from the nature or virulence of the bacteria, and these will now be con- sidered.
Simple Endocarditis. — Articular rheumatism is the disease jxn* excellence in which acute simple endocarditis is most frequently observed.
Whv this is, is not as vet satisfactorilv established, but there appears to be a growing belief among pathologists in the bacterial
ACUTE ENDOCARDITIS
153
origin of rheumatism, as opposed to the once prevalent notion of its dei>eudenee upon lai-tie acid in the blood* The relative fre- quency with which the^^e two affections are associated is variously estimated. Of 32 cases of intlammatory rheumatism that termi- nated fatally, Fagg fonnd the valves affected in all but 12. Ac- cording to Ilayden, PfaccK'k found endocarditis in 16 per cent of his cases of rheumatism, while Fagg puts the ratio as high as 40 or 50 per cent. French as well as English oliservers put the propor- tion much higher than do the Germans; thus Bouillaud, 55 per cent ; Budii, 48 per cent ; Fuller, 23 per cent ; while Wunder- lich and Lehert give it as 23 per cent, and Bamberger 20 per cent. These differences pniliably depeml upon the severity of the rheu- matic attack, since ail observers agree in the statement that the valves are far more likely to become inflamed in acute than in sub- acute or chronic forms of articular rheumatism. Endocarditis is especially liable to occur in a first attack uf arthritis, partienhirly when this is severe and several joints are involved. There is no donbt, however, of its development as u result of subacute or chronic rheumatic manifestations. Hayden is of the opinion that in rare instances endocarditis may be the only manifestation of the rheumatic poison. The period in the course of acute rheumatism at which endocarditis may occur is given by Hayden from the sixth to the ninth day, and by Fuller as from the sixth to the twentieth day. The earlier the time of life at which acute rheu- matism develops, the greater is its liability to set up acute endo- carditis.
The next most frequent predisposing cause of this form of en- docardial inflammation is generally stated to be chorea. End<> carditis of this origin is numerically less frequent than the rheu- matic, whereas the relative frequency of chorea and endocarditis is thought by some observers to be greater; thus, of It] cases of fatal chorea occurring at Guy's Hospital during tv\Tnty years, Fagg found post-mortem evidence of endocarditis in 14. Here, again, there has been much speculation concerning the reason of the asso- ciation between chorea and endcK^arditis. By some the latter is attributed to acute articular rheumatism, which is now recognised to be fretjuently associated with chorea. Thus in 40 cases of the latter affection manifesting organic heart-disease, Gowers found in all a trustworthy history of associated rheumatism. There are
154 DISEASES OP THE HEART
some observers, on the other hand, who hold that chorea is capable of causing endocarditis independently of associated or antecedent arthritis. Since girls are undeniably more subject to chorea than are boys, endocarditis of this origin is obser\'ed more frequently in the former sex.
Scarlatina and measles are also accredited with the causation of endocardial inflammation. This may be either a secondary re- sult, or the endocarditis may be due to a mixed infection. Inas- much, however, as scarlet fever is not infrequently followed by rheimiatic manifestations, the endocarditis is held by some to be referable to the latter and not to the former affection.
Other irruptive diseases, particularly enteric fever and small- pox, are also capable of setting up endocarditis, but as subse- quently stated, this is more likely to be malignant than merely simple.
Although gonorrhoea is more likely to cause the ulcerative form, vegetative endocarditis undoubtedly occurs as a result of gonococcus or perhaps a mixed infection, a conclusion that would seem justified by the entire absence of any other etiological factor in certain cases of valvular disease.
As previously stated, there is both clinical and pathological evidence of the occurrence of acute endocarditis in the course of crou}M)us pneumonia or in consequence of pneumococcus infection. Although such an endc>c*arditis is more likely to be ulcerative, it may nevertheless be benign. In a fatal case of pneumonia, which had exhibited no evidences of endocarditis during life, Ilaushalter found a colony of jmeumococci in the interior of one of the mitral cusps, while the other showed an almost invisible swelling of the endothelium near the point of insertion of the valve. From this he concluded that not only is acute endocarditis a probable se- quence of pneumonia, but also endocarditic changes of a slow sclerotic tyi>e may be ultimately set up. His conclusions were as follows: (1) The absence of murmurs during life or of naked eye changes ])ost mortem does not prove the integrity of the valve, since during the course of the pneumonia the ])athogenic organ- isms may be carried into the interior of the valve, and thus prove the starting-point of future valvular mischief. (2) The possi- bility of such an endocarditis should be remembered, since a latent period may exist between the primary disease and the develop-
ACUTE ENDOCAHDITrS
155
ment of the entlwanlitis. (3) The possibility of such an occur- rence renders it advisable for tlie physiciim to keep a patient under prolonged obser%'ation after ref:overy from piiennionia, and to make repeated examinations of the heart* tliat lie may thereby detect the earliest manifestations of a valvular lesion.
Injury of the valves through strain is generally recognised as one of the conditions predisposing to the occurrence of acute endo- carditis. By some it is contended, ho%vever, that strain alone is not sufficient, but must be united with some previously existing defect. Strain is probably cai)able of setting up fresh intlamma- tion of a valve, already the subject of a former though slight endo- carditis. Rupture of a cnsi> may undoubtedly pro%'e a starting- point of acute infiauimatory change.
Age is an undoubted predisposing faetorj acting in most cases, however, in the way of rendering individuals susceptible to articu- lar rheumatism, the exanthemata or other diseases, themselves capable of bringing about eudocarditis. Supporting this view or interpretation of the influence of age is the statement that rheu- matism is more likely to occasion endfx^arditis in childhood than in the later ]>eriods of life. Both sexes are liable to endocarditis, yet according to some this affection is more frequent among fe- males, although males are said to be more subject to articular rheumatism. To my mind there is nothing in sex, per se, render- ing the endocarditmi more vulnerable in females than it is in males.
Females are more subject to chorea and, by reason of their sex, to puerperal septicicmia and infections from pelvic disease, and hence it nuiy well be that they furnish a greater numerical proportion of cases of acute cmdocarditis, benign as well as ulcera- tive. With increasing experience^ I find myself growing in the conviction that hereditary inHuence plays a not unimportant role in the development of endocardial disease. Cardiac* and particu- larly valvtdar lesions, as such, cannot be inherited, but it seems to nie tl»at in s^mie families whose members evince pronounced rheu- matic diathesis, there is an inherent vulnerability, possibly heredi- tary^ of the endocardium in the presence of rheumatism.
Ulcerative Endocarditis. — ^Tt is a welbkno^Ti fact, established both by clinical and post-mortem observation, that the malignant form is particularly prone to develop as the result of fresh bacte-
156 DISEASES OP THE HEART
rial invasion in valves already the seat of chronic endocarditis or sclerotic change. This is particularly true of the aortic-valve apparatus.
Infectious endocarditis is also specially liable to attack indi- viduals suffering from exhausting diseases or cachexia?, chronic alcoholism, cirrhosis of the liver, hepatic abscess, cancer, etc.
General infection, as pyipmia, puerperal septicemia, influenza, diphtheria, variola, and localized septic processes or abscesses, predispose to malignant rather than to simple endocarditis. Flex- ner found staphylococcus aureus in a case of endocarditis in which the atrium of infection was leg ulcer ; in another, staphylococcus, the point of entrance being the intestine ; in still another, strepto- coccus and staphylococcus, the atrium being hepatic abscess. This form of acute endocarditis has been particularly frequent in aSv<(> ciation with puerperal septicaemia due to infection either of the uterus or its adnexa. It has been known to follow tonsillitis, and even so apparently trivial a local process as a funmcle.
Croupous pneumonia or a pneumococcus meningitis has not infrequently been found as the primary infection in cases of ulcer- ative endocarditis. Although the pneumococcus may occasionally give rise to the simple form, it is much more frequently respon- sible for ulcerative inflammation of the valves. This malignant form is also stated by Dreschfeld to have been associated with 7 cases of gall-stones '* with or without suppuration of the biliary passages.'^ Dreschfeld thinks that the discovery of the bacterium coli commune in diseases of the biliary passages nuiy explain their connection with acute endocarditis. In this connection it is inter- esting to note that Flexner, in one case of endocarditis associated with carcinoma of the pylorus, identified the bacillus coli, together with the bacillus pyocyaneus; and Hasenfeld has reported arti- ficially produced endocarditis in animals infected with the bacillus pyocyaneus. Of further interest is the fact that, despite the severe infectious process, distinct hypertro]>hy of the heart was observed to develop in so short a time as a week.
Finally, this form of endocarditis, although much less fre- quently than the simple, may exist in connection with articular rheumatism, as mentioned by Osier and others.
Its dependence upon the diphtheria bacillus, though rare, is undoubted. Howard has reported a case in which a bacillus was
ACUTE ENDOCARDITIS
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discovered ideiitionl in all respects with the Klebs-Looflfler bacillus* It is DOW gt'iR-nily rt-cognised that .septic endocarditis, although capable uf heiny^ set uj> by pathogenic organisms, is most fre- qiieiitlv caused bv j^treptocricci and staphylucncci.
Symptoms. — Just as it is sometimes difficult from a patho- logical stand iNjiut to say whether the soft, easily detached thrombi belong to the vegetative or infective variety, so a sharp dividing line cannot always be drawn clinically between the two forms of eiMloi'arditis. Nevertheless, I think it will conduce to clearness if, as is usually done, they are described separately.
Acute Simple Endocarditis. — As this process frequently occurs in the course of arlieuhir rheumatism, of which it may be regarded as a manifestalioHf and not a complicaiiouy its symptoms are often masked by those of the arthritis. If the endcwarditis be of a mild ty2>e, it may pursue a latent course, and only l>e deteeted by its results when years subsequently the individual is found to have a vahndar lesion, probably dating back to some almost forgotten rheumatic attack. Such a i>ossibility should always lye borne in mind by any [ihysician attending a case of articular rheumatism, however mild, and should incite him to a daily examination of the heart, since many times acute endocarditis is only recognisable by stich means.
If in the course of rheumatic fever, especially towards the end of the first week, the temperature unexpectedly rises, and can- not be accounted for, by involvenicnt of a fresh joint or some com- plication, attention should be at once fastened upon the heart. If the endocardium lias Itf'come intlamc^d, with or without implica- tion of the pericarditmi, the fact will eventually declare itself by the physical signs subsequently to be described, even though sub- jective symptoms are wanting.
In some cases stibjective symptoms become manifest from the start, and are then due probably either to the severity of the endo- carditis or to associated myocarditis or j>ericarditis. These symp- toms are precordial pain more or less pronounced, or an ill-de- fined sense of oppression and discomfort in the cardiac region, pal- pitation, the heart-action in some cases being quite tumultuous, and particularly a suhjpctivc sense of di/spno'a. By this term is meant a sensation on tlie part of the patient of air-hunger, which may not be evinced by laboured or hurried respirationj but which
158 DISEASES OP THE HEART
is usually greater than can be accounted for upon examination of the chest. I cannot now recall a single case of acute endocarditis, recognised as such, in which this symptom was not present. In some instances this feeling of breathlessness actually amounts to orthopna^a; in others dyspnoea is paroxysmal, compelling the pa- tient to sit up in bed during the continuance of the paroxysm. In mild cases the pyrexia is likely to be mild, and possesses no pecu- liar character.
In other instances the disease produces profound constitutional disturbances, with fluctuating fever and profuse perspiration, plainly suggesting infection, and with a pulse so empty, irregular, and perhaps accelerated, as to at once direct the physician's atten- tion to the heart. These are the cases difficult, if not impossible, of differentiation from the malignant form.
Embolic phenomena are less frequent in the benign than in the malignant form, yet when embolisms occur the sjTiiptoms they induce are referable to mechanical interference with the circula- tion, rather than to a local or general septic process. The most usual seat of infarcts is in the kidney, intestines, and brain. They undoubtedly occur many times without giving rise to recognisable S}ini)toms ; yet when such are produced, they are a sudden, sharp pain in the affected part or organ, chill more or less pronounced, and })vrexia. If the emlx)lus lodge in a kidney the urine is likely to contain blood, albumin, and even pus. Hemiplegia and apha^^ia, the result of cerebral embolism, may in rare instances furnish the first, or i)erhaps the conclusive, evidence of the existence of acute endocarditis. The following case is instructive: W. J. ^f., male, aged forty-eight years, height six feet, weight 176 pounds, first consulted me Xovember 0, 1806, not, he said, because he thought himself in poor health, but because, having some heart-trouble, a friend advised him to get my opinion. Family history wa^s un- important in its bearings upon the patient's condition, but it was stated that one sister had died of consumption, another of insanity, and a third, then living, had heart-disease. Patient declared that he had not been ill since his twelfth year, but had had syphilis at the age of twenty. After his death, it was stated by his wife that the patient had known for seven years of the existence of some sort of heart-disease. Symptoms such as dyspncea and palpitations were denied, but the patient, when questioned
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159
T?p?3iTi^min, said, *' Oiiee in u while n little, dovm near the heart/'
The pulse was noted as 60, not distinctly collapgingj the left Beeming slightly smaller. Carotids and aubelaviana throbbed strongly. Apex-betit in sixth left intercostal space, 3^ inches from the sterniinj, antl the eardiuc impulse was heaving; diffiised from the fifth to the seventh, bnt niaximvnn in the sixth interspace. Absolute cardiac diibiess was practically normal, but the relative was increased to the left, extending 5^ inches to the left of the breastbone, downward to the seventh rib, and but 1 inch to the right of the sternum (Fig. 28). The first sound at apex was muffled and the sei^ond was wanting; throughout tlie pnecor<liuiu the sounds were obsenreil by murmurs, both systolic and tliastolic, which were auflil>le over the entire cardiac area, but were of maxininm inten- sity in the aortic area and on the IkkIv of the sternum. A snapping systolic tone was audible in the femoral artery. In the aortic area bimanual palpation with sliiiht pressure brmigbt out a systolic shock and thrill. Examinatiun of abdomen and urine was negative.
The diagnosis lay between aneurysm of the ascending aorta and insufficiency of the aortic valves, but the lesion was subse- quently decided to be a valvular one of sclerotic, possibly syphilitic origin.
For the next few months th** patient was seen at rather infre- quent intervals until the last of March, 1807. In February of that same year patient was knocked down by a runaway horse, but did not think he sustained special injury. Towards end of March he began to complain of insomnia, great nervousness, and restlessness. The heart was rapid and pounding, and there was
Fio. 2S.— Apex-beat akd Rrlative Dul- wEssi, Caiik of Acutb £Ni>ot:AtiuitiA (p. 158).
160 DISEASES OF THE HEART
dyspnoea, even in reix)se, which increased paroxysmally without cause. Urine analysis showed pus, blood, and albumin.
Patient was ordered to keep to the house and confine himself to milk diet, with potassium citrate and tincture of digitalis in small doses, with saline cathartics daily. After about two months the urine lost all traces of blood and albumin, but patient's gen- eral condition grew worse, and he was ordered to keep his bed. Heart's action was still rapid and pounding, but regular, and dysp- noea with paroxysmal exacerbations very marked. Patient sweated profusely, but the thermometer never showed fever.
One night complained of pain in right hypochondrium below ribs, embolism was suspected, but subsequently doubted. Liver reached 3 fingers below costal arch, was moderately tender, firm, and with rounded border. The condition was thought to be pass- ive congestion without infarction. About the last of May patient developed mental symptoms, as shown by ugliness of temper, espe- cially towards wife; it apj^eared to be a mild acute mania, and the wife stated that the mother as well as a sister had died insane. Hyoscine hydrobromate was ordered, supplemented subsequently by valerianate of anmionia, with improvement, the delirium being only occasional and ugliness less.
June 2, 1897, examination showed the following: Radial pulse distinctly collapsing, venous pulsation in forearm, but external jugulars not turgid and without pulsation. Apex-beat in sixth left interspace, anterior axillary line, systolic impulse in second and third right inters})aces near sternum, followed by diastolic thrill, also a more feeble jnilsation in fourth, fifth, and sixth right interspaces, slight systolic shock in second left interspace near sternum. Absolute dulness, patient in dorsal decubitus, reached 6 centimetres to right of median line, and from second to sixth costal cartilage, the note being flat, with marked resistance from second rib to fourth interspace, and slightly less dull below this point. Dulness also reached 10.5 centimetres to left of median line (Fig. 29).
Auscultation showed first sound at apex, dull and muffled, but no distinct murmur, a double tone audible below left clavicle and down along left axillary line; a systolic tone and soft diastolic murmur in second left interspace and outward 1^ inch from ster- num. There was also a faint second sound in the pulmonary area,
ACUTE ENDnCAEiDITIS
161
and wli€*n the patient took a deep in-s|»irntion and held his hreath the second sound seemed to be elianged into a soft miinnur.
The soft diastolic niiiruinr at left of sternum was transmitted faintly downward. A painfully loud and harsh diastolie and systolic inurniur was heard in second iind third rijudtt irUerspaees, and transmitted more feebly into tifthj out to nipple and up to neck.
The condition was interpreted as follows: Acute endocarditis ingrafted on a chronic endocarditis, atfecfing aortic valves and aorta, and producing dilatation of this vessel Xo evidence could be fuiind of iiiHanmiation of other valves, and yet the great extent of dulness to right of sternmn was thought due, in addition to aortic dilatation, to dihUa- tion of the right auricle, sec- ondary to mitral insufficiency. Cough was at no time a marked symptom, except two or three paroxysms a few hours before death, when patient seemed to have pain in left lung. During tlje last few weeks of life tliere was moderate ledema of ankles and shins, also pnffiuess, l>ut no pain^ in left wrist and hand. Forty-eight to sixty hours lie- fore death patient became comatose, with cold extremi- ties, very rapid, feeble, and irregular pulse, and the tnmk and lower extremities became studded with small lirownisli-red spots, that had all the characters of cutaneous eudwdisms. Death, which tm>k place June 24rth, seemed to be the result of gradual cardiac asthenia.
The autopsy, made Ijv Dr. W. A. Evans thirteen hours after death, was briefly as follows: Very large numbers of petechia? over abdomen, chest, and legs, about the size of a pea. Some inter- stitial splenitis and perisplenitis and zones of connective-tissue growths representing old infarcts. These were generally subcap sular.
11
Flo. iiV^.— Al'EX-BKAT ANU AbsoLI^TK UlL-
jfXM LATXtt I3r Sams Ca«x as Fio. i8.
162 DISEASES OF THE HEART
Liver. — Fatty infiltration — nutmeg. Large numbers of small islands of connective-tissue increase, quite generally distributed in subcapsular zone. A small mass of calcareous material in lower portion of right lobe, superficial. In left lobe a small fresh in- farct about 6 millimetres in diameter.
Left Kidney. — Slight parenchymatous nephritis.
Bight Kidney. — In the cortex an old infarct 1 centimetre in diameter, over this the surface of the kidney depressed. This in- farct, fatty in appearance, reddish, surrounded by a reddish zone. It was this infarct which in March had occasioned the bloody and albuminous urine.
Left Pleural Cavity. — No fluid, no adhesions except to dia- phragm.
Left Lung. — Congested and crdematous. In anterior edge of inferior lobe an apoplectic focus about 1 centimetre in diameter, quite recent.
Right Pleural Cavity. — Extensive old, firm, fibrous adhesions quite general.
Right Lung. — Congested and CDdematous, single hemorrhagic infarct 2 centimetres in diameter.
Pericardium. — No effusion, uniform adhesions between peri- cardial layers. They strip easily, appear gelatinous or mucoid.
Aorta. — Tubular dilatation of aorta in its first portion. The lumen is somewhat ovoid, measuring 9 by 8 centimetres. The aortic ostium dilated with compensatory stretching of the aortic cusps. The aortic cusps, measured along their free edge, show a length of 5 centimetres, 4^ centimetres, and 3^ centimetres re- spectively. All of the cusps show ridges of atheroma, with con- siderable thickening and stiffening. At the base of the largest cusp, a calcareous plate. Thickening, redness, and some deposit of fibrin on each of the cusps, especially towards the free edge.
The valves not competent. Aorta atheromatous. Areas of calcification, atheromatous ulcers, and some vegetations around these losses of substance. The left ventricle enormously dilated, its wall 3 centimetres in thickness at its thickest portion. Myo- cardium is not especially fatty. Mitral valves show multiple foci of acute endocarditis, consisting of small, round red masses, the size of a pin-head.
Left auricle very much dilated, right heart otherwise normal.
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103
Cnhnres made from the vegetations give no growth of micro* organisms.
Diagnosis, — -Tubnlar aneurysm first portion of aorta ; ather- oma of aorta and aortic cusps ; hypertrophy and dilatation of the left heart; acute endocarditis and endaortitis, vegetative in char- acter. Recent infarcts in liver and lungs.
This case illustrates the proneness of acute inflammation to attack valves that have undergone sclerotic changes. It is prob- able that the aortic regurgitation diagnosed in the fall of 1896 was dne partly to incompetence of the cnsps from stiffening and rigidity and partly to stretching of the ring consecutive to the dila- tation of the ascending aorta^ the valves not being able to ade- quately close the ostium in spite of tlieir compensatory stretching* With the exception of the lack of febrile temperature the sjiufj- toms strongly suggested idcerative endocarditis, and show how difficult and unwise it is to attempt a sharp clinical distinction between the two forms of endocarditis. The anatomical changes were those of the vegetative variety, and yet in its rapid course and fatal termination the process may be said to have been ma- lign nnt.
Course and Termination. — As already stated^ in soma eases rheimiatic endocarditis of a mild type may be easily distin- guished from infective endocarditis, while otlier cases seem to occupy intermediate ground, and clinically, at least, cannot be classed with either one or the other type. It is plain, therefore, that the course and termination are equally variable.
Simple rheumatic endocarditis may pursue a favourable course, and terminate in the recovery of the patient, nay, may even subside without serious impairment of the affected valve. In the majority of cases, however, the patient is usually left with a chronic vahiilar lesion.
Ulcerative Endocarditis. — Under this head are reckoned those cases of inflammation of the endocardium which manifest more or less pronounced s^TTiptoms of general sepsis, whether the ter- mination is in death, by far the more frequent occurrence, or in recovery, of which instances are now and then reported. As might be expected from a consideration of the etiology and mor- bid anatomy of this class of cases, the clinieol picture varies much, according as the local — that is, cardiac — or the general symptoms
1
164 DISEASES OF THE HEART
predominate. In the majority of cases the symptoms are those of general sepsis, with very subordinate, or it may be with no mani- festations on the part of the heart. In such cases the inflamma- tory changes in the endocardium are to be regarded as merely an incident of the general infection, and therefore Rosenbach classi- fies these cases as merely local manifestations of a general infec- tion. The endocarditis is but one of the many possible local ex- pressions of the infection, in consequence of the profound disturb- ance of nutrition there induced.
In this class of cases the conspicuous features are phenomena characteristic of pya»mia, an irregularly continuous pyrexia, with few if any rigors, sweatings, great prostration, anannia, emacia- tion, anorexia, diarrha*a, a dry, bro\vnish tongue, abdominal dis- tention, stu}K)r or low muttering delirium, persistent dorsal decu- bitus, and enlargement of the spleen. The pulse is only moder- ately accelerated, in most instances impressing one as being chiefly remarkable for its feebleness and want of tension, while the heart may display absolutely no evidence of disease, or may be slightly dilated, with a faint, soft systolic a]>ex or basic murmur, the same as in typhoid fever. Indeed, this whole condition is so like enteric fever as to be frequently, it may be said usually, mistaken for that disease.
In other cases the fever is much less typically septic, remit- ting or intermitting, not drop])ing suddenly below normal, and again abruptly shooting up several degrees, but running so mild a course as to scarcely merit the appellation of pyrexia.
In others, again, the elevation of temperature is of irregular type, or there are diurnal fluctuations, to possibly 101.5° or even 102.5° F. The feature that mainly attracts attention in such cases is the progressive amemia, and the trifling changes discov- ered in the heart are commensurate with those of anivmia.
The last of July, 1900, I was consulted by a German, aged fifty-eight, who was a merchant in the interior of Indiana. His family history was unimportant, and his personal anamnesis was meagre. He had always considered himself well until about a year previously, when he had suffered from bronchitis, for which he had received medical treatment, at which time a heart-murmur was discovered. In March, 1000, he had been troubled with night-sweats that had resisted treatment by belladonna. Since
ACUTE ENDOCARDITIS
165
FlO. aO, — ApKX BEAT AT£1» RULATtVE OaKDIAC
thai time ho had been losing pfround, -and altogether his weight had declined from 180 to 137 pounds. He gave a vague account
of some gas tro- intestinal dis- order ill the spring, hut could m^t recall any attack of pain that might have heeu an at- tack of appendicitis, hepatic or renal colic. Neither could he remendier any injury or local suppurating process, and he had never had rheu- matism, pneumonia, gonor- rhira, or other infection.
The patient was tall, ema- ciated, ]ialc, and of a slight yellow hue, and hu conjiuic- tiviv were faintly icteric. The radial arteries were thick- ened, and the pulse, of only moderate tension, was regular and equal, 100 to the minute. A feehle cardiac impuke was diffused from epigastrium to the apex- beat, whieh» weak and accompanied by soft thrill, was situated in the sixth interspace, 10 cen- timetres to left of median line. Relative cardiac dulness It the level of the tifth costal irtilage extended from 5 cen- timetres to right of the mid- stomal line tt) 14 centimetres to Ipft of the same (Fig. 30). The first sound at the apex was obscured by a murmur and the second was impure, but over right ventricle both were more iHstinct, while at the base both wei'e faint, the and being sea reel v audible, ihe pnlnmnic seeund the loiul- ^'•'■. «^— ^"^^ 'I' «*'""" A.n.B.uTv
' , It^HADED) ANH TltAjrilf l««|0|f Of MlTltJIt'R
er of the two; both aortic m Case ^jKUtfi).
166
DISEASES OF THE HEART
tones were distinct* but feeble In the eervical arteries, A Itarsh systolic miinmir was heard at the ajiex, and was transiiiitted into the middle of the axillary region and to the median line in front, yet not above the third interspace (Fig. 31). The lungs were negative and the abdomen was flabby, moderately tym- panitic, not tender, while in tlie bx'atiou of the gall liladder a s^ift roundish body could be plainly made out. The urine collected over night and analyzed next day gave following results : Quan- tity, 800 cubic centimetres; chnidy^ spei4tic gravity, L015; reac- tion acid; etdour, reddish-yellow; urea, 1,4 per cent; mucin pres- ent; a slight trace of albumin; no sugar; no bile; no blood; 2 granular and a few hyaline casts; a few eylindroids and uric-acid crystals, but no pus; not examined for |ieptone. The blood-ex- amination *m that day showed hannoglol*in» 40 jK'r cent ; red cells per centinjetre, 3,660,230, percentage of red cells, 73.3; eorpus- ele index, 54,4, and number of leucm^yteB per centimetre, 13,700, His tem]R4'ature at 11.15 a. m. was 08.4"^ F.
As there was nothing in the examination thus far to lead to a susi)iciou of endocarditis, the diagnosis was made of chronic arteriosclerosis, with chronic myocarditis and an atheromatous mitral incompetence and a mild interstitial nephritis, amvuiia. The patient was advised to go into a hospital, where he could re- ceive treatment by rest, approiiriate diet, and niedication, lie did as advised, but got ehilleil in driving to the hospital, and at my visit tliat same aftenioou his tem|>erature w^as found to be 101. S'' F,, respirations normal, nnd pulse only moderately accel- erated. This febrile reaction was thought to Ik? the result of his chill, and fearing he might develop unemia on account of his nephritis, he was ordered to drink very freely of hot water, so as to promote eliuiiuatiou. The result was that by G i\ m, he had passed 15 ounces of urine, and his temperature was normal. Be- lieving this rise of tem|)erature to have been but a transient flurry, I was surprised and disappointed to find that later that same even- ing his tc*mperature again rose to 1UL4'^ F. The chest was then gone over carefully, but with negative results, and accurate record was kept of the amount and character of the urine, also without the discovery of anything of importance.
During the succeeding six days, as shown by the annexed chart (Chart I), he had a low morning temperature and a raoder-
ACUTE ENDOCAaDITIS
167
lie afternoon pv- Bxia with slight perspirations, Imt no rigors, and lie asserted that he felt well. As the pa* tient had come from a State in whieh malaria is common, liis blood was examined on Aiipist 1st for plas- mtxlia, hut with negative results. Nevertheless it was decided to test the effect of quinine, and on August 2d 20 grains were ex- hibited iu the early morning. On that day he had no fe- ver, but on the next day, without qui- nine, his tempera- ture went up as usual to 10L4^ F. On August 4rh 15 grains kept it down to 100- i\, and on the 5th to IOU.8'^ F., while on the 6th, without tlie reme- dy, the temperature again reached 10L8° F,, auil with 20 grains on the 7th it did not go over 99° F. On the 8th,
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168 DISEASES OF THE HEART
without quinine, his temperature was 102.2^ F., on the 0th a degree lower, while 5 grains t. i. d. on the 10th kept fever down to 100.2° F.
The results thus obtained convinced me that the quinine acted as an antipyretic, but that, in spite of doses sufficient to exert a more lasting influence in case the symptoms were due to malaria^ the fever reasserting itself so soon as the drug was stopped, there was some other cause at work. The urine was now tested again for peptone, and with |)ositive results. I therefore became satis- fied that the case was one of pyaemia. It should also be stated that the blood had been tested for the Widal reaction, and this proved to be absent.
As the gall bladder had been found enlarged at the first ex- amination, and was still palpable, it was thought highly probable that there might be an empyema of this receptacle as the source of the infection. Accordingly the patient was seen .by Dr. Bayard Holmes, who corroborated the gall-bladder enlargement and con- curred in the opinion of a probable empyema. This seemed all the more likely to be the focus of infection from the fact that no disease could be discovered in the rectum or elsewhere. A few days subseipiently Ur. Holmes operated on the gall bladder, but although it was enormously distended with fluid, this was not purulent, the condition being a catarrh and not an empyema.
No ill effect followed the operation, but the wound healed very slowly. For a day or two the temperature fell somewhat, but then resumed its former characters, beiiig down nearly or quite to normal in the early ])art of the day and rising in the afternoon or evening to between 101° and 102° F. Rigors were never manifested, and repeated queries concerning chilly sensations al- ways elicited a positive denial of them. Perspirations were also absent, or at the most amounted to no more than a scarcely per- cei>ti])le moistness of the skin where covered.
Week by week the patient lost in strength and flesh, and grew more anaemic in api)earance, although his ability to take consider- able nourishment persisted. lie also displayed slight apathy, lying flat in bed, and changing position but seldom. Pain was not com- plained of, and in vain was a daily search kept up for signs of embolism. During these weeks the pulse slowly and gradually became a little more accelerated, reaching 116 or thereabout. Its
ACUTE ENDOCAKDITIS
169
striking feature 'U'as its feebleness. This want of tension, together with tlie growing weakness uf tlie heart-sunmls, iniluced iiie to
linister strychnine in doses of ^ of a grain 4 times daily, along with 5, and aftenvard 7 drops of tincture of strojihanthua thrice daily. He was also given moderate doses of wine and whisky.
It w'Es always ditlieult, owing to the rigidity of the chest-wall and the volumiiumsness of the huigs, to satisfaetnrily ma]) out deei>seated cardiac dnlness, but I became convinced that the heart gradually increased somewhat in size, though no more than could lie attributed to myasthenia. Pari passu with the increas- ing feebleness of the lieart-sonnds the systolic apex-murmur aug- mented in intensity and extent of audibility until at length it spread throughout the entire pnecordium. It remained to the last a rather hiirsh blowing murmur, and no new^ bruits ever devel- oped. Xeither did ledema become more than a very slight pitting over the tibiiv, and I could not make out any increase in the size of the liver or more than u tritling increase in the area of splenic dulness^ the organ not being distinctly palpable^
In brief, the entire clinical history was that of an ever-growing anaemia, or better, marasmus wntli moderate intermittent pyrexia. In this respect I should think it a fair example of the type of cases deserilK^d by Romberg as amemic rather than markedly sep- tic, and yet there was no doubt of the existence of a mild pyannia. Peptone was repeatedly found in the urine, and thus, w^ith the in- creased lencocytosis, confirmed the conclusion drawn from the tem- perature record. This is well shown by the annexed chart. Death ocrurred the middle of September, about eight weeks after he came under observation. No autopsy was had, hut I believe this was a pyjcmia, with implication of the endocardium as a seeondary and not a primary event.
In still other cases of ulcerative endocarditis there are rigors, sudden high elevations of temperature, and profuse sw*eating, fol- lowed by sharp decline of the pyrexia, the i>ictnre not unlike the paroxysms (*( uudaria, excepting that the septic phenomena lack the periodicity of malarial infection. Jfurchison has narrated an instance of this kind that lasted three months, and was so sug- gestive of malaria to the friends that in deference to their wishes quinine was freely adniinistered, but without appreciable effect on
170 DISEASES OF THE HEART
the disease. In his ease, however, there was physical evidence of an aortic valvular lesion.
There are other cases, again, in which the temperature pursues a still more erratic course, rising and falling abruptly for days, and then suddenly sinking to normal, or it may be to below normal. Remaining thus for days or even weeks, it again assumes its for- mer irregularly intennittent type. During the apyrexial period the pulse still remains conspicuously feeble, and the patient fails to regain strength, so that by these symptoms it becomes manifest that actual improvement is not taking place.
Thus, whatever the various manifestations, they are in them- selves indicative of sepsis, and there is nothing to show that the heart has become affected. Occasionally, on the other hand, the involvement of the endocardium is evinced by the appearance of cutaneous infarcts or by phenomena of embolic plugging of vessels in the intestinal organs. The lodgment of emboli in the skin is shown by the appearance on the extremities or trunk, still more rarely upon the neck and face, of reddish spots of variable size, from that of a pin's head to a pea, or somewhat larger. These petechia' may be few and scattered irregularly, or they may come in showers and at irregular intervals. Septic infarcts in the liver, spleen, kidneys, etc., are productive of abscesses, which may be miliary and escape detection during life or be of recognisable size. In some instances the clinical picture is dominated by these embolic phenomena.
I recall a case in which it was the detection of a splenic abscess which seemed to justify the diagnosis of septic endocarditis. I was asked by Dr. Haskin, of Highland Park, to see a gentleman of about sixty who had been having irregular chills, fever, and sweatings suggestive of malaria. Ilis illness had begim six weeks before with malaise, and had speedily developed the symptoms of sepsis. Three days prior to my visit he had suddenly com- plained of sharp pain in the left hypochondrium with tenderness. I found him unconscious, and lying turned to the left side, with his thighs flexed, skin hot and moist, pulse moderately rapid, but notably weak and soft. There was a distinct blowing systolic murmur in the mitral area. Splenic dulness was greatly in- creased, and although palpation evidently caused pain and was resisted, a rather soft tumour having the form of the spleen could
ACUTE ENDOCARDITIS
171
be f€*lt extenfling well down below the left costal margin. The case was tliuiiglit to be an instance of abscess of tbe spleen, prob- ably secondary to acute ulcerative endocarditis. Deuth took place a day or two later, and, althoogli an autopsy could not be ob- tained, permission was granted to make an abdominal incision for tbe pnrpi>se of verifying tbe existence of tlie al»seess. Tbe abdo- men was opened accordingly, and so soon as tbe doctor's finger pressed npon the spleen the organ burst and pus welled up over bis finger* In this case no etiological factor conld be obtained, and yet it seemed plainly one of septic endocarditis with infective infarct in the spleen.
When emboli of this character lotlge in the kidney, they are declared by albumin, pus, and Idoml, with casts in the urine. There is a class of cases characterized by Romberg as atypical which run their course with all apiK^arance of an acute ha?mor- rbagic nephritis, albuminuria, pus^ blood in varying amounts, casts, renal epitbcliuuij and cylinJroids.
This condition of the urine persists throughout, but with re- missions and exacerbatioiis. A mildly irregular, continuous fever accompanies the nephritis, and the patient displays pronounced and increasing amemia. It is this feature, together with the per- sistent pyrexia out of proportion to the temperature usually ob- served in nephritis, which throws light on the nature of the case. The discovery of an old-standing valvular lesion contributes great- ly to the establisbment of the diagnosis.
Lastly, cases are encountered which display such manifest car* diac symptoms that by some clinicians they are classed in a special group. These are such as either develoj) upon a chronic valve- lesion or occasion such rapid ulceration and destruction of the valves that objective car<liac phenomena become apparent, Sym]> toms of general sepsis may not be marked, or if pronounced, de- pend largely upon infective emboli. The pulse is peculiarly soft, regular or irregular, and more or less accelerated out of propor- tion to the degree of fever. The patient usually manifests dysp- ncea, and it may be cyanosis. Both liver and spleen are enlarged from congestion or infarcts. Exceptionally one may upon re- peated examimitions of the heart detect some evidence of changes going on^ such as increasing fe<*ldeness of impulse, slight increase in tbe area of duluess, and perchance a soft murmur where pren-
172 DISEASES OP THE HEART
oiisly none existed, or an alteration of one already present. More often such examinations are futile, and the diagnosis is largely conjectural or has to be made from the symptom-complex.
Course and Termination. — The duration of acute ulcera- tive endocarditis is exceedingly variable. The disease may run its course to a fatal termination within a few days from its com- ing under observation, or its course may be dragged out over a period of weeks and even months. Some cases progress steadily to a fatal issue, while others show periods of seeming improve- ment, followed by exacerbations and more rapid decline. When death is the result it occurs either in consequence of local changes in the heart and cardiac asthenia, or as a result of acute pulmo- nary a»dema or pulmonary infarcts. In other cases the patient is worn out by prolonged sepsis, or death is directly attributable to the effects of embolism in the brain, kidneys, spleen, etc.
A gentleman of about forty, who had a perfectly compensated mitral regurgitation of rheumatic origin, became ill in the fore part of February with what, from the history, appears to have been an acute follicular tonsillitis. It subsided in a few days, but the man did not regain his accustomed health. He felt weak and slightly feverish, had vague pains, dull headache, and lost appe- tite. Thinking his liver was at fault, he went to French Lick Springs, Indiana, and there drank the waters, took a course of baths, and exercised, but without improvoment. While there he was annoyed by tenderness and pain in the ends of his fingers, and observed that at such times there was a faint reddish colour of the skin immediately above the roots of the nails. He was told it was rheumatic.
At length, failing to regain health, he returned home, and towards the end of April sought my opinion, partly on account of a frequent dry cough that had recently developed. I had known him in health, and had previously examined his heart. The change in his appearance and general condition shocked me. His voice was weak and tremulous, his hands shook, his face was pale and sallow. His eyes were not perfectly clear, the skin of his arms and trunk was flabby, faintly yellow, and although at first dry, became bedewed with moisture upon the exertion of undress- ing. His temperature in the mouth was 90.8° F., and the pulse of 105 was weak and small, but regular. I was struck by the fact
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ENDOCARDITIS 173 ^^H |
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^ that Its rate did not tall ^H appreciably, even while ^H he was resting on tlie ^m lounge after my exami- ^H nation. The hi<art tttd ^H not seem to be enlarged, ^H but the apex-beat was ^m feeble and preceded by a ^m short, scarcely percepti- ^L ble thrilh ^^^1 Tlie old mitral $ys- ^^^^ tolic murmur was pres- ^V ent, but in addition the ^K first sound had a siigges- ^H lion of a presystolic ^1 bruit, and the second ^H sound was feeble. The ^M lungs were negative, the ^M liver barely palpable, and ^^^H urine contained a trace of ^^H albumin with granular ^M and hyaline casts. ^H From the history of ^M tonsillitis and the synip- ^H tonis, I at once suspected ^m endocarditis, and sent ^m him home to bed. His ^M temix^rature, whieh was ^H carefully recorded four ^M times daily, showed a ^M fairly continuous py- ^M rexia, from about 100^ H F. to 101^ F. and a frae* ■ tion (Chart II). His ^m pulse remained persist- ^m ently in the neighbour- ^H hood of 105, and the ^M heart-finding? were un- ^H changed. He was ^iven |
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174 DISEASES OP THE HEART
Strychnine and yeast-nuclein in full doses. The diet was as hearty as his feeble digestion would permit. He felt so com- fortable that he was kept in bed with difficulty. Things remained in this condition for two weeks, when he one day complained of localized pain and stiffness in the calf of the left leg, but with no objective phenomena.
His cough was so persistent that repeated examinations of the lungs were made, at first with negative results. At length I dis- covered moderate dulness of the right upper lobe with ill-defined bronchial breathing, but no rales. About this same time enlarge- ment of the spleen became demonstrable. At a loss to account for the changes at the right apex, I requested Dr. Arthur R. Edwards to see the patient. He agreed in the view that there was probably septicaemia with endocarditis, but could not give a satisfactory ex- planation of the pathological condition in the lung. The pain in the left leg he thought was due to embolism. The faint blush at the root of the nails with tenderness, pain, and moderate clubbing was also observed by him, but without special comment.
Coincidently with the appearance of distinct signs in the right apex the fever rose a degree or two, headache was complained of, and cough without expectoration became troublesome. This con- dition, which I now believe was a pneumonia of the same bacterial ^origin as the general sepsis, persisted for about two weeks, and then gradually disappeared, the lung clearing up, and the patient's general condition returning to what it was before this attack.
For the next month or six weeks the clinical picture remained nearly in statu quo. Occasionally he s{X)ke of sudden pains in the shoulder or elsewhere, wliich lasted for a few days and then vanished. Once he complained of pain and tenderness of the liver, and the organ became slightly more enlarged. This condition per- sisted for perhaps a week, and then disappeared slowly. All this time there was the same relentless pyrexia, which at times fluc- tuated rather more than before — but with exception of its becom- ing somewhat weaker in action and sounds, the heart showed no distinct change.
The character of the temperature is shown in the annexed chart. Credo's ointment was rubbed into the skin freely for two weeks, and was then succeeded by daily injections beneath the in- tegument of an old antistreptococcus serum in doses of 10 cubic
ACUTE ENDOCARDITIS
1T6
centimetres. Altlioiigh kept up for more than a week this treat- ment pnxhieed nu rt-sultSj unless perhaps a feeling of soniewhat greater strength and a slight reduction of temperature.
At length, near the middle of Julv, the patient, who all the time dechired he did not feel very ill, suddenly experienced an excrneiating pain in the third linger of the left hand. The finger became cold, pale, and exquisitely sensitive to touch, as well aa so painful that it prevented sleep. Examination made it apparent that an emholus had lodged in the artery near the middle of the third phalanx. Plugging was so complete and the patient's suf- fering so intense that it became necessary to amputate the finger on the fourth <lay. It was now apparent that he was failing stead- ily, although slowly. The heart-rate increased to 12Uy the apex- impulse less defined, the first sound inaudible^ but the murmur not appreeiaUy more distinct, indeed rather less intense^ and the fever increased, but without rigors or sweatings. Indeed, throughout the illness these had been eonspieuoos by their absence.
I saw him for the last time on the afternoon of July 22d, at which time he declared he felt so eonifortable and happy that he believed he was going to get well. His countenance was slightly sniFused, and as he had not emaciated greatly, his friends could not realize how ill he in reality was. During the forenoon of the 24th he was suddenly seized with jmin in the limgs, which was followed hy violent coughing and the expectoration of blood, Ev^i- dently pulmonary infarcts had taken place and betokened the near approach of the end. The cough grew so incessant aa to require considerable doses of morphine hypodermically for its control. These were followed by unconsciousness, in which condition he lingered until the afternoon of July 25th, when he suddenly expired.
The course of this undoubted ease of septic endocarditis occu- pied five months from the attack of tonsillitis. It was plainly one of sepsis from the date of his visit to my office, yet without the occurrence of embolisms there was little to direct one's attention to the heart, I was familiar with the previous condition of the heart, and hence able to detect slight alteration in the physical signs which might have been otherwise unrecognised. Yet the thing that riveted my attention from the start was the almost un- swerving persistence of the pulse at very nearly the same rate,
176 DISEASES OF THE HEART
105, in spite of rest in bed, until near the termination of the case, when it rose to 120.
A highly interesting feature also was the condition of the ter- minal phalanges of the fingers. The faint redness, pain, and, it seemed to me, slight increase of heat, were due to capillary dilata- tion, which caused the ends of the fingers to become distinctly bulbous in the course of a few months. During the preceding winter I had observed this same phenomenon, only to a much more marked extent, in a young woman who was in the ward at Cook County Hospital suffering from mitral disease, and, judging from the s;vTnptoms, from endocarditis. She subsequently left the hospital, so that I cannot 8tat« the cardiac condition definitely. In her case the finger-ends became distinctly red and unmistak- ably bulbous. In Loth these instances there was pyrexia associ- ated with cardiac disease. May not this phenomenon in the finger- tips point to buinething more than mere capillary paresis, perhaps to such a disturbance of the cardio-vascular apparatus as may sug- gest involvement of the heart as well as general infection ? It is a matter of profoimd regret that an autopsy could not be obtained in the case which has been narrated at such length.
Physical Signs. — Inspection is of very negative value, since although it may enable one to detect signs of circulatory disturb- ance, it does not furnish proof of such disturbance being due to endocarditis. Besides, valvulitis is so often masked by the symp- toms and physical signs of the primary affection that inspection of the patient reveals only such changes in the patient's appear- ance as belong to the rheumatism or other original disease.
Palpation is likewise of minor aid in the detection of acute endocarditis. It may assist in the recognition of some old-stand- ing valvular lesion, or in determining the presence of abnormal pulsations, variations in the force, position, and extent of the ai)ex-beat, the possible development of thrills in the course of the affection, enlargement or not of the liver, etc., all findings that bear in certain cases on the condition of the heart, but, like inspec- tion, it cannot furnish direct evidence of the existence of acute endocarditis. Its chief value is in the study of the pulse, which in all suspected cases should be carefully studied, changes in its tension being often of greater value than alterations of rate or rhythm.
ACUTE EKDOCARDITIS
177
Perciismon* — This is indispensable if one will correctly appre* ciate the significance of ansciiltator;\ phenomena, since the condi- tion which occasions an organic murnuu" also leads to dilatation or hyjK?rtrophy, and therefore to a corresponding alteration in the area of cardiac dulness. If endocarditis occasions mitral incom- petence, it will also eventnally occasion secondary enlargenient of the right ventricle. Consequently daily percussion over this cham- ber should be made in order to detect the earliest evidence of any alteration in the outline of the right and lower cardiac border. On the other hand, aortic disease prodnces increase of dnhiess on the left side with gradual alteration in tlje position of the apex- beat. Accordingly [>ercnssion is of very great value, since without the information derived from it a carefnl diagnostician would scarcely venture on an opinion concerning the nature of an endo- cardial niiirmurj especially an apex-nuirnnir, which, as is well known, is of frequent occnrrenee in febrile affections without inflammatory changers in the valves.
Ausculiaiion. — Even this furnishes only exceptionally a trust- worthy means of re(T>gnising endoearditis, for, as will be shown later on, a murnuir is not always to be accepted as an indication of val\i:ilitis.
It is not so much the detection of an actual murmur that is significant, as it is the recognifion of changes in the eharacter and relative intensity of the cardiac tones. Daily careful study of the sounds must be made therefore. The earliest evidence that all is not right at the mitral orifice (the seat of inflammation in 50 per cent of eases) is said by English observers, who it must be acknowledged have given Hose attention to this subject, to be not a murmur, but a mnffluig or indistinctness of the first sound at the apex. A blowing murmur, whieh is purely accidental, may ac- company the first sound in a given case, and hence the occur- rence of a murmur with the sound is not so significant as an alter* ation in the sound itself, since it is reasonable to assume that if the production of the sound is interfered with it may be by inflam- matory changes. Such altera Hon of (he second sound at the base is likewise suspicious of endocarditis aflfecting the semilunar valves.
If in a case impurity of any of the tones is observed, it is very likely to grow into a more or less distinct murmur in the course
12
1
178 DISEASES OP THE HEART
of time, while there will also develop the secondary changes in the heart appropriate to the lesion, whatever it may be.
A diastolic murmur developing in the aortic area may be set down as not accidental, and therefore indicative of inflummution at this ostium. If this inflammation seriously impair the integrity of the valve, it will be sho^vn in time by the occurrence of the secondary cardiac and vascular signs, which are described at length in the chapter on Aortic Regurgitation.
A presystolic murmur rarely develops as a result of acute endo- carditis unless the process is ingrafted upon an old-standing mitral regurgitation. Inflammation attacking previously healthy valves usually produces incompetence of these, or this combined with a minor degree of obstruction. Therefore, the murmur is apt to be purely systolic, or systolic with a very short, scarcely recognisable presystolic one. When, however, an old endocarditis affecting the mitral valve becomes rekindled, as not infrequently happens, then a presystolic bruit may develop, and so developing it furnishes almost indubitable proof of endocarditis being present. This cir- cumstance has more than once enabled me to diagnosticate correctly the occurrence of endocarditis, as proved by subsequent events.
A systolic murmur in any of the cardiac areas must always be regarded with doubt until its true significance is shown by the development of secondary physical signs. This is true of such a murmur even in the aortic notch, for experience has taught that even here a murmur may be accidental. It is, however, in the case of an apex systolic murmur particularly that caution must be exercised. (1) Because accidental bruits are most often mitral, or mitral and pulmonic. (2) Because such a mitral systolic mur- mur may be the result of a previously existing regurgitation, and not at all due to the rheumatism in the course of which it may happen to be discovered. (3) Because, as sho^^^l by a case re- ported by James W. Walker, of this city, an endocarditis may exist without its giving rise to any murmur whatever. In his case the anterior and left posterior aortic cusps presented on their surface large masses of soft, friable, nodular vegetations, which had filled the ostium, and yet repeated and careful examinations during life had utterly failed to detect any murmur.
Diagnosis. — These three considerations make very plain the fallacy of depending upon the presence or absence of a murmur
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179
in making a diagnosis of acute endcM^arditis. Inaaoiueb, therefore, as acute sLuipie endocarditis may et^cape dL'toetioii entirely or may be only suspected^ one is frequently conii>elleJ to leave its diag- nosis an open question until after it lias occasioned sufficient structural change to produce sect mil a rv pliysical signs. One miisit therefore dejiend upon the hL^torf/ and sympioms even more than on distinctive objective signs.
Even the pyrexia, acceleration of the pulse and respiration, pnecordial pain, nervousness, and restlessness may all be attribu- table to the rhcuoiatism. When the endwarditis is mural — i. e., confined to the lining membrane of the cavities — the valves escap- ing altogether, a positive diagnosis cannot be made without the occurrence of enilKilie j>henomena.
Differential Diisgnosis, — Acute pericarditis is scarcely likely to be mistaken for acute simple endi^carditis, and yet it is con- ceivable that such might l>e the case when the friction-murmur hap^)ens to coincide with one of the heart-sounds, and hence siuin- late an endocardial bruit. In such a case the greater pain and the subscH|ncnt development of signs of eflFusion ought to set one right. Should an inexperienced auscultator mistake a to-and-fro pericardial rub over the base of the aorta for the double murmur of aortic insufficiency of recent origin, he may be able to correctly interpret the rub by noting the absence of the secondary cardiac and vascular signs of an aortic valve-lesion.
Pernicious atut^mla may imder some circumstances very closely simulate acute endocarditis without embolic phenomena. I have seen such a case, in which the systolic a{>ex-murmur of ever-in- creasing intensity, the low irregular pyrexia, great prostration, pain in the hepatic region, with nausea and vomiting, were^ to- gether with a hiatury of infection of the forefinger and lymphan- gitis four months earlier, highly suggestive of a low grade of en- docardial intlammation, particularly as the patient gave additional history of rheumatism. The blood-examination and ultimate au- topsy findings estal>lished tlK* corrert diagnosis.
Tbe BiagnoslB of Ulcerative Endoearditis may in some easea be easy, in others only a matter of conjecture. What has been said concerning the physical signs of the simple applies equally well to the malignant form. In some instances the entire clinical pic- ture is that of general sepsis, and there are no findings to betray
180 DISEASES OP THE HEART
its localization in the heart. In others characteristic signs of valvular insufficiency develop or the tokens of an old lesion un- dergo modification, or indications of a new lesion become added to those of a pre-existing defect. For these reasons repeated and minute examinations of the heart are necessary. The detection of a murmur is in itself of small moment sometimes, but the dis- covery of changes in the rhythm of one already existing, as by a presystolic being prefixed to a systolic bruit, or an alteration in its timbre, a previously soft one becoming harsh or musical, or the addition of a diastolic murmur to a systolic one, all such modifica- tions are of great significance, and should be carefully noted.
The most reliable aid in the diagnosis of malignant endocar- ditis is found, however, in the history and symptoms. One must always seek for an efficient etiological factor. For example, it was not a great while ago that I was asked to see in consultation a young woman who was running an irregular course of fever, was emaciating, losing strength, and had a cardiac murmur. It was evident at a glance that she was suffering from pronounced sep- ticaemia, but the question that the physician wanted cleared up was whether the cardiac findings indicated septic endocarditis. There was history of an old rheumatic mitral disease. It did not require very long search to find evidences of cutaneous infarcts, and when in response to inquiry concerning a vaginal discharge, the nurse stated that there had been an extremely offensive one earlier in the illness, and when a vaginal examination disclosed cervical laceration, the chain of testimony was complete. An abor- tion had led to uterine infection, this to septicirniia, and this lat- ter to an ulcerative process within the heart, which was predis- posed to inflannnation by its old-standing mitral lesion.
Symptoms of pyaemia — i. e., chills, fever, and sweating — in- dicate general sepsis, but do not warrant the inference that the endocardium is involved. This can only be assumed when embolic phenomena are discovered or there are some cardiac findings as well as symptoms of general sepsis. It is very necessary, there- fore, to make daily examination of the skin, spleen, and urine for detection of the changes already mentioned as forming an essen- tial part of the symptomatology of this form of endocarditis.
In the very obscure cases in which embolic phenomena are not present and there are no cardiac findings to explain the pyrexia
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181
^ncl other features that point to infection, yet in which the feeble- ness of pulse and heart-sounds suggest the possibility of a primary focus of infection in the endoeardiuni, information is likely to be obtained from examination of the blood. Usually in infections there is pronouneed leucocytosis, but in a few cases Neusser found an absence of increase, and he consequently concluded that when in a given case of septioemia there is either an absence or possi- bly a decrease of leiieocytosis, it points to the likelihood of ma- lignant endtx'arditis. Eacteriok^gical examination of the blood in a suspected ease is not often productive of results, and yet should be made when all other means of arriving at a diagno- sis fail.
Differeuiial Diagnoms. — It is not sufficient to merely make a diagnosis of acute endocarditis; one must also determine its na- ture. Therefore in making a differential diagnosis the following points may be of assistance: (1) The possible etiological factor; in the simple fornij articular rheumatism, chorea, scarlatina, or m other generally recognised cause of benign endocarditis; in the ulcerative, some antecedent pus infection or focus of suppura- tion, erouiKms pneunmnia, gnuorrbcta, rectal abscess, otitis media, quinsy, trauma, furuncle, carbuncle, leg ulcer, etc, (2) The char- acter of the temperature. In simple endocarditis fever may be absent or due to the primary disease, sulisiding with the disap pea ranee of the rheumatism, etc., or it uiay pursue a mild con- tinuous course. In the ulcerative form the temperature-curve is that of pus-infection of the characters that were described in the sym|»toms. (3) Elnnd changes and bacteriological examination of the blood are negative in the simple form, while in the malignaut there uuiy t>e pronounced leucocytosis. The occurrence of septic phenonjena without such increase points to septic endtx'arditis,
(4) Urinary findings. The discovery of albumin, pus, and blood with easts is in favour of mycotic eudiu-arditis, since luemorrhagic neidiritis is not a part of the clinical history of the simple form.
(5) lla^uuu'rbages into the skin or from the mucous membranes may occur in the ulcerative, but not in the licnign variety of endo- carditis* (6) Embi^lic phenomena, although occasionally observed in the simple, are yet generally found in the malignant endocar- ditis. (7) Enlargement of the spleen is in favour of rhe mycotic as against the sirFiple form. (8) Recovery is the rule in simple
182 DISEASES OF THE HEART
and the exception in ulcerative endocarditis, although its course to a fatal issue may be slow.
Typhoid fever is the disease above all others for which ulcer- ative endocarditis is likely to be mistaken. As a matter of fact, most cases of the latter affection are diagnosed as enteric fever, and so regarded until in the dead-house they are found otherwise. The points of difference are the following: (1) In typhoid fever the temperature is not so erratic, and in the first week often dis- plays the characteristic gradually ascending curve. (2) The pulse in this disease is usually slow, out of proportion to the degree of temperature. In its want of tension during the height of the malady it may be like that of endocarditis. (3) Splenic enlarge- ment comes at an earlier period in enteric fever, and is more con- siderable. (4) Rose-spots usually appear between the eighth and twelfth day, are apt to be in crops upon the trunk, disappear temix)rarily on pressure, are of a nearly uniform size, and have a darker centre, fading out towards the periphery. Cutaneous em- bolisms, on the contrary, apj^ear most often ujx>n the extremities, are irregularly distributed, of variable size, do not fade on pres- sure, and have a necrotic pale centre, becoming of a deeper colour towards the edge. (5) The stools of abdominal typhus are often, though by no means always, diarrhopal, have the pea-soup appear- ance, and contain the Eberth bacillus. (6) Typhoid-fever pa- tients are very apt to manifest signs of bronchitis. (7) Except- ing cpistaxis early in its course and possible hiomorrhage from the bowel during the middle or latter i)ortion, haemorrhages are not common in typhoid fever. (8) In the Widal agglutination test we now possess a reliable means of differentiating enteric fever from malignant endocarditis, and it should invariably be made in every doubtful case.*
The value of this differential test was shown in a case under my care a few months ago. A young man with extreme aortic regurgitation of rheumatic origin was under treatment for attacks of pnwordial pain, and as there were s^^nptoms pointing to a rup- ture of compensation he was put to bed. A few days thereafter he l)egan to manifest a low grade of irregular temperature, but without any other symptoms. His pulse remained disproportion-
* According to MacFarland, there was in 4,000 cases only 4 jx^r cent of error.
ACUTE ENDOCARDITIS
188
ately glow, and I at once siisi>eeted typhoid fever, although not unmindful of the po^sibilitY of endocarditis. Rose-spots were never discovered, notwithstanding repeated daily inspection of tlie trunk, and splenic enlargement could never be satisfactorily made out either hy paljiation or percussion. There was no diar- rha'a at any time, the bowels being rather contined. The Widal test was resorted to at the end of the first week, and settled the diagnosis as one of enteric fever. Had this means of differential diagnosis not hecn available I should have felt exceedingly uneasy as to the nature of the ease and its possible outcome. As it was, I felt no more anxiety than would be natural in such a severe valvular lesion, comirlieated by the occurrence of the abdominal typhus, and a possible infection of the chronic endocarditis in con- sequence.
The error of mistaking ulcerative endocarditis for malarial infection is so easily avoidable nowadays by the discovery of the phisinudia that it ought never to he committed, and is inexcusable.
Prognosis. — ^This deiH*nds not only upon the nature of the endocarditis, whether Wnign or ulcerative, but also upon certain moilifving conditions, as the extent and seat of the inflammation^ the concurrence or not of acute pericarditis or myocarditis, whether it is a first attack or has been ingrafted upon a chronic endiK*arditis, and lastly upon the presence or absence of septic in- farcts. If the inftammation expend its energies in a hxial deform- ing process through ttie development of new connective tissue * within the valves, or the formation of vegetations upon their sur- face, or that of the contiguous orifice, the endocarditis does not usually destroy life directly, but leaves the individual with a jK^r- manent valvular defect* This statement must be modified, how- ever, in acconlance with the seat of the inflammation. If this is confined to the left auricuh>ventricnlar opening, which fortu- nately is the case in at least one-half of the instances, the imme- diate prognosis is nnich less grave than when the endocarditis attacks the aortic valves, rendering them incompetent, Ropidly induced insuthciency occasions dilatation of that chamber inlo which the blood regurgitates.
The secondary effect of endocarditis of the mitral cusps is dilatation of the left auricle, of the aorflc cusps, dilatation of the left ventricle, and there is abundant proof, both clinical and other-
•184 DISEASES OP THE HEART
wise, that dilatation of the auricle is less dangerous to life than dilatation of the ventricle. Moreover, in mitral regurgitation, the resistance offered by the walls of the left auricle is re-enforced by the column of blood in the pulmonary vessels and by the right ventricle, while in insufficiency of the aortic valve there is not only danger of paralysis of the left ventricle from overdistention, but if in consequence of stretching of this cavity and of the left au- riculo-ventricular ring the mitral valves become relatively incom- petent, the evils and dangers of mitral are added to those of aortic regurgitation.
If the inflammatory process extend also to the myocardium or pericardium the prognosis becomes far more serious, since the myocarditis favours a rapid dilatation of the organ. Sturges directed attention to the liability in children to inflammation of all of these structures, giving it the name " acute carditis,'' and pointed out the extremely serious nature of this condition. The gravity of the prognosis in these cases is attested by the following figures, to which reference has already been made in the chapter on Acute Pericarditis: Of 150 cases of fatal rheumatic endocar- ditis in children, Poynton found the pericardium healthy in only 9, while in 34 the myocardium showed changes of one kind or an- other. Death was thought attributable to the condition of the myocardium rather than to that of the endocardium.
If an acute endocarditis becomes ingrafted upon the chronic process, or attacks valves already the seat of sclerotic ehanp:es, the prognosis becomes very doubtful, since it is a well-known fact that under such circumstances the inflammatory process is very likely to prove septic, iloreover, even if the endocarditis should not be malignant, it is certain to intensify the changes already existing, either by causing still greater destruction of the valves or by trans- forming a predominating insufficiency into a stenosis through the development of thrombi about the edges of the opening. Thus a lesion which was compensated may be converted into one of such gravity that compensation is never again possible.
The occurrence of embolisms renders the prognosis exceed- ingly serious, both as to the immediate and remote effects. Even in simple rheumatic endocarditis an embolus may be carried into the brain, the left middle cerebral artery being the one most fre- quently plugged, and occasion hemiplegia. In the case of endo-
ACUTE ENDOCARDITIS
185
carditis of the rig:ht heart, pulniaiiary infarcts frequently con- tribute to the fatal termination. Should the emboli be septic, more than a mechanical effect is produced. Single or multiple abscesses in the spleen, liver, kidneys, or even scattered throughout the body, set up symptoms of general infection* These are the cases properly classed umler the category of malignant enducarditis, since in them death is the inevitable result* Should the urine at any time display the characters of ha^morrhagic nephritis, it is to be regarded as an omen of evil import.
The very interesting and practical question arises, Can acute rheumatic endocarditis subside, leaving the valves uninjured! This (piery has been answered in the affirmative by some writers, their belief being based upon the disappearance of a systolic apex- murmur that had been observed to develop during an acute rheu- matic attack. My experience has been too limited to warrant my forming an opinion upon the subject, yet I frankly state I would be loath to accept any other than post-mortem evidence of the cor- rectness of such a belief. Under the influence of infection and pyrexia, weakening of the myocardium and papillary muscles may verv readily occasion dilatation, and a systolic murmur in the mitral area be developed. With returning health these may re^ gain their tone, and the dilatation and murmur disappear. Can any one assert therefore, without fear of contradiction, that the appearance and subsequent disappearance of such physical signs indicate recovery from acute endocarditis, and not from cardiac dilatation 'i The following case observed during convalescence from pneumonia is one in point: A healthy young married man of twenty -seven passed thnnigh a pneumonia of the right lower lobe iu the fall of 18D0, Aliout a week after the crisis, when convalescence was progressing finely, he arose from bed early one morning and walked into the adjoining bath-room to pass his urine. lie sud- denly became weak and dizzy, and upon returning to his bed- chamber his pulse was observed to be 135 to the minute and weak. ^Tienever during that day he attempted to walk about the room his pulse immediately arose in frequency and became correspond- ingly diminished in strength* I was asked to see him that same evening, and found him reclining on the sofa, his pudsc about 100, regular, but compressible, the apex-beat feeble, in the fifth left interspace slightly outside the nippk*-line.
1S6
DISEASES OF THE HEART
Relative cardiiK* diiltioss was increased transversely, partieu* larly to the left, reaching 12-5 centimetres to the left of the niedi* an line. The temperature was normal, respirations tranquil, and the patient had no sense of dyspnoea. Cardiac sounds were every- where audi hie, but the aortic second was weak, and accompany- intjj the tirst sound at rlie apt'x was a faint systolic hlowiug mur- mur. There was no history of previous attacks of rheumatism, and until the date of his pneumonia the patient had indulged in niucdi athletic exercise with«nu shortness of hreath or palpitation. Kcalizing the possibility of an acute endocarditis of pneuniococ- CU8 origin, 1 insisted upon absolute ]>hysical repose, ordered light diet, and a gentle saline aperient.
On the following day, the condition being essentially the same, xV *^f ^ grain of strychnine sulphate three times a day wae or- dered. As the teuijK*rature remained normal and the murmur had nut increased, two days later tincture of digitalis was cau- tiously administered. Within twenty-four liours the left ventricle had come down 0.5 centimetres, and upon the digitalis lieing incrt^ased^ the next twenty-four hours wit- nessed a still further diminu- tion in the extent of relative ' ardiac dulness to the left. In the course of the next week or ten days the heart meas- ured hut 10 centimetres to the left of the median line, and was normal at the right (Fig. 32).
Two months subsequently, after the patient luid l>een without medicine it^r several weeks, and hail returncfl to his usual mode of life, the left ven- tricle measured but t* centimetres, a reduction of more than 3 centimetres since the date of my first examination. Was this ease to be regarded as one of acute endocarditis following croupous pneumonia i Certainly not. It was one of simple acute dilata-
Fio. 112.— DiMiNiTto^ mk Relative CARitlAO DiLSE&<« IX Onh Webk« und£r Tkkat- M£3rr. Case ip, 186).
ACUTE ENDOCAHDITIS
187
tion, cliieflv of tiie left ventricle^ resulting primarily from asthc- Bia of the lieart-uiuscle in cunseqiienee of the effect of the toxins of the pnemnoeoecus.
Treatment. — Clinical experience the world over accords with the conelusiiin naturally drawn from a cfjnsi deration of the pathol- ogv and morbid anatomy of acute endocarditi^^viz., that when the prtM^ess has once heeome established, we possess no means of causing absorption of inflammatory product or restoring the endo- cardium to a healthy state. It should l>e our aim, therefore, to prevent where we cannot cure. Our first duty is to study the etti* cacy of prophylactic measures. Our efforts in this direction should not be re^stricted to prevention of endocarditis, but shoiild first be directed against that disease, articular rheumatism, which is so largely responsible for inflammation of the cardiac structures. Proper sanitation and attention to the diet^ clotliing, habitSj and oeeupation of patients may do much to this end.
Of special value are all measures calculati^d to maintain a high standard of nutrition, and persons of distinct rheumatic diathesis should be impressed with the danger of exposure ix) wet and cold. Children in whom rheumatic manifestations are ol>scure, should be carefully examined whenever ailing, f«>r ]w>ssil>le evidence of rheu- matic infection, and if this be discovenMl, should promptly be given some preparation of a salicylic acid.
Much has been written concern in*,^ the prevention of cardiac involvement during rheumatic attacks; and when the salicylic- acid treatment of rheumatism came into use, strong hope was entertained of its ability to prevent en<locarditis. Even now there are those who believe that by dituinishing the severity of, or even cutting short, the rheumatic attack, this treatment lessens the lia- bility to cardiac inflammation. The same also may be said of the alkaline treatnicnt, or of the combinations of the alkalies and salicylates. For the njost part, observers of long experience have come to the conclusion that whereas the salicy late-treatment does not assure the prevention of endocarditis it would better be per- severed with, since if properly administered it is not likely to do hann. For my part I do not Ijelieve in the prophylactic power of this drug over the cardiac manifestations of articuhir rheu- matism.
Given a case of this disease in wdiieh salicylate of soda is em-
188 DISEASES OP THE HEART
ployed, and acute endocarditis or pericarditis does not develop, can any one assert it would have occurred had the remedy not been administered i Are there any statistics to show that endocarditis has been less frequent than before the use of the salicylates ? Even if one or more series of rheumatic cases treated with this remedy show a smaller percentage of endocarditis than others not so treated, how can one be sure that the difference in results is not purely accidental, since all rheumatic attacks do not iii6?r(tably lead to cardiac inflammation ?
By all means during a rheumatic attack resort to salicylic acid, or one of its salts, to potash or soda, local applications to the affected joints, to regulation of the diet, and any other approved means of antirheumatic treatment. But do not be too confident that endocarditis will not develop. Should it not, consider your- self and the patient fortunate.
I confess to the same scepticism concerning the efficacy of local treatment of the pnwordium, as leeches, blisters, and cold ap- plications, in preventing acute endocardial inflammation. The only prophylactic measure that appeals to me as rational is the pro- curement of as much rest to the heart as possible, by keeping the patient quiet during his attack of rheumatism, that the valves may not suffer trauma by reason of strain. Fortunately, in an acute attack of severity the urgency of the s\inptoms compels the patient to remain at rest; but in eases of subacute rheumatism, particu- larly if an old valvular defect already exists, the patient should be urged to remain at rest, so as to lessen the tension of the valves and the possibility of having inflammation rekindled in them. This is often irksome to the patient, but if he has the reason ex- plained to him he is likely to acquiesce, although i)erhaps with no very good grace. Even after all the rheumatic symptoms have disappeared the patient should be cautioned against violent exer- cise, and should be kept under rather frequent observation, that the earliest evidence of endocarditis, should such arise, may not be overlooked.
Upon the occurrence of acute endocarditis, or of subjective or objective symptoms suspicious of such an inflammation, the pa- tient should promptly be put to bed, if not there already, and kept there as quiet as possible, both mentally and physically. The ob- ject of this is apparent ; bodily exertion as well as mental excite-
ACUTE ENDOCARDITIS
isa
ment aii^fments the freqiR'Ufv of cardiac contractions and subjects the valvc'-ciirtams to increased strain. The same prinvipfes should apply to the treatment of inflamed valves as to Ihal of inflamed joints. The use of the latter not only causes pain, hnt intensifies the inflanmmtion* L'nfortunatelv, the heart cannut be pnt at en- tire rest^ but by slowing its contractions its^ diastole or period of rest is lengthened and its contractions are less violent. Theoret- ically, at least, the inflammatory process wonld thus be less active and the dnnger lessened of rupture of the intlanied and tender cusps, or of dislodgnient of a soft, not firmly seated thronihus, and the formation of embolism. If the heart's action is violent or too rapidj attem|>t shonhl Ije nuide to quiet it by plaeing iee-bag to the pnreordium or by the administration of bromides.
Digitalis is very commonly administered for this purjx>se, but it cannot be stated too emphatically that this drag is inndmissihle in the Ireatmcnt of acufe endoeardiiis. It not only does no gmid, but is positively harmful. Althmigh capable of slowing tiie heart, digitalis at the same time increases the strength of systole, and thereby subjects the valves to more than ordinary strain. The benefit to be derived from a slowing of the contractions is offset by the injury to the valves and by other dangers possible from this more forcible closure, as already explained. It is better to let the hear! keep its own gait than attempt to control it by possi- bly injurious means.
Aconite or veratruiu viride are likewise injurious, but in a different w^ay* They are depressoi^s to the myoeardium; and if thia be inflamed or weakened by serous infiltration, there is danger of these drugs causing serious dilatation. The san*e objection can- not l)e urged against the local employment of cold^ and as a matter of fact this therapeutic agent is highly praised by those who have given it an extended trial. As staled in the chapter on Acute Pericarditis, the ice-bag is preferalde to cloths wrung out in ice* w^ater, since they do not subject the patient to the danger of taking cold by wetting the clothing, and for the same reason are more comfortable. The ice-bag should not Ixf applied directly to the bare skin, but a dry, light cloth should be interposed. Should the heart and circulation have become very feeble, cold had better not be resorted to, because cardiac depressors are no longer indi- cated.
190 DISEASES OF THE HEART
• Hot applications to the prtBcordium are then more serviceable
on account of the stimulating effect they produce. Vesication of the pra?cordi\mi, either in the form of one large blister, or of re- peated small blisters, is a treatment that once met with much favour, but is objectionable, since it occasions more nervous irri- tation than it is likely to do good. The application of mustard or the tincture of iodine or of a turpentine stupe are less objec- tionable because less severe, and are sometimes capable of alleviat- ing pain.
Mercurials and tartar emetics are now known to exercise no restraining influence over the inflammatory process, and are there- fore no longer used by the best authorities. 3kIoderate doses of iodide of potash have been recommended, in the hope of restricting the formation or promoting the absorption of the inflanmiatory products. It is, however, doubtful if this remedy possesses any such influence in the course of acute endocarditis.
When medicines are powerless to cut short an attack, or even probably to diminish its severity, we are left to a purely sjTnp- tomatic treatment. Pain and restlessness should be alleviated by the use of opiimi, and in the case of adults morphine hypoder- mically is the best mode of administration. In children great care must be exercised in its use, and it is always well to first try the efficacy of bromides in conjunction with cold applications and soothing liniments. Antipyrine, phenacetine, and other remedies of this class are capable of exerting depression, and if employed at all should be in small doses and with strychnine or some stimu- lant.
The pyrexia of acute simple endocarditis is usually not high, and therefore such antipyretics are not likely to be needed for the reduction of temperature. If this should become necessary, it would be best attempted by judicious sjMDnging. Insomnia may be prevented by bromide, paraldehyde, sulphonal, or trional, or, best of all, by some preparation of o])ium.
So soon as the endocardium is found to be the seat of acute inflammation the physician should constantly bear in mind the possibility of the heart finally succumbing through weakness, if not structural change of the myocardium. The organ should be sustained, therefore, by that best of all heart-tonics, strychnine. Opium is also a heart-tonic, and while being given for the relief
ACUTK ENDOCARDITIS
191
of pain, also supports the heart, provided it be not adiiiiniisrt'rcd with greater frequency or in kirger doses than are required to alleviate the symptoms* Sulphate of strychnine is, however, the remedy on whieh chief reliance should be placed. Given in mod- erate do^cs, at first ^V ^^f a grain to an adult three times a day, it may be increased to ^, or even to fV, if signs of myocardial weaknejss super\^ene. Should the disease assume a grave eharac^ ter, and attacks of threatening asystoli^ni make their appearance, by cyanosis, feeljle and irregular pulse, paroxysms of dyspmea, or signs of pulmonary ledenia, the heart should be* promptly stimu- lateil by ammonia, eamj>hor, ether, brandy, and the like. Itihala- tions of uxygen nuiy alsu \>e resorted to, and are likely to prove temporarily, if not permanently, benetieiaL
The patienfs general strength should likewise be sustained by nutritious, though light, diet, llilk, beef juice, an occasional raw egg, soup, broth, and wine jelly are all serviceable. A cup of soup (prepared from ilosquera's beef jtdly), trojinn and somatose, form admirable adjuvants to the dietary. The nourishment should be given frequently, every two to three hours, and in small amounts, care being taken to avoid all articles of diet which occa- sion gaseous distention of the stomach and intestines. C onstipa- tion should not be permitted, and even if the action of the bowels is regular, benefit is likely to accrue from the ocx^asional adminis- tration of a blue pill or small dose of calomel, followed by a gentle saline aperient. The urine should be watched, and if it become bloody or albuminous the diet should be restricted t(/ milk, and the patient urged to drink freely of pure water.
Acute IHcerative EndocarditiB. — Fortunately there are grada- tions in the severity of this type of the affertion; were it not so the physician would be but a helpless spectator of the ravages of this dreadful malady. Indeed, such is his attitude in severe cases, or in those that have made considerable progress before recog- nition of their true nature. The first duty of the medical attend- ant is to search for (he cause — that is, the source of the primary in- fection— and, if this is discovered and can be removed by surgical interference, to promptly resort to such treatment. This, alas! is not generally possible; but if, as Sir Douglas Powell thitiks, un- sanitary environment and exposure to sewer-gas emanation^ are capable of setting np fresh infection in a case of old-standing valvu-
192 DISEASES OP THE HEART
lar disease, then the patient should be promptly removed to a healthful location.
The next indication is to resort to every means which affords any hope of re-enforcing tissue resistance, as a nutritious and easily assimilated diet. The lines of treatment already laid down for the sustaining of the heart and protecting it against the injury resulting from unnecessary work in the simple form are equally applicable to the ulcerative. Indeed, they are still more urgently required; for not only is inflammation more destructive and likely to invade the myocardium, but even when this escapes ulceration or abscess formation the heart-muscle is likely to suffer from the enfeebling effect of the toxaemia.
In severe cases the prostration of the patient generally calls for the administration of small, frequently repeated doses of brandy or ammonia. The use of alcohol in conditions of sei>sis is very generally employed, and, in the opinion of many clinicians, is highly useful. Some indeed advocate whisky in large and fre- quently administered amoimts. Strychnine should be given in full doses, and will yield the best results if administered hypodermic- ally. Quinine was formerly exhibited in doses of 15, 20, or more grains for the control of the fever; but with a clearer knowledge of the etiology and pathology of this affection, we now know that this remedy can exert no controlling influence over its course. Iron and arsenic have also been employed, and Powell speaks highly of the latter, not as a curative agent, but simply as a car- diac and general tonic.
Attempts have been made to introduce into the system antisep- tics in sufficient quantity to exert at least a modifying influence upon the sepsis. The one deserving s})ecial mention is sulpho- carbolate of soda, which has Ix^en thought in mild cases to exert a favourable influence. Sansom has reported one case in which during its use such improvement took place that the patient left the hosj)ital ; she returned, however, and succumbed to a fresh attack or accession at the end of ten months. " At the autopsy the diagnosis of septic endocarditis was confirmed, the mitral, tricuspid, and aortic valves being diseased and infiltrated with micrococci."
Drechfeld, in speaking of this remedy in ^-drachm doses, men- tions a case reported by Sansom (probably the one just quoted)
ACUTE ENDOCARDITIS
193
in which, when death unyk phic^ at a later {leriml, '' distinct cica* trifial ti^wue was found at tlie site of the old ulcerations/'
If this or any other antiseptic remedj, as salol and salophen, is to do good, it must be in very large, frequently repeated doses, so as to rapidly bring the system under their influence, and should then l>e continued for a C€»nsiderable time. These latter remedies recommend themselves in cases with a ^heiunatic element, beeause composed of salicylic as %vell as carbolic acid; but the depressing effect *d the former uj>on the myocardium must not l>e forgotten. For my part I am inclined to attribute whatever benefit has seemed to follow such treatment to their local antiseptic action upon the intestinal tract. Fermentative processes and diarrlirea, as shown by factor of the distdiarg^es, are very common within the digestive tube of patients suffering from sepsis. Such a condition may not only intensify the pyrexia and other symptoms of infec- tion, by itself setting up an infection of intestinal origin, but it prevents the proper digestion and assimilatii>n of nonrishu^'^ut. If now this putrefactive fermentation can be prevented by inte**- timil antisepsis, the patient's nutrition will improve and his tissue resistance be augmented. It is possible, perhaps, by having this additional enemy thus removed, the system may be able to cope successfully with the primary invader. At all events, the physi- cian should employ these and every other means that affonl possi- ble chance of improvement in dealing with so formidable an ad- versary.
The universal success of the antitoxin treatment of diphtheria, and the fueouraging reports that have come from the use of anti' streptococcus serum in some eases of pyaemia and puerperal sep- ticac*niia, indicate the dawn of a new era in therai>euties. It is to l>e hoped that in the not very distant future we shall possess a serum fMitent against each kind of pns-pnulucing microbe. At present we are limited to the serum just mentioned; and inasmuch as the streptococcus is the agent frei]uently at work in cases of spticjemia^ and the jutHcious employuient of this serum appears fnot to be injurious, we are certainly warranted in giving it a trial in cases of septic endocarditis. This has already Ijeen done> although to what extent I am not able to say, nor have I been al»le to find how many cases of this disease treated in this manner have appeared in the literature to date, 13
194 DISEASES OP THE HEART
Douglas Powell has tabulated 14 eases of ulcerative endocar- ditis in which antistreptococcus serum has been employed in Lon- don. The results are as follows: Three recoveries, 9 deaths, and 2 in which no favourable result ensued. Powell is of the opinion that these results appear more discouraging than they really are^ from the fact that the serum was employed in the late stages of the disease, owing to a natural hesitancy to try a new remedy, and after " large embolic detachments had set up fresh centres of cultivation in many positions." He concludes therefore: " It may be laid down as a principle, governing treatment by this particular serum, that the more distinct the history of a previous endocardial lesion and a subsequent exposure to an infection through a suppu- rative mediimi, or a sewer-gas sepsis, the more appropriate the case for the treatment. This rule would discourage its employ- ment in cases in which the pneumococcus, gonococcus, or some other microbes divergent in character from the streptococci and staphylococci were concerned ; and if with the recognition of this principle, and its earlier and bolder carrying out, more encourag- ing results are obtained, it will certainly follow that analogous measures will be foimd for the circumvention of the other forms of microbic action."
If the primary source of infection, an abscess for instance, be not discovered, and therefore not removed by the surgeon, or if fresh emboli laden with pus cocci rej>eatedly discharge into vari- ous parts of the system, to maintain the already existing sepsis or set up fresh centres of infection, then assuredly antistreptococcus serum will prove of little or no Ixmefit.
If, on the contrary, the patient is suffering from pyiemia, the original portal of infection having been closed, and no fresh intoxi- cation having taken place, then this sennu would be of service, even though the streptococcus be not the only microbe concerned in the process. With this formidable streptococcus disposed of, the system ought, theoretically at least, to he able to cope success- fully with the other kind of bacteria. Of course, hope of recov- ery or even improvement can only be entertained in comparatively mild cases, or when, as Powell says, the disease is recognised and treatment begim early. A process with a pronounced destructive tendency cannot probably be checked, but there are cases of septic endocarditis which are shown by the clinical history to be not thus
ACUTE ENDOCARDITIS
195
rnpidly degtrnctive or malignant. Since no one can foresee how virulent the endocarditis is to prove, the patient should be given the benefit of a doubt, and the sernni tried, Gibson suggests that in every case an examination of the blood should be made for possible detection bv culture, in^jculation, experiment, or other- wise of the nature of the infective agent; but their detection, it must be remenibered, is extrenjely unlikely.
Endocardial intlannnation following pneumonia^ or in which the pneumococcns has been identified, promises no hope of iui- provement frijm this treatnient. It is to he hoped that we shall pfjBseas some day an efficient antipnemnococcus serunij and indeed the researches of the Kleuq>erer brothers and others afford some promise of this being attained.
Personally 1 liave had but little experience with antistrepto- C0CCU8 serom in acnte endocarditis. The wife of a physician had suffered for years from an aortic r^'gurgitation of rheumatic origin. At the time 1 saw her she had been ill for several wt^eks with moderate fever of a remittent type that fluctuated l)etween about 100'^ and 102'^ F., or a little more. She complained much of pnecordial distress and paroxysms of pain, also of pain in the lower extremities about the joints, although the latter were not appre* ciably swollen or tender. The usual antirheumatic remedies — sal* icylates, alkalies^ etc* — did not appear to exert any influence over the affection, and as I believed she was suffering from fresh endo- carditis, possibly of a septic type, I advist^d a trial of antistrepto- coccus serum. This was obtained from St. Louis, and was given in two doses of 10 cubic centimetres eacli. Her husliaud subse- quently sent me a report, from which the following has been extracted :
'* Mrs, B. had been very sick about one month when you saw her. The attack set in with a spell of tachycardia, lasting be- tween three and four days, pulse-rate near 200 during all that period. The joints were only slightly inflamed, temperature about 102*^ F., with but slight variation. I gave two doses of antistrepto* coccus serum three days apart, as you directed, without immediate effect on temperature or symptoms. At end of two weeks, how- ever, temperature subsided nearly to normal. A very heavy ery- thematous rash followed the use of the serum. She gradually crept from her perilous condition, dropsy disapjieared, appetite
196 DISEASES OF THE HEART
returned with a fair degree of strength. She had a good deal of bronchitis, and was much worse after you saw her than she was then. No one who saw her at her worst thought she could possibly recover."
The nature of this case was very doubtful, and from Dr. B.'s report the serum appears to have been of doubtful utility. Yet I recall distinctly having subsequently met another practitioner, who had been present at the time of my examination, and who stated in no unequivocal terms that in his opinion the senmi had been of benefit.
About a year ago I saw in consultation with Dr. Lovewell a man of about forty who had been ill for a number of weeks with an intennittent fever, rigors, and sweatings, s\'mptoms of cardiac disease, and distinct evidence of an aortic valve-affection, which had not existed before his illness. The origin of the infection could not be ascertained. There were well-marked signs of aortic insufficiency, which from the general septic phenomena and albu- minuria could not have been other than a malignant endocarditis. As everything in the line of antiseptics had been tried to no pur- pose, I advised the use of antistreptococcus serum. The patient survived a number of weeks longer, but died suddenly as a result apparently of emotional excitement. I did not see the patient again, but had news of his condition from Dr. Lovewell, wEo stated more than once that under the use of the serum the tem- perature became lower, less irregular, and the other indications of sepsis less pronounced. In fact, the general condition im- proved so much that the doctor at one time began to entertain the hope of his patient's ultimate recovery.
It will be remembered that in the case reported of my patient of forty, who died of pulmonary infarcts, this serum was likewise employed. It failed to exert any other effect than to slightly re- duce temperature and produce a feeling of somewhat greater strength. In this instance it was not used until late in the illness and after embolic phenomena had more than once appeared. I regret that the treatment with the senim was not begun earlier, although I am very doubtful if it would have materially affected the ultimate result. These experiences are too limited to be of value in forming an estimate of the utility of the serum, but inasmuch as its use was not attended by unpleasant effects
ACUTE ENDOCARDITIS
19*
I shall certainly continue to give it a trial whenever this seems indicated.
Such cases are so desperate, and the prospect of recoverj so slrglit, tliat 1 believe one is justified in resorting to whatever affurtls even a chance of benefit; and if an old prejiaration is em- ploved, there is not much danger of producing erythema or articu- lar inflammation, and the remedy cannot prove more hurmful than the disease itself, unchecked.
J. iiichell Clarke lias reported a case of a w^oman of twenty- two who had had an attack of rheumatism at ei^^hteen, followed by left-sided pleurisy with effusion. She complained of weakness, dyspntea, pntcordial pain, and tixlema of the ankles. While under treatment for these symptoms she had a sudden chill, followed by a temp»erature of 103^' F. After remaining high for f^mr days the temperature fell to normal, and after so remaining for about a week, again rose, and prevailed for nine days witli a very irregu- lar course. There was a systolic afiex-murmnr, another loud sys- tolic murmur in the pulmonary area, and a faint diastolic one at the right base. Bacteriologic examination of the blood from a vein was negative. A diagnosis of ulcerative endrjcarditis was made, and treatment with antistreptococcus seriuji was instituted* In- jections were given from December 31, 1809, to February 0, UtOO, sometimes daily, at other times every other day, and once five days intervened between injections. The doses varied from 10 euluc centimetres to 20 cubic centimetres, though as a rule 15 cubic centimetres were given. The patient recovered, and exami- nation revealed the apex in the fifth interspace nippledine with a loud, blowing murmur throughout the praNL-ordiuui and posterior- ly, but loudest in the aortic area.
Douglas Powell speaks of the administration of yeast, and re- ports a case in which recovery apjieared to be due to thi^ remedy. It is probable that the efficacy of yeast is due to the nuclein ol the yeast-cell, therefore in Vaughan^s yeast-nuclein we possess a preparation more efficient than a solution of yeast. This may be adniinisterHl either by the mouth or rectum, a solution, No. 2, being sjiecially prepared for this purpose, or solution Xo. 1 may be injected under the skin up to 60 or 80 minims in the course of the day. Nuclein or nucleinic acid acts by increasing the numlier of the jKilynuclear leucocytes, which are the forms chiefly in-
198 DISEASES OF THE HEART
creased in the leucoc\io8is observed in infection, and by the in- crease of which the germicidal action of the blood is augmented.
Many encouraging reports have been made of the favourable effects of yeast-nuclein in cases of pus-infection and cryptogenetic infection. I employed it in one case of acute endocarditis super- vening uiK)n an old valvular lesion, which followed a follicular ton- sillitis, that may have been rheumatic, but if so was the only mani- festation of rheumatism. The remedy was administered by the rectum, owing to the patient's dread of hypodermic injections. Under its influence, or at least during its administration, the mild pyrexia which had existed for about ten days, without showing indication of subsiding, gradually sank to normal. The patient subsequently died. From the foregoing it is evident that the most the physician can do in the treatment of acute endocarditis is to aid nature by helping to maintain the vital ix)wers and by removing obstacles that lie in nature's way.
CHAPTER V CHRONIC ENDOCARDITIS
Morbid Anatomy. — Two forms of cliroiiic endociirJitis are fciniid, (JUL* the rusiilt of the proliferative processes following an acute iutlaniniation, and the other a part of a general tibroid trans- formation of the vascular system, arteriosclerosis.
In the form fullowing tlie aeute disease the developm^ent of fihruns tissue begins with the organization of the vegetations and thrombi that have formed in the earlier stages. As a rule the vegetations are for the most pnrt absorbed, but the process of or- ganization leaves a slight nodular thickening on the surface of the endocardium* The formation of new connective tissue goes much further than the mere repair of the acute lesions, however, for what reason we cannot say, and the entire substance of the valve is infiltrated by fibrous tissue, which in the course of time undergoes contraction that causes a thickening and deformity of the valve-cusps. This process, then, though initially of an in- flamnuitory nature, eventuates in a sclerosis.
The second form is of sclerofir orifjui f roiu the l>eginning, and is usually associated with a similar process in the blood-vessels, particularly the arteries. In this process the aortic valve is the one most frecpienfly involved, and the process seems to be often a direct extension of the disease from the aorta. It is, however, by no means rare to find the mitral valve involved, and often both are affected tf>getlier,
The stiffening and deformity of the valvedeaflets leads to dis- turbance of their function in two ways: The segments may be retracted or their edges curled in such a ivay as to permit the pas- sage of blood in the wrong direction (RegurgitBtion). The con- dition is then spoken of as insufficiency, incompetence, or regurgi- tation. If, however, the deformity of the valve is of such a nature
m
200 DISEASES OF THE HEART
as to cause a narrowing of the orifice, the condition is known as stenosis.
Stenosis may be brought about by thickening and rigidity of the valve-segments so that they cannot open perfectly for the passage of the blood, or the remains of vegetations or thrombi, which have undergone organization or calcification, may encroach on the opening. The special ways in which these lesions are pro- duced will be considered in detail under the head of the individual valvular diseases. It should be noted here, however, that stenosis of an ostium and incompetency of the corresponding valve are usually associated conditions, though as a rule one or the other predominates and gives its character to the lesion.
Fibroid thickening of the mural endocardium is not uncom- mon in connection with chronic valvulitis, especially of the sclero- tic type. It may also occur as a part of an interstitial myocar- ditis. The membrane is thickened and of an opaque whitish or yellowish colour — the latter when fatty change is prominent. Mural endocarditis is often associated with dilatation of a heart- cavity, and is then probably due to the stretching of the membrane.
The secondary changes in chronic valvulitis are mainly those due to the circulatory disturbance occasioned by the stenosis or in- competence, as the case may be. If a valve is incompetent it per- mits regurgitation into the cham])er behind during its diastole, and this chamber then receives blood from two sources, the normal one, and through the incompetent valve. Such an oversupply of blood leads to an overdistention of the chamber, and to an in- creased effort in order to completely empty itself. The continu- ance of these conditions leads to a permanent increase in the capa- city of the chamber, while the increased work thrown on the musculature of the wall causes an increase in its strength and thickness (Hypertrophy).
If the deforming process results in stenosis, the chamber behind the defect experiences increased difficulty in expelling its contents, and develops hypertrophy of the kind known as concentric, because associated with little or no dilatation. The chamber in front of a stenosed orifice, on the other hand, is apt to become atrophied and reduced in size, since it receives a diminished supply of blood, and its work is correspondingly lessened.
The disturbances of circulation secondary to valvular disease
CHRONIC ENDOCARDITIS
201
are by no means limited to the heart itself, but affect the various organs and tia^ues of the body. The blood -siijiply to the arteries h lessened, obstruetion to discharge of blood from the veins exists^ and thus is indueed passive congestion, which affects not only the organs drained l>v the veinSj but in well-marked cases also the arterial system which supplies them. In the course of time this congestion reacts injuriously on the heart in a manner to Ije fur- ther elaborated under the head of the respeetive valve-lesions.
Acute endocarditis is often found associated with the chronic, and indeed the latter predisposes markedly to the former, ilianges in the niyc»eardinm are also frequent, usually in consequence of nutritional disturbance, which is secondary to the dilatation and hyj^ertrophy, or to asscK-iated atheroma of the coronary arteries. Pericarditis is also not infretpiently associated with eh runic endt> carditis, and is generally of the adhesi\^e variety. This is, of course, due to the two diseases having had the same remote origin.
Etiology. — The strictly sclerotic form of endocarditis is not of microbic origin, but is either an expression of nutritional change inci<lent to age, gout, renal and vascular disease, or is the result of strain. That some individuals evince a family tendency to sclerotic changes in the entire circulatory apparatus, as w^ell as in the kidneys, appears proved by the frcHjuent observation of atheromatous valvular disease in two or more members of the same family.
Age is thought to be a factor in the causation of this form of chronic valvular disease; and yet the occurrence of tlie disease in some individuals at a comparatively early age indicates that there is some other influence at work besides senility.
Chronic endocarditis is so fre<]nently observed in persons of a distinctly arthritic habit that gout has come to be regarded as an important etiological element. With resjiec^t to such gouty influ- ence, it seems to me that it is rather the entire manner of living which has to be taken into account. For example, I recently ex- amined a physician's father, whose case illustrates w^hat I mean very well.
Dr. W., from the interior of Illinois, lirought his father to me with the following history: The patient was a German, sixty- nine years of age, who had enjoyed robust health up to two years
202 DISEASES OF THE HEART
before, at which time lie developed redness and swelling, with some pain of the great-toe joints. This was regarded as gouty, and under appropriate tlierai>eutic and dietetic management dis- api)eared. Six months before his visit to me he began to complain of shortness of breath upon exertion, whereupon his son made an examination of the heart and detected a murmur. The routine treatment with digitalis, strychnine, nitroglycerine, and cathartics had failed to produce appreciable benefit, and twice there had been expectoration of bloody sputum. During the previous two weeks he had had two nocturnal attacks of dyspnopa that came on in the small hours, while still a third took place after an evening meal. The son furthermore stated what was of special interest from an etiological standpoint — viz., that his father had always led a seden- tary life, getting exercise by driving instead of walking, had always eaten heartily of rich food, indulged freely in beer and other alcoholic beverages, after the German custom, and had been a heavy smoker. lie had never had inflammatory rheumatism or any other illness.
The patient was a man of j)owerful physique, and in spite of his gray hair did not look at all like an old man. His normal weight was 207, but at date of examination was 190 pounds, while his height was 0 feet. His chest was broad and deep, his bones large and strong, the muscular system well developed, abdo- men not corjnilent, and subcutaneous fat not excessive. The nails were moderately ridged, the radial arteries stiff but not beady, the temporal and carotid arteries not stiffened, and the subclavians did not stand out prominently nor throb strongly, as they often do in old men. There was a i)ronoimced, visible, and palpable epigastric pulsation reaching at least 2 inches below the xyphoid cartilage, but the apex-beat could not be made out. In the aortic area was a systolic thrill, palj>able upon moderate pressure during expiration. The thoracic parietes were so hard and resisting that percussion was diflicult, but the lungs were everywhere resonant and resj)iratory sounds were faint and vesicular. Absolute car- diac dulness was not increased, but by resort to palpatory, aus- cultatory, and ordinary plessimetric percussion, relative dulness was found greatly increased upward, to the left, and downward, but not notably to the right. The left border reached an inch outside of the left nipple, in all 5 inches from the left edge of
CHRONIC EXDOi'ARDITIS
203
the sternum (Tig, 33). With exception of the pulmonic second sound, itself fiH.*bie, tlic heart-tones could not he heard. There was, however, a loud systolic murmur of (lidtinet sawing quality audible throughout the pra*cordia and for a distance beyond the left nipple into tlie axillary region* Fpon eareful study of this murmur it wa;* fouud to have two areas of uiaximuiu intensity, one in the second right interspace near the sternum, the other in the vicinity of the left nipple. Moreover, in these two areas the pitch was slightly yet distinctly different, heing lower and harislirr in the aortic and more nuisieal in the mitral area. The beartV rate was 9n, and its rhythm regidar. The liver was pal- pable.
The audible pulmonary second tone and hypertrophic dilatation of the right ventri- cle continued the evidence obtained from the mitral mur- mur and established the ex- ii^tence of mitral regurgita- tion. The aortic systolie bruit and loss of the aortic second sound, together with the sys- tolic thrill, gave evidence of stiffness, and |>erliap9 steno- sis of the aortic valves. The absence of a rheuuuitic history, the patient^s age, the late ilevelopmeiit of symjitoms, the moderate arteriosclerosis, and lastly, the heart findings, all seemed to war- rant the opinion that the valvular changes were due to sclerotic endocarditis. The condition of the kidneys was not ascertained at that time, as the son had not examined the urine, but inasmuch as there was nocturnal micturition, renal cirrhosis was thought probable, and it was advised to have the urine collected for tw*enty- fonr hours and examined.
In this case I bcdieve the cause lay in the strain to which the valves of the left heart had been subjected for many years in con* sequence of the abnoruud h!c«-)d-pressnre brought about by his ex- cessive consumption of food and ah^ohulit' liipiids without suffi-
Fio. S8.^ — Relative DiLNK^a, Ca^e nv CiittaNic ENttocAttDiris ip»20l).
204 DISEASES OF THE HEART
cient physical exercise. How much, if any, influence can be attrib- uted to tobacco and waste products I cannot say.
The influence of strain has long been recognised in the produc- tion of the sclerotic changes now being considered. High blood- pressure, lasting for years, is a cause of valvular as well as of vascular strain, but inasmuch as the individuals in whom such in- jurious blood-pressure is observed generally lead inactive lives, dine well, and often suffer from indigestion and constipation, it is likely that the products of defective metabolism circulating in the blood act as chemical irritants, and play a not unimportant part in the development of sclerotic changes.
Disease of the aortic valves is frequently observed in men who pursue laborious occupations, as smiths, carpenters, etc., and hence arduous physical exertion is also accredited with the pro- duction of valvular and vascular strain and consequent sclerosis. It is in this class of workers that rupture of an aortic cusp is most frequently observed, with its disastrous sequels. It has always seemed to me not an easy thing to correctly estimate the influence of physical strain in working people, since they are so often given to the immoderate use of alcohol and tobacco, and frequently be- come victims of syphilis. We should probably consider that in these people all these factors are at work, and attribute their chronic endocarditis to their mode of life in general, without at- tempting to isolate any one etiological factor. Syphilis is un- doubtedly capable of setting up sclerotic deformity of the valves, although endocardial changes follow luetic disease far less often than do myocardial and vascular degeneration.
Of that form of chronic endocarditis which is met with in the young, and which is of true inflammatory origin, the one great cause is rheumatism. Although these valvular lesions may un- doubtedly begin in an acute vegetative endocarditis, which merges gradually into a chronic process, it is often a low grade of sub- acute inflammation from the beginning that brings about this form of chronic endocarditis. This inflammation may originate in an acute rheumatic attack, and be recognised clinically at the time, or it may develop so slow^ly and insidiously as to create no symptoms, and remain undetected for years. Indeed, it is not at all uncommon for valvular diseases originating in this manner to be first diagnosed after compensation has begun to wane. This
CHRONIC ENDOCAHDITIS
205
slowly forming endooiirditii? gives rise chiefly to stenosis, and, in aecordancc with the liiw uf numerioal frequency, to stenosis of the left auriciilo-venlriLnilar orifiee.
Physicians sometiines fall into the loose manner of speech of the laity and call the pains of myalgia aJid an intraetalih* or oft- recurring neuralgia, rhenniatic. They shouhi remeniher, however, that these so^alled rheumatic pains are etiologically and patho- logically very different from the articular rlieurnatism that sets up endocarditis. When a student in Munich, I questioned Prof. Jiiseph Bauer on this subject, and received iIr* emphatic reply that ** muscular rheumatism never produces valvular disease." For further discussion of the etiology of endocarditis the reader is referred to the chapter upon Acute Endocarditis a!id those deal- ing with the individual valve-lesions.
Syniptoms*^ — The reader of the following chapters will doubtless be impressed by the fact that the different forms of valvular disease present considerable similarity as regards those derangements of circulation of a mechanical nature and those dis- turbances of visceral function w^hich give rise to subjective symp- toms. Such differences as exist are not so much differences in kind as in degree. Any one of the valvular defects may, so long as it is perfectly corai)ensated, exist for years without revealing its existence to the consciousness of the patient, Init when compensa- tory hypertrophy is no longer adequate, conditions result which must of a necessity force themselves upon the notice of the patient with greater or less prominence.
In mitral disease the sensations are mainly due to passive congestion, while in lesions at the aortic orifice they are the result of a diminished or defectively sustained supply of arterial blood; yet in both it would l>e inaccurate to draw sueh a strict diW- sion. In mitral disease there is defective arterial circulation as well as venous stasis, and when in aortic valve defects compensa- tion fails, there is more or less passive engorgement added to the im[x*rfe<?t arterial flow. Consequently, the clinical picture takes its colouring from both conditions, but in varying proportions, and hence in all forms of vahnilar disease there comes a time in the stage of destroyed compensation when whatever individual features each affection may have once possessel l>ecome blended into the SNinptom-complex of cardiac inadequacy in its broad
206 DISEASES OF THE HEART
sense. Some of these characteristics are plainly recognised as the effects of mechanical pressure in the venous system, as the dull, tense pain of hepatic congestion, the scanty albuminous urine, the hscmorrhoidal congestion and fluxes, and, in large part at least, the serous transudations and the digestive disorders.
Other symptoms are probably owing to the incomplete elimi- nation of the normal products of metabolism; or to the manufac- ture and accumulation in the system of abnormal products which result from perverted function on the part of the stomach, liver, and other chylopoietic visc»era; or there is a combination of these various toxins, with a lessened supply of oxygen and other neces- sary nutritive principles, that may explain some of the subjective phenomena, such as the dull, oppressive headache, the insomnia, ner\'ousness, and in some instances the low, muttering, or even ac- tive delirium occasionally observed in the terminal stage.
The dyspnoea of advanced heart-disease is probably a manifes- tation of both mechanical pressure in the pulmonary vessels and upon the lungs by the dilated heart and by hydrothorax, but also of deficient oxygenation through sluggish blood-flow and from bron- chial obstruction by mucus and serum. Since, then, so many factors enter into the production of the manifold symptoms com- plained of or manifested by sufferers from vahnilar heart-disease, it is not possible to satisfactorily account for them all or to explain why some are present in one and absent in another case.
We have also to reckon with individual tendencies, neuroses, intercurrent affections, complications, etc., all of which serve to modify the legitimate clinical picture. For example, I recall a certain young woman who first came under my care for an im- compensated mitral regurgitation of rheumatic origin in 1893, and who during the ensuing five years presented some highly in- teresting and puzzling phenomena.
At the beginning hers was an ordinary case of mitral insuffi- ciency with slight oedema, which readily yielded to treatment, and she was lost sight of for two years. She then reappeared, having shortly before had a recurrence of rheumatism, and had thereafter been married, both of which occurrences were imfortunate for her. Compensation was so defective, probably in consequence of a fresh endocarditis which had passed beyond its acute stage, and which could be recognised as having existed only by its effects, or in
CHRONIC ENDOCARDITIS
207
consequence of a pericarditis tliat had led to adhesion between the lac anil jinterior chest-wall^ that the patieut manifested hoth ascites and anasarca.
Besides this very ohvions disturhanee of eircnlation she suf- fered greatly from insouniia and a degree of emotional instability that could reasonably be considered liysterieal and made her ex- tremely hard to control. But the particular feature that puzzled me for a time was the fuet that the secretiuii of urine, scauty at all times, became almost suppressed whenever for the sake of sparing the overburdened heart she was subjected to rest in bed. Whether or not this was due to the abolition of those accessory aids to venous flow residing iu muscular moveiuents of the lower extremities and in deepened insijinititju incident to gentle exercise about her apartment 1 ei>uld not decide, liut this seemed probable from the subse(|UL*nt fact that the* enornious hepatic engorgement and ascitt^s did not disappear until she was given a course of re- sistance exercises.
Pari passu with this removal of the mechanical hindrance to circulation the insomnia vanished and her normal meufal state re- turned* Compensation was at length regained and retained for a number of months. Six months later, however, she suddenly de- velojied an exeniciaTing and obstinate neuralgia in the course of the right brachial plexus, for which I could discover no adequate eause^ and which resisted all treatment. It was accompanied by agh with scanty mucous expectoratiim, of which repeated care- Lil examinations of the heart and lungs failed to detect any cause ftside from the old-standing valvular lesion. At length, discour- aged by her failure to obtain relief, she returned to her home in the covin try, where during the next few weeks she expectorated masses of tenacious sputimu which were said whcm put in water to spread out and look like the branches of a tree. Whether this was an instance of fibrinous bronchitis or not 1 cannot say, but certain it is, that when finally her hroucbitis subsided her neural- gia also disappeared. I have always l>elieved this was a manifes- tation of infection, since, as we know» cardiac patients are particu- larly prone to obscure infections, and that the neuralgia could not be regarded as anywise a sjanptom directly attributable to her heart-disease.
The next event in this patient^s series of experiences occurred
208 DISEASES OP THE HEART
about a year later. She had again been suffering from rheuma- tism, as I was told, when, according to her sister's statement, she suffered one night from severe pain in the region of the heart, for which hot cloths were being applied. Suddenly the sufferer exclaimed, "There I something has broken, and the pain has all gone." She then seemed to sink away, her pulse becoming too weak and rapid to be counted, her extremities cold, and her coun- tenance blue. Stimulants revived her, but all night she continued to have sinking spells, which necessitated the administration of restoratives.
The explanation of this attack has never been clear to me. Whether a tendinous cord snapped, or a pericardial adhesion gave way, or whether the pain may not have been due to a muscular cramp, I cannot say. Under the influence of heat the muscle may have suddenly relaxed, and thus caused a sensation, which to the suffering and highly nervous apprehensive girl was naturally at- tributed to the heart, and threw her into a condition of mental shock which reacted on the weakened heart. At all events, the attack was fraught with no less alarm to the friends than to the patient, and an explanation was sought, which could not be given.
Six weeks subsequently the patient was again brought to the city in a truly deplorable condition. There were marked evi- dences of cardiac asthenia and consequent circulatory embarrass- ment, pronounced icterus, a?dema of the ankles, ascites, enormous hepatic congestion, a^dema of the left but not the right arm, and in the heart signs of double mitral disease, relative tricuspid in- sufliciency, and adherent pericardium.
The feature of chief interest, however, was connected with the dropsy of the left upi)er extremity. This was strictly local- ized, extending from the fingers up to and ceasing with the shoul- der. Palpation of the axilla disclosed that-the axillary vein had been converted by thronilK>sis into a firm cord. To what distance the thrombosis extended down the arm could not be determined, but it did not involve the jugular veins. The " swelling," it was stated, had made its appearance a week earlier, but aside from the annoyance did not appear to occasion pain or distress.
This highly interesting and comparatively rare condition was an instance of venous thrombosis occurring in some cases of valvu- lar disease. It has formed the subject of an instructive paper
CHRONIC ENDOCARDITIS
209
bv Dr. William Weloli, wbieli was read at the sossion of the \mo- tnannn of American Physieians in liHKK Welch was able to col- lect but 2S recorded instances, including his own, although, as stated by him, the condition probably occurs more ofren than it is recognised. Of these 28 cases, all but 4 involved the veins of the npper extremities and neck, a fact which lends to it addi- tional interest and importance. Tw*enty-t\vo cases showed throm- bosis of the left side alone 15 times» bilaterally 8 times, while only twice was it confined to the right, Welch found tliat the thrombosis nii^ht be limited to the veins of the arm, to those of the uvi^k, or might in%'olve all the veins — ^that is, the superior vena cava, the iiinujuiimte, botli internal and external jngidar, sub* clavian, axillary and brachial, and eveUj as in one case^ the supe- rior thyroid.
Although throml>osis niay and tloes soraetimes occur in indi- viduals suifering from chronic arteriosclerosis and nephritis, yet in Welch's 2^"^ cases there was in every instance valvular disease as follows: ilitral regurgitation 0 times, mitral stenosis alone 6 times, mitral stenosis with insntticiency i\ times, and aortic regur- gitation with relative mitral incumpetence once. In 10 instances there was associated aortic and mitral disease- The thrombus was either red or reddish-gray, and although in some instances it was softened at its centre, it for the most part was firm through- out, and occluded the vessel excepting at its extremities. In one case it was a " wall thrombus/' It is also interesting to note that the thrombosis appeared to have begiui at the lower end of the in- ternal jugular in those instances in which it involved tlie cervical Teins, This fact led Welch to conclude that the formation of tlie thrombus was favoured by the j>eculiar anatomical arrangement of the cervical veins r>n the left side, together with the conditions governing the blood-flow in them.
As jminted out by Hanot, the left innominate vein is longer and more oldiqne than tlie right, which, together with the right- angle junction of the left internal jugular with the subclavian and the bulbous expansion of the internal jugular, favours, in Welch's opinion, the formation of eddies or whirling currents at that point, and thus furthers the development of thrombosis. Moreover, he thinks there is probable pressure upon the sub- ckviau vein by the dilated left auricle and dilated pulmonary 14
210 DISEASES OF THE HEART
veins, so that circulation in the cervical and arm veins becomes extremely sluggish, and thus provides another favouring factor. Finally, in one of his cases Welch was able by cultures to identify the streptococcus pyogenes, which, he thinks, warrants the hypoth- esis that in these cases there is an infectious origin for the throm- bosis, a conclusion which is strengthened by recent observations going to show that in all cases of venous thrombosis there is an infection.
In my case there is good reason to believe that the patient was still suffering from some infection, for she had but a few weeks earlier gone through with what was called rheumatism by her home physician, yet which may very well have been a strepto- coccus infection, which so often presents the appearances of artic- ular rheumatism. Moreover, there were three small, distinctly in- durated Ijnnphatic glands situated just above the left clavicle, near the outer border of the left sterno-cleido-mastoid muscle, while the patient displayed a slight elevation of temperature. In other re- spects my case conformed with the most of Welch's requirements — namely, she was a female, of but twenty-three years of age, and was a sufferer from mitral disease. Her symptoms too were char- acteristic in the localization of the oedema to the affected arm below the location of the thrombosis. She did not, however, suffer pain, at least not at the time the interesting condition was de- tected, the occluded vein was not tender, and I failed to discover any enlargement and tenderness of the lymphatics of the arm, as is often present. If such existed, they were hidden from observa- tion by the (Edematous condition of the extremity. Welch states, finally, that in at least one of the cases collected by him there was mild delirium, which was attributed to the cerebral oedema discov- ered at the autopsy.
In the matter of the diagnosis of this form of venous throm- bosis there is no difiBculty, provided the thrombosed vein can be felt, and even when not, strictly localized dropsy in one arm or one side of the neck renders the existence of thrombosis very likely. Nevertheless, according to llanot, the greater length and obliquity of the left innominate vein may sometimes cause unilateral and circumscribed oedema even when venous thrombosis is not present.
The prognosis is unfavourable to recovery from the dropsy if the veins are extensively plugged. If the thrombosis is not com-
CHRONIC ENDOCARDITIS
211
plete, or is of limited extent, it is possible for collateral circulation to become establislied and absorption to take place. Finally, the condition is likely to occur in the terminal stage of the valvular disease, and if very extensive it may coutribnte to the patient's death.
It is not common for patients witti chronic valvular disease to suffer from embolism, and yet such a ix)ssibility should always be borne in mind. It is stated that such an occurrence is more fre- quent in mitral than aortic disease; and I have under ol>serva- tion a female patient with mitral insufficiency who has perma* nent eontracttire of tlic fingers of the left hand and but partial use of the arm as a result of an embolus that ^vas thrown off pre- sumably from her mitral valve nearly six years ago. The symp* toms of embolism are usually said to be pain in the part where the plug lodges, nausea, and even vomiting, a chill, and rise of temperature. To judge from eases of embolism observed in acute endocarditis and from pulmonary infarcts, I should say that pain in the affected part is the most constant symptom.
The splenic artery is a frequent seat of embolism, and it may well be that the transient pain from which cardiac patients not infrequently complain in the region of tlie spleen may be of this origin. It is unsafe to make such a iliagnosis, however, unless one can detect enlargement and tenderness of this organ following the pain. This is emphasized by the fact that these patients are very prone to sudden and sharp pains of a neuralgic character in various situations, particularly in the abdomen.
I recall an instance that was narrated to me by an ophthal- mologist of sudden blindness of one eye resulting from the plug* ging of the retinal artery, and as the lady possessed a blowing sys- tolic apex-murmur, tlie embolus was thought to have been a minute vegetation from her mitral valves. I have also been informed of a young lacly with valvulur disease who^ upon awakening one morn- ing, was found to have lost during the night all recollection of certain members of her own family* This |:>eculiar lapse of mem- ory was attributed by her inedical attendant to emb(dism.
Pulmonary infarcts are not at all uncommon in cases of ad- vanced valvular disease, and are evinced by sudden acute pain in the affected lung, together with frequent cough and the spitting of clear blood. These cases must not be confounded with instances
212 DISEASES OF THE HEART
of hsemoptysis due to sudden increase of pulmonary congestion, as not seldom occurs in mitral patients who have overtaxed their hearts. In these cases the history of some exertion and the ab- sence of sudden, sharp pain will usually aid in the differential diagnosis. Embolism of the middle cerebral artery is attended by such manifest sjTnptoms that there is usually but little difficulty in determining the cause of the phenomena.
In a single instance I have observed the conjunction of true epilepsy with valvular disease. The patient was a man of about forty who presented well-marked signs of mitral stenosis. His valvular lesion was of rheumatic origin, and his convulsions ante- dated his cardiac disease by some years. There was every reason to conclude that the association of these two affections was purely accidental as regards their etiology. The fits were usually excited by indiscretions in diet, and required bromides for their control. Although never assuming any causative relation between the two, I yet believed they exerted a deleterious influence upon each other. I am very certain that the epilepsy affected his mitral disease unfavourably by serving to maintain and aggravate the dilatation of the cardiac chambers. Such cases as this arc not to be regarded as instances of cardiac epilepsy, which term has been employed to designate attacks of pra'cordial pain accompanied by loss of con- sciousness and succeeded by twitchings of the muscles of the face.
The association of epilepsy and heart-disease in my case serves to emphasize the fact that valvular diseases may be complicated and have their clinical picture modified by other affections. I speak of this because inexperienced physicians are apt, when treat- ing patients with valvular disease, to attribute all symptoms to the cardiac complaint.
Cardiopatlis frequently become aniemic and neurotic, hysteri- cal or neurasthenic, and then complain of all sorts of sensations, which it is clearly impossible to attribute to their valvular affection.
The French describe what they term " cardiac cachexia " in distinction from cardiac asthenia, and which is analogous to the cachexias of malignant or tuberculous disease. They ascribe it to some chemical change in the blood. It is not at all uncommon to see cardiac patients who, while presenting no very marked sjinp- toms of cardiac inadequacy, yet display an appearance of mal-
CHRONIC ENDOCARDITIS
213
nutrition that might not inaptly be termed a cachexia. In such iherv are often svmjttonis of weakness, inahility to take and assim- ilate food, and variinis either features that^ even if referable pri- marily to a vahidar defect^ are nevertheless attributable to their general state rather than to their heart.
Patients ivith valvubir disease sometimes become victims of attacks of palpitation and prarordial pain that place them in the category of cardiac neuroses, although, strictly speaking, this term should be applied to cases in which the attacks are independent of any discoverahle heart-disease. iVt such times there may even be irregidarity or intermittence of the pulse. This is naturally thought due to the cardiac lesion, and yet it may he wholly inde- pendent of the heart disorder, being the result of si>me toxin per* haps, or of some ubseure nervous excitation. T]iis is proved by the observation that, when tlie attack subsides, tlie beart-s action returns to its former regubir and tranquil state. 1 recall such an instance in a young man with a mitral regurgitation who was sub- ject to attacks of i>alpitation that invarial>lv tlirew Inm into a perfect panic of fright and apprehension. Yet when his attacks subsided he resumed his ordinary duties without a symptom of his cardiac lesion.
I am in the habit of assuring such patients that their attacks of palpitation are not indicative necessarily of a serious state of the heart — for persons witliout auy demonstrable cardiac disease often manifest similar disturbance — hut that l>ecanse the heart ifl not structurally sound, it is more easily thrown out of balance by indigestion or other conditions that would not l>e noticed were it in perfect health. Xutbing is worse for cardiopaths than to get into a state of introspection and constant apprehension. I have knowTi some who were so alarmed over their valvular defect that they might be said to be possessed by a veritable {ihobia. Such patients not only imagine all sorts of symptoms that play no part in the clinical history of their particular lesion, but they are afraid to venture out alone lest they get an attack or be hrought home dead. The me<lical adviser should therefore carefully dis- tinguisli symp^toms due to the valve-defects from those that belong to some associate*i disorder, and reassure the patient accordingly.
Before completing this subject I desire lo add a few remarks [leerning derangements in the rhythm of the heart's action.
214 DISEASES OF THE HEART
Irregularity and intermittence of the pulse are common in all forms of valvular disease, yet they are by no means always ob- served. The regular and rhythmic contraction of the heart-muscle depends upon its receiving regular and uniform stimulation by the presence of the blood. Doubtless there are many disturbing factors of which we are yet ignorant, and which may be transient in action, such as emotional or other impulses acting through the nervous system, toxins of various kinds, etc. But aside from these there are degenerative or other alterations of the cardiac muscle itself that lead to arrhythmia. Such a persistent derangement of the pulse is therefore an unfavourable omen. It is quite likely to be obser\'ed in mitral disease, particularly regurgitation, it is said. Why this is, is not clear, unless it is dependent upon dila- tation or degeneration of the auricles.
A mere lack of uniformity in the force, volume, and frequency of the pulse-waves, to which form of arrhythmia is applied the term irregularity, is far less serious than intermittence, by which is meant a dropping out of some of the pulse-waves. This lat- ter may be due to actual intermissions in the cardiac contrac- tions, or it may be caused by the failure of all the blood-waves to reach the wrist, the heart itself beating regularly all the time, although with unequal force. Many interesting varieties of pulse- rhythm have been described, but I do not know that they possess any special clinical significance aside from the fact of their being an indication of disordered cardiac action. Thus pulstis alternuns is a term employed to describe an irregularity consisting in the appearance first of a large and then of a small wave that follow each other in regular succession. When the pulse-waves occur in pairs that are separated by distinct intervals they are spoken of as pulsus higeminus, and when in groups of three as pulsus tri- ge minus. Pulsus intercidens or intercurrens denotes the occur- rence or interpolation of occasional small waves between the regu- larly occurring large waves. Pulsus tardus is a slow pulse, mag- nus a large pulse, parvus a small pulse, etc.
These variations may exist alone and for a considerable time, or they may be blended and display their individual characters for but a few seconds; so that a pulse results that is strikingly irregular and difficult or impossible to count.
It has been my observation that when a patient with organic
CHRONIC ENDOCARDITIS 215
heart-disease displays a persistently arrhythmic pulse he is usu- ally not aware of its existence by any sensations within his chest. On the contrary, persons with so-called functional derangement are very apt to experience a sensation as if the heart jumped or turned over whenever it intermits.
In studying the pulse in any case of valvular disease it is not only necessary to observe its rhji:lmi, but one should take particu- lar notice of its force and volume. In conditions of stenosis the pulse is very likely to be small and of poorly sustained tension, showing that the arterial system is defectively flushed. In some cases, however, of mitral stenosis the pulse is small and tense in consequence of obstruction to the flow of blood out of the capil- laries. Peculiarities of the pulse of aortic regurgitation will be dwelt upon at some length in that section.
CHAPTER VI MITRAL REGURGITATION
By this term is designated an abnormal escape or leakage of blood from the cavity of the left ventricle through the left au- riculo-ventricular orifice into the left auricle. Such regurgitation may be due to structural defect of the valves or to their relative incompetence from dilatation of the ventricle, or to imperfect function on the part of their muscular apparatus. In this chap- ter will be considered only the form due to valvular defect. Other terms applied to this disease are mitral incompetence or insufficiency; but inasmuch as the term regurgitation is more commonly employed in this country, this is the one that has been selected and is preferred.
Morbid Anatomy. — Tlie structural changes of the mitral valve permitting regurgitation of the blood are mainly thicken- ing of the cusps with increased rigidity that prevents perfect co- aptation, or the shortening or retraction of one or both of the leaflets in such a way as to permit the reflux of blood. The segments lose their normal j)inkisli transparent appearance, thin delicate feel, and become thickened, stiflF, and of an opaque whitish or grayish colour. Contraction of tlie fibrous tissue may cause retraction or shortening of one or both of the cusps, or curling of their edges in a manner to prevent effective closure of the valve. In the valvular disease following acute endocarditis the shrivelled and often calcified renuiins of old vegetations may be found on the auricular surface of the valve along the line of maximum contact. When these old vegetations are numerous the mitral ring is usu- ally fibrous and contracted, leading to a condition of stenosis as well as regurgitation (Fig. 34). Very commonly, also, the ten- dinous cords are found more or less matted together, stiffened, and shortened, so as to still further interfere with perfect action of the valve. The deposit of calcareous matter is by no means limited to 216
MITRAL REOURGITATION
217
the old v€*gc tat ions, Imt may fsifert tlie valve-enspSj the chorda* tend imp, or evtMi the luiiru! eiuhx-ardiiuii in the neighhyurhood» In fact, the deposit of liiiiO'Salts may in some instances be so
Flo. 84, — Siiowsi Condition of iliTRAL Valve, caumiwo Reouboitatiot* Ain> Oasriivvrios. Licrr Aikicle has been dibsected awav.
extensive as to convert the fiitire valvular ajiparatus into a firm calcareous mass, having un resendjlance whatever to the original stnictnre.
The local changes in tlie endocardimn, however, form but a small part of the niorl>id changes fnnnd in a ca.se nf mitral insnffi- eiency. The changes in the circulation, and the effect on the heart-wall ami on the otiier organs of the body that were consid- ered in a general way under chronic endocarditis, take place here and rt^piire descrij>tion. Whenever mitral regurgitation occurs a portion of the contents of the left ventricle is forced back during systole inti> tlie left auricle, which at the i^iunp time is receiving the normal tlow of hlnud from the pulmonic veins. The chaml>er is consequently surcharged, and as the two streams enter it during its diastole it hei'omes overdistended. At the same time, in consequence of its dilatation, the auricle has greater work to i>erform in emptying itself of this increased amount of
218 DISEASES OP THE HEART
blood, and in accordance with the physiological law that an organ which has increased work to do will, so long as its nutri- tion is unimpaired, manifest increased power for work, the walls of the auricle at length become thicker and stronger. In time, therefore, the auricle comes to be both hypertrophied and dilated.
If these changes in the circulation come on slowly, and time is afforded for compensatory changes in the heart to develop, the nutrition of the heart-muscle, and indeed the integrity of the cir- culation, may suffer no serious injury. Furthermore, if the auri- cle is able to deliver an increased volume of blood to the ventricle, this chamber is able to discharge into the aorta, in spite of the regurgitation, an approximately normal amount of blood, and ade- quate arterial circulation is maintained. So far, then, the hyper- trophy and dilatation of the auricle compensates the valvular de- fect, which may consequently exist for a long time without pro- ducing any inconvenience.
If, however, the leakage is extreme, or if it becomes so with lapse of time and the auricle is unable to completely empty itself, a residue remains, which interferes with the inflow of blood from the pulmonary veins. Thus takes place an accumulation of blood (passive congestion) which, acting as increased peripheral resist- ance to the work of the right ventricle, leads to hypertrophy and dilatation of this chamber. Moreover, the stasis within the lungs induces in them the condition kno\\'n as brown induration, in which the connective-tissue elements are increased, the veins engorged, and the whole organ is of a dark-brown colour in conse- quence of pigment deposited by the disintegrating blood. In ad- vanced stages there may also be pulmonary opdema and hydro- thorax from transudation of serum out of the engorged vessels. There is always more or less bronchial congestion in consequence of stasis within the pulmonic vessels.
When at length blood -pressure in the pulmonary artery grows ex- cessive, the wall of the right ventricle finds its work too great, and, yielding to the strain, permits dilatation to supersede hypertrophy. This chamber is now unable to fully empty its contents, stasis within it grows, and at length causes tricuspid leakage either from mus- cular incompetence of the valve or, more often, from great dilata- tion of the ventricle. In cases of long standing and extreme pressure
MITRAL REarRGITATIOK
219
in the pulmonary artery, stretoLing of its ostium is also occa- sioned, and leadi* tu relative pulmonary incompetence.
So long as the left auricle and right ventricle are capable of coping successfully with the back wash from the left ventricle the work uf the right auricle is not especially increased. When» on the contrary, the right ventricle begins to yield to the strain, par- ticularly when it becomes dilated, back pressure is exerted upon the right auricle and great venous system. Veins e\'eryw^here grow more or less turgescent, and the internal organs display the effects of eugorgeinent. The liver in particular becomes enlarged and in time indurated, and on section show^s the peculiar mottling that has given to the organ in this condition the nanie of nutmeg* liver.
In the stomach and intestines passive congestion leads to chronic catarrh of the mucosa, and in the kidneys to cyanotic in- duration or even chronic nephritis. Xone of the internal viscera escape, while the veins share in the distending effects of stasis and become relatively larger than the arteries. Back pressure creeps downward into the vessels of the lower extremities, and as circulation grows still more sluggish serous transudation finally makes its appearance. Comnicncing in the feet, dropsy gradually extends upward, invades the peritoneal cavity and walls of its contained viscera, and in extreme cases the serous cavities within the chest, and finally the lungs (Fig. 35). Thus far we have con- sidered the secondary effects that are produced 1:»ehiud the seat of the original lesion. There are, in addition, certain effects of mitral regurgitation in front of the lesion. These are the hypertrophy and dilatation of the left ventricle found in cases of free and un- comf»!ned mitral insufficiency. This enlargement seems rather re- markalde at first thought, since one would naturally think the chamber ought to be smaller rather than larger in size. At one time this condition of hypertrophic dilatation was explained on the hypothesis that in consequence of venotis and capillary stasis blood-pressure was inrreased in the arterial system, and that hence there was augmented intravetitrieular pressure wliieh resulted in dilatation, with increased demand for work which led to liyper- trophy.
This theory is now known to l>e incorrect, and has been re- placed by the following: Owing to the abnormal volume of blood
220
DISEASES OP THE HEART
contained hy the left aiiriele at the close of it3 diastole, this cliamber^ which has become liypertrophied, discharges with great force an unnatural amount of blood into the ventricle. This
Q^atKMlAof face
of Aiiffttn
oriuip
BnisorgcmiTit »t portal
Cotitfoiloti and adtm^
Fio. 85.— Divt-itAM w|i4jwi?fG Effect* on the CruouLATtoN o? a MiTltAL Leak.
MITRAL REGUHGITATION
aai
cavity is in a state of diastole when it receives this iiinisli, and, being relaxed, beeomes after a time dilated. At the same time it is forced to handle a larger volume of blood, whieh it can only do by undergoing hypertrophy, and thus at last this ventricle come?^ in its turn to feel the secondary effects of the circulatory disturbance.
In rime, moreover, when stasis has become everywhere apjiar- ent, the left ventricle umlergoes still further dilatation, for which it has become prepared by certain structural changes within its niy<»cardium. Its myocardinni is flahliv and of a hrown itistead of the normal beefy red colour, \vbile iU fibres are found micro- scopically to be reduced in size and to contain granules of brown pigiTient, especially near the nucleu?^. This increased dihitution of the ventricle at this time is explained by some as due to the liigh blood-pressure in the arterial system secondary Uy stasis in the veins, which abnormal arterial bltK>d-pressure interferes with the easy emptying of the ventricle. This is a defective explanation, however, since physiologically the abnormal blood-pressure in the venous system leads to lowered instead of heightened blood-pres- sure in the arteries. The dilatation of the left ventricle is now due to the w€*akness of its own wall, which iloes not permit it to completely empty its cavity with each systcde. Thus is estab- lished a residue which auguuuits the amount of blood received from tlie auricle with the next diastole, while at the same time its wall is powerless to withstand the dilating force of this stream that pours into it. Thus is at length set up a vicious circle in conseipience of wliich tlie effect of the original valvular incom* petence intensities the regurgitation.
The typical heart, then, of mitral insufficiency is enlarged. The enlargement is mostly of the right ventricle, and the organ has in consequence a rounded apex. The tricuspid orifice, and often the pulmonary, is found to be wider than usual, owing to the dilatation of the right ventricle. The left ventricle is mod- erately and the left aurifle greatly enlarged, while the mitral valve shows rhe structural changes already descril»ed, which have been the cause of the whole trouble.
Etiology. — What has already been said concerning the causa- tion of elironic end*»carditis applies equully to mitral insufficiency, since this is but one of the manifestations of that affection* I shall
HM
DISEASES OF THE HEART
therefore only add a few general considerations bearing on the localization of the deforming process at the mitral orifice.
Incompetence of the left auriciilo-ventricular valve is a very frequent cardiac affection — is indeed the most frequent of all valvular defects. This is particularly the case in children and young adults, forming in this period of life the coimterpart in point of frequency of the sclerotic changes at the aortic orifice in persons, chiefly men, past middle age. The influence of childhood and youth in the generation of mitral regurgitation lies doubtless, not in the fact of the age, per se, but in the prevalence in the yoimg of those diseases, inflammatory rheumatism, chorea, and the exanthemata, which set up endocarditis. The greater liability of the mitral than of the aortic valves to suffer from endocardial inflammation in the earlier decades of life is probably owing to their being exposed to relatively greater strain, which their more delicate structure fits them less well to endure.
As regards sex, it is generally stated that mitral regurgita- tion is more frequent among males than females, but in analyzing my case-records I find no predominance of either sex. After throwing out all cases that from the history, age, or symptoms cannot be safely considered as organic, there remain 126 cases in which regurgitation was due to structural alteration of the valves. These were divided equally between the two sexes. Classifying these 12G cases according to decades, there were 6 boys and 6 girls between one and ten years of age, 12 males and 16 females be- tween ten and twentv, 18 of each sex between twentv and thirtv, 14 each between thirty and forty, and 15 males and 7 females over forty. Examined with reference to rheumatism and other diseases, it was found that 32 males and 28 females gave a history of rheumatism alone, 4 males and 6 females of scarlatina alone, 5 males and 4 females of measles alone, 1 female of chorea alone, while of more than one disease 1 male and 3 females had had rheumatism and scarlatina, 4 each had had rheumatism and mea- sles, and 4 each rheumatism, scarlatina, and measles, 2 males and 5 females scarlatina and measles, 2 females measles and pertussis, and 1 female all four diseases, 2 males and 5 females chorea, in combination with some of the other diseases mentioned. Two males gave a history of venereal disease. Of the remaining cases, in which no definite history of previous disease could be elicited,
MITRAL REGURGITATION
:>23
organic nature of the lesion was rendered probable either by the existence of arteriosclerosis or by the youthful age of the pa- tient and the absence of antemia or other factors pointing to a rela- tive niitntl insutiiciency*
Symptoms, — The presence or absence of distinctively cardiac syTiiptoiiis depends uptm the degree of the leak and of the com- pensatory hypertropliv that has been established. Consequently we have to distingnish cases in which subjec*tive manifestations of circulatory disturbance are wanting from those in which tliere is more or less evidence of cardiac inadequacy. In the former class such symptoraa as are conxplained of arc probably referable indirectly to the valvular defect, Init are nevertheless such as we encounter in persons without disease of the heart. In some in- stances they direct the experienced physician's attention to the possibility of mitral disease, while in others they seem to point rather to disorders of other organs, and the discovery of the re- gurgitation is accidental. In such cases the indiviiiual iirst learns of his malady on applying for life insurance, or upon subjecting himself to physical examination preparatory to atldetic trainingj or upm considting his physican for some tritling ailment, Tlie dam- age to the valve is slight and compensatory hypertrophy is perfect. It would in some instances be l>etter for such persons not to be infomierl of their defecfj since although tlicy are able to endure games of skill and considerable exertion, as tennis, without con* scions s\^nptoms, they are likely after learning of their lesion, par- ticidarly if of a nervous, excitable tem]>erament, to be alarmed by palpitation, which prior to their knowledge did not attract their attention.
In other instances regurgitation is free, yet there is a truly re- markable absenc^e of subjective consciousness of its existence. This is generally due to the completeness of the compensatory hypertrophy on the part of the right ventricle and the left auricle. Yet I have known individuals of a not very impressionable tem- perament who, in spite of rather inadequate compensation, were unconscious of symptoms referable directly to their mitral dis- ease. Some excitable neurotic persons, like those first alluded to, consult physicians for symptoms referable to the digestive tract, or nervous system, rather than to the heart itself. These are anorexia^ or discomfort after food, constipfition, or an irregular
224 DISEASES OF THE HEART
state of the bowels, distressing prsecordial pains, which either set up or are accompanied by palpitation, and which greatly alarm the patient and friends. In a multitude of such cases there is no objective evidence of loss of compensation, and the patients are able to enjoy outdoor sports or to participate in feats of endurance without subjective symptoms.
Again, cases occur in which the only symptoms are such as are usually classed under the head of litha?mia, or the irregular mani- festations of gout, and occurring in persons of sedentary habits, are removed by regular outdoor exercise.
In other cases the most that can be said is they appear to have an imstable nervous system, and their sjTuptoms in nowise differ from those of other individuals of the same category whose hearts are healthy. In all such the valvular lesion does not appear to be directly responsible for the manifestations, and yet it may well be that these can be referred to defective nutrition and elimination in consequence of the circulatory disturbance.
It is not uncommon for females with organic mitral insuffi- ciency to present evidence of simple secondary anaemia or of chlo- rosis without symptoms of cardiac inade(juacy. If in such cases there is shortness of breath upon unusual exertion, it is no greater than may reasonably be attributed to the blood-state. I recall a remarkably interesting and instructive instance of this kind. In March, 1001, a young married lady of twenty-four sought my opinion because of *^ a grating sound in the heart," which first attracted her notice in the fifth month of her pregnancy, and which still annoyed her at times of unwonted physical effort, as during rapid walking. Aside from this symptom, there was nothing that made her conscious of her heart. She admitted getting a little out of breath, but this was so slight she had not given it any attention. Both her j)arents had died of pulmonary tuberculosis, but of her brothers and sisters, seven in all, none had shown signs of the dis- ease. She had had pneumonia when but a year old, scarlatina at eight, measles and pertussis in childhood, but never rheumatism, and up to the time of her marriage, at twenty-two years of age, she had considered herself well, being able to romp and play like other children without trouble. With exception of the " grating sound " mentioned, her pregnancy and confinement had been uneventful, and she could not recall having suffered from more dyspnoea than
MITRAL REGURGITATION
225
tlo otlier women towards the later months of pregtianey* She had nursed her baby for nine months, and during that period lost 2*J pounds, of which seven had been regained in the seven months fol- lowing the weaning of her infant. Her apjjetite was poor, bowels were irrt^^iilar, and she was apt to suffer from sour stomach and eructations. The menses were reguhir hut scanty* Uands and feet were generally cold, and she said she had grown nervous, being easily excited. Pain of any kind was trifling, forming a marked contrast to most of the eases I encounter.
In all this history and description of symptoms there was nothing to point to the heart outside of her < led a rat ion that she sometimes heard a queer sound, which she wanted to learn the meaning of. The pulse was 85, equal, regular, but to<j small and weak. The broad, strong ai>e.\-beat was in the normal situation, and no increase of either superficial or deep cardiac dulneas could Iw made out. However, the first sound was ]>art!y obscured by a loud, rasping murmur that was au<lible throughout the cardiac area and transmitted around the left side to the lower angle of the scapula. The pulmonary setxind sound w^as accentuated, and in the dorsal decubitus a softer blowing systolic murmur could Imj heard in the p id mo nary area. Thinking this last might be a chlorotic murmur, I had the blood examined, and found that the luem<igltjbin was reduced to G5 per cent, red and white cells being normal in nunitK*r.
In spite of the absentee of a rheumatic history and despite chlorosis, tljcre seemed no good reason to duubt the existence of a mitral regnrgitation of endocarditic origin, but as compensation was preserved, the jiatient was reassured as to the harndessness of the sound she had tioticed. In fact, she was given to understand that tlie more serious ciiuditions were the blood-state and loss of weight, whicli in the light of her family history certainly required attention. She was given a little strychnine and a few drops of digitalis to improve the strength of her pulse, but main attention was I>estowed upon the matter of nutrition. Milk, raw eggs, and fresh air were insisted upon. The patient obeyed instructions to the letter, and soon was disposing admirably of tw^o quarts of milk and ten raw eggs daily in addition to three good meals. Her colour, weight, and general cuntlition improved steadily, until at the end of two months she looked the picture of health. Nevertheless, the 15
226 DISEASES OF THE HEART
murmur persisted, and once in a while she heard that same endo- cardial sound. It no longer worried her, however, and she never complained of any other symptoms referable to the heart or dis- ordered circulation.
In this case it would be difficult to say how much the mitral regurgitation was responsible for her condition. I believe the leak was so slight that it did not materially affect the chylopoietic and blood-making organs, but that the state of her general health was attributable to her child-bearing and lactation, which in a woman with hereditary predisposition to pulmonary tuberculosis proved too great a draught on her vitality. Had she been allowed to go on in her reduced condition she would in time have devel- oped symptoms either of cardiac inadequacy or of tuberculosis. As it is, she is now likely to remain free from symptoms of valvu- lar disease for an indefinite time.
I have notes of the case of a young man who, because of a mitral regurgitant murmur and not very severe symptoms of car- diac strain, was ordered to bed by his physician, and there re- mained for two years. When I saw him he had mitral insuffi- ciency sure enough, but his prolonged rest had established perfect comj)ensation, the heart being not demonstrably enlarged and the liver of normal size. Yet he declared he could not get up .or stand^ much less walk. I compelled him to get on to his legs, and little by little to walk about, with the result that he found he could exercise without harm or 9yinj)toms of heart-weakness. He was easily frightened about himself for two or three years, but did not manifest dyspna-a or other cardiac symptoms even when riding his wheel over hilly and sandy roads. The last time he was seen by me, now several years ago, he was as well as nine-tenths of the young men who, like him, are school-teachers. At the most he had to be careful of his stomach and guard against constipation.
A medical student, aged thirty-four, sought medical opinion on account of attacks of palpitation. In childhood he had measles,, pertussis, and chicken-pox, and dimly recalled having had a swollen knee when five years old. At twelve or thirteen was so pimy and frail that he was given cod-liver oil and kept in the house during the winter, but after fourteen took a start and be- came rugged. Fourteen years ago he had gonorrha»a; had used tobacco from the age of seventeen. In 1893, 1894, and 1895 he
MITRAL REGLTRGITATION
22T
played football a good deal, and again two years ago, 1898, with- out any distress eoimeeted with his heart, excepting on one ocea- sion when, after having dnink a number of ghisses of beer, he played in a very rough game. lie then noticed considerable short- ness of breath and several times had to drop out and lie down on the grasSj heeanse experiencing great difficulty in getting breath. He attributetl his dyqniiea to the fact of having attempted to play on a full stomach. About a month later he began to notice his palpitations. He now does not notice dyspnoea except on nmning upstairs, and then no more than he thinks anybody woidd who was soft and out of training. In spring of 11*00 he consulted me, but nothing positive was discovered to explain his palpitations, and he was advised to give up his tobacco. This he did, and his palpitations disappeared. Upon attempting to smoke again a few months subsequently his symptoms returned and he again aban- doned his smoking permanently, but his palpitations still con- tinued.
Examination of his urine tw^o years ago showed it to be nor*, mah Last spring he observed for the first time that a prolonged and severe attack of palpita* tion was followed by the pas- sage of a large amount of pale urine. His digestion is not good, he thinks, tliere being a '* rumbling and roaring '' in the bowels, some enietations, and occasionally heart-burn. Sometimes his ilatulence is followed by diarrhrea, but or- dinarily his bowels are regu- lar. His sleep is good and his habits are now excellent.
The pulse varies much in its irregularity, being steady for twenty or thirty seconds, and then intermitting every few beats ; it is equal, of good volume, and of normal rate. There is no perceptible cardiac impulse except when rhe heart gives a more than usually vigorous contraction. Absolute dulness is nor*
Fj«. 36. — RtLATlVl DtL!CKi«« C'ai*K mF
Mitral iNscrriciKKCY,
228 DISEASES OF THE HEART
mal, but relative dulness measures 1^ inches to right of the sternum and 4^ to the left of the median line in the third interspace (Fig. 36). The sounds are distinct, but the pulmonic second markedly accentuated. At the apex and roimd about the nipple there is a faint, soft systolic murmur, which is heard distinctly only when the heart makes a strong contraction after an intermission. In the fifth interspace, within the left nipple-line, there is a sugges- tion of a very short presystolic murmur. The systolic murmur is increased somewhat in the recumbent position.
There can be no doubt of the existence of a mitral leak, but it is not quite clear whether it is of rheumatic origin or resulted from a degree of cardiac overstrain during that game of football, and from which the heart has not recovered.
The effect of tobacco and emotional excitement on this patient is interesting. After having both smoked and chewed for seven- teen years he has at length been compelled to abandon its use, because it now invariably induces an attack of palpitation, which is described as a *' fluttering." He notices also that the excitement attending a quiz or examination in class will set his heart to flut- tering. Also an attack is pretty sure to come on about an hour and a half after a meal, whereas if he misses a meal the palpita- tion does not occur until the usual length of time has elapsed after the next meal. This individual is highly nervous, not being able to keep still, continually moving a hand or foot. It is this insta- bility of the nervous system that accounts for the readiness with which his heart resj^nds to stimuli that do not disturb cardiac action in most individuals.
In contrast thereto is the patient's statement that even vigor- ous effort does not produce palpitation and only a moderate degree of breathlessness. Lastly, he is not conscious of the habitually intermittent action of his heart when he is at rest.
The treatment advised was a blue pill once in two weeks, to be followed by a dose of salts next morning, tincture of fat-free digi- talis in 5-drop doses, and ^ of strychnine thrice daily, the avoid- ance of immoderate physical effort, and a dietary rich in proteids and containing a restricted amount of carbohydrates.
Intense cardiac pain of the kind to merit the term angina pectoris is rare in mitral regurgitation, particularly in the young, or when of endocarditic origin. In some, however, there are neu-
^IITRAL REGURGITATION
m>
ra%ic pains aViove tbe pni'cordinnu whiclu by reason of an asso- ciated riense of oppression, may be called not inaptly anginoid pain?^, Tbe pain inot^t frequently eoii»plaine<l of by tbesc patients h a left infranjanuriary neuralgia, wLicb is varimisly described, a^ if a knife wenj beinj»: tbnist tlinnigh tbe heart, or as if the pain \vf»nid take tbe breatli away^ or an if the heart were being ehitehed or twitched or screwed together. This pain is ajit t<j appear sud- ilenly, to be sharp and lancinating, to last a few secondsy and recur after varying intervals, to be conlined to tbe prarordia* or to radi- ate around the back, down int<i tbe hypuebunilriuiii, u]j into the neck, or even into the left arm. OecMsiHually the cutting pain subsides, leaving a feeling of soreness behind. Tliis heart-pain, as it is called, is not angina p€x*foris, but a true intercostal neuralgia, and is very apt to be assrieiated with palpitations. For this reason the patients are all tbe more convinced that the p;dn is iu tbe heart itself. I have knmvn strr^ng men, an*l even physicians, dreadfully alarmed by sneb an attack. Its association with cer- tain tender areas pointed out by Head indicate its origin in dis- orders of indigestiun, and hence its frecpient occurrence in patients \nth mitral disease. It is not to be supposed^ however^ that it is at all peculiar to this class of eardiopatbs.
Xot long ago I was consulted l>y a woman of thirty-six on ac- count of a sharp pain in the left side near tbe heart. She gave a history of intlannnatory rheumatism eighteen years before, at which time she was ill two or three months. She renieiubered having had scarlatina iu childhood, followed by dropsy for an in- definite jx-riod. She bad bad two attacks of measles, once in childhood, and again at the age of twenty. Thirteen years prior to my examination she had suffered from la grippe. She had been married sixteen years, given birth to one child, and for many years had been a hard-working, active woman. Her chief com- phnnt was a sharp pain about the heart, and yet in response to query concerning shortness of breath said that when she ran up- stairs, as w^as her wont in order to get up quickly, she w*as so out of l)reath that she had to sit down to recover breath. At such times she also lM?came blue. F]X)n rising suddenly she felt dizjsy, her hands and feet swelled sometimes, was annoyed by gas in the stomach and bowels, and bad a poor appetite. Bowel movements and menses w^ere regular, though the last were scanty. She
230
DISEASES OP THK HEART
sonietimes heard a grating noise that seenied to come from the heart.
Her puke, while sitting, was 80, small, weak, and regular.
The apex-beat in the fifth left interspace, nipple-line» was weak, but without thrill. Absohite cardiac dulness was normal, but reia* tive dulne!>^ extended to the sixth cosial cartilage below, 4 inches to the left of midsternuni, ncjt increased to right (Fig* 37). The
first sound at the apex was tV^eble, being partially ol> seured by a murmur and suc- ceeded by a feeble second tone^ while the pulmonic second was distinctly accent uati'd. All over the cardiac area was a loud, sawing murmur of sys- tolic rhythm, most distinct at the apex, and transmitted around the left side to the back. The liver was barely piilpahle, yet tender in the re- gion of the gall-hhidder, but in other respects the abdomen was negative. The condition was plaiuly a mitral regurgi- tation of rheimiatic origin, with iniperfeet compensation because of the daily strain to which the heart was subjected.
This case is interesting because of the fact that although the patient admitted dyspna'a and cyanosis upon unusual physical effort, she was yet chiefly disturbetl by the pnecordial pain. This was undoubtedly an intercostal neuralgia that was in reality due to her gastric and intestinal fermentation and only indirectly to the valvular lesion.
The only s^^Tlptoul of which one of my male patients com- plains is an intermittent pulse that annoys him wheuever he breaks away from his strict diet or confines himself too closely to his ofKce. lie is always benefited by outdoor exen-ise, particu- larly fishing, and declares he has no shortness of breath and no uncomfortable palpitation unless his exercise is too violent* An-
Fio. 37.— Arist-BKAT *!fft Relative Di l-
KCM^ Ca«S or MjTIUL KEaLItOtTATKiJi
MITRAL REGURGITATION
231
Other patienty who has pronouneed yet perfeetlj compeBsated mitral rt^fi^irgitationj is able to endure any form of exercise, even running, without any other symptom than a rapid, strong heart- action ; wliile still a third bears without any apparently injiirioua effect broadsword practice and sparring*
Between such cases as these and those in the last stages of cardiac incompetence there are all grades of sufferers. In what may be called an infrrmcdiaie .stage — that is, when comj>ensation is no longer complete — the symptom most commonly exjierienced is dyspna^a. Some patients do not notice this breathleasness dur- ing ordinary walkingj bnt only %vhen they hurry or ascend stairs rapidly. Even then they sometimes say in response to queries concerning their ability to endure exercise, they do not think they get any more out of breath than does anybody in hurrying up- stairs. The fact is, such persons have been so accustomed to breathlessness, even for years perhaps, that they do not attach any iniportanee to it, and do not consider it a symptom of heart- weakness. Indeed, so long as dyspncea is not more pronounced, the mitral lesion may be considered in a state of fair though not perfect compensation.
In this internii^diate stage there is a degree of chronic pulmo- nary congestion which renders these patients particularly liable to couglis and colds. These may be transient and troublesome only during damp, cold weather, disappearing altogether in summer, but in not a few eases there is a very obstinate chronic bronchitis. When this last is present^ it possesses no pecxdiar features that distinguish it from the chronic bronchia] catarrh so often observed in persons without valvnlar disease. It has lieen my experience, however, that a persistent and frequent cough is very apt to inten- sify the already existing dyspna-a by reason of the strain it puts Ujmu the right ventricle. (Consequently, whenever cough makes its app€*arance in a case of mitral regurgitation it is not to be re- garded as of no importance and likely to " wear off." It may gradually wear away if the season is propitious, but it is far more likely to run on into a chronic condition. It should be borne in mind, also, that in these mitral patients cough may be attended by blood-spitting from rupture of a congested capillary in the bronchial mucosa, and is not at all significant of tuberculosiH. Oc- casionally cough is induced by unusual exertion or excitement, and
232 DISEASES OP THE HEART
is, of course, due to the irritation of excessive pulmonary hyper- a?niia. In two instances coming under my notice it was attended by a profuse serous frothy expectoration that betokened acute oedema of the lungs. In both these cases the attack subsided with- out treatment after the patients had betaken themselves to absolute physical repose. Such attacks are not without danger, and often necessitate energetic treatment.
The following case is an example of the occurrence of haemop- tysis in mitral regurgitation. In March, 1901, a tall, slender girl of nine was brought to me by her parents, who were in a state of great alarm because of her having spit up a little blood a few days previously. One of the child's maternal uncles was in Colo- rado on account of his hmgs, and consequently it was feared the little patient might be developing pulmonary tuberculosis. It was ascertained that there had been no antecedent cough, but that the hirmoptysis, which had occurred more than once, had followed upon rather more than the usual amount of running. There was a history of measles, but not of scarlet fever and not of rheumatism, although the child had in earlier years suffered a good deal from pains in her legs, and been wont to cry out in her sleej) from night terrors. Upon examination I readily discovered a loud, blowing systolic apex-murmur that was propagated to the back. The heart was unmistakably enlarged and the liver was palpable. As a re- sult uf these findings and in the light of the history I had no hesi- tation in j)ronouncing the case one of mitral regurgitation, prob- ably of rheumatic origin, and also in explaining to the parents that the symptom causing their alarm did not denote tuberculosis. They were told that it was the result of congestion of the lungs brought on by a degree of physical effort that was too much for her damaged heart. It may be added that the knowledge of their child's valvular lesion did not serve to allay their apprehension. This case also illustrates how remarkably unconscious of dyspna^a children often are who have mitral insufficiency, for this eliild not only was fond of running and playing hard, but said such sports did not make her feel bad or get out of breath.
In cases of imperfect cornpeusafion there are likely to bo symp- toms of stasis within the vessels of the abdomen as well as of the lungs. Disorders of appetite and digestion are now quite com- mon. Some patients lose their appetite altogether, or if they feel
MITRAL REGUKGITATION
233
liiiTigry when sitting d<t\vij to eat, stHJii find themselves full and imconiifortalde, not because of Laving taken too niucb^ but on ac- count of the formation of gas that distends the stomach and pro- duces a sense of repletion with, in some cases, an intensification of the already existing dvsjmcea. These patients declare they bloat up after meakj and often complain of annoying eructations. The escaping gas is either tasteless and odourless or tastes strongly of some of the ingesta. Others snffer from acid indigestion, pyrosis, burning or gnawing in the pit of tlie stomach, colicky pains, etc* Some [latients are constipated and annoyed by tlotulency, wliile others have a tendency to diarrhu?a, particularly in the morning be- fore breakfast. In a few instances I have known a veritable bu- limia, which it seemed to me might reasonably be attributed to the irritation of fatty acids and gases. It is not uncommon for these patients to be tormented by tbirst, wliieli, compelling them to drink largely and often of cold water, aggravates their trouble. The con- dition of chronic gastric catarrh responsible for these symptoms is not peciiUnr to mitral patients; it is only one of the nuiny manifes- tations of secondary visceral congestion which bring the patients to the physician. The digestive defect is often the result of dietetic indiscretions, yet their mitral leak pretlisposes them to suffer from errors in diet which woidd not aff'ect them were they healthy.
In females chronic hypencmia of the pelvic organs is shown V*y leucorrbaa and menstrual derangements. In some menstruation is profuse and irregular, while in others again the catamcnia are scanty or suppressed.
Stasis in the haniorrhoidal plexuses may lead to piles and con- sequtmt constipation. Kenal congestion is shown by scanty, light- coloured urine, rich in urates. Albumin and casts do not appear as a rule until in the latter stage of the valvular disease, when dropsy has come on.
Exaiuiiiation of tlie Hver in this intermediate stage of de- fective compensation may or may not distdose enlargement of the organ. In most instances hepatic dulness is found to reach a finger's breadth or so below the inferior margin of the ribs, while the lower border of the organ feels smooth, rounded, and firm. Palpation may also disclose more or less tenderness of the organ, so that the patient winces and invohmtarily resists further pal- pation. If the congestion has affected the biliary pas.«ages and
234 DISEASES OF THE HEART
led to their catarrhal occlusion, more or less complete, this may be shown by icterus. As a rule this is slight, and combined with capillary congestion produces a muddy hue of the face.
In the most of these cases of partially destroyed compensation there is not actual cyanosis, but instead the lips and cheeks present a dark-red colour that by the uninitiated is very apt to be mistaken for an appearance of ruddy health. If the hands and arms are inspected their superficial veins are seen to stand forth too promi- nently, while by night the ankles display, if not actual pitting, at least a degree of puffiness and tension which is but a little way removed from oedema and betokens marked capillary stasis.
The patients now find their breath uncomfortably short on hurry, and even when they walk leisurely they are conscious of slight breathlessness. In addition, they notice a feeling of fulness or tightness in the heart-region, which if not actually painful is very akin to pain. They find also that they become fatigued more easily than formerly, and that talking requires more effort than is quite comfortable, while if they converse during walking they pant noticeably. Efforts before endured without conscious effect now throw them into perspiration, and make them glad to sit or perhaps He down and rest. Such symptoms constitute the earliest evidence of cardiac inadequacy, and if not heeded will go on to symptoms of j>ositive loss of compensation.
In some persons in this stage there is marked tendency to drowsiness after meals or whenever they sit quiet and strive to fix their attention on a speaker. This is especially noticeable if the atmosphere is close and hot. Some persons find the heat and closeness produce a feeling of faintness or suffocation which neces- sitates their seeking the open air. Sleep is heavy, with frightful dreams, or there is insomnia, so that in the morning the patients are intensely weary and unrefreshed. Headaches are not imcom- mon in this stage, and for the most part are dull frontal pains accompanied by a sense of mental weariness and confusion.
A still more advanced stage of lost compensation is shown bv a yoimg lady with free mitral regurgitation and adherent peri- cardiinn whom I have imder observation at this present writing. The skin along the shaft of each tibia can be indented slightly by firm pressure; the external jugulars stand forth as large as my little finger, are painful, and show the positive venous pulse of
MITRAL REGUKGITATION
235
tricuspid leakage; tbe waist kxiks and feels disproportionately large, while below the ribs the big resisting liver extends to the level of tbe nmbilicus, causing the abdonien at its upper zone to stand out unnaturally; the veins on the hands and arms are turgid, wliile the pulse is siuallj weak, and faltering, but not mueh aeeeleraledj seldom reaching 100. Examination shows a diffused unsteady impulse throughout the pnecordiitm, while the broad, rather strong, immovably fixed apex-beat is in the sixth inter- 8]iace, almost to the left anterior axillary line; absolute cardiac dulness is so enormously increased both by reason of dilatation and the retraction of the lung-borders, as to nearly c-orrespond with relative dulness. All over the left chest can be heard an in- tense systolic murmur, %vliieh is unmistakably a mitral regurgitant one, while to the right of the lower portion of the stenumi is a somewhat softer systolic bruit that is probably tricuspid. The scanty urine contains 0 per cent of all>umin, hyaline and granular casts, while menses have been absent for the last six months. In the way of subjective s^inptoms there are the following: Short- ness of breath when walking or conversing, an occasional short, dry cough^ pain in the distended jugulars, when these are unusu- ally full, a sensation of fulness and tightness in the region of the liver, at times an intense uncontrollable nervousness and restless- ness, but almost no sense of digestiv^e discomfort, and the appetite is remarkably good.
This patient's first breakdown occurred ten years ago, and has been f<jllowe<l by two or three others. This present manifesta- tion of rupturtnl comi>t*nsatiou began six months ago, and for sev- eral months was so bad that she had ascites, dropsy of the ankles, and \vas confined to her apartment. She was not then under my care, but was at her home in an adjoining State. In this case there are to me two features of particular interest : ( 1) The com* plication of i>ericardial adliesions, which utterly preclude the pos- sibility of reducing the dilatation of the left ventricle by which the regurgitation is intensified, and (2) the absence nf dropsy, although the tricuspid- valve is incoriipetent. Compensation is de- stroyeil, and I fear irretrievably so, but the disturbance of circu- lation has not yet reached the degree nor produced the distressing subjective 8\Tiiptoms sometimes witnessed in cases of mitral re- gurgitation.
23G DISEASES OF THE HEART
When in this disease compensation is wholly gonCy there is a marked aggravation of all the objective and subjective symptoms that have been described. There are now evidences of extreme stasis. Dropsy is generally a pronounced feature, and in many cases dominates the scene. Beginning at the ankles, it creeps upward until it involves the integument of the trunk, and it may be of the upper extremities. There is also in this stage transuda- tion into the serous cavities, ascites, hydrothorax, and puhnonary oedema. This condition leads to orthopncra, cough, and frothy or even bloody sputum. I recall a female who in this condition of hopeless suffering was sitting on her bed, supporting her elbows on her knees and her face in her hands, and was coughing pure blood. She had been in this plight for days and had abandoned hojx?, having been told by more than one doctor that her condition was hopeless. Thrive months thereafter she was walking about the house free from anlcma. This case is described more fully in the chapter on Treatment. Another female patient who now visits my office was, four years ago, so dropsical that she appeared water- logged, and for six weeks had been obliged to get what skvp she could in an easy chair and resting her arms on a table in front of her.
When stasis reaches such an extreme degree as in this last case it has generally been preceded by dilatation of the right ven- tricle and signs of tricuspid insufficiency. This condition of the right heart may precede and seem to usher in dropsy, or serous transudation may anticipate the appearance of relative tricuspid incompetence. There is such a difference in the extent of ana- sarca, and in the stage of the disease at which it begins to develop, that there is something more than mere venous stasis to account for it. Accordingly, it is now known that serous transudation takes j)lace when, in addition to stasis in the venous system, there is an increased j)ermeability of the capillary walls due to dis- turbed nutrition, as well as a condition of hydnemia.
In some cases dropsy becomes so excessive that the skin of the legs becomes red and shining, or even forms blebs, which, bursting, permit the serum to ooze forth, and thus diminish the tension of the surrounding parts. Under such circumstances the nutrition of the integument becomes so impaired and infection is so easy that a simple scratch or abrasion may set up inflammation.
MITRAL REGUKGITATIOX
237
In this staire of things extreme gastra-intestiiial congestion and abdominal distentiun from tluid and tlatiis prevent tlie taking of adequate nourishment. Cerebral e<jngestion and a^dema pro- duce lieadaehe, insomnia, or somnolence, an unreasonable fret- fulness and irritability, or a low, muttering delirium. Tlie pa- tient's condition is now one of inde:?cribable juul unendurable suf- fering, so that physician and friends alike breathe a sigh of relief when, after weeks or months of such luirdship, deatli ends the struggle.
It nnly remains to say a word concerning those cases of mitral regurgitation wlach are either mmplieated by chronic nephritis or arc stH^'ondarv to the dilatation of tlie left veiitricle conse<]uent upon the Briglit*s disease. These cases do not ditler essentially from those of the class just considered. Tliere is, how^ever, an ele- ment of uraemia in these cases wliich is apt to in<xlifv the picture somewhat. These patients ure apt ti> suffer from a form of dysp- nfea that is very distressing and dithcult to relieve by treatment It consists of sudden paroxysms or intensifications of their ha- bitual shortness of breath which come on independently of exer- tion or any other exciting cause. These may be worse at night— ai*e so generally, but are not necessarily so, for I have known them to occur by day. They have always seemed to nie to l>e of toxic origin or to be partly renal and partly cardiac. He^adache and nausea arc also likely to torment the patient, and inflamma- tions of the serous membranes are not imconmion. Dropsy ia often very pronounce<l, and is peculiarly soft and rebellious to treatment. In other cases pnlmnnary and cerebral symptoms pre- dion! iuate. They all furnish an absolutely uufavouralile prognosis on account of tlie as80ciate<l or antecedent kidney lesion.
Paroxysms of dyspnoea, sufficient to l>e termed cardiac asthma, are not very connuon in mitral incompetence, unless some compli- cation, such as chronic nephritis, is present, to which the regurgi- tation is sometiuies secondary. In these latter cases asthmatic seizures are fretjuent, or the dyspnrea asi^^umes the Cheyne-Stokes type. Likewise, other sA*mpfoms properly WdongiJig to mitral regurgitation may, when associated w*ith chronic nephritisj be modified by uriemic manifestations. There may be very distress- ing nausea and vomiting, and tlie physician may Vh? at a loss to know whether the symptoms l>e due to renal inadequacy, or to
238 DISEASES OF THE HEART
passive congestion of the stomach depending upon the regurgi- tation.
If in a given case of mitral regurgitation ascites appears prior to or independent of anasarca, it is due to some compli- cation, and in my experience this has most frequently proved to be adherent pericardium. These are the cases sometimes de- scribed as pseudo-atrophic cirrhosis of the liver.
Embolism from the detachment of a vegetation is not common in mitral insufficiency unless it be complicated with acute endo- carditis, yet this untoward event may occur, and then produces symptoms depending upon the organ in which the embolus is arrested. If this be the kidney, there is likely to be bloody urine, and yet it is not uncommon to discover post-mortem evidences of infarcts produced by emboli of such minute size as to have escaped detection during life.
Cerebral embolism produces symptoms too characteristic to escape notice. As the left middle cerebral artery is the one most commonly plugged, it is followed by aphasia and right-sided hemi- plegia. An embolus entering the hepatic artery produces acute icterus and symptoms closely resembling acute yellow atrophy of the liver. In the case of the spleen, the sudden, sharp pain is likely to be followed by tenderness and enlargement of the organ. If an artery of one of the extremities is thus occluded, characteristic pain is followed by loss of pulsation in the artery below the seat of embolism, by weakness, numbness, coldness, and panvathesia, and even by gangrene of the limb, if the main artery happens to be plugged. Usually, however, these symptoms grad- ually disappear with the establishment of adequate collateral cir- culation. A by no means uncommon effect of the terminal stage of mitral regurgitation is the occurrence of pulmonary infarcts due to the lodgment in the pulmonary capillaries of minute frag- ments of thrombi that have formed in the dilated right chambers of the heart. Pain in the affected lung may or may not be felt, but if the patient suddenly begins to cough up clear blood it is very suspicious of pulmonary infarction.
Very exceptionally, a mass of considerable size may be swept off from the cardiac thrombus, and entering the pulmonary artery or one of its large branches, may produce instantaneous dyspna?a and speedy death.
MITRAL REGURGITATION
239
Physical Signs. — Inspedion, — There is nothing in the ap- peanince of imJiviJuulri with a hitent mitral insiiifieieni'y to sug- gest the existence of their disease. In some instances capillary con- gestion is just sufficient to impart to the lips and cheeks a slightly heightened colour that is easily mistaken for the hne of health ; it is, however, deeper than the rosy glow of perfect circulation. In a still more advanced decree of congestion the lips become of a bluish or even pur]»lish enlour, the capillaries of the face are in- jected, and the tingers also display more or less cyanosis* There is, however, nothing in this appearance to indicate more than im- peded circulation, and hence it is not peculiar to mitral regurgi- tation.
In children with long-standing mitral disease the fingers are apt to be cluhbed^ the stature stunted, the shoulders 8t(X>ping, and the pneeordiun^ bulging. In adulfs, ou the other hand, inspection of the cardiac area reveals no alteration of the kind seen in children.
The apex may be displaced somewhat to the left, depending on the degree of left-ventricle hypertrophy, and if serious dilatation is not present is broatler and stronger than in health. If the right ventricle is also sufficiently enlarged to lie well dowTi in the sulcus formed by the union of the diaphragm with the anterior cheat- wall, its pulsations are seen more or less distinctly directly below the ensiform a impend ix. This epigastric putsntion forms an im- portant sign of right-ventricle hypertrophy, and hence is a second- ary sign of mitral disease. It should be carefully distinguislied from the throbbing of the abdominal aorta, so often observed in this situation in neurotic individuals with thin abdominal parietes. Of course the information to Ix* derived from inspection depends largely upon the condition of tlie thoracic walls, and hence in- spection is of greatest value in i>ersons whose hearts are dispro- portionately large as compared with the size of the chest.
Palpation, — ^In compensated and uncomplicated mitral regur- gitation the pulse possesses no distinctive characters aside from its lowTiess of tension. Its rate is usually somewhat accelerated, its tension low, and in compensated eases at least, it is regular in fre- quency, force, and volume. As the energy of the heart wanes, as its walls become degenerated and its auricles dilated, the pulse grows strikingly irregular and intermittent, the pulse-weaves dif-
940
DISEASES OF THE HEART
fering from each other in size and srrotigth. cnming at uneven dis- tunces, and often dmppinj;: out altosretber even when the heart- beats are not themselves intermittent (Fig, 38). Such a pulse is exceedingly ditiieult to eoiintj and if ^uhjected to a little pressure by the linger, for tlie pnrjiose of havinir its characters brought
(Perf-'nui 'i.M-rvftTianJ £u1 urged.
out more distinctly, it disai>]x»ai-s from beneath the palpating finger in a manner that makes it very ehisive. This extreme irregidarity of the pnlse is itiost fretpient when regurgitation is eoiHt>ine<l witli stcnc^sis or an adherent [MTicardinm.
The pulse in the two wrists is generally equal, but cases have been described in which the ri£^ht was distinetiv smaller than the left, owing to relative tricuspid insufficiency and consef|ueut pres- sure of the dilated right auricle on tlie subclavian artery. Balfour Btates that if the arm is elevateil the peculiar characters of the pulse — i, e,, its irregular it tf and hwness of leftsion^nre brought out more distinctly.
Palpation of tlie prax^-ordia crmiirms the information obtained by the eye, but in addition taiables one to l>etter appreciate the strength of cardiac contractions. It may also detect thrill or pul- sations that cannot l>e perceived by inspection. Palpation is often a valuable means of ascertaining the size of the heart, particularly in females in whom excessive raammary development may prevent accurate percussion. By pressing the fingers gently yet firmly into the intercostal spaces beneath the breast one can ascertain the position of the apex-beat» and thus judge of the size of the left ventricle.
Authorities clifFer as regards the existence of a I brill at the a|>ex in cases of pure and uncomplicated mitral regurgitation. When J however, such a thrill is present it is systolic, and felt
I
MITRAL REGURGITATION
241
with greatest intensity at the immediate seat of apex* impulse, since it h the pjilpable expression of the innrniur. For my part I am perfectly sure of its oecasional existence in cases without eon- joined mitral stenosis.
Lastly, by palpation of the epigastric notch one can also judge of the degree of coinj>ensatory enlargement and vigour of the right ventricle. In this way one can often determine that the ventricle is hypertrophiedj when for one reason or another it is dLflicult or impossible to outline the chamber by jjercussion.
Percussion, — This means of cardiac examination should never be neglected, since as a general thing it furnishes the most valu* able and reliable information conet'rning the heart's eonditiom Indeed, i)ercussion is almost our only means of ascej'taining the size and shape of the heart, and hence of learning what and liow extensive have been the secondary changes wrought by the valvular defect. If in the lesion now under consideration percus- sion does not (h^teet increase of absolute or rehitive dnluess to the right and downward, the inference is w^arranted, even though there Iw? an in- tense systolic bruit, that the leak is not free, or that being free it has nevertheless been jierfectly comi>ensated. In most eases of mitral regurgi- tat ion, however, the lesion has led to enlargement of the right ventricle, and in such an event, deei>-seated if not sujier- ficial diilness is increased to the right and inferiorly; and hence the e-xtent to whicli dnlness is increased is a criterion by which we can judge of the freedom of the leak or of the comyiensation. Secondary enlargement of the left ventricle is shown by increased dnlness of the left (Fig, 39),
Mitral regurgitation, it will be rememliered, leads to dilata- tion of the left auricle as well as hyiK^rtrophy ; hence in pro- nounced cases the outline of the deep cardiac dulness at its upper 16
luK 3i>. — Kklativr Dllskw IK A Typicau Cass or Mitraj. KconiAiTATioK,
243
DISEASES OP THK UEAKT
and outer corner, so to speak, is broad and rounded, corresponding to the' enlargement of the auricle. It is not always easy to deter* mine this alteration of shape by jiercussion; yet if firm percus- sion 18 made, and the chc*sr-wall is thin and yielding, it is some- times possible u* determine the extent to which the left auricle has been affected by the regurgitation.
AuscutfafiofL — This forms a very valuable means of cardiac examination, for without the information thus obtained one can- not safely assert that mitral regurgitation does or does not exist. It should not be relied upon to the exclusion of other methods of investiyaiion, however, for reasons that will be statcnl presently. The auscultatory evidence of valvular disease lies in certain acous- tic phenomena which are produced by soniferous currents in the blood-stream, and are called murmurs* It is plain that many dif* fercut factors iullueuce the character of a murmur, and that if relialJe infonmitioTi is to W^ derived froui the study o{ a iiiunnur
the characters peculiar to each must he imdersttxKb
The auscultatory indica- tion of mitral regurgitation, then, is a systolic murmur heard with maximum inten- sity in the mitral area^i. e., at or close to the ajiex-heat (Fig. 40). Such u hruit is not, however, an in variable sign of mitral incompeieiice, since it may k* accidental, and hence there are of her facts crmceruiug a mitral re- gurgitant murmur wliich must be understood.
The niunuur is systolic be- cause pHMJuced during the con- traction of the ventricles, and therefore it is strictly synchronous with tlie first sound, although it not infrcfiuently lasts a little longer, and may even persisr and increase in distiuctuess through the short pause up to the succeeiling second sound. It is so common for some degree of obstruction to be combined with regurgitation
Fla, 40.— PoiWT OF MAXIMtli ALiUlhlilTV (SIIJLDSU) AXD AltiA OF TRAN»MI».<4]i».V
(OtTLINlD) OF MrmAL RtOUHQltANT
MITRAL REGURGITATION
243
that a shorter or longer presystolic oiurnmr often ushers in the systolic bruit. It forms but an added element, and in nowise alters the fact stated above — namely, that the time or rhythm of the mitral regurgitant murmur is slridlif systolic (Fig. 41),
i ihoWD
2 liiiii? tjf
41.— Time ok Mithal RisuufiotTAi^ MtriiMt?!!.
iiiuniiur Ciirdiiic ^fciti «s iu Fig. 9, Read from left to nghL
The next element of iijjjwrtanee is its position of maximum intensity. The bruit in some ca^es is heard most elearly near the anatomic situation of the mitral vah'c — i, e., at the level of the fuurtli costal earttlage near the left border of the sternum, but as a general rule the murmur is conducted along the chest-wall to the point where the apex of the heart strikes with greatest force. Hence the murmur is heard most loudly iu the immediate vicinity of the ajiex-beat, sometimes slightly within ^ sometimes just above the nipple, and sometimes a little to the outer side of the apex. It is, howeverj louder in this than in any other cardiac area, and by reason of this circnmstanee rc^rognised as mitral
Very rarely a mitral regurgitant bmit is heard more plainly in the tricuspid area — i* e., on the ensiform appendix or close to its left ularaiu — when it is likely to be mistaken for a tricuspid bruit. I have knuwii such a mistake to be made iu more than one instance. The error can he avoided by attention to the signs of tricuspid regnrgitatiou, as described in that chapter.
Inexperienced anscultators are apt to attach a wrong inipor-
244 DISEASES OP THE HEART
tance to the intensity and the quality of a murmur. It goes with- out saying that all possible differences in these respects are to be found in mitral systolic murmurs depending upon conditions gov- erning their generation. Neither the loudness nor the quality of a bruit furnishes any evidence per se as to the gravity of the lesion. A very intense musical murmur may be produced by the blood-stream being forcibly driven through a small aperture, and conversely a very widely open and unguarded orifice may permit the blood to regurgitate so easily and noiselessly that only a very soft, scarcely audible murmur is generated. Hence neither inten- sity nor quality of a murmur is of importance in determining whether or not it is mitral; they only facilitate the detection of the murmur, and sometimes aid us in determining the seriousness of the lesion.
Furthermore, the intensity of the murmur is governed by other circumstances than the leak itself. The bruit of mitral re- gurgitation is generally loudest during energetic action of the heart, hence during excitement and immediately after exertion. It is consequently brought out clearly by having the patient jump about, swing the arms violently, or do something else that causes the heart to beat rapidly and energetically. By such a procedure it is often possible to detect a mitral bruit which before was in- audible or so indefinite as to have left the examiner in doubt of its existence.
The position of the patient's body also influences the audibil- ity of the murmur. It is in most cases heard most plainly when the patient sits or stands, but I have frequently seim cases in which it came out far more distinctly in the dorsal decuhittiSy which ]>er- mitted the heart to beat more forcibly because more slowly. Con- sequently, it should be an invariable rule to auscultate a suspected case of mitral insufficiency, and indeed any suspected case of car- diac disease, in all three positions. It will often protect one against a serious blunder in diagnosis.
Mitral systolic murmurs are usually spoken of as blowing and soft. They are as a matter of fact softer than direct murmurs of stenosis, but they are by no means always soft. They may be harsh and rasping, or filing, grating, sawing, whistling, etc., in which event they are designated as musical, a character of patho- logical but scarcely diagnostic interest.
MITRAL RKUUROITATIUN
245
Finally, mitral systolic murmurs should always be studied with rt^8peet to tlie direction in which they are transmitted from the apex. This is es|)i*eiidly important in eases in whieh secondary physical signs of mitral regurgitation are ditticult to ohtain, for in such cases it is necessary for correcr diagnosis to determine whether or not the apex systolic bruit is an accidental one. Such inorganic murmurs are of limited propagation, whereas mitral regurgitant bruits are often, though not invariably, widely trans* milted. Their direction of propagation is towards the left rather than the right, and therefore they may be traced into the axillary region, or, as sometimes happens^ even on to the back. It is not at all rare to hear an intense mitral murmur at the inner side of the left scapula near its tip, and in children such a bruit may be heard throughout the entire thorax. When in any case the murmur is audible in more than one area it is indispensable to detenu ine by careful comparison in which area it is of maxi- mum iutcnsitv, for onlv in this wav can one decide to what car- diac area the murmur belongs.
One is not to contant himself with studying only the murmur, he must also carefully ansiitUaU the several heart-sounds. If the first tone at the apex is not replaced by the murmur, it offers a certain amount of evidence in favour of the valve being not wholly destroyed J but able to still partinlly clnse the orifice. If, on the other hand, the murmur alone is heard, it indicates great freedom of regurgitation. Then one should note the degree of accentuation and purity of the pulmonic second sound, especially in all cases in which the interpretation of the murmur is not clear. Regurgi* tation by inducing pulmonary congestion leads to Intensifkatwn of the pulmoHic second tone^ and hence such intensification is the earliest recognisable secondary i)hysical sign of mitral insnfli- cioncy, and greatly strengthens the inference dra^^Ti from the rec- ognition of a unirmur.
Diagnosis. — The diagnosis of mitral regurgitation is not diffi- cult as a rule, being in some instances one of the easiest of all valvular lesions to make out. When, however, the leak is slight, the murmur obscure, and the secondary changes in the heart and general circulation insignificant, its diagnosis may be anything but easy. It is also occasionally difficult when there is dropsy, a rapi<l, tmnultnous action of the heart, extensive dilatation, and
246 DISEASES OF THE HEART
serous accumulation in the pleural cavities. One may then make a diagnosis of the condition with reservation, and wait for treatment to clear up the case. Attention to the secondary physical signs will usually help out amazingly under such circumstances.
The history of the patient is also of great importance, not alone to the diagnosis of mitral insufficiency, but to the recognition of the etiology, and thereby to the relative or organic nature of the regurgitation. Its gravity is to be determined by the second- ary effects which the heart-walls and cavities have undergone, and by tlie presence or absence of s^^nptoms referable to the car- diac disease. Xot until all this has been accomplished should the physician rest satisfied, remembering that the detection of a mur- mur does not constitute a diagnosis.
Prognosis. — In general, it may be stated that mitral regur- gitation affords a more favourable prognosis than does any other valvular disease, yet in this respect each case is a law imto itself. Furthermore, the prognosis of each case dei)ends upon many dif- ferent factors: (1) On the etiological nature of the defect, (2) its severity, (3) the degree of secondary effects, (4) the complete- ness of compensation, and (5) the existence or not of complica- tions, such as other valvular lesions and adherent pericardium.
Insufficiency of the mitral valve from sclerosis furnishes as a rule less favourable prognosis than does that of endocarditis, because of the progressive tendency of the sclerotic change and of the age of the patient, which renders it likely that the myocardium is no longer healthy. If the regurgitation is free, if secondary hypertrophy and dilatation are extensive, if engorgement of the general viscera is apparent, even though compensation seems ade- quate, the prospect of the disease remaining stationary is not good. If mitral regurgitation is united with defects of other valves or orifices, the prognosis is correspondingly unfavourable. Complications on the part of the pericardium and of chronic nephritis render prognosis very unfavourable. Finally, prognosis stands in direct relation to the completeness of the compen^sation.
The curability of this lesion resulting from endocarditis has been much discussed, and, as pointed out by Balfour and others, seems certainly possible. This is considered particularly true after chorea.
The influence of age, sex, occupation, environment, etc., will
MITRAL REGURGITATION
M7
be considered in a subsequent chapter devoted to the Prognosis of Valvular Disease in Generah
Mode and Causes of Deatli,— A jjatient with imcorapH- cated mitral iHcoiiipetence rarely dies suddeniy and without warn- iijg» as in some other forms of heart-disease. When, however, this lesion is united with fatty or tibroid degeneration of the heart- nmsele the individual may drop dead from suilden diastolic arrest. I have known oiw such instaiiee in a man of sixty, A long period of suffering may l>o terminated by a rather rapidly fleveloped pulmonary a^dema, but usually the end comes slowly through grad- ually increasing cardiac exhaustion and weeks or even months of most distressing symptoms.
Very rarely, death may take place from embolic plugging of the pulmonary arlery or one of its main branches, but snch a sequence is usiudly preceded by symptoms of cardiac asthenia.
In one instance a young woman died suddenly under the fol- lowing circumstances: About a week before her death she had sought medical advice on account of increasing dyspna:»a, and was found to present signs of combined mitral incompetence and ob- struction due to articular rheumatism some years before. Be- cause of failing compensation she was ordered to rest quietly at home; notwithstanding this, she a few days later carried a hiick- etful of coal upstairs. The next morning her speech was thick, she complained of stiffness in tlic back of the neck, and showed a degree nr so of temperature, but evinced no paralysis. She was then sent to the hospital, and a day or two later, uj>on sitting up in bed to drink a cup of tea^ suddenly fell back upf>n the pillow and expired. A post-mortem examination couhl not be obtained.
Another female patient wlio for eleven years had evinced symptoms and physical signs of a double mitral lesion with adher- ent pericardium, at lengtli began to suffer from increasingly fre- quent attacks that seemed to indicate a sudden augmentation of stasis within the pulmonary vessels, yet without other manifesta- tions of more than usual cardiac weakness. Serous transudation could nowhere l»e detected. The final attack lasted but a few hours, and seemed to he the result of a rapidly increasing failure on the i>art of the right ventricle. No necropsy was permitted.
A lad of twelve years with chronic mitral regurgitation of rheumatic origin in whom a badly broken coinpensation had I>een
248 DISEASES OF THE HEART
partially restored, and who a few weeks before death seemed to have contracted a fresh inflammation of the mitral orifice, arose from bed early one morning to pass urine ; he had scarcely made the attempt when he fell on his pillow in a condition that alarmed his nurse. Two hours later I found him partly unconscious, and with a moderately slow and irregular pulse. He was pronounced moribund, and death occurred an hour or two subsequently. Un- fortunately, post-mortem examination could not be obtained, and as in the two preceding cases, the immediate cause of death could only be conjectured. It was probably due to an acute overdisten- tion of the heart, leading to gradual paralysis.
Hustedt examined 491 cases of heart-disease at the Patho- logical Institute at Kiel, with a view to determining the causes of death. Of 15 cases of mitral insufficiency, without associated car- diac lesions, he found the following causes of death: Cardiac asthenia (Ilerzschwache), 7 cases; pulmonary infarct, 2 cases; apoplexy due to embolism, 1 case, while in the other 5 death was due to some accidental or intercurrent affection, such as nephritis 1, peritonitis 2, marasmus 1, pulmonary collapse 1.
CHAPTER VII
MITRAL STENOSIS
This term denotes a narrowing or constriction of the opening between the left auricle and ventricle, in consequence of which there is an obstruction to the free flow of blood from the former into the Jatter chamlter. A narrowing is ahrays the result of druc- tuml defedj either of the ring itself, of the valve, or of both, and ean never be of a functional or relative kind, anab.igoiis to relative incomj>etence of the valves. The stenosis may he congenital in consequence of defect of development, or of endocarditis during intra-uterine life, but in the great raajority <if cases it is acquired after birth, and forms one of the most frequently enconntered of all valvular lesions.
Morbid Anatomy. — In a well-marked case of mitral steno- sis the cusps ure thickened and rigid, they are adherent, and bound firmly in place by tlie thickened and contracted chorda^ tendineae and papillary muscles, Tiie whole valvular structure is thus often converted into a rigid funnel-shaped ojiening, with a narrow slit- like extremity of size scarcely to admit a snuill probe. This is the S4>called butlonkole fnilral (Fig, 42), and in this form of steno- sis the endocardium may present no evidence of old vegetations, but be perfectly smooth. This has led s^jme French authors to consider the condition one of congenital malfortnation rat Iter than of riieumatic origin. Sansom, nn the ntber band, thinks it due to inflanmiation, and that its smootliness results from the ** quasi- cicatricial tissue " being subjected to pressure by the blc»od on both its auricular and ventricular asj>ect.
The stenosed valves often show, however, marked evidence of past inflammation in the form of organized or calcified thrombi, especially on the auricular surface. These may be so large as to almost completely obstruct the orifice* while their presence always leads to shrinkage and defonnity of the valve, and almost always
219
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' 1 |
|
^^^B ^^"S^L.^* |
■^ |
6 |
|
^F termiues the amount of the discharge. The shape of an |
orifice |
|
|
^H and the passage leading up to and away from it in |
fiuenfe rht |
' cjiian- |
|
^^t tity of fluid that can pass tlirough it in a given tin |
le. " If a |
ronnd |
MITMAL STENOSIS
251
tole he punctured in a can full of Avater, the cross-section of the fluid jet eoniiiig from it is much less than the area of the aper- turCj little niore than half of it. The relation of one to the other is termed the coeflicieut of discharge. If now the small end of a funnel hr acenratelv fitted to the inuer side of the aperture, so as to imitate the eunditifm of things uhtaiuiu^ in the fnuuel mitral, the eoetHcient of discharge is almost doulded. Again, if instead of making a nmnd aperture in our can we make a linear one, so as to imitate the buttonhole liiitral, we in a siniilar way nearly double the eoethcient of discharge. This form of the mitral oritice results from the flattening out of the funnel through cicatricial contrac- tion, so as to form a uiore or k^ss t!at diaphragm, and it is indeed a remarkable fact that in this process the round aperture of the funnel is invariably converted into a slit Sometimes it will seem to be sHt-abaped before the flattening-out process begins. Hence it is clear that in mitral obstrnetion the heart avails itself in a very cunning way uf principles well knuwn to the engineer, so as to secure the maximum flow through the narrowed mitral orifice — a brave attempt to make the best of a had job."
It seems possible, however^ that the fact of the mitral valve being comjmsed of two approxinnitely triangidar leaflets, which become adherent nlf»ng their sides, and leave a suudl oi>ening at their apices, where the two flat cusps come together, may have something to do with the slit-like shape of the stenosed orifice.
The effect of narrowing of the mitral orifice is to increase the difficulty with which the left auricle expels its contents into the ventricle. The reaction of the uuisculature to this increased de- mand for work is shown by the production of hypertru|>liy. This 19 the primary effect ; and dilatation, when it does occur, is a later event. In mitral incompetence, on the other hand, dilatation comes first and hyiiertrophy afterward. Yet there arc mnny cases of mitral stenosis in wliich the auricle is found post mortem to be thin-walled an<l dilated. This is probably in most cases due to associated regurgitation, fur in a series of cases taken from the records of Guy's Hospital, Sam ways found that the ilegree of dila* tation was nearly always proportional to the amount of leakage , asaociated with the stenosis.
The left ventriele presents a condition in marked contrast to that found in regurgitation. The narro%ved orifice allows only a
252 DISEASES OF THE HEART
reduced amount of blood to pass into the ventricle with auricular systole, and hence the work required of the ventricle is reduced. The chamber becomes diminished in size, and its walls thin and weak. At times this atrophy of the ventricle is so marked that the chamber is almost rudimentary in appearance.
The effects of mitral stenosis on the circulation, pulmonic and systemic, are practically those of insuflSciency, being primarily due to obstruction of the blood in the pulmonary veins. The obstruc- tion is more constant and unyielding in* stenosis, however, and hence the congestive effect is even more marked than in insuffi- ciency.
The effect on the myocardium in producing brown atrophy, and the congestion of the various organs of the body, are the same as in mitral incompetence, and do not call for repetition.
Etiology. — Much of what has been said concerning the causa- tion of mitral regurgitation applies equally to narrowing of the mitral ostium. There is one great difference between the two, however — namely, stenosis cannot be anything else than a struc- tural defect, and therefore it results either from changes during foetal existence or from endocarditis or sclerotic changes after birth. Acute inflammation usually produces clinical phenomena of incompetence and not narrowing, but changes initiated during an acute attack may subsequently develop into such as cause pro- nounced obstruction.
Mitral stenosis results most often, therefore, from subacute or chronic rheumatism, and on this account is a progressive lesion. Accordingly, as pointed out by Sansom, it is especially apt to be observed in persons who either give no history of acute rheumatic attacks or have suffered from vague joint pains. It is probable, therefore, that in the majority of cases mitral stenosis is of rheu- matic origin, but of the insidious or masked type, and not of the pronounced form. Nevertheless, as previousy stated, a valvulitis initiated during an attack of rheumatic fever may in time even- tuate in a predominating obstruction.
Another interesting view of the etiology of this lesion, and one that merits consideration, is that it has its origin in tubercu- losis. This opinion was announced bv Teissier as a result of his study of a large number of cases. Although positive evidence of the correctness of his views cannot be obtained, as he himself
MITRAL STENOSIS
25a
ail rn its, lie vet helieves that titl^onnilosis lies at the bottom of the cases of mitral stenosis whieh are progressive.
While verv loath to accept Teissier's conclusions, I am never- theless greatly interested in the possibility of sueh a causative rektionshii>, for the reason that prior to my kiiowleilge of his views I had lieen struck with the fact that several times I had encountered narrowing of the mitral orifice in young women be- kmging to tuberculous families. I recall distinctly a young Irish girl who had lost a sister from consumption and sought my opiuiim and treatment l>ecause she feared she was going into a decline* The character of the respiratory murmur at the left apex made me very uneasy, and hesitate about expressing an opinion until after I had kept her under ohservatiou for a suthcient tiuje to note any changes that might take place for better or worsie. To my great surprise I at length, after repeated examinations, discovered signs that indicated a very slight and progressive mitral stenosis. After the lapse of a number of months, during which she occasionally complained of vague leg pains without other definite indications of rheumatism* a very pretty but short presystolic murmur l>ecame unmistukalfh".
In another woman of twenty-nine, who also had lost a brother and a sister of consumption, 1 found a %*ery c^^nsiderahle narrow- ing of the mitral os^tium, as evinced by the secondary signs and Bymptuius as well as by a long, rough, loud presystolic bruit and corresponding thrilL There were also impaired resonance and broncho-vesicular breathing at the right apex, which made me very suspicious of latent tuberculosis. In this case most careful and searching in<pdry failed to elicit a history of previous rheuma- tism or leg pains in childhood that might have been construed as rheumatic. Nevertheless, I should be most reluctant to say that in this case the stenosis w^as of tulierculous origin. To my mind it is far more reasonable to assume that she had had unrec- ognised rheumatism. Are w^e to conclude because tubercle bacilli have been identifieMl in endocarditis that these slowly progressive and often latent cases are neces.sarily of tuberculous causation i The natural delicacy of constitution in these individuals who come of tuberculous stock, and the frequency with which rheuma- tism of chihiren is overkxjked, makes far more plausible, as I take it, the conclusion that the valvidar defect dates from early
254 DISEASES OF THE HEART
years of life, and has taken years to reach that degree at which it becomes clinically recognised.
Based on the teaching of Rokitansky, the view was formerly held that there is a natural antagonism between narrowing of the mitral ostium and pulmonary tuberculosis because of the conges- tion of the lungs produced by the stenosis. This is now known to be erroneous, for pulmonary tuberculosis and mitral obstruction have been observed conjointly in a considerable number of in- stances. Thus Sansom has collected 31 cases in which these two diseases were found associated at the necropsy. It is worthy of note also that of these 31 cases mitral stenosis and tricuspid steno- sis were combined in 11, while in 5 others there was also aortic valve-disease. Sansom explains the connection of pulmonary con- sumption with mitral narrowing on the ground that the latter lessens the natural resistance of the organism to the inroad of tubercle bacilli. The union of aortic and mitral disease intensifies this susceptibility, while tricuspid stenosis predisposes to pulmo- nary tuberculosis in the same way as does obstruction at the pul- monic orifice.
Syphilis and gout are etiological factors that should not be dis- regarded ; but they lead to the sclerotic or atheromatous, not to the end(K*arditic form of stenosis.
Tlie influence of age upon the type of the disease is also inter- esting. It is the rheumatic or endocarditic form that is encoun- tered in the young. This is shown even in the case of an infant that lived but twenty-four liours, and in whom Benezard Smith discovered mitral stenosis post mortem, and likewise in the infant of four months observed by Gerhardt, since in both these cases the stenosis was evidently the result of endocarditis during fcrtal life and not of defective development. This prevalence of mitral ste- nosis in the young ( it being detected most frequently at or about the age of fourteen, Sansom) is undoubtedly explicable by the fact that the young are most liable to articular rheumatism. On the other hand, individuals of middle age or over develop the sclerotic form of this valvular lesion, and in such it is probably but a manifestation of a general tendency to fibrosis.
The association of mitral stenosis with renal disease is shown by Goodhart's statistics, who found it present in about 1.4 of 102 cases of chronic nephritis that came to autopsy, while Pitt, in the
MITKAL STENOSIS
255
post-niortera records of Guy's Hospital, foiiiid mitral stenosis and granular kidney three tiojcs as freijiieiitly as stenosis without this form of renal disease.
It is a striking faet, on which al! writers comment, that mitral stenosis is encouutered far more frequently in the female than in the male sex. This is especially true of the disease in iKn-^ona below the age of forty, in whom it is jrrobably of inflammatory origin, while the selerotie fnrni of the lesion does not appear to predominate greatly in either sex* Of 42 cases of pure mitral stenosis of which I have records, 28 occurred in fenuiles and 14 in males, and of the entire number but 20 gave a clear history of rheumatism. It is thus seen that of my eases females numbered twice as many as males, bearing out the statement that mitral obstruction is par excellence a disease of the gentler sex.
Symptoms* — Inasmueli as the eff'ects of mitral regurgitation and mitral stenusis on the eircukition are practically the same> there is a close similarity in the symptoms of the two affections. Therefore, much of what was sai*l under the head of mitral regur- gitation also applies to mitral stenosis. I juhnd>tedly this affec* tion may remain latent for vcars, but it is less likelv to do so than is regurgitation. Nevertheless, hard and fast lines in this regard cannot be drawn, for the manifest reason that the degree of the effect stands in direct proportion to the gravity of the lesion. If compensation is adetpiate, symptoms re^ferable to the heart, or that call the attention of the patient to his heart, may be entirely ab- sent; and yet a patient with any eonsideralile degree of stenosis is not likely to be robust, or to jkjsscss much physical endurance.
Children are likely to be more or less stunted in development, both mentally and bodily; M'hile in the case of adult females I have been imiiressed by the frequency with which they are tall and thin, with evidence of anaemia. Their circulation, as might be expected, is defective, as shown by coldness of the hands and feet and great sensitiveness to low temjierature. Even when not suf- fering from symptoms referable to pulmonary congestion, as dysp- na*a, they are a]>t to complain of digestive and menstrual disor- ders, sour stomach and Bcanry menstruation being particularly common. They are generally constipated and their urine is diminished in amount, of correspondingly high specific gravity, and loaded with urates.
256 DISEASES OF THE HEART
Patients with mitral stenosis are also very prone to attacks of bronchitis, which ultimately run into chronic bronchial catarrh. They are also particularly liable to acute pulmonary oedema upon extra exertion, and in such instances the cough and hsemoptysis or frothy, perhaps blood-tinged, sputum often give rise to the fear of pulmonary tuberculosis. I have this very day seen a well- marked instance of the kind.
In other cases there is persistent dry cough due to bronchial congestion, which may attract attention from the heart to the lungs. I well remember the case of a lady who consulted me for an obstinate dry cough, which was found due to a mitral stenosis, the existence of which had not been suspected. Indeed, I myself had examined her about a year previously during an attack of tachycardia, and at that time was unable to detect any implica- tion of the valves.
As a rule breathlessness on exertion is an early symptom with patients suffering from pronounced mitral constriction, even though in all other respects compensation seems good. When the narrowing of the orifice is extreme, when the heart-muscle begins to fail from degeneration or preponderating dilatation, dyspnoea becomes an exceedingly distressing symptom, and may be present, though in a less degree, even when the patient is at rest. Palpi- tations may also be an annoying feature, and there may be sharp or dull pni'cordial pains with areas sensitive to pressure, the same as in mitral regurgitation. I am imable to recall a single instance in which there was typical angina pectoris.
In other cases there is a sense of pra:K»ordial fulness or dis- tention, particularly upon exertion. ^lore or less vertigo declares itself upon the patient suddenly assuming the erect position, or he is annoyed by a feeling of fulness or confusion in the head. This, which is a symptom of passive cerebral congestion, often amounts to actual headache. Insomnia, disturbing dreams, and other effects of venous congestion become more and more pronounced, and the patient passes into the stage of completely destroyed com- pensation.
Oidema, which is at first confined to the ankles and tends to disappear over night, creeps upward into the thighs, rendering locomotion difficult and painful. Owing to the feeble, rapid, and arrhythmic action of the overdistended heart, the pulse is thready,
MITRAL STENOSIS
257
perhaps unequal in the two wrists, intermittent, an J often ex- tremely ditMeult to count. This intermittence niav be due to cardiac intermissions, or to such an inequality in the force of the heart's contractions that some of the blood-waves fail to reach the wrist. The hands and forearms may be cold, and the superficial veins stand out prominently in striking contrast to tlie emptiness of the arteries.
Pulmonary congestion declares itself by increased dyspnipa tliat may even amount to orthopno*a, hy cough and sero-mueous or sero-sanguinolent sputum, Julness at the bases of the lungs, par- ticularly behind, and by copious, moist rales. If the tricuspid valve gives way, permitting regurgitation into the auricle^ the turgid jugulars pulsate. The liver, already swollen, perhaps ten- der, growls still more engorged, and likewise pulsates synchro- nouslj with the epigastric throbbing of the dilated right ventricle and the so-called positive pulse in the cervical veins. The taking of food is attended with firrnuition of gas that distends the stom- ach and bowels, adding greatly to the patient's distress, and ren- <Iering ade*]uate uourislunent ditficult. The sufferer frequently e^imjdains of dull or burning pain in the pit of the stomach, and is t*»ruu'Ut*'d by an intolerable thirst. Congest i<ju of the liead is ghnwn by duskiness of the countenance, swimming of the head, or headache, and insonmia. In some cases there is a eiuidltion of somnolence, and the sniTerer falls into short, un refreshing oaps, which are disturbed h}' dreams, and from which he awakes w^ith a start. The skin is not infrequently bedewcfl by a cold sw^eat, which about tlie bead and neck may be so copi<*us as to run off in trickling streams.
Stasis within the renal veins leads to scantiness of the urine, which is dark in colour, loaded with urates, and often contains albumin and easts. The action of the IkiwcI becomes irregular and constipated, or as the dro[)sy invades the abdominal structures the patient may he annoyed by frequent scanty, liquid stools. Con- gestion of the btemorrhoidal veins sometimes gives rise to addi- tional distress. Disorders of the pelvic viscera are common at this time in the female; the catamenia are apt to be scanty and irregular, and lencorrlwea is not uncommon. Day by day the dis* tress of the patient increases ; during his w^akiug hours he longs for the relief of sleep at night, and by night his discomfort makes him 17
258
DISEASES OF THE HEART
long in turn for tlie days. Days drag on into weeks, and not infre- quently weeks into months^ with ever-auginenting dropsy, whieL at length invades the serous cavities (Fig. 43). Ascites and tumefaction of the abdominal walls intensify pressure iip«:»n
the diaphragm and abdominal vesseU^ rendering breath- ing still more la- boiired* The pres- sure thus occa- sioned still further imiM»*les the re- turn tlow from the veins of the low- er extremities, and euuses an increase of anasarca. If hvdrothorax now sets in, the pa- tient's shortness of breath becomes ex- tronio, and he is- obli^fd to 8ii]ijK*rt I) is bixly by resting his arms on a table in front of him. I have knowm a suf- ferer from mitral disease in this stage to remain thus for several weeks, not venturing to leave her chair. Fortunately for tliese patients, nature is not able long to maintain the uneipial struggle, and unless treatment brings relief^ death does so ere long.
Occasionally in this extreme stage the end comes through sud- den stoppage of the heart, but as a rule it is the result of some one of the causes that will be narrated in the part of this subject de- voted to the mode n{ death.
Physical Signu.— Inspection is apt to detect more or less cyanosis, and in pronounced cases there may be distinct bluenesa
^ Ai-K fJF MiTKAL STENO.mr*, showing AsCITlS AKl> (^LLBBI?(0 or FlNC}£K-Ttr».
. AU|>erficm] aiiU duefMcated dulnoAS are indioatc^L
MITRAL STENOSIS
259
of the lips and finger-tips. Patients, particularly children, who have had the disease for years usually display clubbing of the terminal phalanges. Often there is bulging of the prtecordium, particularly at the lower end of the sternxim, as well as visible epi- gastric pulsation. If compensatory hypertrophy is great, and lung- borders are retracted, the eye may discern a systolic pulsation over the body of the heart and a short diastolic shock in the pul- monary area the same as in regurgitation. The apex-beat is usu- ally feebk^j and not likely to be outside of the nipple or belo%v its usual situation.
Palpation eoiifirnis the impression received by the eye, but in addition detects a thrill at the apex, which, preceding the ventricu- lar impulse, is known as presi/stoUc. This thrill resembles the purring of a cat, and hence is called ** fremissement cataire." It may be short and soft, or rough, and extend throughout the greater part of diastole. In some instances a sliorter, feebler thrill fol- lows the second sound, oeeupying the forepart of the diastolic period. The presystolic thrill is found to lead up to, and termi- nate in a short, sharp systolic 8b€>ck or ** thumping "' apex-beat. This thrill is often so short as to convey the impression of the apex-beat being split, the second of the two impulses being the shari>er and stronger. A shar]» stroke, imparted by tlie sudden closure of tlie pulmonie valve*, is sometimes felt distinetly in the second left iutersimee, close to the sternum. Kpigastrie pulsation is generally pronounced, and gives the impression of a powerfully contracting right ventricle.
In compensated cases of stenosis the pulse is small, feeble, and regular, and less rapid tiian in mitral regurgitation.
There has been much controversy j chiefly among the English, as to whether tlie pulse of uiifral obstruetion or of insufficiency is the more likely to be irregular. This, in rny opinion, is a matter of slight practical imivortanee, and yet in my experience I have found the pulse to be more often irr^ular in regurgitation than in stenf>sis.
The annexed sphygmographic tracing (Fig, 44) is from a case of pronounced mitral stenosis in a female, and shows the pulae small, of high tension, and regular. When pulse-tension is pro- nounced, it is due to capillary resistance and not to tl;e energy of left ventricular contraction. Concerning the irregularity of the
260
DISEASES OF THE HEAHT
Fio. 44. — SrHVuMooRAM rROH Casv: of
MiTicAi, STRhfwta,
(Persotud observaUoti. I
pulse in mitral disease, it may be again stated that observations of Radizewsky appear to prove that the character of the pulse in this respect de|>enils upon the state of the niyoeardiuni of the au- ritdei^. When this is healthy, the pulse is regular; when degenerated, either fibroid or falty, the pube l>c*eoine§ irreg- ular, even arrliythiiiic.
Popoff has called attention to the occasional oceiirrenw of a pnlsus differens in this disease, by whitdi term is iiu»atit an ine- quality in the two radial pulses, the left l>eing the smaller. As this is oliserved when t*onippntiation is destroyed, and may dis- appear with restoratinn of i-ardiae energy, PopotI attributes the iuoijuality to pressure of the greatly dilated k^ft auricle on the left suhcdaviau artery. Preble has also notieeil its occurrence in some of his cases. As pulsus differens may also be produced by aneu- rysm, embolism, thrombosis, arteriosclerosis, etc,, it is important
that Jill such causes Ik* ex- cluiled l*efure the phenomenon is atrrilKited to extreme dila- tation of the auricle, a matter that nuiy l)e of some moment in prognosis.
Percussion shows a simi- hir t'haiige in absolute and Illative canliac dulness as de- -^•iibe<l in the article on mi* tral regurgitation — viz., an inrrfase of vardUic dulness towards the right side and dottnirfit'd (Fig. 4')). This increase bears a direct rela- tion to the degree of stenosis. According to Leu be, percus- sion shows a more pronounced enlargement of the right heart in this form of mitral di'^ease thnn in insufficiency, a point he regards as of importance in the differ- ential diagnosis between these two affections.
I
Fio. 45.-— Location or Apkj«-brat and
AbKA or IlEEf'fltATEP Dui*l«^Rftl IN Mr- TKAt StEKOSIS.
MITRAL STENOSIS
261
Another diiference lies in the fact that, owing to atrophy in- stead of hvpertrojihy of the left ventricle, diilness is not likelj to be much if at all increased to the left
Auseultation. — In pronounced eases of mitral stenosis, auscul- tation at the apex of the heart detects a murmur of such intensity and distinctive character that it at once fastens the attention of the examiner. In most instances it is a lon^-drawn, rough bruit, which, beginning after the second sound, runs up to and termi-
Fi«. 4<k— RuYTHH or Characteristic MiRHrR of Mitral Stsiko«ia,
" AuBICULAB-SYiTOUa*'
nates abruptly in a clear, sharply accented first sound* The mur- mur is spoken of, therefore, as presystolic, an<] in tins respect cor- responds exactly to the thrill already described. When well marked, this presystolic murmur is so striking as to be almost pathogiu>monic of mitral oltstrur-tion (Fig. W).
The rhythm of this bniit, by which is meant the time of its occurrence*, has been the subject of considerable controversy, for the reason that some observers have declared it to be in reality systolic and only seemingly presystolic. The generation of the first sound, say they, is delayed in consequence of the rigidity of the mitral valve, and hence, although the murmur begins with the contraction of the ventricle, its occurrence prior to the first tone gives it the appearance of preceding ventricular systole. The arguments in support of this opinion have never convinced me of
262
DISEASES OF THE ElEART
its correctness, and consequeiitlv I regard the bruit as tnily pre- systolic.
When we reflect on the physiology of cardiac action we see that a mil rum r which is audible before ventricular systole is generated during dias*tole, and iliat therefore the ninmnir of mitral stenosis is diastolic* This is not all, however; the bruit in most case.s is plainly heard to Ix^gin in the latter portion of the long pause— i. e., the diastolic interval — and to end exactly with the first tone* It h sviiehrMnous, tlierefi>re, with the contraction of the left aiiri- e!t% wliieli, UA we know, takes idaee imniediately before that nf the ventricle. For the reason, then, that the murmur is generate dur- ing auricular systole, (iai rdner long ogo proposed the name for it of rlie '* auricular sy.Hiidic *' tiiiirnmr.
This term is too restricted, however; since, as is well known, the bniit in some eases commences before the contractiou of the
auricle, in fact inunediately after the second sound, and lasts throughout the lung pause. It is conseipiently a diastolic and not always an auricnlar systolic murmur, and as such is in contrast to the systolic one of mitral re- gurgitation. If has also been called the *' mitral direct " murmur, l>c*eause transmitted in the <li reaction of the ldoo«b stream — i. e., from the mitral opening directly to the apex of the left ventricle. Indeetl, it may be state<l en passfnity that all limits of stenusis are called direct and those of re- gurgitation indireet nnirmurs. Considering, then, the designa- tions that have l>een given to the murmur in question, the Viest is the one in most general use, wliich is presystolic.
The nuirmur is heard most distinctly close to the apex-tteat, not directly at tlie seat of impulse, but slightly within and above, at the point, in fact, where the thrill is felt moat plainly (Fig.
Fi«. -17.— Akea or AruiiiiLi'n* or tub Pre*
gYKTCILIi? MtRMl'tt or MiTHAL StKNOSIA.
It b frequvnllf litnitfed to this area.
MITRAL STENOSIS
263
47). Its area of audibility i« sometimes very limited, being con- fined to the immediate proximity of tlie apex, but I have knowE the murmur to be audible for a considerable distance in all direc- tions, although even then it is not transmitted so widely outside of as inside of and above the apex-beat.
The quality or timbre of the bruit is exceedingly rough and harsh, so that it is frequently described as rolling, blubbering, spluttering, etc. Balfour Impjdly describes it in some instances as sounding like V-cM>t or the soimd produced by the attempt to roll out the letters R-r-b, or when still more prolonged R-r*r-b. The final consonant of these combinations is supposed to represent the short, sharp first sound that terminates the bruit. The mur- mur never possesses the soft, blowing quality of the mitral regur- gitant murmur, since obstruct Ive bruits are ahvays rougher Ikan those of refjurgitafion.
The length and intensity of a presystolic murmur are influ- enced by posture and ihe rate of cardiac action* Thus a bruit, which is short ami rather indistinct when the heart is beating rapidly, or when the patient is standing, is very likely to increase appreciably in duration and to display its true character more dis- tiiictly after the individual has lain down and the heart's action has lieeome slower. In other instanees the reverse obtains, the bruit being most distinct in the erect pr*sture. One should aus- cultate in all positions and under varying conditions of cardiac action.
Another peculiarity of the mitral direct murmur is its change- nbiliiy^ by which is meant that it is not ahvays the same in dis- tinctness at ditferent times. I repeal 1 vividly a woman in whom on several occasions I felt certain of the existence of a mitral presys- tolic nmrrnur. On one f>ccasif>n, however, after an absence from observation of several months, her heart presented no such mur- mur as I had heard before, but instead a feeble first sound accom- panied by a faint systolic whiff. Some weeks subsequently, after having taken iligitalia and strengthened the contractions of (he left auricle, the old-time presystolic murmur reappeared. Broad- bent regards this changeability as of great significance in the dif- ferential diagnosis V)etween stenosis and regurgitation.
The foregoing description applies to most cases of mitral ob- struction^ but not to all, and as it is the exceptions that are every
264
DISEASES OF THE HEART
now and then encountered, they will now bo de§erihed. In some iiistanees the bruit is so short that it is scarcely recognisable as separate from and jtreeeding the first sound. T have generally noted in i^nch cases, however, that the first sound is short and thumping, and aiijicara to have pretixed to it a short thrill, which causes tlie impnise to convey to the hand the impression of its having stidden up to its maximnm instead of having given a clean thrust, as does the healthy heart. Difficult as it is to recognise tliis indistinct or abortive muriuurj it is extremely important to lie able to do so, since it is in the detection of obscure signs of disease that the skilled physician differs from his unskilled enllengno.
The reverse i»f this short, scarcely recognisable bruit is the h:»ng-drawn nuirmur, wiiich Traube first described and designated the '* nuHlitied presystolic uiurmnr/'' This is the murmur which, eouuuencing directly at the close of systole — i. c, immediately after the second sound — extends through the long pause of dias- tole» and ends witli t!ic next first sound (Fig. 4s). A nut at all infrccjuent auscultatory finding is a short murmur occurring after the second sound and known as earfy diastolic^ and which is
Fi». 4S.— Rmytmm of Ooca«iofal Vabtfty c>f Mithal Stenotic; Mi^kmor, throuoh
EKTtni VltNTRIC?ltLA« DlAsTOLK,
then succeeded l>y a short period of silence, and then a character- istic presystolic miiruair (Fig. 49). This anouiiily is therefore a breaking in two, as it were, of the long murmur, and by Fraentzel
MITRAL STENOSIS
265
was called the " interrupted modified presystolic murmur.^^ It is very dia/^iiostic, but may easily mislead an inexperienced auscul- tator. Should such difficulty of interpretation arise, error may be
'-I
FlO. 49,—^ IlO'ERRtTPTED Moi»lFlED pRE»Y«n>LlU ** MuRMUa OF MtTRAL STKyoetS.
aroidecl hy due attention to the associated secondary physical signs and to the njoditications of the heart-sounds soon to he described.
Another departure from what is usnally heard in mitral ste- nosis is tlie retention of the presystolic luniit and of tlie first sound without a second sounds or of the miinnur alone ivithout either of the cardiac tones. Attention h directed to these anomalies by Broadbent, who states that under such circumstanceB it is posaihle for the murnnir to he mistaken for a systolic one followed by a second sound, or for the bruit to be considered systolic, and to have replaced the sound altogether. Care should be taken to avoid such an error, since a systolic nnjrmur means regurgitation, and for sake of prognosis as well as treatment stenosis should be recog- nised as such whenever it exists. A mistake can probably be avoided by palpation of the carotid pulse, when it will be found that this is preceded by the murmur.
Such comparison of the time of the murmur with that of the carotid pulse is likewise valuable when, as stated by Fraentzel, the presystolic murnnir disappears in the last weeks of life, or be- comes merged into a systolic one.
The various modifications in rhythm and intensity of the
DISEASES OF THE HEART
mitral obstructive murmur are due to differences in the rapidity and force with which the blood flows through the narrowed orifice. It is conceivable — e. g., that during the fore part of diastole blood flows too gently into the relaxed ventricle to produce sonorous eddies and vibrations. When, however, it is energetically pro- pelled by auricular contraction, eddies or currents are generated of sufficient force to give rise to the presystolic murmur. In the same manner a diastolic murmur following the second tone owes its production to sonorous eddies generated as the blood gushes out of the auricle into the ventricle. Then as blood-pressure in the ventricle is raised, vibratory, and hence audible currents cease for a time, imtil auricular systole again throws the blood-stream into sound-producing currents and eddies. Xarrowing and rough- ening of the mitral orifice furnish all the conditions essential fori the generation of eddying or whirling currents in the blood-stream' as it passes the ostium. Yet if the blood-flow is languid the eddies within it may fail to set up vibrations of sufficient force to be con- ducted to the ear or hand of the examiner. This explains why shortly before death or during times of great cardiac feebleness the presystolic murmur may disappear, and why it reappears as heart-power is restored.
Heart-sounds. — The recognition of the characteristic murmur of mitral obstruction is not enough ; it is necessary to also study and recognise })oculiarities in the heart-sounds. In well-marked cases the first tone at the apex is short and valvular, or, as is said, " thumping." This quality is so peculiar and striking as to be quite distinctive and of itself sufficient many times for an experi- enced auscultator to make a diagnosis on it alone. It is the audi- tory impression of the sharp, quick tap that forms the apex-beat in this disease.
The second sound at the apex may be distinct, but in most cases it is indistinct. At the base of the heart it is sometimes split or reduplicated in consequence of the pulmonic valve being closed a fraction of a second later than the aortic, according to the law that the valve closure is delayed in that artery in which blood- pressure is the higher. In addition also the pulmonic second sound is accentuated.
The phenomenon, however, which is of greatest interest in many ways is what is termed the simulated or apparent doubling
MITRAL STENOSIS
267
of the second sound. Tliis is to be distinguished from the split- ting of the second sound at the base. It is limited strictly to the mitral area, soinetiines to the very site of the apex-thnist, and con- sists in the occurrenoe of a third tone, which immediately follows the normal second sound. English clinicians have given much study to this apparent doubling uf the second sound, and have offered a variety of explanations for its occurrence. The most reasonable theory is, as suggested by Sansom, that it is in some way a sound of valve-tension being prod need as the blood gushes forci- bly out of the auricle into the ventricle. This seems borne out by the observation that this sound sometimes becomes changed into, or replaced by an early diastolic murmur. Sansom states also that tliis double sound is board at some time or other in all cases of mitral stenosis, and indeed may in some instances be the only indi* cation of the lesiom
When this auscultatory phenomenon is present^ together with a presystolic murmur, it forms a very striking assemblage of sounds that cannot possibly be mistaken for any other condition than mitral stenosis.
I have known this duubling nf the second sound to be inappre- ciable when the heart was not strong, and to come out clearly and beautifully as treatment restored cardiac power. When the heart beats slowly and regularly it is a matter of no ditlicultv to differ- entiate the several sounds and murmurs beard in mitral stenosis. When, on the contrary, the rhythm of the heart is disturbed, the impression may be received of an indistinguishable jumble of sounds, both uurmal and adventitirms. Thus, I have a nuile pa- tient with a rheumatic mitral narrowing combined with a slight degree of insufficiency who presents such a jumble, Wlien, as now and then hai>i>ens, his heart's action is tolerably slow and regular I hear the foil owning: A rough presystolic murmur ending in a thumping first sound, then an exceedingly brief pause, followed by a doubled, or apparently doubled, second sound, which in its turn is succeeded by a short, early diastolic murmur and a short silence preceding the next presystolic bruit. At times a short sys- tolic murmur accompanies the tirst sound, and as this heart is gen- erally very irregidar in rhythm it can l>etter be imagined than de- 8cril>€Hl what an unintelligible mLxture is made by its sounds and murmurs.
268 DISEASES OP THE HEART
Diagnoflis. — The diagnosis of mitral stenosis is usually a comparatively simple matter. It may, however, be difficult and next to impossible to say whether it or insufficiency is present. Such a diflFerentiation is important, however, from the standpoint of prognosis and treatment, and should be made when possible. As aids in this direction are the following: (1) Sex, stenosis being more common in females, regurgitation in males. (2) The short, sharp apex-beat preceded by a thrill of longer or shorter duration. (3) The greater extent of dulness over the right heart in stenosis with stronger and more distinct epigastric pulsation.
(4) A rougher lower pitched murmur occurring in some portion of the diastole, usually presystolic, but often also early diastolic.
(5) Doubling of the second sound, limited strictly to the mitral area or to the apex. (6) The likelihood in stenosis of more pro- nounced secondary effects in other organs than the heart. (7) The greater smallness and feebleness of the pulse in stenosis, and the greater likelihood of arrhythmia in regurgitation.
As a matter of fact differential diagnosis is not likely to be difficult except in the stage of lost compensation, and then less de- pendence must be placed on the auscultatory findings than on the evidences of greater secondary effects in stenosis.
In all cases the question of ascertaining the exact nature of the lesion is not all of diagnosis. One has also, or in addition, to decide the degree of the lesion and the severity of its effects, and whether or not the findings account for the symptoms complained of. The degree must be determined by careful consideraticm of the munmirs, sounds, and secondary effects. The longer the pre- systolic niurnnir, the more thumping the first sound and apox-beat, the greater the enlargement of the right and the smaller the left ventricle, the feebler and smaller the pulse, the more ])ronounced the evidences of secondary effects on the liver — then the more pro- nounced will be the degree of narrowing. The association of a mitral regurgitant bruit points to a medium degree of stenosis, and so, according to Sansom, does the simulated doubling of the second sound at the apex.
Dyspna^a on even slight exertion, as slow walking, great prone- ness to cough, and other signs of bronchial congestion, a feeling of weakness and fatigue out of proportion to the effort occasioning it, scantiness of urine, emptiness of the arterial system — are all symp-
MITRAL STENOSIS
%fm
^ns indicatire of serious circulatory eiubarras^ment, and atlribu- table to the valvular disease.
On tbe other hand, neuralgic jmins in the prt>»eordia and a feeling of fulness or uneasiness in the canliac region, coldne.*^ antl numliiiess of one hand and not the other, or of tlie hand?^ and not the feet, heudaehej and prolonged vertigo, tlie paiient hein^ <)niet and the pulse not feebler than usual, a feeling of nervout^nesH luul restlessness — may all be neurotic iiiaHifestatiniis ih^peiiding on de- fective nutrition or elimination, and in sneli cases are a[M to Iki out of proportion to the degree of the lesion and to symptoms dii- tinetive of cardiac disease.
Prognosis. — ^In general, tins is less fiivonrMlde llinn I hut of mitral jncunipctenee, and for two reasons: ( 1) Olislnict'hni is con* Slant and tends to greater stasis in the pulmonic vessels, in conse- quence of which the left auricle and right ventricle arc HtdtjecUMJ to greater strain. They are likely, therefore, to break in (heir com- pensation at an earlier period. (2) ilitnd sfiTiohiK in a profjtrH§' ive lesion^ and oiay under the influence of rej>eated attaekj^ of Huh- aeute rheumatism become at length so extreme that life cannot lie maintained.
When the narrowing is pronounced there in but a jninall vol- ume of blood ejected into the arterial system, general nutrition U correspondingly poor, complications on the part of the lungn ii r6 more likely, outdoor exercise is difficult if not impcjssihk% normal metabolic processes are interfered with, and ^meral nutrition becomes verj^ defective.
In a word, even when tineomplicate*! and apparently well cfnn* pensated, mitral stenosiii offers an exceedingly grave prifpitmit^ Hy some authorities tbe average length of life i§ Mrt d4>wii aa not far from ten years. It sUii<U next to aortk mguigitatjoii to point of gravitT-
Tlte following figures are of mWiregt as fbowing tbe Brerug^ t age at which death took place in iereral i0rt«« of emtm. Of San* ■V ^1 caaea death oeenmd af 32.7 jwari^ In Ha/dra'a 42 cmm Fdealh look plan at 37J» nam Of Bmadbenl'i M emtm k ^ eurred at Z3 years fm niaka, and 37 to Z^ for f«nial«a. Saanrnji found that at Gtiy^f Hovpital dirriof a paf4od of tJfi y«afi tbi ararage kngib of lif'' ff^ brjtb aasaa vaa S$JiZ jears ; in Ims pifi^ nomittd fonnay 4Z.^ yean ; mmm mumum mmB, 98.$
270 DISEASES OP THE HEART
The influence of age, habits, occupations, environment, etc., will be considered in the chapter devoted to Prognosis in General.
Mode and Causes of Death. — Death in cases of mitral stenosis results most commonly from increase of cardiac asthenia, the same as in mitral regurgitation, or from the overpowering eflFects on the heart and lungs of hydrothorax and stasis in the pul- monary system. Pulmonary infarcts are particularly liable to occur, and are then the immediate cause of death. Sudden death is possible, but is not likely except in the terminal stage, when sudden exertion may bring about diastolic arrest of the already overburdened heart.
Even when compensation is fairly good the patient may at any time succumb to an attack of acute bronchitis or pneumonia. A lad of sixteen, whose compensation allowed him to occasionally enjoy a hunting trip, contracted a cold on such a trip, and died two days thereafter of what was thought by his physician to be extreme pulmonary congestion. An attack of acute pulmonary (rdema is also a possible cause of death the same as in mitral re- gurgitation. In one case coming under my knowledge obstinate vomiting contributed largely to the fatal result by preventing retention of food and remedies. The end apj>eared to come as much through general as cardiac exhaustion. Death may be preceded by mild delirium, or consciousness may l>e retained to the last.
Of 24 cases analyzed by Hustedt with reference to causes of death, he found heart-weakness in 8 cases, pulmonary infarct in 1, pneumonia in 4, pulmonary collapse in 1, emphysema in 2, apo- plexy in 3, bronchitis in 1, pleurisy in 1, meningitis in 1, perito- nitis in 1, and delirium in 1.
The following cases illustrate so well many of the features that have been dwelt on in the foregoing pages that they are here appended :
Mrs. C, Irish-American, aged thirty-four, was admitted to St. Anthony's Hospital, Xovember 20, 1900, complaining of breath- lessness on exertion, cough, and frothy white sputum. Both par- ents had died of heart-disease, but three sisters and one brother were living and healthy. The patient had had measles and pertussis in childhood, but no rheumatism. She had been married thirteen years, had six children, of which the youngest was three, and had
MITRAL STENOSIS
271
had six abortions, all of whicli she had herself induced* and which had not been followed by ebill or fever* During the first pregnancy she had had a^dc-ma of the left leg^ passed no urine for two days, and had come near '* smothering/- Her physician declared she had *' water around her heart/' and had tapped her, but she could not say whether water had been obtained or not She had been troubled with dyspna^a on exertion for a number of years, and this had always been particularly bad durinsj her pregnancies.
Exanjination showed a wonum of medium height, weighing 114 pounds, slight cyanosis about lips, cold, moist extremities, and pulsation of the external jugu- lars, tongue having a whitish coat and indented by the teeth. The pulse was KH, compres sible, and irreguhn- in ftirc* and volume, but tliere was in* pitting €»f the skin over the ankles or elsewhere. The aj^M?x4>eat was in the sixth in- terspace, 4r^ inches to left of the midsternal line, of tlie cluiracter of a faint tap in an area of diffused impulse (Fig. 50), A presystolic thrill ran up to and ended with this faint, sharp tap, and there was marked ejiigastric pulsa- tion. Relative dulness wm in- creased in all diameters, from third interspace to sixth, and from 2 inches to right of median line to 5 inches to left of the same. The first sound was thumping, beard throughout pra'cordia, and followed quickly by a scarcely perceptible second sound, the aortic second being weak and the pulmonic second markedly ai-eentuatctL A harsh murmur of greatest intensity in the mitral area Ixgan im- mediately after the second, ran up to and ended with the next ensuing first sound, and was not transmitted into the axillary re- gion. The lungs revealed impaired resonance at the |)osterior baseSy with some moist rales. The liver was palpalde two finger- breadths below the inferior costal margin^ but the spleen was not
IHl>e#« in Ca«i uw UvntAh Stxmoau (p. t2T0),
272 DISEASES OP THE HEART
palpable, and there was no evidence of free fluid in the abdomen. The urine was scanty, dark-coloured, and contained a trace of albu- min. The temperature was 98.6° F. and respirations 28. Her stomach was very irritable, and for several days she had not been able to retain nourishment.
Four hours after her admission her pulse had increased in rapidity and feebleness, and so few of the pulse-waves reached the wrist that the heart-rate had to be counted with the stethoscope. It was beating 180 per minute. Cyanosis had deepened, cough and dyspnoea were very bad, rales had grown more numerous, and the liver had increased in size. Her condition was so critical that she was given a hypodermic injection of ^ of a grain of morphine with ^ of atropine, nitroglycerin yj^j^, and ^ of sulphate of strych- nine, this latter to be repeated every two hours during the night. An ounce of sulphate of magnesia was also administered, and a few hours subsequently she was put upon 10-minim doses of tinc- ture of digitalis every four hours. By the next day her condition had improved materially, the pulse coming down to 134, and being rather more regular, but the strychnine, digitalis, and a daily dose of salts were continued. Without detailing all the fluctuations of this patient for the ensuing ten days, it may be said that the pulse showed ever-recurring vagaries, being at one time fairly regular, all waves reaching the wrist, and at others being rapid, irregular, and intermittent. The liver also varied in size, dimin- ishing and increasing according to the persistence and regularity with which the salts were administered. The cough, however, gradually grew less, expectoration diminished, pain left the epi- gastrium, she retained nourishment, and as a rule got several hours' good sleep each night. As the condition improved, the strychnine was lessened in frequency of administration, but the digitalis was continued. At one time indeed its action was sup- plemented by strophanthus. At length, bv Xovember 80th, her pulse-rate averaged 84, and it was recorded that all the waves reached the wrist. Dulness and rales had left the lungs, but the liver still remained palpable, although smaller in size. The pa- tient then left the hospital abruptly. Two months subsequently she again re-entered, complaining as l)efore of cough and expec- toration, but showing no dropsy. Treatment again benefited her, and she again withdrew from observation. I am indebted for
MITRAL STENOSIS
273
the notes of tkis case to Dr. J. K. Yung, one of the internes at
the time.
This ease illustrates fairly well the sraiptoms and amenabil- ity to treatment of a case of mitral stenosis in which compensa- tion was broken, bnt not irreparably so, and in which, with signs of stasisj amounting even to a relative incompetence of the tricns- ]>i»l valve, there was no cede ma. In fiii't, the brunt of the dis- turbance was borne mainly by the lungs, the duluess auj rales, the dyspnci^a, cough, and frothy expectoration being the result of the great pulmonary engorgement. It is hard to explain why in such a case oedema is absent, whereas in other individuals with afiparently no greater stasis, dropsy will be a marked and dis* tressing feature. It certainly seems tu uorruborafo the view that dropsy depends upon the state of the blood mid nutrition of the capillaries, as well as upon the degree of capillary and venous engorgement. This patient subsequently succumbed to a third attack ill the hospital.
Mr. B., aged twenty-nine, tailor, consulted iiie January 9, 1900, on account of great breathle«sness u]h»u rhe slightest effort He gave a history of rheuma- tism four years previous* since which tiiue he had suffered with subacute articular pains. Gunorrhu'a six years ago, with stricture at present time. With the exception of a *' bad eye/' nature unknown, at six years of age, has had no other illness. Heart l>egan to trou- ble him one year after the rheuuiatic attack, but was not treated for heart-disease until the summer of 181*9. His symptfiins were great dys- pnoea on effort, coiigli once in a while at morning and evening, vertigo upon exercise, some pain between the shoulders, and poor appetite, but sleep good, Uis pulse %vhile sitting was weak, small, regular, and 00. The 18
Fio. 5L— LofATinx OF Apex and Rklativ* DcL^Eim ijr Caas or MiTUAL Srsifoftw
AJfO REOCRrtlTATION (p. 27S).
274 DISEASES OF THE HEART
examination of the heart discovered the weak apex-beat at the fifth interspace, nipple-line, 3J inches from median line, and preceded by a short thrill (Fig. 51). The apex-beat was not thumping, but there was marked epigastric pulsation. Abso- lute dulness was increased from right border of sternum, at fourth costal cartilage, to left of parasternal line. Relative dulness from lower border of third costal cartilage above to junction of sixth and seventh costal cartilages below, IJ inch to right of median line and to f of an inch outside of nipple. The pulmonic second sound was found accentuated. Second sound was not doubled at base, but limited to area of the apex-beat was an apparent doubling of the second sound, the second element at times having the character of a short murmur, and separated from the following presystolic murmur. At lower inner edge of the apex-beat the first sound was also doubled at times.
A short, rough presystolic murmur was found just within, and a blowing systolic at the apex. The murmurs and sounds made a rolling, tumbling rhythm. In dorsal decubitus the appar- ent doubling of second sound was very marked at inner edge of apex. As the heart occasionally slowed, the first sound was found also doubled, the first element replacing the presystolic murmur. The systolic murmur became plain and whistling with a very pro- nounced blow 2 inches to left of nipple. The liver was palpable a finger-breadth below the costal arch.
The diagnosis made was mitral stenosis and insufficiency, with secondary cardiac hypertrophy and dilatation.
Mrs. A., aged thirty-three years, weight 115 pounds, height medium, American, was examined March 29, 1901. Her father was living, but had cough, while a maternal uncle and a maternal aunt had died of consumption. At eighteen she had suflFered from a severe attack of inflammatory rheumatism, and had had more or less joint pains for three or four years subsequently. Of chil- dren's diseases, she had had a mild attack of scarlatina when a child, and thought that during her childhood she had also had pleurisy. She had had a second pleuritis a year prior to her examination by me. Her present illness dated back to 1S91, when she first began to have a cough, but lior symptoms had grown much worse for the last year, and she had grown percep- tibly paler. In the way of symptoms, she complained chiefly of
MITRAL STENOSIS
275
chronic cough, which was most troublesome at night, and of con- siilerable yellowish sputum, in which tubercle bacilli were said to have been discovered. She noticed shortness of breath in walk- ing and ascending stairs. The appetite was prmr and the diges- tion weak, although bowel movements were regidar, as also were the menses. Sleep was disturbed by the cough, and there was slight pain in the right hip and the left side of the chest near the shoulder. The voice was husky, but it may be said in passing that laryngoscopic inspection revealed no infiltration of the larynx.
Hxammaiion, — The pulse was 105, small, regular, and of no- tieeably low tension. The temperature taken at 12 m* was 99^ F- Respirations were shallow, but not hurried. The chest was mod- erately emaciated^ 'rery shallow in its antero-posterior diameter, and flattened both above and below the right clavicle. Vocal frem- itus was increased at both apices, particularly the right. Upon the right side, dulness extended from the apex to the third inter- space in front and to the middle of the scapula behind^ shading off to impaired resonance as far as the tip of the scapula and below this point, becoming again more pronounced towards the posterior axillary line. In the right infraelavieular region there were bronchial breath-sounds, looist riiles of varying size, and the voice-sounds were so concentrated and hollow as to strongly suggest a cavity. Posteriorly, respiratory sounds were also bron- chial, and the act of coughing developed numerous tine and coarse crackling rales os far do\m as the inferior scapula angle. At the left apex there was impaired resonance both front and back to the level of the second rib, and over this area breath-sounds were broncho- vesicular, and cough produced crumpling rales that ex- tended below the limits of alight duJ less.
The apex-beat was situated in 'he fifth left interspace slightly within tlie nipple-line, was feeble, and of tlie character of a quick thum]>, and was preceded by a s^hort yet distinct thrill that ended with the cardiac impulse. Relative heart's dulness was somewhat increased towards the right and downward, but did not reach beyond the vertical nipple-line at the left (Fig. 52). Upon aus- cultation the first sound at the apex was short, sharp, and thump- ing, the second sound was not doubled, and the pulmonic second tone was markedly accentuated. A rather short, roiighj distinctly
276
DISEASES OF TlIK !TEART
presystolic Biiiriunr ran up to and ended abruptly with the sharp first sound, and was of greatest intensity in the i^tanding i^osition.
A high-pitehed systolic whiff accompanied the systole in the mitral area, but was not trans- mitted to any appreciable dis- tance outside this area.
The alMlomen was flat and .'«-'-- thill, the lower hepatic border
I \ distinctly palpable and tender
to pressure, and hepatic dnl- ness reached from the upper margin of the sixth rib in the mamillury line to slightly he- low the inferior costal arch.
The dia^osis was clearly chronic pidnionary tuberciilo sis with softening and vomica in the right lung, incipient disease of the left npper lol>e, mitral stenosis of first degree, with probably some regurgitation, the vahnilar lesion being of rheiunatic origin and in good com- pensation.
This case is interesting because of the rather rare association of pulmonary tuberculosis ami mitral stenosis, and would seem to corroborate the view that this valndar lesion is sometimes of tuberculous origin, were it not for the very definite history of inflamnuitory rheum at ism at the age of eighteen. It likewise shows the fallacy of Rokitansky's statements concerning the an- tagonism between mitral stenosis and consumption. It is worthy of note, however, that in this case the narrowing was not extreme and was combined with regurgitati€*n, a form of mitral disease wdiich is m^t so infrequently associated with pulmonary tubercu- losis as was once thought.
Furthermore, this case raises the very interesting query if this stenosis may not have exerted a retarding influence ujwn the progress of the lung affection, although in this connection it should be stated that her residence has been in southwestern Kan- sas, where the air is dry and the altitude not far from 2,000 feet
Fit!. .Vl — LtHATI^tK **t AfEI AKD RkLATIVK
MITRAL STENOSIS 277
For my part I am much more inclined to attribute the slow ad- vance of the pulmonary affection in this case to other factors, possibly to climatic influences, possibly to inherent mildness of the tuberculous infection itself, rather than to the mitral obstruc- tion, since, as suggested by Sansom, it is reasonable to assume that a valvular lesion would have a tendency to impair the resistance of the organism, particularly in one inheriting a predisposition to tuberculous disease.
CHAPTER VIII AORTIC REGURGITATION
In this fonn of valvular disease a portion of the blood dis- charged into the aorta with each ventricular systole leaks back into the left ventricle during its diastole. Although relative in- coni]>etence may be proiluced by dilatation of the aortic ostium, the disease in question is in the vast majority of cases due to structural defect of the valve itself.
Morbid Anatomy. — Defects in the aortic valve leading to regurgitation are as nearly analogous to those found in mitral re- gurgitation as the anatomy of the valve will allow. They may follow acute endocarditis, or may be the result of a non-inflamma- tory sclerosis. The latter is more often the case here than at the mitral orifice because the aortic valve has to bear the brunt of the increased blood-pressure due to muscular exertion.
The leaflets, one or all, may be retracted, curled, or shrivelled, so as to permit a free regurgitation. Old vegetations on the ven- tricular surface may interfere with tlu^ir complete apposition. In short, the conditions parallel those found in mitral insufticiency, with exception of the influence of contraction of the chorda^ ten- (Hneie and papillary muscles.
Acute incompetence may oc^cur during ulcerative endocarditis by the perforation of one of the valve-cusps. Very rarely a cusp may rupture during violent muscular exercise. The aortic semi- lunar valve is one of the most delicate structures in the body, and yet one of the strongest, sustaining as it does the whole blood- ])ressure of the systemic circulation. It is hence extremely un- likely that muscular exertion could be severe enough to raise blood-pressure to a height sufficient to rupture a healthy valve. Probably in such cases the valve has been weakened either by de- generation or inflammation.
As in mitral disease, regurgitation is often combined with 278
AORTIC KEGURGITATION
279
mwM'ifg^ of stenosis, but regurgitiition may occur without nar- rowing, and oecasionally, in cousequenee of dilatation of the ven- tricle, even with stretclnng, of the aortic ring. That such en- largement of the ring, leading to relative insufficiency, could take place, was long cluubttHl, owing to the great strength of the annuhis fibrosns, hut so many instances of the kind have been observed that there is no longer any room for doubt
The first effect on the heart is dilatation of the left ventricle. This is due to the impaet on its inner surface of the regurgitant Btream, which in very free n^gnrgitation re-enters with nearly the force with which it was driven out of the ventricle. Such lesions, however, are of grachial development, and the increasing work leads to a corresponding hypertruphy of the wall of the ventricle, which enables it not only to withstand the strain of the regurgita- tion, hut to exj^el the greatly increased volume of blood present in the chiimlH r at the beginning uf its systole. This by|>ertropby in aortic insuthciency is of early develoiJUient and often becomes so extreme that some of the largest hearts on record are those show- ing this defect. The wall of the hypertrophied ventricle may be as thick as 4 centimetres (If inch). The apex of the left ventricle projects far beyond that of its fellow, and the interventricular steptum is displaced, encroaching largely on the cavity of the Tight chamber.
As long as the mitral valve remains intact the effects of aortic f regurgitation upon tlu* heart are limited to the left ventricle. If, however, the mitral is incompetent, either from disease of the valve or rehitively from the enlargement of the ventriclo, the phe* nomena dcscrik-d as the results of mitral incompetency are added to those of the aortic lesion. In such an event, of course, the right heart is also enlarged, and the largest hearts have been those show- ^ing this coTul>ination of lesions. Such a henrt may weigh as much ras 3 or 4 ponnds. Indeed, von Ziomssen has reported 6 pounds as the weight of a specimen obtained from one of the great Stokes's patients. On account of its size such a heart is spoken of as cor hovinum. The heart presented to me by Dr. C, C O'Byrne weighs 2\ pounds, and in it the regurgitation could not have been extreme (Platp II). The point of interest in this specimen is the swinging vegetation, 3 centimetres long, and containing calcareous nodules, which evidently swung in the bloodstream, now in the
280 DISEASES OP THE HEART
ventricle, and again in the aorta, for on the intima of the aorta and on the mural endocardium of the ventricle, at the points where the vegetation must have struck, are marked atheroma- tous patches. There is said to have been a musical murmur during life.
The greatly increased force with which such a ventricle pro- pels the blood into the aorta throws great strain on the walls of that vessel, and hence atheromatous changes are often found not only in the aorta, but in the whole arterial system. That such change is due to this valvular disease is indicated by the fact of its occurrence in young and otherwise healthy individuals, in whom it would not be expected to exist.
When this valvular disease is the result of a general sclerosis, the myocardium is apt to be so degenerated as a result of coronary involvement that hypertrophy is not great. It is when the disease develops in young and healthy individuals as a result of endocar- ditis that the enormous heart is usually found.
Etiology. — Endocarditis affecting the semilunar valve may have the same origin as that of the left auriculo-ventrieular valve, and hence the discussion of its causes does not need to be rejieated.
Aortic regurgitation may be met with in persons of both sexes and of all ages. It is a striking fact, however, that this lesion, even when duo to rheumatic endoc»arditis, is far more com- mon in nudes than in females. When developed at or after mid- dle age, it is usually due to those conditions which bring about sclerosis, and which are fully considered in other chapters (pages 201 and 741). This sclerotic form is also undoubtedly met with more frequently in males than in females, and for the reason that arterial degeneration is more common in the former — and there- fore the etiological factors leading to sclerotic change in the aortic cusps are essentially those of arteriosclerosis.
In a considerable portion of males suffering from aortic re- gurgitation there is a history of syphilis and the abuse of alco- hol. In a most typical case of this lesion recently seen in a man of thirty-nine, syphilis and whisky were the only two causative factors to be elicited. Gout and bodily toil, particularly if com- bined with alcoholic excess, also seem to be causative agents of considerable importance.
As already stated incidentally in Morbid Anatomy, severe
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rioK
281
strain may bring about acute incompetence of one of the aortic ciispt3 through rupture at some point that bad been previously weakened by inflauimatiun or atheroniatoua tiegeneration.
There is a form of aortic insufficiency which, although not due to valvular defect, yet presents the same clinical features as the organic form, and h so frequently encountered that it may here be brietly dweh iipi>n. This h a rehvtive ineomfietence of the semi- lunar valve, and its causes are found in conditions that predis- pose to stretching of the ventricular wall and of the basal ring of the aorta. They are therefore (1) degenerative changes in the myocardium, (2) diseases of the aorta that greatly narrow its lumen, or, per conim, hml to its dilatation, and (3) tnediasti- na! tumours, which hy p>ressure diminish tlie calibre of the aorta. The most frequent cause of this relative insufficiency is aneurysm affecting the ascending arch, or a general dilatation of the aorta secondary to sclerosis. In one instance of the latter kind coming under my notice it was ass^K?iated with mitral regurgitation, also of atheromatous type, but which had existed for years. During the later weeks of life iu this case aortic incompetence developed^ and after death was found flue to extensive atheromatous degen- eratiun and dilatation of the aorta, reaching from its origin to the beginning of the descending jKirtion of the vessel.
In another case in whieh regurgitation through the aortic valve had run its course to a fatal termination within a few months, post-mortem examination disclosed stenosis of the ascend- ing aorta, about ^ an inch almve the insertion of the valve, so pronounced that the lumen was diminished by at least a half. This narrowing was caused by a growth of fil>rous tissue which comjilett^ly encircled the aorta, and froni the history ap{>eared to have originated in acute inflammation a year and a half pre- viously.
As already stated, relative aortic incompetence may be tlie ultimate effect of chronic myocarditis, which is associated with sclerosis of the aorta, and which so seriously impairs the resist- ing power of the ring tliat it gradually yields to the distending force of the blood-wave as it recoils against the chised valve. I have seen more than one instance of the kind as disclosed by the necropsy, although during life the regurgitation had been attrib- uted to structural defect of the valve-segments.
282 DISEASES OP THE HEART
Of 53 cases of aortic regurgitation of which I have records, 46 occurred in the male and only 7 in the female sex. Seventeen of the males and 4 of the females were below the age of forty. Eleven of the former who were less than forty years of age gave a history of rheumatism or scarlatina, while 10 over forty also had had one or the other of these diseases. Of the females, 2 below forty and 1 over that age, gave a history of rheumatism or scarla- tina. Of the total number of cases, therefore, 24 were probably due to endocarditis. It may also be stated that of the 29 males and 3 females over forty there were 19 males and 2 females in whom the lesion, owing to the absence of probable endocarditis, could be reasonably attributed to atheroma. In whatever way these figures are looked at they exhibit the striking preponder- ance of men over women afflicted with this particular valve-defect.
SjrniptOlllS. — It goes without saying that in this as in other valvular diseases it is the degree of compensation which deter- mines the presence or absence of distinctively cardiac symptoms. In other words, if the lesion is of inflanmiatory origin, and if the state of the myocardium has permitted the development of great hypertrophy, the disease may remain entirely latent for many years. Arduous occupations requiring great physical eflPort, feats of endurance and skill, mountain-climbing, running, boat-racing, football playing, tennis, etc., are often endured without discom- fort. I recall an attorney with pronounced aortic insufficiency of rheumatic origin who consulted me soon after his return from a six-weeks' vacation in Colorado. He had ridden his wheel at an altitude of 0,000 feet with no more discomfort than he would have experienced in Chicago. The only time he had suffered any inconvenience was when he had taken the train up Pike's Peak. Upon reaching the sunmiit, 13,000 feet, he fainted away, yet upon returning to the foot of the mountain he got on his wheel and rode away as if nothing had happened.
Dyspnoea is not experienced in this stage, and aside from vio- lent action of the heart, patients are totally unconscious that the organ is anywise different from that of their fellows. If any dis- turbance of bodily function exists, it is not such as arises from venous congestion, for so long as the mitral valve remains com- petent stasis back of the left ventricle is impossible.
The state of the circulation is one of intermittent ancemia on
AORTIC REGCRGITATIOX
283
the part of the arterial system. At each systole the arteries are flushed, and with each diastole they are relatively depleted. The teiideiieVj therefore, is to a hick of mitritioii of the various organs and tissues throughout the body. This is not specially manifest in some persons, while in others there is more or less pallor and delicacy of body. The muscular system in particular is weak, and some children show inability for sustained menial effort, yet as a rule young persons with aortic regurgitation show nothing either in appearance or deportment to indicate the existence of their k^sion.
A well-compensated aortic insufficiency is not likely to inca- pacitate an otherwise healthy young adult for the active and even the arduous duties of professional or mercantile pursuits. Many a hard-worked medical man with tliis lesion is able to sustain the severe mental and physical strain of a hirge general practice with- out more fatitrue than his more fortunate confreres. The only symptoms experienced by some patients are palpitation or slight vertigo, or both, and yet trivial as they may seem to be they are Bometiuies the earliest announcement of faltering energj^ on the part of the left ventricle. In one instance, more than twenty years before the patient's death, any effort or excitement iK^yond a certain moderate degree, brought on attacks of such violent pal- pitation as to necessitate absfdute repose for hours in the recum- bent posture. These attacks were also produced hx even small doses of digitalis^ and as they were allayed by aconite they were thought due to extreme hypertrophy. In most cases such violent cardiac action is an exprc*ssion of weakness rather than of ex- cessive strength, as sometimes supp<3sed. When dizziness is expe- rienced, it is usually, though by no means always, induced hy sudden exertion, and in such cases it is generally found that the regurgitation is very free.
The cerebral arteries are flu^lnMl with each systole, but in consequence of the regurgitation bUxxl-pressure within them is not sustained, and when for any reason the reflux into the ven- tricle is intensified, transient anaemia of the brain restilts and vertigo is felt. In some cases dizziness is prwluced by intermit' tenee in the heart's contractions, and it is then a mild manifesta- tion of what in other cases becomes a syncopal attack. Indeed, fainting is an occasional symptom in this disease, in consequence
284 DISEASES op' THE HEART
of the fact that the state of the cerebral circulation is the opposite of what obtains in mitral stenosis. This explains, I think, why it is that aortic patients are able to lie low in bed, whereas those siiflFering from mitral disease usually prefer to sleep with their head and shoulders propped up on two pillows. In the former there is an unconscious attempt to overcome the force of gravita- tion upon the cerebral circulation, while the latter class of patients seek to aid venous flow out of the head by that same force of gravi- tation.
Disorders of digestion are not so common in aortic as in mitral patients, and when present are referable not to interference with the circulation, as has been explained is the case in lesions at the auriculo-ventricular orifice, but they are due in most instances to errors in diet or whatever deranges gastro- intestinal function in individuals who have no heart-disease.
The comparative immunity from symptoms enjoyed for years, it may be, by persons w'hose disease is the result of endocarditis, is not the fortunate lot of those in whom the aortic valves have become incompetent in consequence of sclerosis, and in whom the my(x?ardium is incapable of maintaining adequate comi>onsatory hypertrophy. In persons, therefore, whose signs of aortic regurgi- tation develop during middle age, symptoms are apt to appear early and to be pronounced. These do not differ essentially from those experienced by i)atients of the other class, and are palpita- tion, vertigo of more or less intensity and frequency, a fooling of general weakness, uncomfortable prax?ordial oppression, more or less pain that may Ik? distinctly anginal or of an anginoid char- acter, and in particular distressing attacks of dyspn<oa. When these symptoms arise a fatal termination is not far distant.
With Dr. G. W. Webster, October 18, 1000, I saw an Irishman who presented a very striking picture of the distress often experi- enced in the terminal stage of aortic incompetence. There was no history of inflammatory rheumatism, but of syphilis and the im- moderate use of alcohol. Three weeks prior to my visit ho had been in the coimtry, and while there had overexerted himself, become greatly fatigued, and had begun to suffer from attacks of sudden weakness with a feeling of suffocation. Upon his admission to the hospital he was suffering from frequent attacks that seemed to portend speed}'' dissolution. Ilis hurried and somewhat
AORTIC REGUHGlTATlUX
2S5
laboured respirations wmild siiddcnlv become so augmented in severity that be would spring into the upright positiun gasping for breath, eonghiiig and raising frothy mneiis, while cyanosis became marked, and the pulse grew rather more rupid, irregular, and extremely feeble. The face beeauiC anxious, and, in a word, the whole ujn^'aranee of the man was one of direst distress. The examination on admission disclosed aortic regurgitation and a secondarily leaking mitral, with very swollen and tender liver. Ilypudermics of morphine relieved tliese attacks in a measure, and under the free use of cathartieSj digitalis an<l iodide of soda, the condition so much improved that the mitral no longer leaked, I found a rather spare man of medium stature who looked much older than he really was. He was semi-reeumbent, and although comfortable was yet breathing with apparent difficulty and greater than nonnal rapidity, Tliere was no ohIcuui, and signs of stasis were not notiee- al>le, Tlie temporal and cervi- cal arteries throbbed strongly, the pulse was quick and of the character known as bis- feriens, and the radial arteries were stiff. The lower border of the liver was paljiahle a short distance Ixdow the costal arch, but the organ was not hard or tender. Cardiac im- fmlse was diflFnserl and weak, the indistinct broad apexd>eat being in the sixth interspace, midway between the left mamillary and anterior axil- lary lines. Percussion showed slight increase of cardiac dulness to the right of the sternum and downward, but very great extension of dulness towards the left and downward. The outer border was broadly rounded, after the manner often de- scribed as indicative of preponderating dilatation of the left ven- tricle in cases of aortic insnlKciency with broken compensation (Fig, 53). When hj^pertrophy predominates, the outline of the
Fi<i ft'i, — L<'«<^ATioN OF Apex Awr« Kelative DcTLNE^f, Ca8» Of Aortic Ixhi fi-icienct
(p. 284).
286 DISEASES OF THE HEART
left ventricle is long and pointed with a rather sharp apex. Upon auscultation there was at once detected a systolic and diastolic murmur of the usual character in aortic regurgitation, but with the exception of the accentuated pulmonic second tone the heart- sounds were scarcely audible. Indeed, the aortic second was quite wanting, and in the neck was replaced by the feeble dis- tant diastolic bruit. At the seat of the apex the ear perceived a dull or toneless thud rather than the normal first sound, and the diastolic murmur was faintly distinguishable. In the femoral artery, pressure elicited the double murmur of Duroziez.
The diagnosis was easy enough. It was an aortic regurgita- tion of atheromatous origin in the stage of ruptured compensa- tion that had led to venous stasis. The congestion of the lungs was shown by the frequent cough and sero-mucous sputum, and the stasis in the general system by the hepatic enlargement and scanty urine. The patient was unable to sleep, and the taking of food was followed by the formation of gas, which contributed its quota to the already existing dyspna*a.
The prognosis was of the worst, for it was only too evident that the left ventricle could not withstand the impact of the regur- gitating stream. That this was free was shown by the absence of the aortic second sound, which had become wholly replaced by the diastolic murmur. The attacks of increased dyspnoea and cardiac feebleness were the manifestation of left ventricle failure or asys- toHsm and portended grave danger. In fact, although as vigor- ous and skilful treatment was maintained as could be devised, it exercised no appreciable effect on the patient's condition, and after lingering another five days he expired in one of his attacks.
There is a twofold reason why aortic regurgitation of the sclerotic type is particularly serious. Xot only has more or less myocardial degeneration preceded the development of the valvu- lar defect, but the reflux of a portion of the contents of the aorta into the left ventricle augments the cardiac ischu'niia resulting from the aortic and often coexisting coronary sclerosis. I will not discuss the much-debated question whether the coronary arter- ies are flushed during systole or diastole, since this is amply set forth in works on physiology, but only state that the weight of evidence is in favour of the systolic flushing of the heart-muscle.
AOKTIC REGURGlTATtON
287
It is siiffieieTit to emphasize the faet that in aortic regurgitation blood-pressure is not sustained within the euronarj any more than ill other arteries, and hence eardiae nutrition cannot be good.
There conies at length a liuiit in all cases to cardiac hyper- trophy because the heart-iuusele btK'onie* more or less degenerated, and tberefiux* ineapable of luaintaiuiug the circulation and o£ withstanding the dilating force of tlie regurgilant stream. Its flagging energy is shown by more rapid and perhai)S less regular contract ions, even, it may be, by occasional inlerinissions.
Therefore, the earliest and most reliable indications of failing compensation are generally shown in the pulse. Eren before sub- jective symptoms bring tlie patient to his medical adviser the pnlse-waves are no longer of uniform frequency, force, and vol- ume. Tlie radial pulse is accelerated, but it does not strike the palpating finger with its old-timed suddenness and vigour, the artery not being so powerfully and quickly distended as when the ventricle contracts with energy, (-onsequently the physician may not so readily distinguish the peculiar characters of the aortic re- gurgitant pulse. At irreguhir intervals the pulse seems to falter a little, or a small, weak beat follows its predecessor more quickly than usual, and is followed by others of normal strength.
This is the expression of an accessory or extra systole, intro- duced now and then into the regular series of contractions for the imrpose of re-enforcement (pulsus intercurrens), or it is the result of the ventricle giving a hurried, ineomplete eontractionj in consequence of fatigue. As muscidar incompetence increases, the pulse growls nu>re irregular, or indeed liecomes permanently intermittent. It increases in frequency, and its distinctive colhips- ing character, to be subsequently described, grows less apparent.
Sul>iective symptoms annoy or even alarm the patient, who begins to nc>tice an unwonted breathlessness. Attacks of vertigo or even syncope supervene* If the patient does not now die sud- denly and unexpeetedly, he is likely to suffer from irregularly re* eurring attacks that are of grave danger because indicating immi- nent cardiac paralysis. These are a more or less sudden feeling of great weakness or prostration, with cyanosis, a feeble, irre^^ii- lar, perhaps accelerated and empty pvilse, dyspmea, and an inde- scribable feeling of impending dissulution. In addition, he may suffer from cough with frothy, it may be bloody, expectoration
288 DISEASES OP THE HEART
and other s^^Ilptom8 indicative of stasis in the pulmonary vessels and general venous system. If the mitral valve has become rela- tively incompetent, regurgitation through the auriculo-ventricu- lar opening is added to that already present at the aortic orifice, and the symptoms become the same as those of the last stages of mitral disease.
Early in my practice I was called to attend a middle-aged woman, whom I found intensely dropsical, orthopnoeic, and pre- senting unmistakable evidence of aortic and relative mitral insuf- ficiency. Rest in bed, infusion of digitalis and catharsis speedily removed the anasarca, closed up the mitral valves, and, in short, so greatly improved her condition that she thought herself fully re- stored. Despite my warning, and contrary to my strict orders, she insisted upon leaving her bed and sitting dressed in the family living room. Only a day or two thereafter, while alone in her apartment, she heard a rap on the door, arose quickly to answer the knock, opened the door, and almost immediiately fell to the floor and died. In this case I believe life might have been prolonged had the mitral valves continued to leak, and thus acted as a safety-valve for the left ventricle.
I am led to this opinion by my observation of a case with Dr. Lowreuce at Chebanse, 111. The patient was an old man, who was suffering from albuminuria, dropsy, congested liver, and orthoj)- ncra. Upon examination, there were the usual signs of stiffened arteries and aortic regurgitation, but, in addition, a mitral regur- gitant murmur, pulsation of the external jugulars, and a murmur characteristic of tricuspid iiisutficienev. The outlook seemed very bad, and but small hope i«t improvement was held out. Xever- theless, upon the daily moderate use of cathartics and nitro- glycerin, the replacement of digitalis by strophantlius, and the hypodermic administration of small tonic doses of morphine, this patient actually improved beyond all expectation, and several months subsequently was reported by the doctor as still alive and in tolerable comfort, being able to drive out in pleasant weather, although, needless to say, compensation was never re- stored. I believe in this instance the leakage of the mitral and tricuspid valves relieved the two ventricles from dangerous strain and threw the brunt of the trouble back upon the liver and general venous system. The stasis thus resulting, of course, produced res-
AORTIC REGURGITATION
289
piratorv embarrassment and fuiietional derangement of tht* ab- dominal viscera, bnt aetuailv served to prolong life.
In my care in the wards of Cook County Hospital there are at the present writing two men with aortic regurgitation in whom mitral iricompetenoe has beeome added. Both present evidence of venous stasis in a moderate degree, chiefly hepatic and pulmo- nary. One complains of w^eakness and but little else, the other of insomnia ; yet in both patients things are growing slowly w^orse in spite of rest in bed and the usual heart-tonics. To all intents and purposes tliey have become converted into eases of mitral di.sease, the most frequent sequel of events in aortic regnrgitation. The chief difference, how^ever, lies in the refractorine:^ to treatment and in the liability, one might almost say certainty, of a sudden <leatli.
In June, 1899, I saw with Dr. Houston a pow^erfully built Irishman, weighing over 200 ponncls, who was suflTering from dyspntra, which had suddenly developed six weeks previously. His personal history w^as negative wuth exception of swelling of one knee some six or eight years befoi'e. This may have been a monarticular rheumatism, and if so, it may have been responsible for the man's valvular disease. It was TH>t followed by any symp- toms, for with exception of a fall that occasioned ]niin near the heart for a day he had been perfectly well up to his present ill- ness. Xo history of overexertion or any other exciting cause for his dyspntea con hi be eliciteiL His slu»rtness of breath had set in abruptly while he was attending bis duties as engineer, and at first had !»een more severe than it was when I saw him, the im- provement being due to treatment. Xevertheless he was incapaei* tated for work, and counsel was sought in the hope of obtaining trome snggestion for his further improvement.
The pulse was arrliythmic and rapid, displaying feebly the usual characters of aortic iusutHcieney, and the vessels did not feel thickened and stiff. The broad, heaving apex-impulse was displaced douTiward into the sixth interspace and outward to the anterior axillary line. There was epigastric pulsation and a sys- tolic tlirill in the aortic area. The heart-tones were everywhere audible, though feebly, and there was a loud, rough systolic niur- ninr at the l>a3e to right of sternum, followed by a very feeble diastolic bruit At the apex could be made out a softer systolic 19
290 DISEASES OP THE HEART
murmur possessing the characters of a mitral regurgitant one, which, together with evidences of enlargement of the right heart, convinced me that the mitral as well as the aortic valves were leaking. The liver was palpable and tender, and the urine con- tained a small amout of albumin. I looked upon the mitral insuf- ficiency as relative and secondary to the aortic disease.
The prognosis was very unfavourable, notwithstanding the degree of improvement that had already attended treatment, be- cause when compensation is once lost in this form of valvular disease it is rarely possible to restore the dilated and perhaps de- generated left ventricle to its former vigour.
The patient was informed of his grave state, and was advised to keep his room for as long a time as was thought best, the dura- tion to be determined by results. In addition to rest, the treat- ment w^as to consist of strychnine, digitalis, and nitroglycerin; food was to be light but sustaining, and cathartics were to be employed daily, but not enough to weaken him. The purpose of the last-named remedies was chiefly to prevent the patient from being obliged to strain at stool, as might be the case were he to become at all constipated. It is well known that effort of this kind is particularly bad, even dangerous, for persons whose left ventricle is in a state of dilatation. In aortic regurgitation the sudden constriction of the arteries incident to straining is liable to cause sudden and fatal diastolic arrest of the heart.
In October I saw the patient a^ain, and was not surprised, althoufrli disappointed, to find that in spite of treatment the dila- tation of the left ventricle and resulting insufficiency of the mitral valves had increased. The action of the heart was more regular, but in other res])ects things had crown rather more ominous. He was now ordered to keep his bed strictly, and was put on larger doses of digitalis. Improvement did not follow, and he began to suffer much from sudden paroxysms of dyspncra, which were very alarming to him and his friends. His liver also became greatly engorged, and his whole condition grew steadily more threatening. Strychnine and nitroglycerin were increased, and he was given daily injections of morphine, ^ of a grain, with atropine to lessen dypsnopa, quiet his nervousness, and sustain his heart.
It was decided to persevere in the use of digitalis, interrupt-
AORTIC REGURGiTATIOIf
291
ing it from time to time and substituting therefor tincture of strophanthusj to prevent the piossible cumulative action of the fox- glove. This was carried out uutil at length a singular mental state developed, eharaeterized by delusions closely resembling a mild mania. A^ Dr. Houston bad obbcrved a similar mental state onee before in a patient whom 1 bad turncil over to his charge, and in tbat instance had discovered it was caused by digitalis, he concluded it was of the same nature and origin in this case and promptly stopped the drug. As in the other case, so also in this, the delusions and otber iiuiuiaeal manifestations lasted abtjut twenty-four hours, and then disapfMmred entirely. This rare effect of the prolongetl administration of ibis agent will be sjwiken of in the chapter on Treatment of Valvular Diseases.
Patient was seen again in January. He was still in bed, where he had remained since the fore part of October, was quite recumbent, and breath ing tranquilly, although he stated be bad Occasif>nal paroxysms of dys]m(ca that compelled bim to spring up for breath. These spells of difficult breathing had returned upon bim about the 1st of January after a i>erio<l of constipa- tion. His pliysieian stated that as a result of vigorous purgation, digitalis, strycbnine, and morphine byiM>dennicaIly, and restricted diet, which was kept up for nearly two months, bis condition bad by late autumn improved wonderfully. The enlarged liver bad re- turned nearly to normal, his colour had grown quite natural, and his pulse stronger, of better volume, and regular, the heart-sounds stronger, and the apex-beat fairly well defined. Recently, how- ever, the patient batl become intolerant of the catbtirtics and pro- longed rest in bed, and liad implored to be allowed to sit up.
I found the pulse about 70, with two intermissions in a min- ute and a half, but %'ery eompressible, and its collapsing character not well marked. The liver was j)alpable, particularly the left lobe, which was very tentler in the ejiigastrium. There was no oedema, although the feet w^ere a little puffy. Cardiac impulse was wanting except for an occasional vague apex-beat consider- ably outside the left nipple in the sixth interspace. Heart's dul- nesfi was pronounced, presenting in this regard a marked contrast to its condition in Octfrber, when it was obscured by pulmonary resonance. It was of triangular outline, reaching to the third interspace, and from 2 inches to right of sternum across nearly
292 DISEASES OP THE HEART
to the left anterior axillary line, well outside of the occasionally palpable impulse. The lungs were everywhere resonant. The heart-sounds were audible though faint, the aortic second being particularly feeble, and the pulmonic second accentuated. A loud, harsh murmur was present throughout the pra?cordium, which was systolic, but could not be traced to any particular area. Over the body of the organ it disappeared on firm pressure, permitting other more distant and persistent murmurs to be distinguished. These were found to be a harsh aortic systolic, a soft mitral systolic transmitted to the back, and a feeble diastolic, which was of aortic origin, as shown by its area of intensity and direction of propa- gation.
The diagnosis was apparent; added to his old-standing aortic insufficiency with relative mitral regurgitation there was a peri- carditis with moderate effusion. The liver was both congested and displaced downward.
The prognosis was most unfavourable, for in addition to the cardiac dilatation depending largely on myocardial degeneration, a pericarditic effusion had taken place. As is well known, this sometimes su|)er\'enes upon a chronic vah'ular disease, particu- larly aortic insufficiency, and is then apt to be a terminal event. It was stated to the family that sudden death was not improbable.
In the way of treatment, compound cathartic pills were or- dered, the patient objecting to elaterium and disagreeable saline waters; digitalis in considerable doses, a grain of codeine thrice daily to promote quiet and to lessen the paroxysms of dyspnoea, and restricted diet. Morphine was not prescribed because of its constipating and other objectionable effects.
In spite of the greatest possible care this patient did not im- prove, and one month later died suddenly and quietly while rest- ing in bed, as usual. This case not only portrays the clinical pic- ture often seen in aortic regurgitation, but also illustrates the powerlessness of our art in attempting to stay the progress of the disease.
In this and Dr. Webster's case there was one symptom com- mon to both — i. e., paroxysmal dyspna^a. In the one case it seemed due to sudden threatening asystolism of the left ventricle, as shown by feebleness, rapidity, and irregularity of the pulse, and pulmonary congestion, manifested by cough and frothy expectora-
AORTIC REGURGITATION
293
tion. In the other there was also threatening weakness of the heart's action^ hut the striking eoneoiuitant was the intense anx- iety amonnting to fear^ so that the patient would spring up in bed gasping for breath and looking wild and terrified. In both xhvi^e instaiiees, moreover, the symptoms of cardiac breakdown de- veloped suddenly, and were ncner again wholly lost, in this re- spect diifering markedly from the gradual onset of compensatory failure seen in mitral affections. In both eases mitral regiirgita- tiiui was superadded, but instead of the end coming with pro- nounced dropsy death was sudden, before venous stasis jirogressed to t!iat degree.
In my experience young persons who hive contracted their aortic insuihcieney in consequence of endocarditis rarely suffer from cat'diae pain, while, on the other liand, I have observ^ed numerous instances of angina pectoris in individuals whose aortic lesion Iiad rc^sulted from degenerative elianges. In 1^^91 I began to treat a marrietl wonian of about thirty who was afflicted %vith aortic incompetence and attacks of prsecordial pain. She was quite stont^ and this made examination of the heart difficult. The radial pulse was collapsing, though not as full and quick as in typical cases, and slie had an aortic reg^irgitant murmur. The apex-beat could not lie distinctly made out, and the large breast prevented my determining the boundary of dcn^p-seated dulness at the left. The ahsence of manifest cardiac hypertrophy rather puzzled nie, but eventmilly led me to conclude tliat the teak was not verj' free, and consequently that there was not much hyper- trophif dihitation of the left ventricle. After she liad been under treatment for a time she called attention to a pulsation in the neck. This was found to be just behind and above the right sterno-ela- viculnr articulation in the kication of the innominate artery. It was attrihuted to aneurysm of the arch uf the aorta, which thus brought the innominate prominontly into view. The patient wa8 taken to several diagnosticians for opinion, and among others to the late Dr. Christian Fenger, by whom my diagnosis was con- firmed. This discovery of a probable aneurysm changed my views concerning the etiology and pathology of the case. Whereas the history lunl led me to regard the aortic regurgitation as of rheu- matic origin, I now considered it secondary to aortic aneurysm, a view that seemed to account for the attacks of angina.
294 DISEASES OF THE HEART
The patient then left Chicago, and I did not see her for sev- eral years. At length I was one day unexpectedly summoned to visit her at one of the hotels to which she had betaken herself immediately upon her return from Europe the day before. She was in a truly pitiable plight. The attacks of agonizing pain had become so frequent and severe that she literally could not walk across the room without one being evoked, and she was taking large doses of nitroglycerin and whisky, though with but slight effect. The circumference of the neck was greater than normal, although the evident congestion had not produced oedema. The old-time pulsation was still in evidence. It did not appear to have increased in area, and the only alteration I could detect in the heart-findings was greater rapidity and feebleness of action. She was given injections of morphine sufficient to somewhat blunt her sensibility to pain, but aside from this there was nothing that could be done. She dragged out a miserable existence for a few weeks longer, and then in one of her attacks death mercifully ended her sufferings.
At the autopsy, which was performed by Dr. Frank S. John- son, who had also seen the case, the aortic valves were found very incompetent and sclerotic, but whether the process had originally been of endocarditic origin or not it was difficult to decide. There was a moderate degree of enlargement of the left ventricle, the walls of which were fatty. The two most interesting features, however, were (1) occlusion of the mouths of the coronary arter- ies by deposits of lime-salts, so that they with difficulty admitted the point of a fine probe, and (2) the size of the aorta. No aneu- rysm could be detected, but careful measurement showed that the ascending [)ortion of the arch was uniformly increased in diam- eter by about 1 centimetre, while its walls were possibly a trifle thinner than normal. It seemed probable, therefore, that when distended by the abnormally large blood-wave it became stretched sufficiently to amoimt to a considerable dilatation, which had caused some pressure on the great veins, hence the congestion of the base of the neck, and the prominence of the innominate artery.
It was now easy to imderstand the frequency and intensity of her angina. The heart-muscle simply could not be flushed with blood through the extremely narrowed coronary ostia. Wh(^ncver physical exertion called for more blood within the coronary arter-
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les it was not fortlieonung^ and cardiac ischtemia was manifested by a cry of agony.
From the foregoing, it is plain that cases of aortic regurgita- tion can be divided into two chisst»s. In the one, tlie lesion is the result ui endocarditis, euntracteJ during a period of life when the myoeardinm and arterial walls are still young and healthy — great compensatory hypertrophy is possible^ and the disease may endure for many years witliont giving rise to symptoms. These appear at length only after the hcart-iiius^i'le can no longer be sustained by the coronary circidation» or the I breakdown occurs as the result of fresh endocarditis ingrafted on the old prcK*ess in the course of acnte articular rheumatism. In my care, five years ago, was a viva* cious young lady of eigliteen, why presented the typical signs of free aortic regurgitation, a quick, collapsing pulse, a broad, heav- ing apexdjeat, sihiated far l»elow and to the left of its normal situation, and a loud diastolic mnrmur. She consulted me because of having noticed that she could no longer run upstairs, dance, ride a wheel, or do other things which before were unattended with consciousness of the heart's net ion. She did not get out of breath, l>ut was annoyed hy forcible pounding id' ihe heart and by the occasional sensation as if it ** gave a flop/^
She had some Hatulent in<ligpstion and was constipated. The pulse was now and then intermittent, and for the purpose of cor- recting this intermittence slie was given small doses of tincture of digitalis, 5 drops 3 times a day. When she next returned, after a few days, she stated that the j>ounding of thv heart was worse instead of l»ettcr. The digitalis was reduced, but still intensified her svmptonis, and was discontinued. Thinking that the inter- misgions might be due to gastri>inte8tinal derangement, she was given remedies to correct the constipation and improve digestion. There was some improvement, but still the heart did not Ijecome entirely regular. One <lay she complained of dull frontal head- ache, some pains and stiffness of the muscles, which seemed to me a muscular rheumatism, possibly of uric-acid origin. Accord- ingly, she was put upon ])otash and salicylate of so<la, and or- dered to drink freely of water. This was a happy hit, for she lost the intemiitfence of the pulse, and was no hunger annoyed by the heart's pounding.
A year later, believing I had discovered evidence of a tendency
296 DISEASES OP THE HEART
to growing dilatation of the left ventricle, I gave her a course of Nauheim baths, which agreed with her, and she felt so well that I lost track of her for some months. Indeed, with one exception, after the baths were finished, I never saw her again. But one day, encountering her mother in the cars, I learned that in Au- gust, eight months subsequent to her last visit at my oflSce, she developed what appeared to be a mild attack of articular rheu- matism. As I was out of the city, a neighbouring physician was given charge of the case, and he very properly confined her to bed. After about a week the rheumatic manifestations had sub- sided, and she was thought to be getting on finely. One morn- ing she awoke in excellent spirits and seemed nowise in imme- diate danger. Nevertheless, during the forenoon, when she sat up in bed to drink ;. glass of water, she suddenly, without warn- ing, fell back upon her pillow and expired. Xo autopsy was held, and I have no means of knowing the exact condition, but I be- lieve that probably the heart had become weakened by fresh endo- carditis attending the mild rheumatic attack, and under such cir- cumstances the exertion of sitting up occasioned sudden diastolic arrest of the left ventricle. It simply illustrates the liability of these patients to sudden, unexpecteil death.
In the second class belong patients whose valvular defect is the local manifestation of degenerative changes, which, if not due to sy[)liilis, the j::outy diathesis, strain, and the like, are associated with advancing age. In such persons com])ensatory hypertrophy rarely proves so enduring as in the young, and may fail early, because the myocardium is already degenerated, or because the state of the coronary arteries does not pennit that degree of nour- ishment necessary to the maintenance of hypertrophy. In this second class should also be reckoned those eases in which the aortic insufticiency is the result of rupture. In this latter group, pain, pra^cordial distress, and other symptoms of cardiac incompetence are apt to appear promptly after the injury, and to persist without relief. Naturally, however, the ability of the heart to compensate the defect depends u]X)n the extent of rupture — that is, the degree of regurgitation permitted — and upon the state of the heart-mus- cle. Dilatation of the left ventricle usually develops rapidly, with little or no hypertrophy, and hence after a few weeks or months the heart succumbs.
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Tn persons suffering froia slowly indnced degenerative changes sjinf»toms ajipear slowly, but are never so delayed in com- ing as in patients whose incompetence originate in endocarditis. In most iustanees the sj^nptonis that initiate breakini^ compen- sation are such as may be referred either to cerebral amemia— i. e., vertigo nnd syncopal attacks — or to cardiac fatigue and de- generation— 1. e,, irregularities of the pulse, palpitation, and angina pectoris.
When, on the other hand, cardiac failure leads to stasis in the lesser circulation, or in the great veins of the general system, the symptoms gradually become those of the terminal stage of mitral disease — i. e., dyspiura, cough, and frothy, or it may be san* guineous expectoration, disturbed visceral functions in general, cedema, and attacks of threatening asystulism. When at last aortic regurgitation has reached this stage the struggle is less likely to be protracted, and death is usually more sudden tlmu in defects at the left auriculo-ventrietdar orilxce.
Physical S%lis. — Inspedion, — In cases of pronounced aortic regurgitation the disease reveals its presence to the skilled eye by the throbbing of the temporal and carotid arteries. In contrast with the cyanosis of mitral disease the aspect of the pa- tient is apt to present more or less paUor, es|>ecially if the disease has develfiped in early life, In.s]iection of the chest usually de- tects strong pulsation of the rardiac area to the left r»f the ster- num, the degree and extent of this pidsation depending upon the thinness and flexibility of the chest-wall, as well as on the hyper- trophy «»f the heart. Occiisionally a wave-like impulse is seen to pass from the base downward towards the apex-bi^at, while in some cases there may be slight systolic retraction of the third and fourth interspaces to the left of the sternum, in consequence of atmospheric pressure, as the hypertrophied heart recedes from the chest-walL
The apex-beat is displaced outward and downward, in some cases even as far as the seventh or eighth left intercostal space, close to the left anterior axillary line. It is broad and heaving, at once conveying the impression of a large and j>owerful organ. In the young, with broad intercostal spaces, the dimensions of the left ventricle may Ijc almost as accurately delineated by the vis- ible impulse as by j>ercussiom
DISEASES OP THE HEART
In middle-aged individuals, on the contrary, particularly if the chest is capacious, the apex-beat may be scarcely perceptible. In some instances, no doubt^ this is owing to the inability of the degenerated heart to establish great compensatory hypertrophy. When very free regurgitation is compensated by great hyper- trophy, the eye sometimes discerns visible pulsation in the periph- eral arteries, as the radial or the dorsalis pedis. This phenom- enon, which is brought out with special distinctness by extension of the hand or foot, is the ocular manifestation of that peculiar- ity of the pulse about to be described under palpation as the pulsus alius el celer.
Quincke has described a visible pulsation of the retinal artery, which may be more or less tortuous and elongated with each pulsation. Capillary and venous pulse will be considered later on.
Palpation. — The hand laid upon the prcecordium detects pow- erful cardiac impulse, and over the apex-beat sometimes perceives a short presystolic thrill, or rather receives an impression as if the tip of the heart slid up to its maximum impulse. The impact of the apex resembles the striking of a huge fist against the chest- w^all, and if the patient l)e slight, the whole chest may seem to quiver with the shock. Systolic thrill is sometimes felt in the aortic area. Under some circumstances a diastolic thrill is also manifest.
The most remarkable feature in this part of the examination is presented by the pulse. Its characteristics are so distinctive that a diagnosis is often iK)8sible from it alone. First carefully stud- ied and accurately described by Sir Dominick Corrigan, it is often called Corrifjnn pulse, while other terms applied to it are the collapsing pulse, the waier-hammer pulse, the locomotive pulse, and the pulsus alius et celer. In well-marked eases the finger laid upon the radial artery, or upon any other readily accessible artery for that matter, is suddenly lifted by a large, powerful pulse-wave, which, advancing swiftly along the vessel, strikes the finger like a shot or ball, and then instantly recedes. The vessel, in other words, after l>eing quickly distended as quickly collapses, hence the name collapsing pulse. It is well shown in the accom- panying tracing (Fig. 54).
This characteristic of the pulse is intensified by raising the
AORTIC UEGURGlTATiOX
299
patient's hand to a level higher than that of the heart, and thus allowing the foree of gravity to hasten the quick recession of the pulse- wave.
Tlie i]iiiekness of the pulse- wave has thus been dwelt upon for the piirpo>=^ of euiphasizing the difference hetween the speed with which it travels along the artery, and the frequenoy with which
Flo. 54,— SFHVrtMoc^RAM ur Auhtic Keol:»«itatiu», Tmclnir by Dr. Kdward h\ WflJtt.
individual pulse- waves follow each other. Consequently, a frequent jnihe is a rapid or accelerated pnlse, whereas a quick pulse is one (hat air ikes the fiufjer suddenly and is not susfained, A pulse may be both frequent and quiek, as in fever, but a qniek pulse does no! necessarily have to he also a rapid one. In aortic regurgitation, liowever, the pulse is Ixith sudden and aeeelerated.
In some cases when the arteries have liccoiue niore or less sclerotic and tortuous the bounding pulse-wave seems to lift the vessel from its bc^d, and hence some writers have spoken of it as the locomotive pulse. To nuike the raison d'etre of this collaps- ing character nnderstofid, it is ncM^pssary to descril>e how the valvu- lar disease under consideration nKKliiies pulse-tension.
Under normal conditions blond iiressure within the arterial system is maintained at a uniform height by the perioilic dis- charge of bhxHl into the aorfa and by the elastic recoil of the arterial walls aided l>y the tightly fdosed semilunar valves. The blood'stn^am driven against the valve liy the recoiling aortic walls IS intercepted and forced onward through the arterial system. If the aortic valves, incompetent by disease*, are unable to check the backward flt>w of the blood a portion of it regurgitates into the left ventricle, and blood-pressure in the arterial system is corre- spondingly lowered instead of being maintained at a uniform leveh Accordingly, the wave of blood constituting the pulse- wave quickly recedes and allows the arterial wall?* to collapse, as it were. The liypertrojjhied left ventricle, made more than nor-
300
DISEASES OF THE HEART
inally capacious bv dilatufion, discharges its contents with a de- gree of energy pro|K^rtionate to its hypertrophy; and as its con- tents are augmented over the normal by the amount that has the moment before regurgitate J, the aorta becomes powerfully dis- teutled by this abnormally large mass of bloi>d. In consequence of the partial emptiness of the arteries caused by the regurgita- tion the large blcKnl-wave meets with but little resistance, and travelling rapidly towards the periphery, distends the arteries in its course.
Hence the greater the comjiensatory hypertrophy of the left ventricle^ the fuller, stronger, and quicker will be the pulse. The freer the regurgitation the ui(»re marked will Ix* the collapse of the vessel- walls. The degret^ of dilference, therefore, between the distention and collapse of the artery is a measure not only of the degree of the regurgitation, but also of the resulting compensatory hypertrophy, for when the left ventricle begins to fail, this jiecul- iar collapsing quulily nf the pulse grows less pronounced, although the regurgitation is nu whit less free.
Very exceptionally the pulse is said to exhibit the character knowTi as bisferiens und represented in Fig. 55. If the linger is
pressed lightly on the artery
ft /^ M M M /ll\ rtl^ ft
W WWW
AilbuUV 8yit. of Med,, vol. v, p.!*.'^!.
it receives a sensation as if the pulse-wave were dividcil into two portions, of which the second is the stronger* The fonnrT represents the sudden distention of the artery, and the latter is tlie palpable ex- pression of the prjedicrotic nr titlal wave. Pulsus hisferiens is u,«u- ally stated to be found in ar^rtic obstruction, but according to Graham Steell, cited by (1iff(»rd Allbutt, undoubtedly occurs in some cases of regurgitation ass*rf*iated with little if any stenosis. In one of SteelTs instances this f>eculiarity was not equally con- stant or pronounced on Iwith sides of the body. Its production is therefore difficult of explanation, as well as inconstant. I have never obtaineil a tracing showing a bisferiens pulse in aortic insuf- ficiency, but I have certainly felt pulses in some cases which, to my finger, seemed plainly of this character.
Not infrequently, pulsation is so pronouuf^od in the arterioles that the fingers of the patient throb appreciably when grasped
AORTIC REGURGITATION
301
and the diagnosis of his malady can be made while in the act of shaking his hand.
Two other phenomenaj the capillary pulse and visible venous pulse, shonld properly have been described under inspection, but have been reserved until now for the reason that they will be bet* ter understood after what has just been said concerning the pecu- liarities of the pulse. In eases in which arterial tension is very low in coiisequeriee of free regurgitation, the capillaries are dis- tended by the blood-wave instead of being kept unifonnly tiiled, and hence display what is known as the capillary pulse (Quincke's sign). This may be well seen in the palm and beneath the nails when the hand is warm, or it may be evoked by friction of the skin — e. g., of the forehead — until an area of hyperiemia is pro- duced. If the periphery of such a red zone is closely watched, its edge will be seen to alternately advance with each systole and recede with each diastole of the heart. Capillary pulsation is also sometimes plainly visible on the soft palate.
By venous pulse is meant a visible pulsation in the superficial veins. This is sometimes well nuirked in the subcutaneous veins of the back of the hand and the forearm when the extremity is al- lowed to hang down until the vessels become turgid. This venous pulse is a slow undulatory wave which, as Broadbent suggests, may be best noticed by laying a filament of sealing wax across the sur- face of the vein. Venous pulsation is specially pronounced when arterial tension has been still further reduced by fever. Neither of these last two phenomena is peculiar to aortic regurgitation, for they may be obser^^d in severe ana^nna which has sufficiently lowered pulse-tension. They are, however, most distinct and typ- ical in aortic incompetence.
Finally, when regurgitation is very free» a distinct thrill may be felt in the cerv^ical arteries and even in the brachials. This was well felt in a man of alx>ut thirty -five, who died suddenly a few weeks subsequently. In this case the thrill was palpable when the finger was laid ever so lightly on the vessel, and seemed to be but the palpable expression of vibrations imparted to the arterial coats by the suddenness and violence of the impact of the blood- stream.
Percussian.—A^ in other cases of valmlar disease, percussion aflfords our best means of noting to what extent and in what direc-
803
DISEASES OF THE HEART
f IQ. .W. — ^TtPIOF KiLATIVK lJl'L?rKMIl?< WtLL-
tion tlie heart lia.s siiffc'red eiilargoment. It is particularly valu- able in eae^es in wbicli tlie size of the ehest or the feebleness of
oarJiau impulse prevents ns troll) jiiJ|iing of the size of the heart by inspect ion and palpation. In coin]>ensated eases eanliac diilneas is in- creased only to the left and downward, and the outline of the left ventricle is rather jiuinted (Fig, 56), As dila- tation conies on, the left car- 'liac border l>econies more ronnded and the apex is blunt and broad, so that one should always strive to percuss out the shajx^ of the left ventricle as well as its distance from the median lino ( Fi^. 57). Increased dulness to the rig:ht is present only sei^ondarily, and is a measure of back pressure important tu determine,
-4 usai//a/torL— Regurgitation through the aortic valves de- clares itself by a murmur syn- chronous with the second heart sound and therefore diastolic iu time, which is heard with greatest intensity over the base of the heart any- wliere between the second right costo-stcrnal articulation and the junction of the fifth left costal cartilage with the breastbone (Figs. 58 and 5^0- Its most usual seat of maxi- mum loudness is on the body of the sternum at the level <jf tlie third costal cartilage, and vet in some instances it mav ^\ '^r.-Tvr. of Relat.v,. d.lke.. .n
be heard most plainly or heard tatjok.
AORTIC REGURGITA^JluN
30;i
only in the fourth left interspace, dose to the breasthone. It is generally moAt dii^tiuct in the ereet iH>sitiijn iir when the heart's action is excited. Never the- Jesa I have eertainly observed cases in which the niunnur he- came more distinct and easily recognised when tlie patient was reeumhent. This ninrnnn' is transmitted downward to wards the ensifonn appendix, and in some instances also towards the left, even as far as the apex. When audihle, with more than nsnal inten- sity at the ajjex, the miinnnr is thought by some to indicate incompetence of the left pos- terior flap.
As previoiiiily remarked w*ith reference to the mitral regnrgitant mnrmur, the intensity jnid the extent of condnetion r»f tliis anrtie diastolic mnrmur furnish no criterion of the gravity of
Flu. 58. — Spot or Maximum iMt^etTif
{8MALL CIUCLK) AJfH AjlKA or TUANsMtn- StOJf OF TVPJCAL AoitTIO KliurUtiJTANT Ml'RUlB.
FicJ. .'9.— RHYTtiit or AoKTic HcorRoiTAXT MrRMUR.
the lesion. Indeed, numerous instances have been recorded in which no bruit at all was audible for a variable time iinmediatelv
304 DISEASES OF THE HEART
prior to death. This is probably owing to a want of sufficient force and rapidity in the regurgitant stream to generate sonifer- ous vibrations. The duration of this murmur is usually short, and its quality is soft rather than harsh, and is unlike that of any other murmur excepting the bruit of pulmonary regurgitation.
In exceptional cases the diastolic aortic murmur may have a true musical tone. I well recall the case of a coloured man, in whom the intra-vitam diagnosis of aortic regurgitation was sub- stantiated post mortem, and who presented this musical quality in a most marked degree, but not with every ventricular diastole. At irregular intervals the soft diastolic bruit was associated with, or replaced by a musical murmur so intense that it was heard by the patient, and imparted a distinct thrill to the hand laid upon the heart to the left of the sternum. A few days before death this musical murmur entirely subsided, and at the post-mortem examination no condition that could explain its production could be discovered, although diligently sought for. The valves pre- sented the appearance ordinarily found in cases of endocarditic insufficiency.
The heart-sounds usually present more or less modification. The first sound at the apex is apt to be muffled or toneless, while the second sound is enfeebled. In the aortic area the second sound may be entirely wanting, being replaced by the diastolic murmur, or there may be a faint rudimentary second sound. The aortic first sound may be audible or replaced by a rough, more or less intense, systolic murmur. This bruit is usually interpreted as signifying an associated stenosis. This conclusion, however, is not always justifiable, since such a systolic murmur may be due either to roughness without narrowing of the orifice, or to sclero- sis of the aortic intima. When both a systolic and diastolic mur- mur are heard, they are often spoken of as a " to and fro " mur- mur, and such a combination is very frequent.
There are also certain auscultatory phenomena connected with the peripheral arteries which furnish valuable secondary signs of this valvular lesion. Over the carotid and subclavian arteries a faint systolic murmur is often found to replace the first sound, while if the regurgitation is free the normal second tone is ab- sent. When one auscultates the femorals, he hears a sharp snap, which is synchronous with ventricular systole and is the audible
AORTIC REGURGfTATION
305
expression of die sudrieii tension into wliieb the arterial coats are thrown as they are distended by the large sudden pnlse*wave» If ratlier more pressnre is exerted upon the vessel by means of the stethoseope, this t^napplng tone diij^appears and becomes replaced by a <liiatinet miirmin\ the innrninr of const riet ion, which can be elicited over any artery of sufficient size when no vaivnlar disease exists. When regurgitation is free, it is usually possible by trying diffcrenr clogrccs of pressure to at length bring out more or less clearly not only this systolic murmur, but also a diastolic one, so that one becomes conscious of a double ninrmnr, of which, in my experience, the systolic is usually the louder. This double femoral bruit was first describes! by Duroziez, and hence is often spoken i>f as Dumzif'zs siya. If is corisiderrd pathognomonic of aortic regurgitation, since in no other disease are the conditions pre- sented for its production. The explanation of this phenomenon is as follows:
Constriction of the artery throws tlie blood-stream into audi* ble vibrations as it passes the point of pressure, and, normally, this is all; but in aortic insuftic*iencv the Idornl-wave recedes during diastole and passes again this point of c<»ustriction, with the result that it is a second time thrown into vilvrations, and a diastolic mumnir is generated. In most cases these acoustic phenomena are elicited tuily over arteries of large calibre, but when the lesion is very pronounced and the h^ii ventrirle is jiowerfob both the sys- tolic snap iuhI the double bruit may Uv heard in suuiU vessels, as the radial aud even the dorsalis pedis,
DiagnosiB, — Ordinarily the rc^cognition of aorlic insutficieney is not ditficult. In some instances il may be detected at a glance, but when tlie individual is past middle age. with siderotic arteries and a voluminous Miorax, the collapsing character of the pul>r and a powerful cardiac injpulse may not l»e pronounced, and care is requisite to determine that the condition is not an aortic aneu- r^-sm that has led to regurgitation. In all doubtful or indistinct cases particuhir study should be given to the vascular signs, since they are conclusive, and a diastolii- bruit is not. Indeed it is to be remembered that w^hen in tlie lust stages the heart has become very weak, the murmur previously present may entirely disappear. Moreover, the diagnosis of this lesion may l>e rendered not easy by the association of relative mitral incompetence, or of other organic 20
S06 DISEASES OP THE HEART
defects. In all such cases one must minutely investigate the vas- cular system and rely on its disclosures rather than on cardiac findings, although even here valuable information miy be obtained if attention is paid to the secondary changes instead of the auscul- tatory findings.
Before leaving the subject of the diagnosis of this disease, I desire to dwell for a few moments on a subject which has given rise to much controversy. Many years ago the late Austin Flint, one of the most careful clinical observers this country has pro- duced, directed attention to the presence of a presystolic apex- murmur in some cases of aortic regurgitation, and declared it was an accidental murmur which did not necessarily denote the co- existence of mitral stenosis. He was vehemently attacked by Bal- four, who declared a functional presystolic murmur an impossi- bility. But corroboration of Flint's observation has come from so many sources that there cen no longer be any doubt of the cor- rectness of his statements.
His explanation of the mode of its production is, however, probably not correct in the light of more recent physiological knowledge concerning the closure of the mitral valves. The mur- mur is now thought due to vibrations of the mitral curtains as they are caught between the regurgitant stream on the one hand, and that pouring out of the left auricle on the other. It is quite pos- sible for mitral constriction and aortic regurgitation to coexist, and in any instance of this latter disease in which a mitral presys- tolic nuirnuir is recognised its correct interpretation is made pos- sible by giving due consideration to the presence or absence of secondary changes in the right ventricle, and the smallness yet collapsing character of the radial pulse.
Prognosis. — A pro])er estimation of the prognosis of aortic regurgitation requires a sharp distinction between the forms due to endocarditis and those of degenerative origin. Furthermore, in each group and in each individual instance, the prognosis is in direct relation to the degree of compensatory hypertrophy, the same as in any other valvular defect. If, in the first class — that is, of endocarditic origin — compensation becomes once well estab- lished, it is possible for the disease to be borne for many years. Mr. W., the description of whose sudden death will be narrated, was known to have aortic regurgitation of severe type for at least
AORTIC REGURGITATION
307
twenty-eight years^ and perhaps longer. When, however, com- pensation begins to fail, the prognosis is very grave, for it cannot be so readily restored as in mitral disease. Indeed, some author's are of the opinion that compensation can never he reinstated; at the most there being hope only of retarding the downward progress.
When in the seeund category of cases, those of degenerative nature, compensation becomes established, it is at the best only for a o*jniiianitively limited period, owing to the probable presence of chronic myocarditis, and when this eomi>ensation once breaks, it is irretrievably gone. Henceforth the progress of the malady is for the most part steadily downward. In all cases the prospect of even partial recovery is slight, and of restoration to a life of ac- tivity and freedom from symptoms is nil.
It is stated that very rarely a regurgitation may be converted into a predominating stenosis by the growth on the valves and ring of vegetatiuns, in consequence of fresh endocarditis; and whenever this occurs the prognosis becomes more favourable, prc^* vided, of course, there be no myocarditis or other complications. This possibility is too remote to be ordinarily taken into considera- tion.
Mode and Causes of Death.— No other valvular disease so often terminates abruptly. The suddenness of the death is due to paralysis f the left ventricle in diastole. In most cases, no doubt, warning has been given of the pending catastrophe by ir- regularities of the pulse, vertigo, or other symptoms which failed at the time to attract the patient s attention, or were too insig* nifieant to impress him witli their gravity. Death follows some sudden effort, as assmning the erect from the recumbent position* springing out of a chair to leave the room, jumping on to a moving street-ear, and the like* The muscular effort iiicident to such sud* den movements abrupt!}^ raises blood-pressure within the vessels supplying the groups of contracted muscles, and drives the bloo<l into the left ventricle during its period of relaxation with a degree of force which the ventricle is unable to resist. It fails to respond by a subsequent systole, and the patient falls to the ground in an attack of fatal syncope.
Fortunately for the patient, as well as for the peace of mind of his friends, assurance can be given that sudden death in the way
308 DISEASES OF THE HEART
just described is not usual. Indeed, it occurs in the minority of cases of aortic regurgitation. According to Broadbent, it occurred in 10 out of 38 cases taken from the records of St. Mary's Hos- pital. Sudden death occurs by far the most frequently as result of fibroid and fatty degeneration of the myocardium, and, there- fore, we should look for it in individuals whose aortic valves are incompetent in consequence of degenerative changes rather than in the young, whose valvular lesion is of endocarditic origin. This does not apply, however, when the heart is freshly attacked by an acute endocarditis. The case of the young lady of eighteen illus- trates that under such circumstances the end may come unex- pectedly and without warning.
AVe have ?oon in most cases of aortic regurgitation that the symptoms showing complete loss of compensation become those of pronounced venous stasis, the same as in the last stage of mitral disease. It is to be expected, therefore, that exitus lethalis should take place in the same manner, and in fact such is the case — i. e., from gradual cardiac asthenia or acute pulmonary (pdema.
Striimpell directs attention to the not infrequent occurrence of pericarditis in aortic insufficiency, particularly when the valves have been attacked by fresh inflammation, and in such the j>eri- carditis is very apt to lead to the death of the patient.
Of 24 cases analyzed by Ilustedt, the causes of death wore as follows: Heart- weakness, S; pulmonary infarct, 0; pneumonia, 2; QKlema of the lungs, 3 ; apoplexy, 1 ; and pleuritis, 1.
The suddenness of death is illustrated by the case of Mr. W., aged forty-five, who had had aortic insufficiency dating from chorea and rheumatism in boyhood, and had shown symptoms of failing compensation for at least two years. These consisted in feebleness and irregularity of the pulse, and attacks of weakness and faintn(»ss of such severity that they com])elled him to seek aid of the nearest physician. Notwithstanding the extreme degree of fatigue and exhaustion occasioned by his duties, he persisted in the daily attendance at his office. The day of his death he left home as usual and proceeded to his place of business. While in the act of stooping over a table, he sank to the floor, and ex- claimed, " I am dying! " His clerk, who was standing near, lifted him into a chair, and asked if he should run for a doctor. The sufferer looked up, smiled, and shook his head, as much as to say,
AORTIC REGUKGITATION
80<J
*'No, it is of no use," and a few moments thereafter he quietly expired, Thar this patient was fully awiire of his heing in daily — yes, hourly — tianger of death was showr* by the fact that he had given explieit rlireetions to his clerk what to do in the event of sueh a fatality* KeticeUng upon this case, one cannot help won- dering by what knowledge this patient recognised the significance of hii3 final attack, and refused to liave a medical man summoned, when in pre\ ions attacks he had always sought the services of the most accessible physician*
The following case is appended because it emphasizes in an impressive way several points with respect to aortic regurgitation. In tlie tiist place it illustrates the important part played by heart* strain; in the second, how h«>pelcss is the jin>gnosis in these cases; thirdly, die tntility of treat nicnt: and, lastly, the manner of death in a eonsiilerable pro|)ortion uf them,
I recently witnessed the death of a gentleman of forty-two who ha<l sought medical advice three months before on the sup- position that his distress was due to some form of stomach trouble. Excepting scarlafiTia at the age of six, he had never known a day's illness, and his habits had been exemplary with the one exception that be had been accustomed to take about two drinks a day of whisky before meals. He bad always been devoted to hunting and fishing, and bad spent much time each year in the woods, at which times he bad always shouldered bis |)uck and tramjied along with his guides, having many a time, as he said, " Done them up and come in at night fresh as a daisy, while they were beat out/' He had thouglit nothing of carrying 60 pounds on his back all day through the woods, and had paddled and |x»rtaged with the best of them. AVlten nut out hunting or fishing he had been untiring in bis devotion to Inisiness, and for the previous seven years bad w^orked with colossal energy in building uj» vast interests in the ^ortli. In addition to tireless work with bis brain in bis office, be had endured and intleed revelled in efforts connected with his business schemes, reijuiring and displaying extraordinary physical endurance, so that he was the marvel of liis friends. On one oeca- sion, in December, 1900, this robust man of medium stature and weight, without an ounce of superfluous fat, all muscle and sinew, started with a crew of men up bis railroad to inspect some work, and, as the engine was forced to *' buck snowdrifts " and make a
310 DISEASES OP THE HEART
way for itself, the engineer suddenly discovered that, having neglected to fill his tank afresh, it was out of water. The weather was intensely cold, and this meant that the fire would have to be dumped and the locomotive be allowed to freeze up, or that in some way a supply of water must be obtained. They were near a river, and this indomitable man of whom I write started on a dead run through the deep snow for a camp of his men a mile and a half distant, where he knew he could obtain some pails. He went himself because he knew he could get there in quicker time than any of his men, and, too, would have the authority to take the buckets. Arriving there, he shouldered a package of half a dozen iron buckets and started back, running all the way through the snow with his load of 75 pounds. He arrived in time to save the engine, but completely exhausted. Nevertheless he recovered in the course of the day, and thought nothing more of it, going about his hercnilean daily work in and out of the office as before. But outraged Nature was to have her revenge yet. In April fol- lowing his almost superhuman effort, this man of affairs took a hard, fast horseback ride of ten miles over a very rough road, and before he reached his destination he became seized with a severe pain in the epigastrium, which, however, ceased to trouble him greatly after he had dismounted. From that time on until I saw him the next October, he had grown steadily less and less able to endure exertion without this epigastric distress, to which dyspnoea finally became added. Tn June following his ride, he had climbed down and up a ladder into and out of a mine several hundred feet in depth, and on reaching the surface again had noticed that he was very much winded, and from this time forward he was obliged to walk slowly if he did not wish to suffer from his pain and short- ness of breath. The night previous to his arrival in Chicago, and on several other occasions, he had been awakened in the small hours by a feeling of oppression which compelled him to sit up on the edge of his bed and breathe hard. On this particular occa- sion he had attributed his attack to the closeness of the sleeping- car, had taken a drink of whisky, experienced speedy relief, and, lying down, had gone to sleep. Such in brief was his history, a;* full of interest as a romance.
From his recital I expected to find a case of simple cardiac dila- tation from overstrain, such a case as I had shortly before finished
AORTIC REOrRGlTATION
311
treating. Imagine my surpri^, therefore, when I discovered a collajising but not large pulse of ahout 110, a diffused, rather indefinite apex-ljeat way below and outside the left nipple, percus- sion evidence of a greatly hype rtropli led and dilated left ven iricle (Fig. 00), feeble heart^soundis, and everywhere a loud dou- ble murmur plainly aortic in origin. Duroziez's sign and capillary pulse were present, and the liver was juilpable and tender a couple of inches below the inferior costal margin. The left lobe was specially swollen and sensitive to pressure. The urine was and always remained negative.
Here, then, was an aortic regurgitation, hut what was its eti- ology i Was it possible that there had been a valvulitis years before and that the eompensation had l)een broken down hy his prodigious exertions, or had the heart - mtisele been not quite healthy and had that run started a stretching of the aortic ring which had been increased by suecc*eding ef- forts^ or had the strain led to an aortitis or aneurysm, and this to insufficiency of the valves? Rupture of a cusp was out of the question, be- cause of the absence of serious 8;vmptonis in the weeks imme- diately succeeding his run. A previous valvulitis was not impossible, for it is well known that the enonnous secondary hypertro|ihy of the left ven- tricle sometimes develoi>ed in cases of rheumatic incompetence of the aortic valves, is capable of enduring an extraordinary degree of strain for years, as witness some of the cases treated by the great Stokes. In this instance there was no history of anyibiog to lead to endocarditis except the scarlatina, and that occurred thirty- six years before, and if that had led to valvular insufficiency ita presence had never been suspected or betrayed by a 8\Tnptom. Moreover, thirty-six years is a very long time for an aortic regur-
Flti, 60,— RlLATt%'E DVLXEW) IW CaBE OF AoRTtC lUllLROtTATlOK ({». 34.^1^
First t'xuminjititm.
312
DISEASES OF THE HEART
gitation to exist without discovery. I therefore considered this explanation as less likely than one of the others. Regarding aneu- rysm as eaiise of iji>rtie ineoiuj>etenee, 1 liad already ol»j^erved a case in which such was the condition, not a very uniisnal one, but for the greater part of a year there had been no symptom to point
r <Hv>r IN Ca?e or Aortu^ Kkouuoitation.
to anenrvsni, and it was not discovered nntil three months prior to death from pressnre on (he left hing. Consequently 1 now had a Roentgen-ray picture taken for the detection «if anonrysni if such existed. It is shown above (Fig. Gl), and slimvs great breadth
AORTIC REGURGITATION
313
of slifidow at the base over the position of the large vessels, but nothing that can hv interpreted to indic^ate aneurvsm. It also shows a very large heart, a veritable cor hovtnum. The only re- maining hypothesis was that of stretching of the aortic ring and base of tire aorta. The vessel cunld be felt pulsating at the level of fhe nj>i>er etlge of the sternum, and in the aortic area could lie bcjtrd u faint tli«itirict click, evidently a feeble aortic second trine.
Another cme that has l>een already narrated (^ee page 15S) had taught me how guarded one shouhl be in attributing to endo- carditis w*hat might turn out to be attributable to myocarditis and stretching of the orifice, esi^ecially in the absence of a definite his- tory of rheumatism or other sufficient etiological factor. In the present instanre this point was of great irnportaiiee in its bearing on prognosis. I l>elieve the subsequent lack of resistance on the part of the left ventricle bore out strongly my original view of the origin of the valvular incomj>etence. The leak was started by the awful strain of that insane run, and was augmented and rendered hopeless of repair by his succeeding exertions.
Tlie num was t*dd bow serrnus bis roudition was, and that bis only hope of reinstating his heart-])nwer lay in at once giving him- self up to entire and prolonged rest in bed. Very reluctantly he yielded to the inevitable, and took to his bed. He was of a some- what |ieculiar nervous make-up and could not be induced to remain as imictive as I tliought w:is ncri'ssary. He would, for instance, get up and go to the toilet in the adjoining liath-room instead of using a bed-pan. Hn would get up an<l shave himself, and be would sit ujT in bed to eat, and on one or two occasions arose to receive a visitor. I now Manie myself for having permitted even 80 much latitude, yet bis annoying symptoms disappeared so promptly on being put to rest and bis left ventricle came down so appreciably in size and tlie apcX'i)eat returned in such strength, that I hoped, against my first judgnif-nt, that the heart was going to recover it5 hypertrophy l>etter than was at first feared.
At the end of a month of this enforccfl inaction the patient be* came so restless that permission was given bim to leave his bed and, by degrees, Ijegin to move about, under the condition that he was to lie down much of the time. He w^as allow^cd also to take iaily drive. A course of Xauheim baths was also begun in the
314 DISEASES OP THE HEART
hope of re-enforcing the effect of the digitalis, nitroglycerin, and strychnine he was taking. For a week he did not seem to suffer any ill consequences, although he ignorantly overdid in various, to him, seemingly trivial ways. He would put on his heavy fur- lined overcoat unassisted, and go into a store to make purchases, and be on his feet for an hour at a time, not realizing that he was still far from well. Then the saline baths did not slow his pulse and improve its quality as they should have done, and after a bath he did not react to my satisfaction. So after two weeks, in which it was clear that he was losing ground, I again ordered him to bed, this time insisting on his having a trained nurse who was to lift him, and in many ways save him from efforts he had made during the earlier weeks. He now remained fairly quiet, though it was very difficult for him to learn to keep still and not to assist his nurse whenever she lifted him, turned him, etc. He simply w^ould not use a bed-pan, and therefore was drawn in a chair to the bath-room, and later on was lifted on to a night- stool alongside his bed. His treatment consisted of digitalis and other tonics, cathartics, and resistance exercises given by a com- petent attendant. Although it was realized that these last were in violation of the principle of absolute physical repose, still they were decided on because they slowed the pulse somewhat, im- proved its quality, and so quieted him that he fell asleep after the seance was over. Xo more Xaulieim baths were given.
As days ran into weeks, however, it became plain to me that treatment was not going to restore what he had lost during the two weeks he had been up. Indeed, he slowly but perceptibly lost ground. His liver swelled again somewhat and gave a very uncom- fortable feeling of fulness below the ribs, which he attributed to his stomach and to indigestion. The outline of the left ventricle very gradually became more rounded, the apex less pointed, and its impulse less vigorous. It was at length clear that if the mitral valve was not already relatively incompetent, a matter for cer- tain reasons difficult of positive determination, it would soon be- come so.
January 1st he was moved from the hotel into a rented house, and the removal was effected as easily and with as little disturbance to him as possible. Xevertheless when I visited him a few hours later I saw at once that the transfer had hurt him. His pulse was
AORTIC REGURGITATION
315
less strong, the heart-dulness a little larger, and his breathing a little less easv.
The feature that especially increased mr anxiety, however, was the peculiar irregularity of the pulse. At varying intervals, from 5 to 20 beats', there would eome a .sudden €[uick wave closely fol- lowing the one before, as if the heart were trying to catch up in its work by giving an extra contraction (pulsus intercurrent). The patientj moreover, appeared totally unconscious of this peculiar action, whicli did not disappear during the remaining two weeks of life until the dilalatiun of the left ventricle had growm so ex- treme as to lead to relative incompetence of all the other valves. One night, apparently in consequence of flatulent distention of the bowels lie became extremely nervous and alarmed over a flut- tering of the heart, which persisted for several hours, and until after a dose of whisky administered liy the nurse lie fell asleep.
To add to the damaging effect of all this strain, the patient became nervous and desfwndent, and so desirous of getting out of doors that I agreed to bis going out in bis wheel-chair provided he was carried downstairs on a stretcher, then placed in his chair, and on his return brought uj) again in the same manner. This was attempted but was bungled in some way so that he was ren- dered extremely nervous, and, after all, was borne down and up in his attendant's arms. This in reality ought not to have injured him had his heart-musi'le been less seriously damaged. As it was I recognised, so sixm as I examined him a short time after* ward, that the walls of the cardiac cavities were still more stretched and the liver still more engorged.
He now lost his appetite entirely, pas^sed rather poor nights, and showed a sUght puffiiiess of the iu,stei>s. One week biter he began to have very slight nausea, and on Sunday forenoon was seized with a sudden attack of vomiting. He rose up in her! and strained violently in the act in a way to make me most uneasy. I bapi:)ened to be sitting by his bedside at the time and took occasion to observe the pulse. This did not become specially accelerated but rather thready, and its irregularity somewhat more pro- nounced. Examination of the heart did not, however, reveal any marked ill effect. He was now put on kumyss, and all internal medication was stopped lest the stomach might be again disturbed. He passed a poor night and the next day complained of rather
316
DISEASES OF THE HEART
more fulness in tlie epigastrium. About noon this feeling of dis- tress increased, a '* harJ lump '* appeared above the umbilicuSj and about 4 p. II. he had a prolonged nervous chill. They succeeded in reaching nie by telephone at this time, and I ordered an injec- tifUi iA* UKO'phinr I witli ^l^ of atropine, thinking, as con&iidered
Ijy the nurse, that the pain ami ** knotting " might lie an utrumulatiuii uf rtatu& in the rulon. Vpon arriving an hour later and examining the nhdiv tien, I at once diseovered that he left lol>e of the liver was ureatly swollen, tt*ntli*r to pressure^ anil was tlimbhing from the propagated pulsa- tion of the aorta lieneath. It required only a luuef exami- nation of the hrart U* perceive that the strain of vfnuiting the day before had dniie its evil Fio. rtsi!.— Kbi,at»vb Di'i,NE» AND LuwKR worfc by setting u|> a marked B»K..« or L,>«« «..HTLv nK,..Hr. increase of back-pressure (Fig.
(i2). The external jugulara were swollen, the ri^hf heart more dilated, and the pubnonie sec- ond tone very muffled. A eathartic was ordered and he was at once pot on a hypodermic of nitroglycerin ^^ with ^^ of strych- nine sulphate every four hours. Half a dozen watery stools the next morning made him feel ermifnrtable, but it was elenr that back-pressure wm on ihv iurrease. By noon he was quite eviiuoBed, and the pulse was small aiul weak, lie was then put on 15 dro|>s of fat-free tincture of digitalis every two hours, the glouoiu, etrychnine, and cathartics being coutiuued,
Wednesibiy mi»rning, in spite of free hydragogue catharsis, bis i*oniIitit»n was still woi*se. The pulmouic second tone was re- placed by a soft diastolic niur!uur, and he was cyanosed. Even turning him in bed itrodut'cd jiroftiuud cyanosis, feebleness of the pulse, and dittit-ulty of breathing. The morphine w*as continued h\'porlernuValIy in doses of J onre or twire in twenty-four hours to prevent restlessness and unnecessary suffering, while the interval
AORTIC REGURGITATION
317
between the injections of nitroglycerin and stry**hnine was shon- eneJ to two instead of four lioiiri^. He then rallied for a few hours and the cyanosiis almost disappearedj but the heart-findings remained about as before, ilorphine gave him a fairly eomfort- able night and Tbnrsday eame. The pulmonic second sound was now audible again, but the pulmonic diastolic murnuir persisted and the external jugulars and liver pulsated nnmistakabl}, while a soft systcdic bruit, evidently tricuspid, could he heard at riclit of the sterniun near its extremity.
The pulse now began to slow down, from 00 to 90, tlien to 88, and by noon to 80, yet did not grow stronger. On the nmtrary, it seemed to grow smaller and weaker, while the jngnhir pidsation increased, and distention of the right an rich* caused iil>sLdute dub ness to rearli across the steriuim and beyond. lie had now re- ceived 24 doses of digitahs, and believing tluit it would only do etill greater harm, I ordered it stopped and ju-ovided elixir of valerianate of ammonia and a 10-per-cent solution of camphor in sterilized olive uil against iiossihle further sinking of tlie pidse. The oil was to be injcetcd un<ler the skin in case of need.
The feet and ankles were now ipiirc ydcnuitous, nrine was vqvj scant, tlie patient perspired profusely, slept njuch of the time, and was profoundly cyanosed with marked puffiness of the neck and lower part of the face, Jlorc bowel niovemcnts of a watery charac- ter were secnrcd withtnit any iuijircshiun on the stasis. The ptUse stayed at 80, V(M'v weak, and whenever tn rest him he was turned on to his back or left side, hecanie distinctly worse. His greatest comfort was when he lay in the right biteral rlccuhitus. His respirations were 28, and his breathing was hihoured at times. Rides of hypostatic congestion were audible at the right base behind.
In this condition things remained until 10.30 p. m., when sud- denly he complained of inability to breathe, turned purple in the face, grew rigid and pulseless. The nurse hastily injected the camphorated oil as I entered the room and hurried to the bedside* I listened for the beart-sonnds, hut all was still; life was extinct, his muscles relaxed and his sufferings were at an end.
This case has heen detailed at this length in the belief that it might prove highly instructive on many of the points that have been already dwelt upon in regard to aortic regurgitation, and
318 DISEASES OP THE HEART
will be dwelt on in considering the prognosis and treatment of valvular disease in general.
It brings out only too clearly the utter hopelessness of the prog- nosis in aortic insufficiency in men of middle age when compensa- tion once gives way, no matter what the cause of the valvular de- fect. The heart-walls are too degenerated to retain any temporary improvement that may follow appropriate treatment.
In the matter of management nothing is so important as rest, and this should be as absolute as possible. One cannot refrain from looking over his management of a case and being inclined some- times to upbraid himself for not having done this or that. In this case I now think I should perhaps have been rather more energetic with digitalis from the very start than I was, and yet at the time I feared its effects on the vascular system might offset that on the heart. In another case I believe I will try pushing the drug to the limit of its usefulness. Then as to the degree of rest which was secured. I might have been less lenient, and yet this gentleman had been so active a man that rest in bed chafed him. It was a nice question to decide whether, as a matter of fact, strictness in regard to complete physical inaction would not have made him so impatient and restless in spirit as to have entirely counteracted the benefit to be had from rest of body, or as to have done him greater harm than did the little exercise he took during the first month of treatment. At all events this was how I looked at it th(Mi, and I am not sure but I was right. As a matter of fact the result was inevitable, and no treatment could do more than retard the fatal issue.
CHAPTER IX
AORTIC STENOSIS
Tins is a comparatively rare affection when existing alone, antl, as its name s^ignilies, consists of a narrowing of t!ie aortic ostinni. It is awavs a structural defect and owes its origin chiefly to iiitlamnmtory changes.
Morbid Anatomy. — There are two types of structural change that iruiy leu J to narrowing of the aortic orifice: (1) The cusps of the valve may hccome adherent and stiffened; (2) growth and organization or calcification of vegetations may take place in such a way as to interfere with the passage of the hlood-strcam. The former defect may l>e tlue to a develoi>jnental error, and oc- curs in congenital narrowing. It may also, however, follow acute endocarditis. The cusps may become so completely adlierent that only a small opening, scarcely large enough to admit the point of a lead-pencil, is left. Fig, 63 shows such a heart, and also ilhis- trates the proneness of acute endocarditis to attack a valve already the subject of chronic disease. Here a tiny row of vegetations is seen along the line of maximum contact during the closure of the valves. In those cases of stenosis of sclerotic origin in which tho cusps are not adherent but interfere with the blood-flow on ac- count of stiffness which prevents their swinging back in the normal way, regurgitation is usiuilly so freely permitted that the ease is classed as one of insufficiency.
In the second class, vegetations on the aortic valve may assume such proportions as to induce narrowing of the orifice. These oc- cur most usually on the ventricular surface of the valve segments, and in that situation of course interfere also with the closure of the valve, producing leakage. The narrowing is usually the pre- dominant effect, however, of a large vegetation in this situation. An interesting type of stenosis, shown well in Fig. 64, is that in which vegetations develop in one or more of tlie sinuses of Vah
ai9
830
DISEASES OF THE HEART
§alva. Calcified thromhi ia this location almost rompletely pre- vent the opening of the valve, and niav prodnce an extreme grade of stenosis.
^ ^ ^
Fia, ($&— HsAitT Of AoBTic Stehosis, wirit Atun.,.
AOITTl E3ftfOCAIlI»lTlS.
r! CuttPB, A»U AUMJ
Aortic stenosis is not always Im'ated in the valve, however, for the aortic rinij, and sometimes the whole trunk of the vessel, may be narrowed. This is probubly mtjst ( iff en a eongenitid defect. Stenosis of the hearty or more properly of the conns arteriosus of the left ventricle, may also produce the secondary effects of ste- nosis of the orifice.
It goes without saying tliat aortic stenosis, according to its de- gree, presents more or less resistance to the outflow of blood from
AORTIC STENOSIS
321
the ventricle. Tii order, tlierefore, to disoliarge a normal volume of blood through tlie diminished opeiiingj the ventricle is obliged to contract more powerful iy and more slowly, Tliis increased work results in the development of hypertrophy.
Fraentzel is of the opinion that dilatation of the ventricular cavity precedoj^ the hypertrophy, heeause the w^all cannot accom- modate itself to its increased task. This would be the case, doubt- less, were the stenosis suddenly developed^ but inasmuch as the changes in the valves leading to stenosis are brought about slowly, the wall of the left ventricle is able, pari passu^ to meet the grow-
Vm. M.— Hcart or AoxTic STKNosta, «howimo CALcirixD VEoiTATioirt lit Sivutu
OF VALSALViL.
ing resistance. It seems clear, therefore, that hypertrophy of the left ventricle is the first result; and that when dilatation of it« 21
DISEASES OP THE HEART
cavity is also present, it is either the effect of associated regurgita- tion or comes on gradually with failing compensation.
Until compensation does fail the secondary effects are limited to the left ventricle. When, however, the ventricle becomes un- able to fully empty itself at each systole, the residual blood forms an obstruction to the complete emptying of the auricle. The stasis thus produced creeps back in the manner already described in pre- ceding chapters, with the result of general cardiac enlargement,* and the manifestations of passive congestion in the various organs of the body.
In extreme grades of stenosis the supply of blood to the coro- nary arteries may be so reduced as to cause degeneration of the myocardium. In this manner the constriction tends ultimately to the destruction of that compensatory hypertrophy by which alone the effects of the stenosis can be offset. It will be readily seen that in such a heart as that of Fig. 64, this factor would be of great importance.
Etiology. — Stenosis of the aortic orifice is in nearly all in- stances acquired after birth and is then due either to endocarditis or sclerosis. The disease occurs more often in the male than the female sex, the same as aortic regurgitation, and, in my experience, more frequently in the young. It is, however, so rarely observed independently of incompetence that of several hundred cai?es of valvular disease of which I have records, there are only half a dozen instances of pure and uncomplicated stenosis of the kind under consideration. This is readily understood when one reflects for a moment upon the conditions which are responsible for the stenosis.
In those cases in which the valve-segments are agglutinated and rigid, projecting like a cone into the lumen of the artery, there is left a small opening at the extremity of the cone through which a certain amount of reflux is possible. In other cases in which vege- tations cause obstruction there is usually such a condition of the thrombi or of the valve-flaps as prevents their perfect coapta- tion, and hence regurgitation takes place.
When in any given case regurgitation is not also recognised clinically, the conclusion is reasonable that either the valve is not too rigid to close the ostium, or that the seat of obstruction is in the ring or conus.
AORTIC STENOSIS
323
The etiological factors respousible for tlie endocarditis or the degenerative clmiiges iiiiJerljiiig the stenosis have already been so fully considered in the causation of the foregoing valvular de- fects that it would be a needless repetition to discuss them here.
Symptoms, — Stenosis of an orifice is justly regarded as a serious alTeciiun ; yet in this particular lesion subjective syuiptoins ^are sometimes entirely wanting. Consequently the clinical fea- tures of each case, as well as their severity, depend npon the de- gree of narrowing. If this is extreme, it is impossible for the disease to remain latent, and the patient suffers either from a too inadequate supply of arterial bbiod to maintain nutrition and nor- mal visceral function, or from the effects of stasis behind the seat of constriction.
In the slighter degrees of aortic stenosis patients are usually capable of ordinary physical and mental activity the same as their companions. I recall a lad of fifteen who presented himself at ray clinic in the Post-Graduate Medical Srhool, liceause of some trivial digestive disorder, ami io wliom were discovered all the signs of uucuioplicated aortic stcnosis» Jndged by the secondary physical signs it was not very pronounced, and the boy stated that be was a newsboy selling papers on the suburban trains, in the habit of carrying heavy bundles of papers, and of jumping on and off mov- ing trains without any shortness of breath or consciousness of his heart's action.
It is in such cases as this that individuals go for years without knowing there is an}i:hing w^rong with them, and at length learn of their defect through its accidental discovery by some medical examiner. Indeed, ]>ersons witli thoronghly compensated aortic obstruction may pass through their entire lives to old age without having ever learned of their disease. The pulse of such an indi- vidual is slower and smaller than normal, and the cardiac impulse denotes hypertrophy, but having grown up, so to speak* with these deviations from the general nilcj he pays them no attention.
If any circulatory disturbances result from the aortic constric- tion wlien single and of minor degree* they are such as indicate deficient supply of arterial blood to the various organs and parts of the body. Even these effects may be too slight to attract special attention. At the most, the circulation is not very active, and the boy may not be quite as vigorous as his healthy play-fellows.
324 DISEASES OP THE HEART
It is stated by some authors that aortic narrowing of consider- able degree may occasionally give rise to distinct symptoms of cere- bral anaemia — i. e., syncopal attacks and epileptiform seizures. Such serious effects must indicate either an extreme grade of ob- struction or periods of cardiac weakness when the left ventricle expels very small amounts of blood, or perhai)s none at all, for a few seconds, in consequence of intermittence. A far more common symptom is vertigo ; and yet even in this there is nothing peculiar to aortic stenosis, since, as well known, dizziness may be experi- enced in any form of valve-lesion. In one instance coming under my observation attacks of vertigo proved a most distressing fea- ture, and yet in this case they depended not so much upon the cardiac defect per se as upon disordered action of the muscle fibres — 1. e., interference with its capacity for conducting motor im- pulses. The case presents features that bring it into the category of Stokes-Adams disease, and will be referred to again in con- sidering that interesting symptom-complex.
In the fall of 1899 an officer of the United States Army de- sired my oj)inion concerning the condition of his heart, which he stated was very unusual. lie was highly intelligent, and had made his heart an object of much study. From his detailed report of his history the following summary is given: He was born in 1873, and with exception of measles had no illness until his eighth year, at which tinio he had a protracted and nearly fatal illness thought to be acute gastritis. For a number of years thereafter his digestion was weak, but he was able to ]>articipate in the games and sports of his playmates without Iwing conscious of ill effects.
At the age of fourteen or fifteen he accidentally discovered that his ])ulse-rate was between 40 and 45, but at the age of eight- een he was pa^^sed for life insurance, the examiner finding his pulse of normal frequency, and not detecting any cardiac murmur. Nevertheless, when a year later he applied for admission to the AVest Point Military Academy he was told that he gave signs of slight aortic stenosis. Thereupon he consulted many physicians in his native town and elsewhere, receiving a variety of opinions. Some declared he had valvular disease, and others as positively asserted the contrary.
On one occasion, after having hopped up and down the exam-
AORTIC STEXOSIS
325
inmg surgeon's office, he was to!d that his pulse was beating 140 ])er uiimite. To iimki* a hmg story shortj it suffices to say he was at k^ugth athiiiftCHl to the Ae:.(leinj at the age of twenty, notwith- standing the (iiscovery of his aortic stenosis, the lesion heing con- sidercMl trilling and coni])en?^ation good During his cadetship he \vm able to endure the arduous drills with apparently no more dis- tress than did his comrades, although he noticed upon a few occa- sions that the veins on liis forehead stood out prominently.
In his si^iiiitu^ year he, like many others of his class, had to go to the hospital with chills and fever that were considered malarial, and which have not recurred since his leaving the Academy. From September, 1897, until the spring of 1801), he was stationed in San Francisco, and while there hail a fudse-rate of 38, but with the exceptiun uf slight hhirriiig of vision and headache, that was al- ways relieved by calomel, he had no illness or sj^mptoms referable to his heart* In the fall of ISiKS, upon being examined for promo- tion, he was told he had aortic stenosis and mitral regurgitation, and was rejected in consequence. Nevertheless, upon his record he at length ohtain<'d his prnmuticni, and was transferred to a post in the East.
In May, 1809, he participated in a bicycle ride, being unac- customed to that particular form of exercise, although he engaged in every other kind of sport and game with his fellows. During this ride he nnnle n s|mrt, and then got out of breath, hut other- wise appeared to suffer n<» inc<mvcnieiice. Two hours subsequent to his return to his quarters, and while standing by a table waiting for dinnerj he suddenly became dizzy and was assisted to a couch. The junior surgeon was sunnuoned, and finding his pulse 30, ad- ministered whisky, which somewhat relieved him and brought his pulse up to 50. From that i-me on he was daily distressed by spells of vertigo for some weeks, ami he noted that the regular slow ac- tion of the heart was every now^ and then exchanged for a more rapid irregular one, with an occasional violent thump against the chest-wall. At this time his dizziness w^as usually relieved by assuming the recumbent posture.
lie received some mediciual treatment, nature unknown, and then for a month w^as free from his distressing symptom. It re- turned again* however, more violently and still annoyed him in November, 1809, the date of my first examination. During the
326 DISEASES OF THE HEART
summer previous he was given digitalis for a short period, and twice after having taken the remedy his pulse suddenly became accelerated to 60, and was regular. During these months he was in the habit of striving to either work off or forget his dizziness by playing golf, and it is worthy of note that such exercise did not aggravate the symptom.
In September, 1899, he suddenly, while studying the action of his heart, made the discovery that during his spells of vertigo, and while his radial pulse was but 2(y to 30, he could perceive by placing his finger above the clavicle a series of " small pulsations which corresponded with feeble heart contractions." These were of variable number, and were interposed between two energetic cardiac contractions which were declared by a forcible apex-impulse and by the radial pulse. He furthermore noted that no matter how slow his radial pulse was, oven as infrequent as 19 in the min- ute, he was not dizzy provided it was regular and the number of small pulsations in the neck was uniform. I shall recur to this striking and peculiar feature again. During that same fall he was treated for a few weeks in the Battlecreek Sanitarium, and while there requested on one occasion that an '* ice compress " be placed upon his heart. Tliis was done, and upon its removal ten or fifteen minutes later his heart grew regular and the pulse at the wrist registered 56. He then fell asleep, only to find next morning that its rate was again 26 to 30.
The night before consulting me had been an unusually bad one, and when I saw him the pulse was 36 and irregular. He admitted no shortness of breath on exertion, but suffered from constipation. He thought that on a few occasions he had lost consciousness. Not to make this narrative tedious, I will say my examination revealed hypertrophy of the left ventricle, the apex-beat when felt being broad and strongly thrusting in the sixth left interspace, 11.5 cen- timetres to the left of the median line and 1 centimetre outside of nipple. Increase of both superficial and deejvseated dulness to the right showed enlargement of the right heart. There was a loud, rough systolic murmur over the entire praK»ordia whenever the heart made an energetic contraction, and this murmur was suc- ceeded by a distinct second sound even in the aortic area. U])on in- vestigating this bniit minutely it was found to have two areas of maximum intensity, one in the aortic and the other in the mitral
AORTIC STENOSIS
337
area, altliough I could not detect tliat the quality iu the two re- gions was dilTerent 1 foimd subsequently, ho\ve%'er, that at the apex the munuur was softer and more blowing.
The murmur at the base was transmitted upward into the neck as well as on to the body of the hearty while that at the apex was pro|jagated outward into the axilla and feebly to the hack. At til-Sit 1 did not observe the small pulsations in the neck, but when my attention was directed to them I perceived them distinctly enough, and 1 also noted that synchronous with these were feebly audible cardiac tones, while at a much later date these feeble heart-suunds were accompanied by a faint murmur and an indis- tinct apex-beat. These small pulsation^, for lack of a better term, were of irregular number, being ordinarily two, but sometimes as many as seyen, and according to the officer even more, before there would come a normal pulse-wave* It was suggested by the patient tliat these were auricular in origin, but I decided that they were due to feeble ventricular contractions, and subsequent car- diograms taken by Dr, Janeway iu New York established the cor- rectness of my opinion,
The very interesting feature pertaining to these incomplete systoles was, that so long a? they were regular and in groups of two, vertigo did not ensue. Wlii^Uj on the contrary, they ran up to half a dozen or more the patient felt dizzy or even fainted. These pulsations were first thought by me to be in the carotid artery, but are now known to be jugular.
My diagnosis of the cardiac disease was the same as that of others: aortic stenc^sis of iriild degree and mitral insufficiency, the heart being in a state of stilbpreseryed cornpcusatiou; for although vertigo was a symptom, there was no dyspnflc^a on effort and no secondary hepatic or other \dsceral engorgement. Two things greatly pnzzh'd me: first, if the mitral valve leaked why did not the obstruction of the aortic orifice render the regurgitation through the mitral more serious, as is usually the effect; and, sec- ond, what was the cause of the vertigo, or rather the irregidarity, in the heart's action.
This latter condition, I believed, was in some manner connected with his digestive organs, but just how I conld not decide. The urine was collected for twenty -four hours and carefully examined in the Columbus Medical Laboratory, but aside from some con-
328 DISEASES OF THE HEART
centration was negative. The genitalia were examined by a com- petent specialist, but showed nothing more than slight urethral congestion and hypera^sthesia. The patient was sent to an expert neurologist, who was not able to discover any cause in disorder of the nervous system. Diffusible stimulants in frequent large doses for many hours were administered without appreciable effect, as were cathartics and remedies to improve digestion; all to no pur- pose. The case was dismissed, therefore, as an enigma and with- out a parallel in my experience. It was not at this time recog- nised as an instance of Stokes-Adams disease.
But now comes the still more interesting sequel. At Christmas- time, 1900, this same young officer reappeared with the statement that during the previous summer he had visited Bad Xauheim and been treated with baths by Dr. Schott without any benefit; had been examined by a number of comi)etent men, among whom was Rosenbach of Berlin. Xo one had given him any help, and no one had decided the precise nature of his heart-trouble. Rosenbach indeed had diagnosticated the aortic stenosis, but was undecided as to what was the condition at the mitral. I found things exactly as a year earlier. But strong in my belief that the vertigo that still continued was in some way related to his digestion, or met- abolism, or excretion, or all together, I persuaded the young man to try for a mouth an absolutely non-animal dietary, by which was meant the exclusion of anything derived from the animal kingdom, including meat, ])oiiltrv, fish, eggs, etc., with exce})tion of cheese and milk. These and butter, of course, were to be allowed, to- gether with all kinds of cereals, vegetables, fruits, nuts, and breads. For several weeks his urine was sent to me for analysis, and was always loaded with indican and oxalic acid, but in other respects was normal. Xearly four months later the })atient reappeared with a perfectly regular pulse of 2C), and was entirely free from his vertigo, which he stated had left so soon as he began the prescribed diet and had not once recurred.
Examination of the heart showed the condition unchanged ex- cepting regularly interposed between every two vigorous cardiac systoles were two feeble contractions that produced palpable and visible small pulsations in the right common carotid, as well as weak heart-sounds, but no perceptible radial pulse. The actual heart-rate was therefore 78. The subjoined sphyginographic tra-
AORTIC STENOSIS
S99
ciiig (Fig. fi5) was taken Kv Dr. Edward F. Welles, and is bv him, a conipetfnt iiidgf% considered entirely nornml exeept in rate.
Fm, 66.— SriiiroMuojtAM MiMU Ta^^e of Aoutio 8TENo»ia (p, 324j. Puky-rutt^ *z5 per ndnute.
The conchisions to which I arn forced by this case are the fol- lowing: 1. That this singular eanliae action is normal to this in- dividual, and rhat it is only its irregidarity that occasions synii> toms of any kind. 2, That this irregnlarity was of an aiito-infec* tioiis origin, dne either to the productir>n of leiieoniaines or to the inthience of constijtariun on the vagus or hcart-nuis<:;le cells, for on this new dietary he has had two or more bowel movements daily. 3. That the lesion is a mild aortic stenosis together with a mitral defect, of the exact nature of which I am not certain. But as I feel sui-e that at my last exariiination I detected a very short presystolic thrill and niurniiir as well as an apex-systolic murmur, I am inclined to the opininn that there is buth narrowing and re- gurgitation at the mitral ostium. AVby this combined lesiun dues not occasion secondary signs and symptoms can only be exphiiucd on the hypothesis tJiat the defects are slighter than %vould be sup- posed from tlie cardiac findings, ])articularly the intensity of the murmurs. The peculiarity of bis normal, or at least seemingly norma ly cardiac action, is still inexjdicable. The symptonis in this case do not as such belong to the usual history of aortic stenosis, but are here narrated because they may be remotely referred to the valvular lesion and illustrate the vertigo said to be sometimes depentlent upon narrowing of the aorti** ostium.
It is apparent that the development of subjective symptoms is determined Iiv other conditions than the mere existence of aortic stenosis. They depend upon either dis<>rdered or dehcient cardiac tion. Wlien at length, either in consequence of overstrain or of extreme narrowing, the left ventricle begins to manifest inade- rjuacy, dilatation sets in, and it is no longer able to completely
330 DISEASES OF THE HEART
empty itself. Symptoms of stasis back of the point of constriction now appear. Left ventricle weakness may be shown by feebler systoles and a more rapid, even irregular pulse. Always small and of low tension, it now becomes still emptier, and at the same time more rapid than formerly.
When in the course of time dilatation leads to relative mitral insufficiency, the clinical features become those of mitral regur- gitation in an intense degree. Even before things have reached this grade, however, the patient has noticed more or less breath- lessness on exertion, and it may be also attacks of palpi- tation.
If now the heart is carefully percussed, it is found that the right ventricle has increased in size, while there are in addition signs of engorgement of the general venous system. This condi- tion may last for months before relative mitral insufficiency be- comes pronounced, but as a rule the condition grows more or less rapidly worse and the individual is no longer able to keep about because of dyspna^a and congestion. A mitral systolic murmur is added to that of the aortic stenosis, the right ventricle, feeling the strain of pulmonary congestion, begins to pulsate in the epigas- trium, the cervical and superficial veins swell, the liver grows pal- pable and tender, the urine becomes scanty and concentrated, and at last (pdenia makes its appearance in the feet and ankles. The case has now become converted into one of mitral disease in the stage of broken compensation.
When the mitral orifice shares in the dilatation of the ventricle, the ensuing regurgitation acts as a safety-valve, the same as in cases of aortic incompetence, and actually serves to prolong life. Not infrequently the strain on the right heart leads also to rela- tive tricuspid leakage, and we have the signs of that lesion added to those of the aortic and mitral defects. When this state is reached the patient's sufferings are often extreme, and may be protracted through many months.
In the spring of 1898 I first took charge of a lady of forty-one who had an extreme and apparently pure stenosis of the aortic orifice of rheumatic origin. Six years before, the late Dr. W. W. Jaggard delivered her of a son, and recognised the gravity of the case because of the valvular lesion. The lady did not subsequently experience distinctive cardiac symptoms until the care of a con-
AORTIC STENOSIS
331
iniptive step-«on eompelled her to reside for many months at a ►vCoiisideTabie altitude. Going with him first to Colorado Springs (6,000 feet), she there suffered intensely from shortness of breath, so that they were obliged to take up their residence in the Pecos Valley at a height of about 2,500 feet. Even there she was not able to walk withf>ut considerable dyspnana.
After the death of the young man this lady went abroad, and in Europe sought medical advice. She was advised to take a course of baths under Dr. Schott^ at Bad Xanheini, and while there had her first violent attack of angina pectoris. This followed one of her baths, Xo s^iecial benefit was produced by the balneological treatment, and she returned to America* During the winter of isliT and isiis she pas^sed through an attack of acute nephritis, but when she consulted nie the urine showed no albuniin or other ab- normal findings. The heart was greatly enlarged, but compensa- tion was still fair. That snmmer she had a violent attack of angina foHowing a fatiguing walk across a very uneven meadow, and thereafter was never again well.
When I saw^ her in the fall I considered it necessary to confine her to b€*d for a number of weeks » and %\hen at length she was per* mitted to get np she was still obliged to remain on one floor and to move about with great slowness. The action of the heart did not quicken ninch under exertion, but the ptdse grew very feelile, the veins of the neck swelledj and she breathed with evident difficulty. She had several severe anginal seizures, which will be described in the article on Angina Pectoris* Strength was gained with great slowness, and she was rarely free from more or less cardiac distress. Tliis tonk the form chiefly of brifathlcssness, distention of ihe ab- domen by flatus, and hepatic congestion.
There was never any tedenui, but the ankles often felt swollen and stiff. She passed the summer of 1899 at the seashore under the care of my frieiul, Dr. Edward O- Otis, of Boston, and in the autumn returned no worse but apparently no better as regarded her heart. All these months she had been kept on approved cardiac tonics and was frequently obliged to resort to hydragogue cathar- tics because of the relief they afforded. The ensuing winter was a hard one for her, as she was most of the time confined to her apartments in the care of a trained nurse. This was necessary by reason of the possibility of an anginal paroxysm and because at
332 DISEASES OF THE HEART
night she would sometimes awake deathly cold, in a drenching sweat, and feeling extremely faint.
The pulse at these times was small and feeble, and the coun- tenance was blue. Prompt stimulation relieved her, but not al- ways speedily, for it seemed as if absorption from the stomach was slow, and hence resort was had to hypodermics of j^^ of nitro- glycerin, followed at once by heat to the surface and diffusible stimulants. During that winter, and indeed I may say most of the time for nearly three years, the pulse-rate did not vary much from 96, sinking as low as 90 when she was at her best, and when at her worst rising to 105. I believe that on a few occasions I noted a few beats less than 90, usually regular. As a general thing the pulse was tense, and exacerbation of symptoms was invariably preceded by a noticeable increase in its hardness.
This patient was much distresse<l by frightful dreams, from which she awoke with a start and a feeling of faintness. She was also easily startled by unexpected noises, although she apjwared to have her nerves under good control. Insomnia was very dis- tressing, and yielded to nothing so well as to hypnotism. She had to be extremely careful in diet, for at times everything seemed to create gaseous distention of the stomach and bowels with imme- diate aggravation of her dyspna»a. During that winter relative incompetence of the mitral valve became constant, and every now and then tricuspid regurgitation was added. Even without actual leakage of the tricuspid valve the cervical veins remained much distended and at times caused pain by their pressure. I have since noted painful swelling of the jugulars in another patient, but as a rule have not known patients to complain of actual pain from this cause.
Whenever an attem])t was made to invigorate the circulation by considerable doses of digitalis or other cardiac tonics, this pa- tient became annoyed by a feeling in the heart, which she charac- terized as *^ pounding,'' so that the treatment finally settled down to an attemj)t to keep down pulse tension and stasis by means of nitroglycerin and cathartics, with strychnine and caffeine in small four-hourly doses, and careful feeding.
Thus weeks dragged into months, spring came and passed, the heated term was at hand, with its thunder-storms, for which she possessed an uncontrollable phobia, and she was again sent down
AORTIC STENOSIS
333
to Dr. Otis, at Rye Bearli. By fall her condition grew so threat- ening from oardiac dilalatiun and visceral congestion that she was not able to return to Chicago initil Thanksgiving. When at last she w^as able to make the jonrney m\d reached home I fonnd her in a defdorable state, Botli aiiriculoventriciilar valves were leak- ing, antl the liver was ennniioiisly increased in size. Tlie lungs were so congested that she was harassed by a froijuent eongh^ which eonijiletely exhausted lier» made the face actually purple, and caused her to gasp for breath for many minutes.
The ditHeult sputum was often bhxKly^ or if not actually san- guineoiis was made np of thick, tough brownish mucus. The bases of the lungs were dull, and everywhere were copious niolst and dry rales. Heroin, strychnine hyj)i>ileruiically, energetic catharsis, and apomorphine in |-grain doses at last pulled her out of her desperate condition, and by Christmas she was reasonably com- fortable. She was obliged to remain in bed, however, or to ex- change this for an invalid's eliair. Whenever she made this effort her pulse grew weak, the veins distended, and she was unable to speak fur a minute or two on account of shortness of breath.
The excitement and fatigue of the holidays nearly used her up. Her cough returned with increased visceral hyjiera'uiia and be- came 80 frequent and distressing that it could only be controlled by hyiioderrnic admini^^t ration of bydrochlorate of heroin ^ of a grain. This, however, after a day or two produced nausea and vomiting, and then I actually feared the strain of emesis would make her heart stop beating altogether. As it was, after each vomiting spell she sank Imck on her pillows, lilue in the face, gasp- ing for breath and too exhausted tu speak, while the perspiration simply poured off of her.
At length, however, things mended somewhat, and if not rea- sonably comfortable, she was at least not miserable. Then albu- min and casts appeared in the urine in large amounts, and this patient sufferer began to fail slowly but steadily. By the middle of January it became necessary to resort to stimulating injections of nHjr]>hine and atropine to keep off the horrible sensation of fainting which took possession of her. Strychnine was increased to the limit of toleration, and in addition h^-podermics of a grain of valerianate of caffeine were also given every tw^o hours.
Stasis became so distressing, although oedema was never a very
334 DISEASES OF THE HEART
marked feature, that cathartics became a daily necessity. I recog- nised that the morphine was a two-edged sword, increasing the danger of uraemia and upsetting the stomach, while at the same time affording her relief from positive misery, and therefore it was not withheld. At length, towards the end of February, this boon became so necessary that more than a grain a day was administered. This sufferer's craving for stimulation be- came most urgent and distressing — so much so that whenever the effect of the stimulants passed off she at once felt a ter- rible sensation of dying. Of course this could not be kept up for long, and finally, five days before her death, the stomach gave out. Whether owing to the morphine, to the gastric hypencmia, to irritation of the nerve-centres, or uraemia, I am not able to say, the vomiting became incessant except when she was under the influence of large doses of morphine, as often as every five hours.
There actually seemed to be no circulation at times, as judged by the state of the venous system, and yet that poor heart kept right on, beating 105 times a minute, and for the most part regu- larly. It seemed as if the end must come at any moment through diastolic arrest of the organ, and yet merciful death was withheld for five weary days. At length, forty hours before the struggle ceased, I stopped all medication, except what morphine was actu- ally required to prevent unnecessary suffering, in the hope that by so doing the end might be hastened. Still that heart went on, although gradually growing weaker and weaker. Twenty hours prior to death she sank into coma — merciful coma — and at five o'clock in the morning the sufferer suddenly gave a little gasp, there came a gush of blood to her lips, and all was over. Death was probably due to pulmonary apoplexy, in consequence of sudden arrest of the left ventricle an instant before that of the right.
No excuses are offered for the detailed narration of this case, since I believe it is highly instructive. Two years and a half elapsed between the time this patient first took to her bed and her death, and during all these thirty months it was one unceasing fight against the inevitable. The original defect at the aortic ori- fice became converted, so far as symptoms were concerned, into a mitral and tricuspid regurgitation ; but with this difference, that
AORTIC STENOSIS
335
the aortic narrowing absohitelv jirecliided all possibility of over- coming the dilatation vtf tlie left ventricle and the closing of the mitral valves. Every now and again treatment closed up the tricuspids, but nothing eould restore adeqtmte arterial circula- tion. The more one tries in such cases to force the left ventricle to contract energetically the more is its dilatation likely to be increased.
In this case there was another element tliat had to be reckoned with — namely, the angina i)ectoris and the prohahle degeneration of the myocardium resulting frtjm the cardiac ischa-mia that led to tlie angina. From the start I foresaw^ the inevitable result, and we only put up as good a iiglit as w^e could.
Physical Signs, — Inspection,— In most cases of aortic steno- sis there is nothing in the patient's appearance to attract attention unless it be some degree of pallor. Cyanosis is not present so long as compensation is preserved, and theref(*re when observed it is indicative either of some associated lesion or of cardiac inade- quacy that has led to stasis. The chief value of inspection lies in the fact that it en allies one to detect the location of the apexdieat. This, in consequence of the hypertrophy of the left ventricle, is seen displaced downward and outward, the extent of displace- ment depending n]inn the degree of hypertrophy. In thin individuals with Ijroad intercostal spaces there is sometimes a diffused lifting of that portion of the chest-wall, overlying the left ventricle, hut this is rarely so pronounced as in aortic regur- gitation,
Palfmiion, — The hand laid n|K»n the pnecordia perceives a slow, broiid, heaving impulse, and at once receives the imj)ression gf a powerfully contracting organ. Palpation is consequenrly a vahialde means of examination by enabling one to judge of the contractile energy' of the left ventricle. In corpulent |K?rsons the thickness of the thoracic parietes may conceal the real force of the apex-beat, l>ut as a rule feebleness of the impact, even when the apex is displaced, is a token that dilatation of the ventricle is weakening its systoles. Furthermore, in many cases of aortic narrowing careful palpation of the base of the heart detects a thrill or fremissement at some point along the course of the ascending aorta. This is generally in the second right inter- space close to the edge of the sternum, but it may be on the
S3<;
DISEASES OF THE HEART
Fm, 66. — SruYoiicKiiuiM or U|tcoiUPttciAfXi»
Aortic i^TKNoaia. PerKOUAi observfttiotk.
bi*c»a8tbone or in the third iiiterspaee^ inutiediately adjoining the left sternal border. The inrensity of this thrill b variable, but iU rhythm ia always systolic. It is needless to remind the reath^r that this vibration i? the palpable expression of eddies or eurrenfs in the blood-stream after it has passed the point of con- striction.
The pulse of aortic stenosis is small and nsnally weak in con- 8et]nence of the diminution in the amount of blood ejected from the ventricle. It^ eize there- ^^^^^^^^^^^^^^^^^^^m furnishes ^^^^^^^^^^^^^^^^^^|
the degree stenosis. So ^^^^^^^^^^^^^^^^^^| lonir as the myocardium is healthy antl compensatory hy- pertrophy is maintained the pulse is regular, and in rate is jrom* rally somewhat below the nof^ niaL Accurdingly, an undue aceelerution, or an irregularity, or intermittence of the pulse is a t^ign of weakness. If aortic incom- petence is associated the puke is likely to be modified in accord- ance with the characters uf tluit lesi^in. The spliygniogrn]duc
tracing of aortic stenosis shows rather distinctive char- acters. The amplitude is not great, the line of ascent is rtliliqne, the summit rounded, the descent gradual, and the s<.fondary waves indistinct. These characters are shown in Fig. i»t), which is the copy nf a tracing obtained from one nf my patients who presented the signs of pure and uncom- plicated narrowing of the ostium, there Iteing no dias- tolic murmur of regurgita- tion, and the left ventricle hj^pertrophied with very little dilatation.
Percussion. — ^So long as compensation is preserved, deep- seated cardiac dulness is increased towards the left and downward
i'u.. t.7.— Tvini'AL Helativk I>ilne»» in
Ca»« ok WKLL-COMPENfkATID AOBTIC
i
AORTIC STKNOSIS
to an extent coinmeusurate with the degree of left ventricle hyper- trnphv (Fig. 67). It is only when failing eonipeusation has led to piihnonary eongestioii, or when aortic stenosis is united with a
Fio«6S. — RnvTHM of Aortic Um^tbuctive MmMuii,
mitral defect, that percussion detects any increase of absolute and relative cardiac dulness to the right.
AiiscuUation. — ^The first sound at the apex is apt to he dull and muffled in conse- quence of the preponderance of its muscular clement, while the second tone is likely to l>e enfeebled. Over the base of the heart in the aortic area the ear perceives a murmur which is synchronotis with the first sound, and is therefore systolic (Figs. 68 and f)S)), In pure stenosis there is only this one bruit, Intt not infre- quently there is also a dias- tolic innnnur due to accom- panying aortic regurgitation. The systolic murmur, like the llurili, is of variable intensity, 23
AuRTic Stknutio MrmKUK.
338 DISEASES OP THE HEART
but as a nile it is heard with great distinctness, and is of a harsh or grating quality. Its direction of propagation is with the blood-stream upward into the neck, and it is not rare for the bruit to be audible in the left interscapular region along the course of the descending aorta. In exceptional instances when very intense it is heard throughout the pnecordia, particularly upon and down the sternum, being sometimes most distinct in the left third interspace over the anatomic seat of the aortic valves. The murmur generally replaces the first tone at the base, and when the valves are too stiff and thick to close, the second tone in the aortic area and in the cervical arteries is wanting or so enfeebled as to be merely a rudimentary click. Consequently, in those cases in which the aortic second sound is retained in its normal intensity and clearness, this fact suggests the possibility that the obstruc- tion is situated in the conus arteriosus or at the ostiimi, the valves themsolvos being but slightly affected.
Diag^nosis. — As a general thing there is but little diificulty in diagnosticating the disease in question. The conjunction of signs of left ventricle hypertrophy with a systolic murmur in the aortic area and enfeeblement of the second tone at the right of the ster- num, is as a rule sufficient evidence for its diagnosis, particularly if the i)erson is under forty, and furnishes a history of a previous attack of rheumatism. There are three conditions, however, that must Ik* differentiated : (1 ) sclerosis of the aorta or its valves with- out obstruction, (2) aortic aneurysm, and (3) an accidental mur- mur, often called anai'mic.
In favour of arteriosclerosis are the following: Middle or ad- vanced age, stiffened peripheral arteries, accentuation and ringing quality of the aortic second sound. The left ventricle alone may be hypertrophied, but in most cases the whole heart is enlarged. A history of syphilis as against inflammatory rheumatism also makes strongly for sclerosis instead of stenosis. The difficulty is still further increased by the consideration that degenerative changes may lead to narrowing of the orifice in one way or an- other. Consequently, a precise differential diagnosis between these two diseases cannot always be made.
As regards an aortic aneurysm — every one knows that when this is small it is often impossible of detection, yet the following differential points may be stated : The patient's age, being forty
AORTIC STENOSIS
339
or more, n history of i^yphilis or of injury or strain, stiff arteries^ sTOiptoiiis of pressure, as pain, dyspiifpa, and eongh^ inequality in the size of the pulses of the iieek and upper extremities^ displace- ment rather than hypertrophy of the heart, pulsation, particularly if expansile and condiiiied with bulging in the aortic area^ circum- scribed didnesa over the manubrium sterni or at either side, and in addition to the syatolic aortic murmur, a booming second tone that is not quite pure or is accompanied by a faint bruit. If doubt is still entertained, resort should always be had to the X- ray. Indeed, if this means of diagnosis is accessible^ it should he appealed to for eontirmation in all cases. Jlediastinal tumours pressing on the aorta are so rare that they will not be considered.
If all the signs of aneurysm just mentioned were present in every case a differential diagnosis wcmld not be difficult, but un- fortunately such is seldom the case. I recall a patient in the wards of CtK»k County Hospital who presented a conjunction of signs that rendered the condition of his aortic orifice a subject of much controversy, and owing to his departure from the hospital were never cleared up. In this case there was a history of syn- <'opal attacks, and this fact, it was argued by some, made strongly for stenosis. On the other hand^ I felt quite certain of a circum- scribed area of deep-seated dulness in the first interspace close to the right sternal margin, and therefore believed the condition was more likely an aneurysm.
Lastly, an accidental murnmr in the aortic area may, wlien occurring in the young, give rise to the suspicion of a stenosis. The error can be avoided by attention to the following points: The id»sence, it may be, of a rheumatic history, the sex (the patient being most frequently a female, in w4iom aortic stenosis is compara- tively rare), the absence of left ventricle hypertrophy, retenticui of the aortic second soimd, the |>resence of other accidental mur- murs in other areas, as pulmonary and mitral, the softer quality of the mnnuiir, greater frequency of the radial pulse, and the detCiHion of anaemia in some instances.
Prognosis, — This depends upon the etiology of the affection and the degree of compensation that has bet?n established. If ste- nosis has resulted from degenerative changes in the valves, there are likely to be associated defects in the aortic walls, and it may be in the coronary arteries, which seriously affect the blood-supply
340 DISEASES OF THE HEART
to the heart, and hence prognosis is correspondingly unfavourable. Under such conditions compensatory hypertrophy cannot be main- tained for long, even if it has been developed. For the same rea- son there can be but slight hope of its reinstatement after it has once shown indications of breaking. In these unpromising cases the assurance cannot safely be given that sudden death will not take place. In this respect it presents a similarity to aortic regur- gitation.
When the stenosis has been produced by endocarditis in the young, the life-prospect stands in direct relation to the degree of narrowing and the perfection of compensation. Cases of moderate severity may exist many years without symptoms, and the patient may be likely to die of some intercurrent disease. This is substan- tiated by the frequency with which aortic obstruction is discov- ered post mortem in cases in which its existence was not known or in nowise contributed to the individual's death.
When, however, compensation has once begim to break down, even though the heart-muscle is not greatly degenerated, the prog- nosis becomes mOvSt serious. The loss of compensation is due to initiation or increase of dilatation in consequence of the resistance having l>ecome disproportionate to the strength of the ventricle. In most instances, to be sure, the myocardium of the ventricle has suflFercd degeneration of its contractile elements, in consequence of the small sup])ly of l>l()od sent to the coronary arteries; yet by reason of the j^rogressive nature of the valvular defect the ostium may at length become so reduced in size that even a healthy ven- tricular wall cannot carry on adequate coronary circulation. In either contingency it is out of the question for the ventricle to again develop predominating and adequate hypertrophy. Accord- ingly, the prognosis is very difTerent from that of failing compen- sation in mitral regurgitation, in which, if not too badly lost, it may In? repeatedly restored.
Mode and Caiises of Death. — Stenosis of the aortic ori- fice rarely terminates in sudden death. Certainly it possesses no inherent tendency to such an end, as aortic regurgitation may be said to possess. In obstruction the failing ventricle tends to grad- ual, not sudden dilatation, and hence the fatal issue is likely to come through the effects of progressing stasis, the same as in mitral defects. In some cases increasing weakness of the heart
AORTIC STENOSIS 341
ends in fatal exhaustion before oedema and transudation into the serous cavities become marked. The last weeks, or even months, of life may accordingly be highly distressing to both patient and friends, and death be welcomed as a deliverer.
Of 20 cases of aortic stenosis Hustedt found the following causes of death : Cardiac asthenia 2, pulmonary phthisis 7, pneu- monia 3, marasmus 2, pulmonary oedema, apoplexy, nephritis, bronchitis, emphysema, carcinoma, and anaemia, each 1. It is noteworthy that but 2, or 0.9 per cent, were attributable directly to the heart, while the remaining 20 were due to intercurrent dis- eases. It is also interesting to note that in 7 cases death was due to pulmonary tuberculosis, and that therefore aortic stenosis may be said to predispose to this disease, probably in consequence of the general malnutrition, w^hich is favoured by obstruction at the aortic orifice. This finds further corroboration in the fact that 2 died of marasmus and 1 of anaemia.
342
DISEASES OF THE HEART
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CHAPTER X
TRICUSPID REGURGITATION
This is the most frequeBt of the valvular lesions which aifcct the right heart. It is divisiKle into three classes: 1, Striietiirah 2, Relative. 3. Miiseular; By the last two is meant ineompe- tenee of the valve clue either to stretching of the ventricle or to incomplete coaptation of the cusps from defective contraction of the ring or pa|>illary muscles.
Organic disease of these valves is one of the rarer cardiac de- fects, and when found as a chronic affection is generally congeni- tal. It is not as a clinical entity that tricuspid insufficiency is rare; it is only the structural deformity of inflammatory or scle- rotic nature that is rare. Concern iug the frequency of relative tri- cuspid regurgitation Gibson says: *' It is incomparably the most common of valvular lesions, and that the reason this fact is not brought out in statistics upon the relative fre<]uency of valve de- fects is to l>e found in the eircu instance that incompetence of the tricuspid valve diH?s not in itself seriously impair the general course of the circulation, and it is therefore often found among those who, although under treatment for various affections, have no cardiac symptoms. It accordingly esca|>e9 observation unless especially sought for.'*
This is a renuirkable statement, and is at wide variance with the opinion generally entcrtainrrh It would seem a piece of temerity for me to take issue with Gibson on this point, but as I am not ^^nlHng to accept the presence of a systolic whiff in the tricuspid area as conclusive evidence of leakage at this orifice, I must conclude that I have overlooked this regurgitation many times when he would have diagnosed it. Doubtless, in conse- t[uence of the readiness with which the safety-valve action of this incompetence is brought into play, there may many times be slight leaks that are not considerable enough to produce positive venous pulse in the cervical veins and liver; but this is a matter of con-
343
844 DISEASES OP THE HEART
jecture rather than of demonstration, and one might argue that the murmur is due to some other condition than actual regurgi- tation.
Morbid Aiiatoxny. — The changes discovered at the tricuspid orifice, whether they constitute a structural or a relative defect, are analogous to those at the mitral, and therefore a detailed de- scription of them is omitted. In most cases in which the incom- petence is owing to defects in the valve itself there is a combina- tion of both regurgitation and obstruction. Consequently, more will be said on this subject under the head of Tricuspid Stenosis. When organic changes at this ostium are encountered, they are usually associated with lesions at other orifices, chiefly the mitral.
When the valves in question are relatively insufficient the right ventricle is found dilated and its wall thin. The trabeculce are apt to show evidence of hypertrophy, the papillary muscles of having been stretched, and the valve-flaps are often longer and broader than normal, in consequence of the prolonged pressure to which they have been subjected. The auriculo-ventricular ring is also stretched, admitting more than four fingers. The right auricle is dilated, in some instances to an enormous extent, and its nor- mally thin wall is still thinner. It is not uncommon also to find that the distending force of the regurgitant stream has induced more or less dilatation of the great venous trunks close to their teniii nation in the auricle.
The inyoeardiuni of the ventricle and auricle generally fur- nishes evidence of prolonged stasis in the coronary veins, or of degeneration. Finally, there are the associated changes in the lungs or left heart, which have served as the etiological factors in the development of the right ventricle dilatation and eventual in- comj)etence of the valve.
Tricuspid regurgitation is a pathological condition, and yet Adams, and later Wilkinson King, have pointed out that it really exerts a ** safety-valve action." It occurs with remarkable ease, and these authors claim it is a beneficent provision on the part of Nature by which the heart is spared from disastrous overstrain. In the chapter on Aortic Regurgitation I pointed out that relative incompetence of the bicuspid valve acts in the same way. But whereas the firmness of the mitral ring renders its stretching a matter of much difiiculty, the tricuspid orifice yields to relatively
TKICUSPID REGURGITATION
345
englit pressure and closes ilowii again so soon as the strain is re- moved. Consequently, as everj clinician knowSj leakage through the right auriculo-ventricnlar valve will come and go many times in the course of any disease that throws excessive strain on the right vontrk^e.
Etiology. — Structural defects at the tricuspid orifice are generally produced during fa4al life, and are the result of endo- carditis. Nevertheless these valves may be tlie seat of an inflam- matory process after birth, as well as^ although but seldom^ of sclerotic changes, the same as other valves. When endocarditis attacks the right heart it is usually associated with inflammation elsewhere in the heart* at one of the oilier orifices, and owes its origin to the same etiological factors, which do not require re- capitulation here.
I shall therefore pass on at once to the consideration of those diseases and conditions that are responsible for the causation of the relafive form.
Comprehensively stated, these are all tliose conditions which raise blooih pressure in the pulmonary system to such a point that the right ventricle is no longer capable of successful resistance. Occasionally this pressure l>ecomes so high as to lead to relative incompetence of the pulmonary valves also, but in most cases the ring into which they are inserted i)roves equal to the strain, so that it is the ventricuhir wall and basal ring of the tricuspid valve which give way. This degree of abuorinal blood-pressure is most fre- quently presented in mitral disease, particularly stenosis, and hence it is in these cases when compeusation is wholly destroyed that relative tricuspid regurgitation is most frequently recognised. Oftentimes it follows the mitral incompetence secondary to dilata- tion of the left ventricle in cases of aortic valvular disease, and it is very frequently seen in the terminal stage of chronic nephritis.
In renal cirrhusis, in particular, blomhpressure is high and sustained, throwing great strain on the left ventricle. In time this chamber, because of degeneration or of the excessive periph- eral resistance, begins to yield, dilatation sufic^rsedes the hypertro- phy, undue pressure is thrown back upon the right heart, and the tricuspid begins to leak. Thus, whatever is the nature of the primary cardiac ilisease, rlic ultimate effect is the same — namely, augmentation of Ului id-pressure in the puhnonic vessels and right
346 DISEASES OF THE HEART
ventricle until a point is reached at which the wall of the ventricle must stretch and the valve become incompetent
Other diseases that produce the same effect are vesicular em- physema with or without chronic bronchitis, long-standing bron- chial asthma, cirrhosis of the whole or even of a part of one Ixmg, fibroid phthisis, and puhnonary collapse in consequence of pleu- ritic effusion. A hydrothorax, itself consecutive to inadequacy of the heart, may by compression of the lung hasten or intensify the effect on the right ventricle of primary disease of the left heart. Xo doubt in some of the pulmonary affections the strain on the right ventricle is intensified by frequent and severe fits of cough- ing. It is probably in this way largely that tricuspid regurgita- tion is produced in cases of chronic bronchitis, although many times there is an associated emphysema.
The wall of the right ventricle is thinner than that of the left, and one can readily understand that loss internal pressure is re- quired to bring about overdilatation and relative tricuspid incom- petence ; and yet I cannot refrain from expressing wonder at what Gibson says concerning the influence of fever and other conditions in the production of this valvular insufficiency. '^ Pyrexia, if of more than brief duration, almost invariably leads to dilatation of the right ventricle and tricuspid regurgitation. It does so some- times from simple relaxation of the muscular substance, but in other cases by means of hyaline degeneration. Toxic influences belonging to almost every class produce the same effect ; the tox- ines produced by micro-organisms (sometimes in the absence of all pyrexia), the organic poisons, such as alcohol, the inorganic poisons, such as lead, act in precisely analogous fashion. ^Mal- nutrition, whether arising from some morbid process, as malignant invasion, from deficient absorption, as in such a simple affection as dilatation of the stomach, or from some deficiency of the food, all lead to the same end. A long experience of out-patient service in our great hospitals enables me to bear witness to the extreme frequency of tricuspid regurgitation in atonic conditions of the stomach. Such disorders as anemia, in which the nutritive power of the blood is lowered, are also to be considered as potent causes of tricuspid regurgitation.''
Severe muscular exertion, as mountain-climbing, may and not infrequently does produce dilatation of the right ventricle and the
TRICUSPID REGURGITATION
347
gafetj*valve aetioo of triciispid iiicoiiipetenee. In such instances the protective action of this leak eomes beautifully iuto play, for did the valve not give way and allow the strain to fall on the right auricle, great veinSj and liver, the continuance of the exertion Would eventually lead to dangerous haemoptysis or fatal cardiac syncope from overditsteution of the ventricles.
I have within the past twelve months seen two stalwart foot- ball players who, judging from the history and the subsequent condition in which I found their right heart, must have gotten up tricuspid regurgitation during a game. In both, the ventricle and cervical veins still showed permanent ill effect of their violent exertions. So long as the myocardium of robust young men is healthy, uUiiuate recovery is the rule; but w4ien after middle age myocardial degeneration exists, individuals should beware of physical efforts that are likely to so seriously overstrain their heart ?i.
S3rinptoms. — As a matter of fact tricuspid regurgitation exists so rarely alone — that is» independently of some other car- diac or pulmonary disease — that our knowledge of its symptoma- tology is in reality derived from our observation of the effects it produces in conjunction with such disorders, or with tricuspid stenosis. Nevertheless, it would not be difficult to deduce the symptoms from onr knowledge of the influence of this affection on tlie circuhition.
The first effpt*r tyi the regurgitation is to hinder the free flow of blood out of tlie right auricle, and tluis bring about its dilata- tion. This reacts ni>on the contents of the two vena? cava*, raising pressure within them from a negative to a positive one. As nega- tive blood-pressure within these two great venous trunks is neces- sary to the maintenance of the circulation, a rise of blood-pressure within ihem and their trihutary veins tends to bring the blrwMl- sti-eam to a standstill. Stasis thus induced shows itself by cyano- sis and turgescenee of the superficial veins of the upper and lower extremities and by passive engorgement of the abdominal viscera. The liver grows large and tense, even to the extent of tenderness and pain, particularly in the epigastrium. Functional visceral disorders in various form show themselves, the feet and ankles swell and ultimately Wcome crdematous.
The patient is weak and easily fatigued, and after a time is
348 DISEASES OF THE HEART
obliged to keep to his room or even to his bed. Dropsy increases, and may invade the entire body, or ascites and hydrothorax may predominate over the anasarca. Indeed, Gibson, who appears to have had a remarkably rich experience in this class of cases, says : " The fact must never be overlooked that right-sided disturbances are more likely to produce interference with the functions of the pleura than affections confined to the left side of the heart, inas- much as the blood circulating in the pleural membrane is in over- whelming proportion returned to the heart by the bronchial veins, which discharge their contents on the right side by means of the vena azygos, and on the left side by means of the superior inter- costal veins. Their destination is therefore the right auricle. When disturbance of the function of the right heart occurs, there is as a consequence considerable liability to backward pressure upon the pleural membrane, resulting in hydrothorax."
If the tricuspid regurgitation is not secondary to heart or lung disease, dyspna*a and cough are likely to come on only after the growing stasis in the venous system has, through its effect on the general capillary and arterial circulation, led to pulmonary con- gestion. In most cases, however, these symptoms are complained of prior to the development of the tricuspid leakage, because form- ing a part of the symptomatology of those diseases to w^hich the tricuspid defect is usually secondary. Therefore, as a matter of fact, the symptomatology of this affection is inseparably linked with that of the antecedent disorders, and does not require recapit- ulation. According to Gibson, it is possible for tricuspid regurgi- tation to exist without producing any symptoms, and this is one of the reasons why it is so frequently overlooked. For my part I cannot see how this can well be, and I am not convinced by his statement, for although tricuspid insufficiency may not produce cardiac symptoms, strictly speaking, such as dyspnoea on exertion, still it cannot fail to exert decided effect on the venous circulation in general, which would be sufficiently serious to bring the patient to a physician.
When this valvular incompetence arises in consequence of long- standing heart or lung disease, it speedily aggravates the pre-exist- ing symptoms. The rapid appearance of general dropsy which usually follows the establishment of regurgitation is due in lar<re part no doubt to interference with the lymphatic circulation. The
TRICUSPID HEGUHGITATION
349
grent veins into whose blood-stream the contents of the thoraeic duet are emptied are so turgid that the stasis retards the ready emptjiiig of the duet. C'ongestion results, therefore, in the duet and its triliutaries, injuriously affecting nutrition and increasini^ the permeability of the eapillary walls. This disturbance of the circulation inevitably results from primary tricuspid regurgita- tion, and hence I cannot conceive of the disease remaining latent.
Physical Signs, — InspecllotL^Contrary to what is usually the case in diseases of the heart, inspection and palpation afford the mo.%t, and according to some the only, reliable nunins of diag- Bosis in tricuspid regurgitation. This is partly due to association of this lesiim with other cardiac or pulmonary diseases that pro- duce conHieting physical signs, and partly to close anatomical con- nection between the right chambers of the heart and the great venous trunks, in eonsei]uence of which the contents of the latter ^are directly exposed to pressure by the reflux stream in the manner llreatly describtMi. Instead of tlie large veins which enter the thorax being invisible, the dilatation of the right heart leads to their perntanent turgeseencej and in extreme degrees even to dila- tation of the venous bnlbs at the root of the neck. This turgid Sty IS specially marked, therefore, in the jugulars^ which may stand forth like great purple cords.
When incompetence of the tricuspid valve permits ^he ven- tricular systole to drive part of its blood back into the auricle, a nearly synchronous wave is transmitted upward into the veins of the neck through the superior vena cava and downward through the inferior vena cava, even to the liver or beyond. This reHiix venous wave declares itself in the neck as a visible and e\*en pal- pable pulsation. This is particularly pronounced in the right in- ternal or external jugular, or in both. This phenomenon has been carefully investigated l>y Riegeb and by him shown to coincide with pulsation in the arteries, as the carotids. This ** positive venous pulse," as Riegel calls it, is usually spoken of as systolic, Iiut is, strictly speaking, presystoHosystolic, and may be correctly timed by comparison with the carotid pulse. Simultaneous palpa* tion of the artery and inspection of the vein wnll show that pulsa- tion in the latter takes place during the rise of the arterial pulse.
In eases in which there is dilatation of the auricle, yet without tricuspid regurgitation^ a venous pulsation may likewise be de-
350 DISEASES OP THE HEART
tected, but its rhythm agrees with the last portion of ventricular diastole, including, of course, auricular systole, and hence is, strictly speaking, diastolic-presystolic. This venous pulsation occurs, therefore, during the collapse of the carotid artery. This diastolic-presystolic or " negative venous pulse," as it is called, never indicates tricuspid insuflSciency.
The positive jugular pulse of tricuspid incompetence must also be distinguished from a pulsation sometimes communicated to the distended vein from the adjacent artery. This can be done by pushing the artery away from the contiguous vein in the case of the internal jugular. To test the external jugular it should be compressed by the finger a short distance above the clavicle, when, if the pulsation is communicated from an adjacent artery, the part below the point of constriction will entirely or partially col- lapse and the pulsation disappear wholly or in part.
Palpation. — The corresponding positive venous pulse con- ducted downward to the liver is to be detected by palpation of the organ. If the congested liver is grasped by the two hands, the left pressing it strongly upward from behind and the right being out- spread upon the organ in front, pulsation of the liver is perceived as an expansile distention in all directions. This positive venous pulse in the liver is therefore quite unlike the merely rising and falling motion imparted to it by the pulsations of the abdominal aorta or the downward impulse of the hypertrophied right ventri- cle above.
This positive venous pulse is the pathognomonic sign of tri- cuspid regurgitation. Without it, in either the cervical veins or the liver, a diagnosis of this valvular lesion is always open to doubt. There are two exceptions, but these occur so rarely that they seldom need to be considered. One is a wave communicated by the mitral regurgitant stream through an open foramen ovale to the contents of the right auricle, and thus to the stream in the jugulars. The other is a systolic pulsation in the jugular veins due to the rupture of an aortic aneurysm into the vein, instances of which accident may be found in the literature.
The radial pulse presents nothing distinctive even in primary tricuspid incompetence without other cardiac disease. It is small and weak, accelerated and regular, or irregular and intermittent, as the case may be. PopoflF has reported diminution in the size of the
TRICUSPID REGURGITATION
351
right radial as eoropared with the left, and attribiitecl it to pres- sure of the distended right auricle and veins upon the right sub- clavian artery.
Dropsy is usually present in cases of relative insufficiency of the tricuspid valve, having in most instances begun before the valve f;ave way; It is not present, however, in all cases, certainly in the early stage of the tricuspid leakage. Consequently this absence of cutaneous trdenia, notwithstanding great venous stasis, is a proof that something more than stasis alone is necessary for the production of dropsy. This additional factor is, as previously stated, an abnormal permeability of the capillary walls dejiending upon defective n'^utrition.
Percussion. — This yields infonnation of minor diagnostic im* portance, because any alteration discovered in the area of cardiac dulness may Ik? due to an associated or antecedent cardiac or pul- monary affection. Vesicular emphysema, chmnic pleuritic effu- sion or hydrothorax, and cirrhosis of the ri^ht lung, nuiy render unavailing any attempt to deteruiine by percussion the accurate size of the right heart. In vesicnilar emphysema the borders of the lungs are distended, pushing the lieart away from t!ie chest- wall and occasioning such a degree of hyperresonance tlnit the limits of ih'Civseated car- diac dulness tH?coine inapprcv ciable. WTien fluid exists in the right pleural cavity, or there is soliditication of the right lung, the dulness thtis occasioned blends indistin- guishably with that of the heart. Under favourable con- ditions, however, cardiac dul- ness 13 found increased to the right and dowmwnrd, the ex- tent of this increase Vjeing de- termined by the degree of the dilatation of the right ventri- cle. In cases of primary or independent tricuspid insufficiency due to endocarditis, the right ventricle is found less enlarged
Fio, 7<X — Relative Dilxess in a ♦as^ of FriMI^KT TlUCtftPJD Be4»i-roitatio^%
832
DISEASES OF THE HEART
FlO. tl.— UliLATIVE l)li.Nt:?iS IN TasR or TrICISI-IO Re«*1 lltilTATJOX, SeC4JI«I»AUI'
ro Dilatation of tmi Ujout Venthicli.
(Fig. TO) than when regiirgiiatiuii lakes place as a result of vcn- trieulnr dilntatir»o (Fig. 71). On the nther hand, in either fHnn
of tlie affection, dulness is greatly iiicrea.sed over the right auricle and the large venous trunks, reaehing far hpyond the right sternal I>or- der, lialf'way or mure to the right niamilkry Hue. In most instances also there is increase of cardiac dulness to the left, depending u'jwn the nature and extent of the act'ompany- iug disease of the left heart.
J mcufifdion. — ^This fur- nishes even less trustworthy data than are obtained by per- cussion. There is generally a blowing, systolic uuirniur, said to have its maximum in- tensity in the tricuspid area (Fig, 72); yet as the dilatation of the several ciirdiae chambers alters the normal relations of the parts, this murmur may be heard most distinctly in any one of several situations. It may be at the junction of the fifth and sixth left costal car- tilages with the sternum, over the ensiforni appendix, or even to the right of the ster- num in the third, fourth, or fifth intercosal spaces, close to this lione,
Gibson, in his remarks on the Heart in Debility, ha> narrated cases showing thai the munuur may be heard in the second left interspace an ^'^*- :±-Vi^cE .v MAxtut,, AvmmuTY
^ . i^MALL CIROLK) AND AhKA OF ProPAUA^
mch from the sternum, in an tiuk or TkictaHD RtouBorTANx Mukmur.
TRICUSPID REGURGITATION
353
area in which a systolic piils^atiou is also often obj^erved. In these cases there was also veiums pukation in the neck^ and hence it seems prcibable tliat the murmur was that of the disease now under diacussiou. This is the site of a systolic nmrniiir frequently audi- hie in chlorosis and aniemia, and variously explained by Xaunyn, Balfour^ Russell, Bramwell, liaiidford, Foxwell, etc. (see intro- ductory chapter), and therefore caution is required in the cor- rect interpretation of a bruit in this situation.
The tricusjud murmur has a bU^wing quality, is of no constant pitch, and ditfers ninch in loudness^ according to the conditions that generate it. It is often obscured by other bruits originating at other orifieet^, particularly at the mitral If the auscultator is experienced, and conditions are favourable^ he timy he able to locate different areas of maximum intensity for the different mur- murs, and thus be able to determine which is tricuspid, which mitral, etc.
Regarding the heart-sounds in tricuspid insufficiency but little need be said. The first tone over the right ventricle is apt to be muffled, even replaced, by the murmur. The pulmonic second sound appears to differ in different cases. It would naturally be enfecbleil, in consequence of the fact that lessened blood is expelled Ito the artery, but as the predisposing mitral or other disease has iiugmenteil blood -pressure in the vessels of the lungs, the second tone in the jnilmonic area may be accentuated. However, if in a given ease of gastrectasis tricuspid regurgitation is suspected, an enfeeblement of this second sound would lend a measure of sup- port to the diagnosis.
Lastly, it is tjuite common to hear a vascular tone, if one aus- cultates the vein in which the positive pulse is seen, and the tone thus f^btained is, of course, synchronous with the pulsation,
DiagnoBis. — Recapitulating, I wish to emphasize the state- ment tluit inasmuch as mitral murmurs may sometimes be heard with great intensity over the right ventricle, and be conducted far beyond the right border of the sternum, it is very unsafe to rely upon a murmur in the tricuspid area in making a diagnosis of re- gui^itation through this valve. Certainly it is so exceptional for any considerable leakage to occur at this ostium without giving rise to the venous ami bcfiatie pulsation already descril>ed, that in the absence of these pathognostic signs it is unsafe to declare that 23
354 DISEASES OF THE HEART
the murmur is that of regurgitation. This has been impressed upon me many times.
There is a certain Russian Jew who exhibits himself to medi- cal students for examination because of his possessing a musical murmur of obscure origin. In his instance the bruit is systolic, and most intense upon and immediately roundabout the xiphoid cartilage. From its location, therefore, it is thought by many good observers to be a tricuspid regurgitant one. The musical murmur is, however, also distinctly audible well outside the left nipple ; and as there is a combination of lesions in this case it is very difficult, if not impossible, to definitely decide whether the murmur in question is tricuspid or mitral. It all depends on the existence or not of a positive venous pulse in the jugulars. Six years ago I did not detect such a pulsation ; two years ago I thought such a venous pulse was present; a few days ago (March, 1002) there was no such evidence of tricuspid regurgitation, and consequently I am obliged to still leave the question sub judice. The heart was in a far better state than two years before, and it is quite possible that a slight relative tricuspid incompetence was accountable for the jugular pulsation at that time. At all events this interesting case is very exceptional, for ordinarily it is not a difficult matter to determine the existence of tricuspid leakage. It illustrates that in the absence of a positive venous pulse in jugulars or liver one is not wise in declaring a systolic bruit in the tricuspid area to be tricuspid.
Prognosis. — This may be said to depend upon the nature and causes of the tricusj)id insufficiency. Relative incompetence of this valve may come and go quickly, but unless its cause can be removed its tendency is steadily dowmward, although death may not CK'cur for weeks or even months.
Mode and Causes of Death. — The fatal termination grad- ually results from either general or cardiac exhaustion, in conse- quence largely of malnutrition, or from pressure-effects of the dropsy, or from pulmonary (iKlema, or from some other terminal manifestation of the primary cardiac or lung affection. In other words, there is no mode of death peculiar to tricuspid insufficiency per se. In 3 cases of this disease ITustedt found as the cause of death cardiac weakness once, phthisis once, and anaemia once.
CHAPTER XI
TRICUSPID STENOSIS
This is the coimterpart of mitral stenosis, but is infinitely more rare. Indeed, it is said to be Ihe rarest of all valvular de- fects— so imieli so that some writers speak of it merely as a patho- logical curiosity, and devote very little space to its consideration. It probably occurs oftener than it is recognised, and yet its ex- treme infreqnency nuiy be judged of by the fact that, although many thousand necropsies are annually made, only 154 cases had bi*en rtH!orded in medical literature up to the fall of 1896. Of these, 114 collected by Lendet occurred prior to 1888, while in the next eight years llerrick collected 40 more. Three of these were his own cases, and the total number was brought up to 154. It is to the Tatter's monograph that I am indebted for much that will he said in the f<>llowing pages*
Morbid Anatomy.^ — This differs according to the group into which the respective case falls, for tricuspid stenosis may be either congenital or acquired. The former class is again subdivided into those due to intra-uterine endocarditis and those resulting from some defect of development. In tlie congenital form there are the usual associated abnormalities, such as stenosis of the pulmo- nary artery, defective closure of the interventricular steptum, and patency of the foramen ovale and cluctns arteriosus.
When acquired as a result of endocarditis tricuspid stenosis presents changes analogous to those at the left auriculo-ventricu- lar orifii'e, thickening, rigidity, and adhesion of the flaps. Vege- tations may also be found on their auricular aspect, and the neigh- bouring endocardium is apt to present the grayish-white appear- ance and thickening characteristic of mural endocarditis.
The shai»e and size of the opening at the extremity of the cusps are variable, the same as in mitral stenosis. The conditions are also such as occasion incompetence as well as obstruction. The
355
356 DISEASES OP THE HEART
tendinous cords and papillary muscles may in some cases also show the changes of endocarditis. In the great majority of cases tricuspid stenosis is associated with other valvular diseases, as shown in the annexed tables taken from Leudet and Herrick :
Letuiet
Tricuspid stenosis alone 11
Tricuspid stenosis with mitral stenosis 78
Tricuspid stenosis, mitral, and aortic stenosis 21
Tricuspid stenosis and pulmonary stenosis 3
Tricuspid stenosis, mitral stenosis, and pulmonary stenosis. . . 1
Herrick
Tricuspid stenosis 1
Tricuspid and mitral stenosis 18
Tricuspid and pulmonary stenosis 0
Tricuspid, mitral, and aortic stenosis 18
Tricuspid, mitral, and pulmonary stenosis 1
Tricuspid, mitral, aortic, and pulmonary stenosis 1
Tricuspid stenosis and endocardium of the left auricle 1
Tricuspid stenosis and aortic stenosis 0
The changes observed in the walls and cavities of the heart are in part secondary to the tricuspid stenosis, and in part to the coexisting lesions of other orifices and valves. The right ventri- cle usually exhibits combined hypertrophy and dilatation, in con- sequence largely of the conjoined mitral defect, but if the tricus- pid obstruction is great, with but little if any regurgitation, the ventricle is diminished rather than enlarged in size. The cham- ber upon which the stenosis chiefly reacts is the right auricle, and hence this is more or less hypertrophied and dilated, according to the degree of the stenosis. It has been known to reach a size of two or three times the normal, but Ix^cause of the thinness of its wall the right auricle rarely undergoes much compensatory hyper- trophy. The degeneration of the myocardium is such as is often found in other valvular diseases, and in one of Herrick's cases the right ventricle was covered by a thick layer of subpericardial fat.
Etiology. — Cases of this disease originating after birth are due to endocarditis, and as in other forms of valvular defect of this origin, articular rheumatism appears to be its chief exciting cause. Herrick states that of the 154 collected cases, 30 per cent gave a history of antecedent rheumatism. He also says that syphilis has been assigned as a cause, and that Leudet regards the puerperium as also an etiological factor. This latter fact may possibly have
TRICUSPID STENOSIS
351
a bearing on the far ^rrfater frequency of tricuspid stenosis in the female than in ilie male sex. The disproportion of the two sexes in this disease is far too patent to he merely accidental, Gibson stat- ing that of 14t} cases of tricuspid obstriiction, 114 occurred in females aii*! *^rj in males.
This disease also occurs uiusr frequently in the early decades of life, the majority of cases falling between the twentieth and thir- tieth years. In this respect it is not peeidiar, for, as we knoW| valvular diseases of rheunuitic origin are uinch more frequent in the young tliiin in persons of middle or advanced age.
Symptoms. — The fact thut the ablest and most experienced clinical t^hservers have failed to recognise the existence of tricus- pid stenosis during liic% and that in most cases it has first been detected on the autopsy tahk% may he regarded as proof that there is no symptomatology peculiar to this affectiim. Its clinical mani- festations, even when such exist, are, rnore<:»ver, apt to lie obscured hy thuse iHLOonging to tlie associated lesions. Thus, although ob- stniction at the tricuspid orifice leads to stasis in the systemic veins, the liver^ and other abdominal organs, mitral disease does the same; and as the physical signs of tliis hitter affection gener- ally mask those of the trieu^^pid defect, the syjiijitctujs are quite likely to be attributed to the disease in the left heart.
Trieus])id stenosis tentls to limit the amc*unt uf bloud sent to the lungs and left auricle, and therefore there is n<ithing in this disease tending to produce dyspntra of effort and other symptoms rc'ferable to pulmonary congestion. In fact, were the tricuspid lesion to exist alone, the v^cct on the lungs wouhl, like tluit of pul- monary stenosis, be one of anu'mia with its tendency to tubercu- losis; and it is here worthy of note that in the single instance in which Ilustedt ascertained the cause of death, this was *" phthisis." It is pbiin, therefore, that wlien we leave out of consideration the puhtionary symptoms due to conjoined mitral disease, we must seek the clinical features of tricuspid stenosis in all those perver- sions of function incident to visceral hypenemia and in the effects and manifestations of general venous engorgement.
The jugulars are distended, and when hypertrophy of the right auricle is marked, these veins are likely to exihibit a negative — that is, diastolic-prf»systnHc pulsation. This was the case in one of my patients in whou* physical signs led me to suspect the exist-
358 DISEASES OP THE HEART
ence of tricuspid narrowing, but in which case, unfortunately, a post-mortem examination could not be obtained. The liver bears the main brunt of the secondary stasis, and is consequently greatly enlarged, perhaps tender, and there is furthermore a growing tend- ency to ascites and cBdema.
I have had the good fortune to observe a patient in whom dur- ing life there were the classical signs of both mitral and tricuspid stenosis, as will be subsequently described, and whose heart pre- sented such interesting post-mortem findings that the case will be here introduced.
The patient was a Polish Jew under the care of Dr. Kaczorovv- ski, by whom he was brought to me. His age was given as forty- three, and for six vears he had been unable to work on account of shortness of breath. There was a history of scarlatina in child- hood and of articular rheumatism fifteen years before I saw him, but further particulars were too vague to be trustworthy.
His symptoms were dyspncra on exertion and a cough, which had existed for six weeks. The liver was engorged and palpable for a distance of 3 inches below the costal arch, and there was distention of the external jugulars.
The heart was greatly enlarged in all diameters, and there were two se])arate and distinct presystolic murmurs, one at the apex and the other close to the xiphoid cartilage. The diagnosis of a double stenosis was made, tricuspid as well as mitral, and the patient was not lost sight of, although only seen twice in the sub- sequent sixteen months, the last occasion being five weeks prior to death. Some four months before the fatal issue he began to have a'donia of the lower extremities, and to suffer much from difiiculty of breathing, amounting to orthopnona. The anasarca increased rapidly and soon invaded the scrotum, which became so distended that he was e()m])elled to let it hang through a large o])ening cut for the piir])Ose in the seat of his chair. Cathartics afforded but slight and transient relief, and upon receiving an urgent request from the attending physician to suggest some means of lessening the painful scrotal distention T advised tapping, although it was realized that this would ameliorate the condition for only a short time.
When at length I found time to visit the poor fellow his plight was truly pitiable. He was in a chair, which he had scarcely
TRICUSPID STENOSIS
359
quitted for many weeks, and he presented signs of moderate as- cites as well as extensive tiHlema of the lower extremities. The scrotum was as large as a chihrs head, of a purplish-red colour^ very hard to pressure, and hathed in hloody serum, which trickled drop by drop into a Imsiii underneath Lis ehair. Owing to the inability of the patient to move or sit in any other position ex- amination was difficult. But so far as it was possible to deter- mine, the oardiae findings were essentially as found nud recorded fifteen months earlier*
The pulse was weak, moderately aceeleratedj and irregular. As cathartics, diuretics, and digitalis had all lieen used freely, and proved of very little eltieacy, no adJitioual suggestions could be offered, and the poor sufferer was reluctantly left to wear out his few remaining weeks of life as best he might. The blessed release came about five weeks later, and lh\ \\\ A, Evans made the autopsy.
There was much subcutaneous crdema and gangrene of the penis, scrotum, and one of the large toes. The peritonaeum and right pleural cavity contained clear seruuL The various organs showed tLe usual changes of long-standing congestion. The heart was enormously enlarged on both sides and was hardened by Kaia- erling's solution without being oi>ened (Plate III), However, au attempt was uuide to discover the condition of the tricuspid orifice by passing the tingers through tjie great v(*nuus opening in the right auricle. The tricuspid ostium admitted three fingers to the second joint instead of four, as is normally the case, and it felt firm and resisting. ^Iore<n'er, the valve could be felt projecting across the opening.
When at length the specimen had bc^come hardened and it was opened an interesting combination of lesions was presented. The mitral orifice was a mere buttonhole slit, and the endocardium of the left auritde showed the whitishi thickened api>earance denot- ing? prolonged high 1drw>rl-pre6sure» and its w^all was hyiTertrophied. The valve projceted like a cone into the cavity of the ventricle, which was both Ijypertrnphit^d and dihitc*d. The cnrds were fused and presented unmistakable evidence of old endocarditis. There was some thickening of the aortic cusps, which had caused moder- ate ohstrncti«»n at that orifice, a conchision justified by the en- largement instead of atrophy of the left ventricle usually found
860 DISEASES OP THE HEART
in mitral stenosis. Yet during life this aortic lesion had not pro- duced recognisable signs aside from enfeeblement of the aortic sec- ond sound, which had been attributed to the smalhiess of the blood- stream ejected into the aorta by reason of the mitral disease.
The pulmonary artery presented a remarkably extensive atheroma, due evidently to the long-standing and extreme pressure to which this vessel had been subjected. The pulmonary orifice was relatively dilated, and the valves were of increased size. Con- sequently, the conclusion seemed warranted that relative insuffi- ciency of this valve had existed and had contributed to the enor- mous dilatation of the right ventricle. This very great hyper- trophy and dilatation had been recognised during life, but had been put down as secondary to the extreme mitral obstruction. The pulmonary regurgitation either failed to produce a diastolic murmur, or it had been overlooked. The pulmonic second tone was noted as feeble, but this was thought due to the diminished amount of blood sent through the tricuspid ring. I feel quite cer- tain that an audible diastolic murmur did not exist.
The right auricle was not only strikingly dilated, but its wall was thickened, and its lining membrane also showed by its appear- ance to what a high degree of pressure this chamber had been sub- jected.
The tricuspid ring was rigid, barely admitting the tips of four fingers. The valve leafiets were very considerably thickened and partially united, so that the opening was considerably smaller than the actual tricuspid ring. It was the thick and rigid edge of the posterior flap that was felt in the preliminary examination.
This interesting s])ecinien was submitted to Dr. Gnstav Fiit- terer, and at first he was inclined to doubt the existence of an appreciable tricuspid stenosis. Yet, after a careful examination of the right heart, he arrived at the opinion that in consideration of the marked dilatation of both the right ventricle and auricle and the disproportionate smallness of the tricuspid ring, together with its firmness and thickening, and the condition of its flaps, one could not escape the conclusion that actual stenosis of the ring had existed.
Moreover, the endocardium of the ventricle displayed slight evidence of previous inflammation, probably the same process that had thickened the edges of the tricuspid valve. Nevertheless, it
TRICUSPID STENOSIS
361
was Dr. Fiitterers opinion that the ^yiuptoms liad been caused more by the mitral narruwing and the relative pulmonary regurgi- tation than by the stenosis of the tricuspid ostium. However this may be, I can only assert that it had been sufficient to occasion very positive clinical signin, else I should not have suspected and diagnosticated so rare a lesion in the jiresence iif a pronounced mitral disease to which one might very natiirally have attributed the symptoms of stasis. I must therefore stand by my belief that to the tricuspid stenosis is to he attributed a not unimportant share in tlie production of the imusnal degree of general venous stasis as compared with the puhnonic. The right-sided hydrothorax, dis- covered post mortem, furnished profif of tlie enormous stasis that had been present in the cavity of the right auricle.
At all events this case illustrates the influence of right heart lesions in the causation of general venous and visceral stasis, while the gangrene bore witness to tlie profiiund emptiness of the aortic system.
Fliysical Si^ns. — -Inspection. — A perusal of IIerrick*s col- lected eases convinces one that there is nothing in the apiK-arance of these patients to distinguish them from those with mitrsil dis- ease in the last stages of broken compensation. In Case 27 of his series venous pulse* was noticed, but ordi- narily there is nothing more tlian the ocular evidence of venous anil capillary stasis,
Palpalion^ — The pulse is small and weak, and nuiy hv regular or irregular, and ukhI- erately or greatly accelerated. In Broad ljent'9 case (No. 25 of Ilerrick'a series) the pulse was reported as 100, small, and irregidar, while in Eustis Smith's case (No. 29) it was recorded as only GO and small.
There is nothing in such statements that might not also apply to the pulse in mitral disease. Palpation of the praxjordia is usu-
Fi'i. T;i -L^M^vTlr^^ or Thrill aitd Mlrmi s i?f A Typh^al Cauk or Tricibko SncKoetP,
DISEASES OF THE HEART
ally negative so far as the tricuspid lesion is concerned, but in some instances there niav be a shcu't, tlminping inipnlse in the epi- gastrium similar to but distinct from that of the assocnat^l mitral stenosis. This was pronoimccMl in the case I have narrated. There was also a shr^rt presystolic thrill in the sulcus between the ensi- form ap|H^ndix an*! the h^ft costal cartilages (Fig. 7*1), which was plainly shorter and less distinct than that felt at the ajjcx. Be- tween these two there was a sjiace in which no presystolic thrill could be detected, and it was this fact that tirst riveted my atten- tion. This short thrill ran up to and ended abruptly with the tbuHiping systolic shock mentioned.
It is conceivaltle tlnU, owning to the hc*art lying nearer to the niediHU line than usual, a presystolic thrill and sharp systolic shock of mitral stenosis might he felt in the tricuspid area. Con- ee«pientK\ the ree<»gnitif»n at these signs in this area alone would not lie so sn^picious as was the detection, in my case, of these pal- patory plienoiuena in two se[)arate and distinct situations.
Percussion. — Cardiac diilness is increased fiver the right auri- cle— that is, at the right of the sternum — but this is not distinctive,
since it *x*curs likewise in mi- tral disease (Fig. 74). In tricuspid stenosis it is likely to be jiiirtieularly well marked. It may be said, tlierefore, that the evidence derived by per- cussion is valuable, I ml not positive,
Aii>icttlitiiion. — T7nfortu- nately the results of this means of examination are also likely tn bf very indefinite. Even if ;i inurnnir generated at the tricuspid orifice exists, it is likely to be ctm fused with or indistitiguisbabJe from mur- murs produced elsewhere, par- ticularly mitral bruits, Tn my case, as in Broadbent's (No. 15 of Herrick's series), there was a distinctive murmur in the tricuspid area. In my patient a presystolic murmur existed in the very
Fiti. 74,— Relativk Cardiac DtLrfrM i?f a Tyficai. Ca»s Of Taicutrip Stkkomh,
TRICUSPID STENOSIS
868
situation in which the thrill was detected^ and it was much shorter than that at tlie mitral area, was of a somewhat different pitch, and teniiinated in a sharp thud, the same as in Broadbent's case. But this was nut all ; when the stethoscope was passed, little by lit- tle, from the long, rolling mitral hniit towards the ensiform, it was noted that there was a space in which the mitral ninrmur became lost, while a trifle nearer the sternum another area was reached in which another and shorter presystolic nuirniur became audible. This fact showed |ilainly that there were two areas of maximum intensity for these two [presystolic nuirmurs, which fact convinced me that I had to do with two entirely separate and distinct bruits.
It may he objected that this murmur in the epigastrium was the pnlnionary regurgitant murmur transmitted to that point. But in rt^ply to this possible objection I need only point ont that although both murmurs are diastolic, that of pulmonary regurgita- tion falls in the early part of diastole immediately after the sec- ond sound, while a presystolic one occurs just before the first sound at the end of diastole.
Theoretically and practically, therefore^ in endeavouring to establish the existence of tricuspid stenosis, one must search for auscultatory signs in the tricuspid art^a, yet must remcniljer tliat <»wing to the enlargement of the right heart the position of the tricuspid orifice beconjes changed, s<> that the tricuspid area is a \*Hde one* Broadl>ent detected the murunir in the fifth right in- terspace, close to the sternum.
Finally, in most cases of this lesion more or less regurgitation 19 permitted, and hence? the tricuspid disease may declare itself by a systolic luurmurT the presystolic being either absent or so short as to entirely escape recognition in the presence of the regur- gitant bruit. In but 12 of the 154 cases was the tricuspid orifice alone tlic seat of dis4*ase, which sliows its rarity apart from asso- ciated defects. 1 should fancy that when it exists alone, it ought to be recognised more easily than when combined, and hence ob- scured by coexisting disease.
Diagnosis* ^O wing partly to the indefiniteness of the physi- cal signs and partly to their being obscured by those of associated valvular lesions, the diagnosis of tricuspid stenosis is generally first made on the autopsy table. Some of the ablest clinical ob- servers believe that an iutra-vitam diagnosis must always be
SM DISEASES OF THE HEART
problematic, and that when made correctly it is a matter of for- tuitous circumstance. One should not feel chagrined, therefore, over his failure to recognise the existence of this disease during life. Conversely, should he be so fortunate as to have his ante- mortem diagnosis corroborated by the necropsy, he should not take pride to himself, but rather congratulate himself upon the fact that in that particular case the lesion had furnished recognisable physical signs.
Prognosis. — Notwithstanding the fact that one of I^udet's patients is reported to have reached the age of sixty-four, the pros- pect of long life is not good in cases of this disease. Death over- took the majority of his cases between the ages of twenty and thirty. This brevity of life is due probably not so much to the tricuspid obstruction itself as to its association with other valve- lesions so pronoimced as to make it a matter of wonder that pa- tients live as long as they do. When compensation begins to fail there is small prospect of its restoration. The immediate prog- nosis dej)ends ui)on the severity of symptoms as well as upon the number and degree of associateil lesions. Albuminuria, ascites, hydrothorax, etc., indicate the terminal stage of the disease, and yet proi)er care and management may extend the life of a patient many months after the urgency of sjinptoms has compelled him to ^ieek medical aid. !Most of the cases reported by Ilerrick were under observation from a few months to a year or longer.
Mode and Causes of Death. — Death occurred suddenly in one of Ilerrick's cases, but nothing was found at tlie post-mortem examination to exj)lain it, further than the ordinarv ehiniges in hearts with other valvular diseases. As a rule death comes slowly from gradual cardiac exhaustion, or probably as a result of an a])proaching standstill in the circulation, due to reversal of the normal blood-] )ressure within the arterial and venous systems. In llustedt's single case already mentioned the cause of death was put down as " phthisis," which emphasizes the fact that death is likely to be the indirect rather than the direct result of this valvular defect.
CHAPTER XII
PULMONARY REGURGITATION
This form of valvular disease is the corollary of aortic insuffi- cienev, but h infiuitely luore ui)Coiuuil>ii, ainl unassociiited with other valvular lesiuns is very rare. AUhougli I have observed a single instance of chronic organic piihuonary incompetence, as detenu ined by the history and clinical signs, I am indebted for the lunst of what will be said to Barie's paper on the subject*
Morbid Anatomy. — This depends largely u]>on the cause of the disease. Thus we recognise two chief groups: (1) A func- tional or relative incouipetence in which the pulmonary artery and ring are so dilated that the valves cannot close the orifice, but are themselves not responsible for the regurgitation. (2) The form in which tlie leak results from structural changes in tlie valve-t=M?ginent^i, Thus far this disease is the counterpart, lM>th pathologically and etiologically» of the other valvular lesions that have l>ecn considered, hut the second group of pulmonary regurgi- tant lesions is again divisible into the congenital and the acquired. In this respect it conforms with what we know nf rightdieart de- fects and differs from valvular diseases of the left heart, since congenital affections of the mitral mid aortic valves are exceed- ingly rare.
In relative insufficiency of the pulmonary valve the artery and ostium are found stretched, and the former may show the changes of atheroma, wliile the leaflets are elongated and broadened in conse<|uence of the strain to wliicli they hnvc been subjected, yet in other particulars are quite likely lo be free from disease. This was the case in the patient with mitral and tricuspid stenosis whose history was narrated in the preceding chapter.
In those instances in which the regurgitation is the result of endfM^-arditis, the changes are the same as in other valvular defects of the same origin, and hence do not need to be repeated in BX-
DISEASES OF THE HEART
tenso. I may only add that the valve-segments have in several eases been found torn into shreds in consequence of inflammatory softening. Not infrequently, according to Barie, the changes are such as to have led to more or less obstruction, as shown in 23 out of 43 cases of pulmonary regurgitation.
Congenital regurgitation at this orifice is certainly rare, and yet Barie is also authority for the statement that it was discovered in 10 out of 34 cases. In this form regurgitation is permitted in consequence of defects in the formation of the valve. In a three and a half months' infant, cited by Barie, there was a rudimentary cusp which allowed a stream of water poured into the artery to leak through into the right ventricle. In Bouillaud's case the orifice was covered by a membranous partition having a circular opening at it« centre 6 millimetres in diameter. A mere hint of an attempt at the subdivision of this membrane into segments was shown by the presence of three folds upon its convex aspect.
The secondary effects upon the heart are important. In the congenital cases there is usually discovered a defective closure of the interventricular sa?ptum or patency of the ductus arteriosus, the same as in congenital pulmonary obstruction. In acquired cases, whether relative or structural, the right ventricle is found dilated, or both hypertrophied and dilated, the same as with the left ventricle in eases of aortic regurgitation, ^foreover, in con- sequence of the easy stretching of the right aurieulo-ventrieular ring, this orifice is dilated, and the tricuspid valve is also incom- petent.
In cases in which pulmonary insufficieiicy has been the only valvular defect the right heart alone is enlarged, the left chambers being small and looking like mere appendages in comparison with the right. This appearance is not usual, however, because of tlie coexistence of other valvular disease at the mitral or aortic ostia that have led to secondary enlargement of the left half of the heart. Finally, the myocardium evinces the degenerative effects of long-standing strain and stasis, which have been already de- scribed in preceding j)ages.
Etiology. — In the form of pulmonary regurgitation most fre- quently recognised — namely, the secondary or relative — the imme- diate causative element is abnormally high and prolonged blood- pressure in the pulmonary artery. This in turn is due to disease
PULMONARY REGURGITATiuN
367
of the left heart or of the kings. It is in extreme and long-stand- ing mitral stenosis, therefore, that secondary incompetence of the pulmonary valve is oftenest encountered.
Obstruction or regurgitation at the aortic orifice may also pro- duce pulmonary incomjx^teiice after having set up stretcJiing of the left auriculo-ventricular ring and relative mitral regurgitation. Great increase of blood-pressure in the pulmonic system is so com- mon and necessary a result of most cardiac and many pulnmnary diseases that it is probable that the regurgitation now considered takes place far more freipiently than it is recognised clinically.
Of those cases in which the valve itself is diseased the most fretpieiit cause is acute endocarditis. This may be of rheumatic origin, but it is more often septic, and therefore a localization of pus or pneumococcus infection. It occurs in the puerperium, therefore, the same as malignant endocarditis in other situa- tions.
The causes of the congenital form of pulmonary regurgita- tion are intra-uterine endocarditis and developmental defects, whetlier due to inHannuation or not.
Symptoms. — ^In those cases in which pulmonary regurgita- tion is second a ry to pre-existing mitral or aortic disease, the symp- toms of these latter affections generally obscure those referable to the former, if indeed any new ones are developed. The patients already suffer from the eifects of pronounced stasis in tlie lungs and venous system, and when the pulmonary valves yield to the strain and leak, the force of the regurgitant stream is thrown upon the already overlnirdened and dilated riglit ventricle. The pro- pelling power of this ]>ortion of the heart is thereby lessened, and the congestion everwhere present is augmented — but as this con- dition has come on gradually, it is put down as only a further manifestation of the inevitable asystolism.
With greater dilatation of the right ventricle the tricuspid ring stretches and tricuspid regurgitation is added. This leak is more easily re(*ognised than ie the pulmonic, and accordingly the still more urgent stasis that now comes on is attributed to the tricuspid incompetence, and the pulmonary insufficiency is overlooked. The seriousness of relative puhnonary incompetence consists, there- fore, not so nuieh in the addition of any new and characteristic subjective symptoms as in the fact that it intensifies those already
368
DISEASES OF THE HEART
existing, while rendering the prospect of the patient's betterment practieallv nil
Objei^tive symptoms^that is, clinical signs of this complica- tion— are present, theoretically at least, and when recognisable consist in a weakening or impurity of the pulmonic second sound, or in a soft diastolic murmur, heard in the second and third left intercostal spaces.
The form which chiefly interests ns at this time is the primary or organic, which, either as a congenital or acquired lesion, exists indepeiHlently of any other vahnjlar or lung disease. D^ies this produce distinctive subjective sTOiptoms? To this query I think one most reply that not only does it not display distinctive symp* tumiitrilugy^ but it sometimes pursues a latent course for many years. In most of the cases cited by Baric the patients displayed dyspntea and other ordinary tokens of cardiac disease, as cyanosis and venous congestion, that every now and then wont on to the product itin of anasarca, albuminuria, etc., but wbieh were not in any way peculiar.
That tlie disease ujay k* latent for many years is proved not
only by Botiillaud's patient who, ii» spite of her congenital ]ndmonary defect, attained tlie age of twenty-ftmr, but also by a ease that came to my notice nearly ten years ago, Most unfortunately an au- topsy could not be secured, and henee a post-mortem con- Hrniation of my diagnosis was not had. Yet if iihysical :?igns count for anything, then this case, as wnll be seen by the reeitid, was one of pulmo- n a ry regu rgitat ion u nassoci- ated with other valve def^x'ts. The patient was a married woman of fifty-eight years of age who had given birth to eight children without, she said, any greater difficulty than is exj)erienced by most healthy women.
Fia, 75.— A»iA OF DKSP'iEATEn CAnnij^c DtfLTCSiia IN Ca«i or Pclmoitaby Rtotni*
QITATION (p. 389 >.
PUL3I0NARY REGURGITATION
369
She was short and slight, and althougli she stated she had known of her heart-disease since her eighth year, it had never oeeasioned her any particuhir discomfort. At the time of her consulting me she had lieen weak, nervous, and aimoyed hy palpitations for sev- eral weeks, l>nt had ohjeeted to seeking medical aid hecause of prejndice and the discovery, years hefore, that the ordinary heart medicines did not agree with her.
She showed mcHlerate cyanosis and distention of the external jugular veins, Imt no cedenia, and she did not eomjilain of short- ness of hreath. The radial pidses were e(|Ufil, nuNlerately accel- erated, irregular in force, and occasionally intermittent, Cnt their particularly iitjticeahle feature was their smallness and feebleness. There was evi- dent, but not great, eidar^^e- ment of the liver. Thus far there was nothing in the ex- amination of the patient to impress nie as unusual.
Wliem, liowever, explora- tion of the heart was begun, I was at onee struck by the for- cible and extensive cardiac impulse, which reached from the left nipple into the, epigas- trium, ipiite across the median line to the right eostal carti- lages, and as far downward as to the level of the eighth. This was not at once reeognised as the impulse of the enoruiously hypertro]ihied right ventricle, but by carefully studying tlie apex-beat, ami by <lerermining tlie area of deep-seated cardiac dulness (Fig. 75), I became convinced that it was the right and not the left ventricle which was enlarged.
Then upon resorting to auscultatirm I at once distinguished a diastolic munuur, which was located at the left fif the sternum in the third interspace, was transmitted <lownwiinl, and possessed the peculiar quality of the aortic regurgitant bruit (Fig, 76). This was quite naturally taken to be aortic, until pondering on 24
Fio. 76. — Arxa or ai&xintiii Iictikwtt
4IHMALL CIHCLK) AND OF PKurAlMTluX Of
Mi iivt'R IN Ca8K of Fllmuaakv Ksarn^ tilTATION (p. 3*58).
370 DISEASES OP THE HEART
the size of the right ventricle and the smallness of the pulse with- out any suggestion of a collapsing character or of other vascular signs of aortic incompetence, the conviction was at length forced upon me that I had to do with pulmonary regurgitation pure and simple.
I may add that both sounds at the apex were clear, while both second sounds at the base were feeble, and both heart-tones were audible in the cervical arteries. If secondary tricuspid insuffi- ciency existed, it was not recognised. I do not believe it was pres- ent, but that the enormous hypertrophy of the right ventricular wall prevented such a degree of dilatation as would have been necessary to set up tricuspid regurgitation.
Xot being able to relieve this patient's sense of weakness, nerv- ousness, and inability to take sufficient food, and above all to quiet the violent action of the heart, all of which constituted her symp- toms, I was not called in often, and after a few weeks was notified of her death, as nearly as could be determined, from exhaustion.
Here was a patient who to her certain knowledge had been the subject of some form of heart-disease for fifty years, a fact in itself highly interesting and unusual. Moreover, it had not inca- pacitated her for attending to all the duties of a housekeeper and mother of eight children. And lastly, when the physical signs were carefully determined, they were found to indicate regurgi- tation into the right and not the left ventricle, consequently pul- monary regurgitation. As no definite and reliable history of dis- eases in childhood and infancy could be obtained, I was unable to decide whether hers was a congenital or an accpiired lesion. It seems to me that there is much matter for reflection in the history of this case and in the long delay of symptoms, which wore those of increasing venous stasis, without, how(»ver, any complaint of dyspncra. It would seem to indicate that if this disease is unat- tended by stenosis, there are no symptoms so long as com]x?nsation is maintained, and that this is capable of being preserved for many yea rs.
Physical Sig^ns. — The diagnosis of pulmonary regurgitation concerns both the secondary and the primary form. The former, it will be recollected, is a relative insufficiency depending upon some antecedent pulmonary or cardiac disease, and therefore its physical signs are likely to be obscured by those of the associated
PULMONARY REGURGITATION
371
affection. The possiliility of its oecurrence in the late stages of mitral or aartie disease shoiihl always be borne in mind, and if in snch a ease a diastolic nmrmur develops in the pulmonic area, the diagnosis of secondary pulmonary incompetence may be assumed. Particulars regarding this niumuir will he coiii^idered under the head of auscultation, to which, therefore, the reader is rt^f erred.
Inspection.— ThiB discloses nothing characteristic in the sec- ondary form, the evidences of circulatory embarrassment being due to the associated affections. Even in the primary form the exist- ence of visible signs of heart-disease is likely to depend upon its severity. So long as comjiensation is preserved » inspection of the pnecordia tk^tceti? nothing more than a forcible and pcrbajvs ex- tended cardiac impulse, whichy to judge from the case 1 have hrietly reiK>rted, is particularly pronounced in the epigastriiun. So soon, however, as the riglit ventricle begins tn fail ocular signs of venous stasis appear, of the same character as in other cardiac affections.
Palpation.- — This is of considerable service in the detection of the right ventricle hvjiertrophy and in the study of the pulse. Pulsation in the epigastrium is forcible and imparts to the palpat- ing band the impression of a powerfully contracting %'entricle. It is in the study of the peripheral arteries that palpation is of greatest value.
Inasmuch aa the murmur is so closely like that of aortic regur- gitation as to often leave one in doubt concerning its real signifi- cance, the pulse must be relied on for differential information, Tn pidmonary iitconif^etcnoe the aortic system does not experience the sudden distention and equally rapid collapse of aortic insuf- ficiency, and consequently the p\dse is not at all like that de- scrihed by the term collapsing. On the contrary, it is likely to be small and weak, presenting in this respe<^t a striking contrast tn what might Ik^ looked for in connection with the diastolic nmrmur at the base of the heart.
The rate and rhythm of the piilse are determined by the state of compensation. If one coidd place his finger on the pulmonary artery he would iliscover that this vessel and not the aorta under- goes forcible distention and sudden collapse.
Perciffision. — Pulmonary regurgitation affects the ^he of the right ventricle, and consequently the area of cardiac dulness is
872 DISEASES OF THE HEART
increased, chiefly do\Miward, while that at the left is but slightly if at all changed. This means of investigation is therefore of great importance in enabling one to differentiate between pulmonary and aortic incompetence.
In the rehitive form cardiac dulness is already augmented to the right, and hence percussion is of less value than in the primary variety of this valvular lesion. It may nevertheless be of minor aid in enabling one to determine a degree of enlargement of the right heart out of proportion to what would be expected did mitral or aortic disease exist without pulmonary leakage.
Auscultation, — Contrary to what is usually the case, and to what has been stated in previous chapters concerning the diagnos- tic value of this means of examination, auscultation is of the great- est assistance in the detection of this particular lesion, not only because of its recognition of a murmur, but also because by it we are able to determine the absence of those vascular j>henomena that attend aortic disease of the same nature. Barie directs attention to the inijwrtance of carefully studying the pulmonic second tone, since, as he says, the earliest and in some cases the only evidence of relative insufficiency of these valves is to be found in a muffling or impurity of this sound. Consequently, if in a given case of cardiac disease, which ought naturally to intensify the pulmonic second tone, there is heard instead an enfeeblement and trifling inijjurity of this sound, it shiaild render one suspicious of dilata- tion of the artery and consequent inconij)eten(*e of its valve.
If a characteristic murmur results, this is diastolic (Fig. 77), acconi])anying the second heart-sound or even replacing that usu- ally heard in the second left interspace. In ]>riinarv lesions this niurniur is probably always present, and when stenosis is com- bined there is also a pulmonic syst(dic nnirnnir, so that there is a double or to-and-fro bruit, the same as when there is re£rurj2:itation at the aortic orifice. The seat of nuixinium intensity of this dias- tolic niurnuir is at the left of the sternum in the second and third left inters])aces. Its direction of transmission is downward along the left sternal margin, and its quality is soft. Indeed, it may so closely agree with all the characters of an aortic regurgitant bruit as to make it absolutely essential that one study carefully all the secondary signs before he can arrive at a differential diagnosis. It should be remembered, however, that the puhnonic murmur is
PULMONARY KEGURGITATION
373
not heard at the right of the sternumj as is generally the aortic. Yet this is not alone sufficient for its recognition, since an aortic diastolic nnirninr is sonietinies inaiidihle at the right and andible at the left of the breasthone. Should a pulmonic systolic murmur
Fia. 77. — Rhythm of Mibmlr in Typical Came or Puimokabt RKi.i'RoiTAnojr.
be as:^oeiated, this i,s not transiuitted into the arteries of the neck, but instead the ordinary heart-sounds are there audible, a circum- stance which is of diagnostic aid.
Diagnosis. — Tlie diliiculty which attends the diagnosis of ibis affection consists not in the recognition of the munnur, but in its interprefation, since it is likely to be mistaken for the bruit of aortic regurgitation. It is indispensable, therefore, to pay atten- tion to the secondary signs, of which the most valuable are those connected with the vascular system. For the reasons stated under palpation, there can be no acoustic phenomena connected with the arterial system in pulmonary insufficiency; and consequently the absence of a systolic snap, and still more of the double soutHe in the femorals, would, in conjunction with hypertrophy of the right, not the left ventricle, and with a diastolic nmrmur at the left car- diac base, cnalde one to state quite positively that the regurgita- tion was at the pulmonic, not the aortic ostium. The foregoing remark applies to the relative as well as the primary lesion; for even in cases of combined aortic and mitral incompetence, careful study of the peripheral arteries detects some of the characteristic
874 DISEASES OP THE HEART
signs of the former condition. WTien, on the contrary, mitral dis- ease has led to puhnonary insufficiency, such vascular evidence is wanting.
If the pubnonic valve becomes relatively incompetent in the last stages of aortic stenosis (as I believe occurred in my patient with aortic obstruction whose case was narrated in the chapter on that disease), the recognition of the secondary defect is very diffi- cult. This is so partly because its murmur is faint and likely to be overlooked, but also because if detected it is apt to be attrib- uted to a leak set up iw some reason at the aortic orifice. In the case of the lady just alluded to such a diastolic bruit developed some months prior to death, and became attended by distressing and at times violent palpitation at the pit of the stomach, the throbbing being visible. Keflection has since convinced me that this exaggerated action of the right ventricle was an indication of its hypertrophy, and hence corroborative of pulmonary regurgita- tion. I believe such an observation might be utilized in the future diagnosis of this lesion.
Prognosis. — Very little needs to be said upon this subject. Not only is the disease incurable, but it is not amenable to treat- ment. In relative pulmonary regurgitation there is already pres- ent a disease that affords a grave prognosis, else the pulmonic valve would not give way, and the addition of this complication ser\'es to hasten the downward progress of the patient. It shows that the original affection has reached an extreme stage, and that the right ventricle will not long be able to withstand the strain.
If the pulmonary incompetence is unattended by other cardiac disease, and if comjwnsatory hypertrophy is good, the lesion being discovered accidentally perhaps, the regurgitation may last for years without producing serious circulatory disturbance, as shown by my patient who had the lesion fifty years. This freedom from symi)toms is the exce])tion, however, for the wall of the right ven- tricle is so thin that compensatory hyi)ertrophy is likely to be easily ruptured, and when subjective symptoms once set in they are likely to be progressive. The occurrence of albuminuria and dropsy is to be regarded as of very evil import and to betoken the not very remote termination of the case.
Mode and Causes of Death. — Barie speaks of the occur- rence of pulmonary embolisms as a not remote contingency and as
PULMONARY REGUKGITATION 375
contributing to the patient's death. The fatal termination is most likely to superv^ene slowly, in consequence of cardiac or gen- eral exhaustion, rather than suddenly, and yet this latter event is not impossible. Congenital cases, particularly if combined with stenosis, may lead to pulmonary phthisis through anaemia of the lungs.
CHAPTER XIII PULMONARY STENOSIS
This is an obstructive lesion which in its effect on the right ventricle is analogous to that of aortic stenosis on the left. It dif- fers from the latter, however, in its origin and anatomical char- acters. It is divided into two great classes, the congenital and the acquired, the former constituting by far the greater number. Even when congenital, this lesion is one of the rare forms of heart- disease. Instances of the acquired affection are so extremely in- frequent that since Constantin Paul's elaborate monograph in 1871 only 8 cases have, so far as I know, been reported. For my knowledge of these cases I am indebted to a thesis by Koehler, of Halle, in 1894. I have not l)een able to ascertain how many of the cases described by Paul belong to each variety. The 3 cases reported in 1895 by Boviard, Holt, and Forlanini, and the 3 in 1890 by Adams, Amozan, and Siredy, all appear to have been congenital, which still further emphasizes the rarity of the acquired form. The first case on record of this fonn was descrilx^d in the Atlas of Pathological Anatomy by Cruveilhior.
Morbid Anatomy. — This can be l)est described by the repe- tition of a report of the 8 cases above alluded to, which was pub- lished by me in the Journal of Medicine in January, 1897.
In 1873 the late Christian Fenger published a case in a male of nineteen years in which the disease was traceable to an attack of articular rheumatism at the age of eleven. The autopsy dis- closed numerous vegetations attached to the pulmonary valve and along the wall of the artery as far as its bifurcation and into its main branches, particularly the left. This condition, although the vessel was dilated, had led to very great obstruction, with consecu- tive hypertrophy of the right ventricle. The septa were intact, the pulmonary artery and its main right branch dilated. Fenger, 376
PULMOXAKY STENOSIS
377
from the history and post-morteii) discovery of recent endi^carditis, concluded that there euuld be no doubt of the postnatal origin of this case.
Moritz Mayer next reported a case in 1874 in a girl of sixteen, who at the age of eleven had sntforcd from some pulmonary dis- ease and from endocarditis. The necropsy revealed cauliflower vegetations attached to the wiill of the conns arteriosus and to the pulmonary valves, with secondary hypertrophy and dilatation of the right ventricle. The ductus arteriosus was closed, hut the interventricular sieptum contained an opening large enough to aduiit the tip of tlie first finger, and Mayer explained this defect as having originated after hirtli in consetjuence of the previous endocarditis.
Rinsenna's case in 18>^;J was in a patient aged thirty-four, who had also had acute rheumatism. On post-mortem examination the pulmonary valves Avere found greatly thiekened, and to have thus caused slight ohstructioUj but without enlargement, of the right ventricle.
In 1884 Krannhals reported 2 eases, of which one was in a widow of forty-three suffering from leucainia, and the pulmonary stenosis w*as attributed to this affect i*in. Neither necrosis of the valves noT micnvorganisms were found to explain the stenosis. In his sectmil case, that of a liousemaid of nineteen, there was a history of good health up to the fourth year, when she had an attack of rheumatism, and her health had been itnpaired since that time. The ftrtal passages were found closed, there were no c«»n- genital defects, but the pulmonary artery was dilated.
Keiidu in 1884 de&crilx'*l a case in a girl of nineteen, who had htid the disease for fifteen years, and after death the pulmonary valves were found fused into an inflexible diaphrnpn having an opening of about -yV <>f ^n inch in diameter. The immediate cause of death was a rapiilly progressing nephritis.
Stybr^s case in 1890 was that of a w^oman of twenty-four in whom the stenosis was found due to an inflammatory blending of the puhnonary segments into a tendon dike cone that projected into the lumen of the artery and contained at its apex an opening 2 millimetres in width. Two oblique lines that passed down the sides of the cone showed where the cusps had become united. The right ventricle was enormously hypertrophied. As the aortic cusps
378 DISEASES OP THE HEART
were slightly sclerosed, Koehler thinks the inflammatorr process must have dated from intra-uterine life.
Finally, Koehler described the case of a housemaid of twenty- one who was admitted to the hospital in July, 1893, suffering from pneumonia, and who gaye a history of acute rhemnatism the May previous. Since that time her health had been poor, and she had suffered from dyspna?a. The autopsy disclosed polypoid vegeta- tions springing from the wall of the pulmonary artery in such a manner as to prevent the complete oj)ening of the valve during ventricular systole. The valve-segments as well as the endocar- dium of the right ventricle were healthy, but similar vegetations were found in the aorta so disposed as to prevent the adequate opening of these valves, and to thus cause a stenosis of this orifice, the same as on the right side. Both ventricles, particularly the right, were dilated. The sseptum was intact and the foramen ovale was closed.
In the foregoing cases, with exception of Rendu's and Stybr's, there were evidences of recent endocarditis, absence of congenital abnormalities, and dilatation, or at least no perceptible narrowing, of the pulmonary artery. Acquired cases present striking differ- ences from most of the congenital in their pathological appear- ances, but they both have the common feature of hypertrophy and dilatation of the right ventricle.
In the congenital form the obstruction is due most usually to a fusing together of the valve-segments, which then form either a diaphragm stretching across the ostium or a cone-like projection into the artery with a small opening at its a])ex (Fig. 78). The foramen ovale is usually open, and the interventricular sa^ptum is sometimes incomplete. The pulmonary artery is always nar- rowed, and there may be atresia of this vessel. The ductus arterio- sus is generally oj>en, yet is in some cases found closed. Very rarely the stenosis is caused by constriction of the right conus arteriosus, in which event this may appear like a third ventricle, and both the interventricular and interauricular septa are defect- ive, the pulmonary artery is narrowed or even occluded, and the ductus Botalli remains pervious.
In other cases there are various errors of development, as trans- position of the aorta and pulmonary artery, or their origin from one common tnmk ; a blending of the two ventricles into one com-
PULMONAHV STENOSIS
8T9
moil cavity with hut one instead of two auriflea; or one ventricle and two auricles, or hut one auricle and two ventricles.
It is not always easy to determine post mortem whether a given cfiso helongs to the congenita! Mr the acquired csitegory. In well-
Flo. 7B. — Ulaut "F 1 H>v,sii 'W[\^ < ii.N<»-i« ^»r tiiiv Plluunak\ Uiiinot,
Spedmen in collection of in Uustav Futtcrer,
marked specimens, like Fenger's, or in such as show striking ab- normalities of ilevelopnjcnt the decision may he easy; bnt in cases presenting some of the cliaracteristica of both forms the exact nature must be left in douht.
Aside from the evidences of recent endocarditis it is the condi- tion of the pulmonary artery upon which pathologists rely for the determination of the intra- or extra-uterine development of the
380
DISEASES OF THE HEART
lesion. Dilatation of this vessel makes strongly for the acquired form, while narrowing of the artery points to the f*ptal origin of the disease.
Etiology, ^-The congenital form can be dismissed with the stateiaent that it resnits eitlier from intra-nterine endocarditis or myocarditis, or from defective uevelopuieut.
Acquired eases also originate in endocarditis either of rheu- matic causation or in the course of other acute infectious pi'ocesses, as shown in tlie histories of the 8 cases ab^>ve mirrated. Its rarity is due to the fact that after birth the right heart is seldom the seat of acute inflammation.
In a ninth case that has come to my notice, that of A. Kasem* Bt'k in 180i>^ the puhnonary stenosis was caused by a gtunma on the ostiuui.
Symptoms, — These depend largely up«»n the congenital or acquired uatiire i>f each case* Moreover, in the latter the clinical history is also influenced by the presence or absence of acute endo- carditis. If the cases are not stumbled up+m accideutally in the course of examination or treatment for some other wholly differ- cut disease, the patients are likely to lie seen when the atfectiou has led to prononuccd diHturbauce of the general heaUh. In such there iin^ dyspncra and other ordinary evidences of cardiac asthenia, or there is a compUiint of vague general distress and ill health. In a word, there are no symptoms peculiar to pulmonary stenosis as contrasted with other valvular lesions.
In the congenital form patients are apt to be weakly, under- sized, sometiuies mentally deticicnt, and to manifeeit striking cya- nosis. This is not always present, however. In the chapter on Congenital Cardiac Affections will also be considered certain changes in the blood that accompany marked cyanosis or the Mor- bus Ceruleus of older wTiters,
Sufferers from piihtioimry stenosis are very apt to die from tuberculoms of the lungs, as is shown in the only instance of this cardiac disease I have observed, and which was published in my paper previously mentioned, A plumber's helper, aged twenty- three, was first seen by me at my clinic at Cook County Hospital, having been sent from Ward 4 as a case of pulmonary tuberculosis. Family history was meagre, Ilis?^ fatlier had died of some wast* ing disease with cough; his mother of cancer; two sisters living
PL'LMOXARY STENOSIS
381
Fio. TO, — Relative Cahoiaij Dilnias in Ca^e or riLM<-»r\KV STESoais (p, 380).
and liealthv. Patient dcclaroj he was heaUliy in infancy and
eliildhoudj iuid had never siiifered from dyspntra nn exertion
prior to his present illness,
and liad nut exliibited cya-
ncrsis. In fact he was healtliy
until his present illness began
three months before his ad- mission to the liospitaL
Without entering tix» nnieh
into detail^ it will sutfiee ti^
state that he presented the
usual syinptonxs of eunsnnip-
tion, eniaeiution, cough, pro- fuse niueo-pnrnlent expectora-
ticaj, felxrile temperature, and
a rapid J feeble pnlse, the fune-
tiuns uf the digestive organs
remaining good. There was
no cyanosis. The ri;ij:ht apex
was retracted, and expanded poorly upon inspiration. Both
apiees showed dnlness, hronehlal breathing, and moist rales.
T 1 1 e pnvco rd i u m b ii Iged from the third rili to the epi- gastrium and from left to right nipple. There was a shortj weak systolic thrill in second left interspace, 1 inch from sternum. AhsohUe dnl- ness was increased from I he level of the st^eond costal earti- laire to the lower border of the tifth rib, and from 1^ inch to right of sternnm to j inch in- side of left mamilhiry line (Fig. 7D).
The heart's rhythm was regidar and accelerated, rhe
Fio. ^x-i.H ATJON nr TuniLi. AiTT, SvirT.atr goinidg hcins? verv feeble, rhe
MrRMiR IS Case of Pulmoxakt 8tex«>- t* i i i" n 1*1
■u (p. sso). first muffled and dulh while thi*
382 DISEASES OF THE HEART
second, in the third left interspace, was short, high-pitched, and so feeble as to be rudimentary. A harsh systolic murmur was audible, having its maximum intensity in the second left interspace, 1 inch from sternum, and corresponding in position to the soft systolic thrill previously mentioned (Fig. 80). It was transmitted with special clearness upward and outward towards the left shoulder and around the left side to the back, but could be distinguished feebly even in the right half of the thorax. The liver was not appreciably enlarged. Tubercle bacilli were discovered in the sputum.
The diagnosis was made of pulmonary stenosis with secondary hypertrophy and dilatation of the right ventricle ; tuberculosis of both lungs and moderate venous and visceral congestion consecu- tive to the cardiac lesion. This was thought to be congenital, although there was no history of cyanosis in infancy, and no evi- dence of other congenital cardiac defects. The patient was kept imder observation until January 10, 1896, when he was foxmd dead in his bed. Symptoms of general asthenia increased in sever- itv, and diarrha*a set in a dav or two before death.
Xecropsy was made by Dr. F. Tice twenty-four hours after death. The lung-findings, briefly stated, were those of pulmonary tuberculosis. The pericardium contained from one and a half to two ounces of fluid. Aorta was not enlarged; the pulmonary artery was larger than the aorta, dilatation extending into the two branches, the left more than the right. The aortic valves were found competent, but the pulmonary valves leaked slowly to the hydrostatic test.
Looking into the pulmonary artery from above, it api>eared as if a ni]>ple with a small opening at its apex projected into the vessel, and at one side near its base was a second small opening, which was closed in below by a thinner membrane (Fig. 81). The right ventricle was liy])ertropliied and dilated, and the right auri- cle was also enlarged. One cusp of the tricuspid valve showed a slight thickening along its base. The mitral valves were negative except a slight thickening; aortic valves were thickened along base and margins, while small atheromatous placpies were found in the beginning of the aorta.
The left ventricle appeared slightly dilated. The interven- tricular sipptum was complete, but in the interauricular sieptum
PULMONARY STENOSIS
383
tliere was a %*alve-likc? passage, which would not quite admit two iriafrhes, was perhaps 3 milliiuetres in diameter, and corresponded
Flo. 81. — Heart from Ck»e cty Pi'l^hnart Stehobki (p. 880). Litto shows imrrowtni pultuoiiury oriJioe»
in sitnation and nhape to the foramen ovale (Fig, 82). Thus it waa seen that the intra-vitam ^liagiiosis was confirmed in its main features. A more careful inspection of the heart, made a year later after having l>een presented in a formalin solution, showed that the cone which projected into the pulmonary artery, and rep- resented the seniiliniar valves, was made up of a uniform mem- brane, sonipwhat thicker than normal valves, and showed no lines or ridges that indicated the points of fusion of the cusps. The opening at the apex was oval, measuring 15 millimetres by 8 milli- metres at its broadest point. The edges of the cone were thick- ened, and the seeond minute o]>ening at its side, near its base, was
884
DISEASES OF THK HEART
found to be a saccular dilatation projecting into the binien of the cone. The diameter of the pulmonary artery wa§ '22 millimetres, of the aorta 18, and of tlie foramen ovale 3 millimetres.
From the foregoing deiiteription it is apparent with what uncer- tainty one eim classify this case as eimgenital (ir ac4]nired. There were no indications of endoearJilis, as it ordinarily ap[>ears after
Fm. H2,— Same Hkart as Fi«, **1- Loft fturfclu is laiit u;xtR, nud tine tIhML•jlU^ pAtont forsimou ovulfii
birth, TIjc pulmonary artery was not contracted, but rather dilated, tire interventricnlar ssrptnm was complete, and the fora- men ovale was not more patent than it is in a considerable propor- tion of hearts witliont a snspicion of congenital disease. Xever- tlielesSj the appearance of the cone, which replaced the semilunar
PULMONARY STEX08IS
885
vaT%'es, rendorod it probable that this case was of congenital origin, and that iiura-iiterint' endocarditis oaused a fusion of the seg- ments at a iieriod subsequent to the closure of the septa, and that the stenosis was not sutficient to prevent the chmure of the furarnen ovale after InrtlK Moreover* the volume of blood driven into the jmhnonary artery conhi nut have been very small, and must have been divideil into fluid veins, which threw the stream against the arterial coat^ in such a way as to maintain ade- quate blrHid-jiressure within the vessel. It is interesting to reflect that, althuu^h the lesion, aeeonling to the patient's hisiorv, gave rise to no subjeetive symptoms, it should yet ultimately have led to pulmonary tuberculosis, the usual sequence in such cases.
Regarding physical signs in this case, it is also of interest to note the wide propagation of the murmur. This was more marked in the left hing^ and as the left branch of the pulmonary artery was found to be rather larger than the right, there was probably direct connection between the size of the artery and the transmis- sion of the murmur; for had the vessel been narrowed, the audi- ble vibrations could n*vt have l:»eeu transmitted to any great dis- tance.
If a conclusion from a single case is justitiable, it is likely that the symptoms directly referable to pulmonary stenosis dei>end upon its degree and upon the association of other developmental defects even more than upon the obstruction itself.
Physical Signs. — Inspertloti, — Cyanosis is not always pres- ent in congenital cases, and when present is not uniform through- out the ImkIv. It is this bluish tint which led old writers to des- ignate the underlying abnormality by the generic term of Morbus C'enileus, Cyanosis is most apparent on the cheeks, ears, fingers, elbows, and knt^es, and is intensified by coughing or physical exer- tion. As shown by my case, it is not so likely to be present when the stenosis lias not led to or is not associated with defects, as, e. g., patency of the foramen ovale or of the interventricular sa^ptum.
In the acquired form patients are more apt to show pallor of the countenance, and there may be turgescenc^ of the superficial veins as a direct result of interference with the outflow of blood from the right heart. Inspection of the pnecordinm detects bulg- ing over the situation of the right ventricle — i. e,, at the hnver end of the sternum and the parts immediately adjacent. Such a bulg- 25
386 DISEASES OF THE HEART
ing is most marked in cases in which the valvular lesion is either congenital or has existed from very tender years. It is due to hypertrophy of the right ventricle, and hence there is associated pulsation in the epigastrium and over the prominent area.
Palpation. — This corroborates some of the information de- rived by inspection, and enables one still better to appreciate the extent and force of the cardiac impulse imparted by the hyper- trophied right ventricle. In addition, there is usually felt a sys- tolic purring vibration or thrill in the pulmonic area — i. e., in the second left intercostal space, close to the sternum. This fremisse- ment may be exceedingly delicate, as in the case observed by me, or it may be distinct and harsh.
The pulse presents no distinctive characters aside from small- ness, feebleness, and increased frequency.
Percussion. — By this means is revealed marked increase of both absolute and relative cardiac dulness, the increase being downward and to the right, over the situation of the right ventricle and corresponding auricle (Fig. 79). In my case this alteration of cardiac dulness was very pronounced, and aided materially in the diagnosis of the lesion by assuring me of the existence of right ventricle hypertrophy.
Auscultation, — The conditions here are favourable to the gen- eration of a bruit, and as it is produced during the passage of the blood from the right ventricle into the pulmonary artery, the mur- mur is systolic (Fig. 83). Its seat of maximum intensity is over the base of the heart, at the left of the sternum, in the second and third intercostal spaces (Fig. 80). At first this bruit may be thought to be aortic in origin, but if its direction of propagation is studied this will be found to be upward and to the left towards the left clavicle rather than to the right and upward, as is the case with the murmur of aortic stenosis. Another point of difference is that the pulmonic systolic murmur is not heard in the cervical arteries, where, on the contrary, the two cardiac tones are usually distinct. If intense, the murmur may be heard throughout the pra'cordium, though in all instances its area of maximum intensity corresponds with the location of the systolic thrill. In my case the murmur was transmitted widely, but was more distinct in the left than in the right half of the thorax. In auscultating towards the apex and over the body of the right ventricle the murmur grows
PULMONARY STENOSIS
38T
less intense, while the two cardiac sounds become more distinct. Tlie imirniur uuiy he rough and loud, or soft and faint The piil- nionie sfrond ^^oinid is dinjinishetl in intensity, or may be absent ahogether, while the two aortic sounds are distinct.
Fjo. 88.^Hbttuii of Ttvical Pllmonjuiy Stenotic Murmur,
Diagnosis, — The diihcnlty of diagnosis in this affection lies in its differentiation from aortic stenosis or p<.^ssihly in deciding whether the hriiit may not be accidental, since it is situated where such an accidental murmur is so often heard. If, however, proper attention is paid to the secondnry physical signs as described above, in particular to the evidence of hypertrophy of the right, not of tlie left ventricle, one cmi scarcely fail to interpret the mnr- mnr correctly. If after such careful study of all the physical signs doubt is still entertained^ the sphvgmograph will be found of service in enabling one to differentiate between this lesion and aortic stenosis, for it goes without saying that pulmonary ohstruc* tion can in nowise modify the characters of the radial pulse. Finally, the discovery of pulmonary tuberculosis and of cyanosia in cases in which the two halves of the heart coninumicate» fur- nishes a certain degree of evidence in favour of the existence of pu hn on a ry obst ruct i on .
Prog:nosifl. — Pntients with pulmonary stenosis rarely live be- yond the tliird decade. Even when the disease dt>es not dire<-'tly destroy life, it does so indirectly by predisposing to pulmonary
388 DISEASES OP THE HEART
tuberculosis. This has been so frequently observed that no doubt can be entertained concerning the intimate connection existing be- tween these two diseases. WTien phthisis has once supervened the prognosis becomes that of the secondary affection, and since the stenosis is irremovable there can be no hoi>e of the arrest of the tuberculosis. The influence of this cardiac defect upon the pro- duction of consumption is througli the ana?mia of the lungs which the narrowing of the ostiimi occasions.
Mode and Caosee of Death. — In Hustedt's G cases of pul- monary stenosis death was caused in 1 case bv heart weakness, in another by miliary tuberculosis, and in the 4: others by phthisis.
PULMONARY STEXOSIS
389
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CHAPTER XIV COMBINED VALVULAR LESIONS
Chbonic valvular defects have been dealt with singly, since by so doing their distinctive individual features could be brought out more clearly and without danger of confusion. It would be a mistake, however, to consider these forms of heart-disease as always, or indeed as generally, occurring alone. As a matter of fact certain of them are usually combined, while it is possible for any two or three, or even for all of them to be united. The most common association is that of both stenosis and regurgitation at the same orifice. Thus it is comparatively rare to find aortic obstruction without also some insufficiency, or the reverse, while in the same manner the two mitral lesions are usually combined in varying proportions. Indeed, a moment's reflection will convince one that the structural alterations set up by endocarditis are very prone to result in both incompetence of the valves and narrowing of the ostium, the clinical features of each case being determined by the predominant lesion.
This is not all ; lesions at one orifice may be complicated by a defect situated at another. To be explicit, mitral stenosis may be combined with either aortic stenosis or regurgitation, or both, and the same way with mitral insufficiency, or a double mitral disease may be associated with either or both of the aortic defects. Let us now consider these various combinations in detail.
COMBINED MITRAL STENOSIS AND REGURGITATION
As already stated, the endocarditic changes that lead to mitral <lisease are very apt to cause both constriction and insufficiency. Extreme narrowing is more likely to exist alone than is free re- gurgitation, and yet even when there is a buttonhole mitral, it is possible for an insignificant leak to also occur, although the insuffi- ciency may not be declared by a systolic apex-murmur. On the
890
COMBINED VALVULAR LESIONS
391
other liand, mitral segments that are too stiff to close are qxilte likely to depend in front of the openin^r in siieh a manner as to oppose some barrier to the free ingress of the blood from the auri- cle. In ebildren the mitral curtains are not infrequently so shriv- elled as to form a mere fringe ahout the ring, and when stich is the case stenosis is abs€*nt. In adults, {>artieularly when dje incom- petence is the result of atheroma, pure and unmixed regurgitation is the exception.
The etTeets on the lieart are essentially those of either form of mitral disease when existing alune, antl yet the left ventricle and left auricle manifest certain modifieatiouB depending upon the as- sociation of stenosis with incompetence. The ventricle is neither so dilated as in unmixed regurgitation, nor so atrophic as when there is extreme ohstruetiyn. Similarly, the left auricle is neither 80 hypertrophied as in predominating stenosis, nor so dilated as in free regurgitatiim. When conjoined, the two lesions, therefore, exert a somewhat restraining intlnence upon each other as regards the secondary effects cm the cardiac cavities directly affected. The changes in the right heart are those incident to retarded pulmo- nary eirculation, and their extent depends upon which of the two lesiims ]ir(Hhiniinates.
Ssmiptonis, — The 8\'mptoms depend upnn the degree of com- pensation, and this on whether the stenosis or the regurgitation is the greater. They have been described in considering the re- spective mitral defects, aiul do not need to be reca|)itulated.
Diagnosis. — ^The diagnosis is as a rule not difficult, for the reason that the signs of the two diseases are comliined with varying distinctness in different cases. The apex-beat is not so displaced nor so forcible as in uncomplicated regurgitation, nor, on the other band, is it so distinctly thumping as in pure stenosis, 1*ut presents the characters of both affeetions. There is usually a presystolic thrill at the apc*x, but it is less long and less intense tlian in stenosis alone, l)eing commonly only a slrort vibration, which seems to be merely a prolongation of the afiex-sboek. Car- diac dulness is increascnl transversely, but chiefly to the right, and the pidmonic secoutl sound is accentuate<h
Auscultation detects a combination of lH»rh a presystolic and a systolic murmur, the latter being well marked as a rule, and the former long and relatively pronounced, or short and difficult of
892 DISEASES OF THE HEART
recognition, according to the degree of narrowing. I have some- times found in these cases that the systolic bruit is the predomi- nant one in the erect position, while in the dorsal decubitus the presystolic murmur comes out more distinctly. This is the reverse of what has been stated as the rule regarding the influence of position upon the two mitral murmurs when uncombined. I have also observed that often, when only the presystolic bruit is audible directly at the apex, the systolic murmur can be detected further to the left and on the back.
Prognosis. — The prognosis is, other things being equal, rather more favourable when these two conditions are united than when either exists alone, and I believe for the reason that they tend to check each other.
MITRAL STENOSIS AND AORTIC STENOSIS
This is an exceedingly serious combination, since at both of the left ostia there is a mechanical impediment to the passage of blood from the pulmonary into the aortic system. The left ventricle re- ceives and discharges an abnormally small volume of blood, de- pending on the degree of constriction, and hence is a thick-walled chamlxT of limited capacity, while in marked contrast are the greatly liy|x^rtrophied and dilated left auricle and right ventricle.
Sjmiptoins. — Symptoms appear early, and are pronounced in consiHiuence of tlie great stasis within the lungs and body gener- ally. Cyanosis and dyspnoea are present, often in an extreme degree, while engorgement of the abdominal and pelvic organs is shown by all of its attendant phenomena, both subjective and objective.
Diagnosis. — The pulse is small, weak, and slow or acceler- ated, according to the state of compensation. The apex-beat is weak and precede<l ])y a presystolic thrill, unless indeed it be pro- duced by the impulse of the hypertrophied right ventricle, when it may be diffused and quite strong between the sternum and left nipple.
Epigastric pulsation and a marked increase of absolute and relative cardiac dulness to the right evince the secondary enlarge- ment of the right heart. There are heard a rough, low-pitched presystolic murmur at or within the apex and an accentuated pul- monic second sound indicative of the mitral lesion, and in addi-
COMBINED VALVl'LAK LESIONS
393
tion, a harsh systolic V>niit in the aortic area with a feeble second tone, showing obstruction at this orifice.
PrognoBis, — The ]irognosi9 is of necessity very unfavourable, since compensation cannot long be preserved, and when broken can he restoredj if at all, only with great difficulty,
MJTRAL STENOSIS AND AORTJC REGURCrTATION
This is iiho a serious conibinationj yet the degree of its gravity IS Jeterrnined by the extent and predominance of the lesions.
The i^econdary effects on the heart are thofee produced by ob- structed outflow from the lungs and left auricle, together with such as are usually caused by reflux into the left ventricle— namely, hypertrophy and dilatation of the left auricle and right ventricle, and in the case of the left ventricle, such a degree of hypertrophy and dilatation as would follow regurgitation of a diminished volume of Idood from the aorta, diminisheil in conse* qiience of the stenosed mitral o]>ening- In one ease the mitral lesion predominates, and the effects on the heart and circulation are essentially the same as in uncomplicated mitral narrowing. In another this defect is subordinate to the aortic lesion, and the secondary changes in the heart are cliiefly such as are found in aortic insntficieney.
Ssrmptoins. — The syuiptoms are consequently determined by the j>retlt»minating lesion. In oil examples of this combination there is more or less tlyspna^a of effort, but when the mitral sur* passes the aortic defect in gravity this symptom is more pro- nounced.
Thus I have observed two female patients with this combina- tion. In one the aortic regurgitation was plainly the greater, and she was able to take a fair anunint of exercise, even slow bicycle- riding, without sjx^cial discomfort. If the effort became to<3 severe it produced palpitatitui and breathlessness* The other woman in wliom the mitral defect predominated^ and was still further com- plicated by pericardial adhesions, showed great hepatic and con- siderable general %-enous engorgement and complained of weakness and decided shortness of bre^ith upon even slight exertion. Both these patients broke dovm their com]»ensation while under my ob- servation, and in both thi^ rupture proved irretrievable. The 1 ni- ter was given a course of baths, after having been confined to bed
394 DISEASES OF THE HEART
for a number of weeks. They failed utterly to reinstate the heart. Digitalis also proved powerless. Dropsy did not appear, but the circulation became extremely feeble, temperature remained per- sistently subnormal, falling on several occasions to 96° F., and once to 95° F., dyspntra grew greater, and death took place one week after she returned to her Dakota home, under what final apj)earances I have not been able to learn.
The other patient considered herself in usual health until mid- summer of 1901. Then, apparently as a result of the intense heat, the fatigue of a short journey, and an attack of indigestion, follow- ing a too hearty sup]>er that same day, she began to suflFer from most annoying palpitation whenever she walked about, no matter how slowly. Weakness also set in, and with the palpitation in- creased in spite of digitalis and other therapeutic measures. These symptoms at length obliged her to keep her bed, and even then her condition grew so much worse that she was brought back to Chicago.
I found her in a deplorable plight. The pulse was extremely small and weak, about 100, and the right appreciably smaller than the left. The right arm and a portion of the right thoracic wall were cpdematous, in consequence of thrombosis of the external jugular, subclavian, and axillary veins. The liver was palpable and hard, but there was no dropsy of the ankles. The bases of the lun^s wi^-e dull with fine crackling rales, and she coughed up bloody sputum. Tlie ri^ht heart was much dilated, and the sounds and murmurs were feeble. She complained much of exhaust i(m, slept j)(K)rly, and passed a scanty amoimt of urine containing a trace of albumin.
After a time dropsy of the legs set in, and towards the close of her illness thrombosis took place in the veins of the left side of the neck, with resulting a»dema of the corresponding arm. There was nothing to indicate acute endocarditis, and hence the thrombosis was probably due to coagulation of the blood from pressure and stasis. This very interesting phenomenon — i. e., venous throm- bosis in cases of heart-disease — has been considered more fully under Symptoms of Chronic Endocarditis (p. 205).
Diagnosis. — The diagnosis of combined mitral stenosis and aortic regurgitation is made by the discovery of the physical signs of both lesions modified and more or less obscured bv each other.
COMBINED VALVL'LAR LEt^IONS
395
Inspection shows the apex-beat displaced to tlie left and down- wardj as in aortic ineompeteneej but to a less extent. If the steno- sis is eoDsiderable, and lias led to right-ventricle hypertrophy^ there is epigastric pulsation^ and there may also be visible engorge- ment of the snperticial veins.
On palpaiion the displaced apex-beat is fuund to be less forci- ble and heaving than in pure aortic regnrgitation, and there is a more or less distinct and prolonged presystalie thrill, depending on the ciegroe of initral eonstrietirm. The characters of the pulse are also found niii<liticd. By reason of tlie stenosis it is small and weak, while the aortic lesion gives it a collapsing character. In one of my patients mentioned above this was fairly well marked, ivhile ill the otber it was not appreciable by the finger, the pnlse being distingiushe<l by sniallness and hiwness of tension. In cases in which the iiiirnil obstnietion is the dominant lesion palpation is also likely to detect more or less liepatic enlargement.
PercuMton discovers increased cardiac dulness in all diame- ters^ and is of great aid in the determination of the coexistence of these two lesions. Mitral stenosis does not cause increase of dulness to the left of the nipple; and, conversely, aortic regurgitation does not occasion increase of dulness t<> the right. Yet in this combined lesion dulness is increaseil in both these directions. Consequently, the results of iwreussion takeu in connection with those of auscultation are of the greatest possible importance.
Ausculiafiofh — This also furnishes valuable information, al- thmigli it shnuld never be rfdied upon to the exclusion of the sec* ondury physical signs perceived by tlie other means oi investiga- tion. The mitral disease is shown by a ehjiracteristie presystolic murmur at tlie a|iex and Ijv accentuation of the pulmonic second sound, the aortic insutticiency by a diastolic bruit in the aortic area or upon tlie sternum, and transmitted downward and to the k^ft, while the second tone in the second right interspace is enfee- bled or absent. If in doubt concerning the siguiticance of this murmur* tme should auscultate the femoral artery, since when aortic regurgitatiuu is also present there is a sharp systolic snap, and it may be also a double murmur in this vessel Extreme mitral stenosis in its late stages rnay occasion pulmonary incom- petence with a diastolic bruit, and therefore auscultation of the
396 DISEASES OP THE HEART
feniorals is of greatest importance in the differentiation of this insufficiency from aortic regurgitation.
PrognOBifl. — The prognosis depends upon the degree of tlie two lesions and upon which predominates ; yet, on the whole, the course is likely to be that of mitral stenosis.
MITRAL REGURGITATION AND AORTIC STENOSIS
A moment's reflection will convince one of the exceeding seriousness of this combination. The obstruction to the outflow into the aorta ser\'es to intensify the regurgitation into the auri- cle, because the blood flows in the direction of least resistance, which in this case is backward rather than forward. If the steno- sis is extreme, it leads to great stasis and exerts all the local and constitutional effects of a most pronounced regurgitation. The heart becomes enlarged in its entirety, but the hyi)ertrophy of the left ventricle, instead of overcoming the obstruction, serves but to intensify the force of regurgitation. The work of maintaining the circulation falls chiefly on the right ventricle, and as this is a thin-walled chamber, capable of but limited compensatory hyper- trophy, it will not long be able to keep up the unequal struggle.
Symptoms are those of mitral disease of an extreme degree, and do not need to be recapitulated.
Diagnosis. — The pulse is small and feeble, while its rate and rhythm are determined by the state of eomj>ensation. The apex- beat is displaced downward and outward, and relative cardiac dulness is increased in all directions. Two systolic murmurs are audible, one in the mitral area, and one in the aortic, which are to be distinguished from eaeli other by their different points of maximum intensity, by their propagation, and by their different quality. The former, blowing and softer, is transmitted to the left, while the aortic, lower pitched and rougher, is propagated upward into the arteries of the nock. There is intensification of the pulmonic second and diminution of the aortic second sound. The chief difficulty of diagnosis does not lie in recognising the presence of the mitral insufficiency, but in determining whether or not this is relative, in consequence of dilatation of the left ven- tricle secondary to the long existing aortic stenosis.
Prognosis. — Under the most favourable circumstances the prognosis is grave, since the compensation on the part of the right
COMBINED VALVULAR LESIONS
397
ventricle is Hkelv to Lie short lived, and when oiwe ruptured can- not jmssildy bo restored, iloreover, iioth puhnonarv and tricuspid iiisiitfieieney are likely to result when eoiupensation fails, and then render the prognosis hopeless.
AORTIC REGURGITATION AND MITRAL REGURGITATiON
This conibiBation is not infrequently encountered in the hite stages of aortic insuificieney when dilatation of the ventriele has led to relative ineomjietence of the auriculo-veutricular valve. It ntay, however, be seen as a enndjined lesion when both deft^^ts are the result of structural alteratio!L The conihination is a grave one, and yet, as stated by Baeelli» a double regurgitation of the kind under discussion does not begin to be so serious as ohstructiou at the a<)rtic and leakage at the mitral ostium.
Symptoms,— The influence of the mitral lesion is to lessen the etlect of the aortic regurgitation on the general system, since a part of the blond intended for the aorta is diverted into t!ie auri- cle, and the arterial system is not so violently distended by each bl(X>d-wave. Arterial tension does not present such a striking con- trast during systole and diastole as in uncomplicated insutficiency of the semilunar valve. For this very reason, however, the arte- rial bkHxl-sui*jdy to the various organs and tissues is diminished, and there is marked arterial anaemia.
In addition there are the symptoms of venous congestion, only limited by such capacity for compensatory by |>er trophy as resides in the right ventricle. The heart is likely to attain enormous size, as shown by the position of the apex-beat far to the left of the nipple and flownward, and by great increase of both relative and absnlnte cardiac dnlness.
Diagnosis. — This is not usually a matter of much difficulty. The pulse is small yet collapsing, and there is increased dulness both to left and right. Aiiscnltation reveals both a basic diastolic and ajK*x systolic bruit, with feebleness of tlie aortic second ac- centuation of the pulmonic second, and often absence of the sys- tolic sound at the apex. Inspection and palpation disclose passive congestion of the venous system and alxlominal viscera. In case the diastolic bruit is likely to be thonglit a mitral diastolic one,
398 DISEASES OP THE HEART
its real nature may be ascertained by auscultation of the femoral arteries.
Prognosis. — ^When the combined defects are both primary, a fair degree of compensation may be attained and preser\'ed for a time. When, however, cardiac adequacy is once seriously im- paired, there is but small prospect of its restoration. If the mitral leak is secondary, it indicates such a grave loss of ventricular tone as to make practically hopeless the possibility of again closing up the mitral orifice by treatment, no matter how skilful and ener- getic it may be. This was shown by the history of the cases nar- rated in the chapter on Aortic Regurgitation.
AORTIC STENOSIS AND AORTIC REGURGITATION
This combination is not very infrequent, but does not exist so often as the diagnosis is made. This holds true particularly with regard to cases of aortic incompetence. The rough systolic mur- mur so commonly heard in persons who present unequivocal signs of free regurgitation through the aortic ostium leads most inex- perienced auscultators to conclude that there must also be stenosis. This inference is erroneous, however, as shown by necropsies. Vegetations about the orifice, the ragged and stiff leaflets, athero- matous patches on the surface of the aortic intima, are all capable of throwing the blood-stream into audible vibrations as it passes through the ring without in the least acting as an obstruction, an important fact in its bearing on the clinical features of the case.
In predominating aortic stenosis, on the otlier hand, some de- gree of regurgitation is very likely to occur, as has been state<l in the cliapter dealing with obstruction at this orifice. Tlie thicken- ing and rigidity of the valve flaps, wliich prevent their being thrown widely oj>en by the emerging stream, also interfere with their complete closure as ventricular contraction ends. Hence a portion of the blood-wave finds its way back into the ventricle. In other cases one of the cusps may be fenestrated, or for some other reason incompetent, whereas its fellows are not, being only incapa- ble of opening in a normal manner.
Sjrniptoins. — The symptoms produced by combined aortic stenosis and regurgitation partake in character and gravity of the features which are special to the predominating lesion. If incom- petence is the greater, compensation is possible for years without
COMBINED VALVULAR LESIONS
399
the individual boing made tnvare of its prosence. If stenosis pre- dominates and is pronoiinci^d, the left ventricle is nut likely to establish sneh a degree of hvpertrophv as will itiaintain eoniplelo adequacy for very long. The reflux, even if slight, as measured by actual quantity, is yet sufficient to cause more or less dilatj^ion c»f the chamber, and hence the drivin^r force of its wall is impaired. Consequently, the patient is more apt to notice some breathlessness and perhaps palpitation under conditions that ought not to affect him were either stenosis alone or regurgitation alone the lesion,
Fliyslcal Si^ns, — The jihysieal signs are nuulified also by this combination, and display in varying projwrtion the characters of each defect. Thus the pulse is neither so large and collapsing as in pure aortic regurgitation, nor so small and sIoav as in uncompli- cated stenosis, but is collapsing and also smalL Capillary pulsa- tion and Durnzicz's double femoral bruit are eitlier a1*seut or very im perfect ly obta i ued .
The impulse of the heart against the ehest-wall is not so forci- ble and extensive as in free regurgitation, and tlie apex-beat in size and displacement partakes ratlier of the character of stenosis. Hypertrophy of the left ventricle is more apparent than is its dila- tation with thickening.
The hand is very ajU to perceive a systolic thrill in the aortic area, and percussion demonstrates that the heart is not so large as in nneombined aortic insufficiency.
There are two murmurs, of which the systolic is likely to be intense and rasping, while the diastolic is of inferior prominence in all respei'ts. The sounds nomially heard in the second right interspace and in the cervical arteries are likely to be absent and replaceil by murmurs.
Diagnosis. — The diagnosis of this condii nation is as a matter of fact very difficult, and it is often impossible to determine defi- nitely whether both conditions are united or not. This is emj>hat- ically true if the ease is seen for the first time after compensation has faileih Relative mitral insnfficiency or pronounced feeble- ness of the left ventricle may then modify the pulse, sounds, and murmurs in the manner just described. However, if the fern* oral artery is auscultatc-d, and the left side of the heart is accu- rately outlined by percussion, Ouroziez's sign will declare the freedom of ihe retlux, and percussion will demonstrate the enor-
400 DISEASES OP THE HEART
mous enlargement of the left ventricle secondary to free regurgita- tion without obstruction.
A moderately slow, small, yet collapsing pulse, a vigorous, rather circumscribed, not greatly displaced aj)ex-impul8e, a systolic aortic thrill and bruit without powerfully throbbing and thrilling cervical arteries, absence of double femoral souffle, and no de- monstrable capillary pulse — these signs, together with a regurgi- tant murmur, would justify the conclusion that stenosis and insuffi- ciency coexist, but that the former probably predominates. The sphygmograph ought to show the rounded summit and anacrotic notch of obstruction and the ill-sustained down stroke of regurgi- tation (see Figs. 54 and 66).
Prognosis. — The prognosis of this double defect is certainly far from favourable, either as to length of life or as to restora- tion of heart-power, when this has once given way. This certainly applies to pronounced stenosis with regurgitation, whereas it is conceivable that a minor degree of narrowing might, by rendering regurgitation less free, serve to protect the wall of the left ventricle against the speedily damaging effects of free reflux through a w^idely patent orifice.
CHAPTER XV
THE PROGNOSIS OF VALVULAR HEART-DISEASE IN GENERAL
Something has been said already on the subject of prognosis ill the chapters devoted to the individniil valve-lcrfioiiSj and there- fore some repetition will be imavoi<lable. In attempting to fore- ciiat the counse and termination of a given ease one should con* sider (1) the special ebaracters of the lesion, (2) the degree of the secondary eflfects in the heart and other organs, and (3) extraneous faetora of age, temi>erament, environment, etc.
The characters of valvidar disease which inflnenee prognosis are its natnre, locationj and degree, and these cannot always be considered separately. As a general proposition, it nuiv be stated that stenosis is a more serious defect than is regurgitation, and yet its gravity depends largely on its hieation. Furthermore^ the amount of disturbance to the circulation is determined so much by the degree of the local defect that this latter may render most serious a vahiihir rlisease, which from its nature and situation alone would ordinarily furnish a more favourable prognosis. In fact the forecast is so largely based on the conditions of each case that one wotild go far astray if he were to he glided by general principles alone.
Although aortic insufficiency is to be ranked first as regards I gravity, still a distinction should be made between cases originat- ing in the young in endocarditis, commonly rheumatic, and those of atheromatous origin, observed at or beyond middle age. In the former group great com];>en8atory hypertropliy and a healthy heart-muscle may enable the organ to functionate adequately for many years, far longer indeed than do many cases of mitral dis^ ease^ although in itself this latter is considered a less serious lesion. On the other hand, when aortic incompetence is due to a sclerotic process, the myocardium is rarely healthy and compensa- te 401
402 DISEASES OF THE HEART
tion is short lived, or indeed is never perfect. In such a ease prog- nosis is grave from the start. It is in this particular lesion that sudden and unexpected death is likely to take place. Indeed, it is almost the only valvular disease which so terminates, since when death occurs unexpectedly in other defects it is very exceptionally instantaneous, and then is the result of some accident, such as em- bolism, or it terminates weary weeks or months of failing heart- power.
In aortic regurgitation it is not very rare for patients to fall dead unexpectedly in the midst of apparently good health. When- ever compensation shows unmistakable signs of failure, sudden death in this disease is not a very remote possibility. Moreover, compensation may be broken at any time by a rheumatic attack, and once impaired it is rarely restored. Absence of the aortic second sound and dilatation of the left ventricle are therefore prognostically grave, since they indicate free reflux and feeble ventricular resistance.
Stenosis of the aortic ring presents a less grave prognosis than does regurgitation at this orifice. The reason for this difference is to be found in the effect of the two lesions on the wall of the left ventricle. A narrowing of the outlet leads to hypertrophy with relatively little dilatation, unless of course the obstruction be so pronounced that the chamber is unable to empty itself during sys- tole, and stasis results behind the point of constriction. So long as the hypcrtrophied ventricle is able to discharge its contents with each contraction, and the effect of the lesion is limited to the ven- tricular wall, the prospect of a continuance of life for many years without distressing symptoms, and even of death at the end through some intercurrent affection, is good. When, however, compensa- tion in this disease is once destroyed, there is small likelihood of its repair, and the prognosis becomes very serious. Yet in this, as other lesions, it is its severity, even more than its nature and loca- tion, which determines tlie degree of its seriousness. An extreme stenosis as regards length of life is even worse than free regurgi- tation. Wlien the two lesions are combined tlie prognosis is as a rule more imfavourable.
Of the two mitral defects, it is generally conceded that stenosis is the more serious. One reason for this is that the disease is not stationary, but tends to grow more pronounced in consequence of
PROGNOSIS OP VALVULAR HEAHT-DISKASK L\ GENEltAL 403
coiitnH-ti(Hi of the iiowlv fitniieil iihroiis tissue imJ of the increase of tibriiif de}»ositetJ uiioii the vege tat ions, Aiiothci" reason^ as we sluill set* litter im, lii^s in the greater intensity of the secondary effects on the heart. AHtnil regurgitation, on the other hand, is under ordinary eirciiinstiinfes the most favourable of the four lesions situated in the left heart. When the leak is not too free and there are no serious eompHcations, such as aortic stenosis and ad- hi'reiit perieardinnj, the defeet in question is not incompatible with kmg life and great mental and bodily vigour. It is possible, how- ever, for the regnrgitation to he so free that this rehitively benign disease is thereby converted into a very serious one. Leyden states that su(hJen death occurs in only 2 per cent of mitral disease.
With the exception of relative tricuspid insiitiieiency, diseases of valves of the right heart are so infrequent that nothing needs to be added to what has been said already eoneerning their prognosis in the respective chapters. Incompetence of the right auriculo-ven- trieiilar vulves secondary to other diseases is generally regarded as of serious inipiu-t, not because it threatens life directly, havings as it is said, a safety- valve action, but hei'ause it indicates serious dis- projmrtion between the degree of the prinuiry disease and the strength of the right ventricle. If it occurs with anything like the fretpieiicy cliiimed for it hy Gibson, then one should not attach to It a very unfavourable |>rognosis. Nevertheless the degree of inijiortanee to be attributed to it de|>ends much on tlie nature of the ju'imarv affection. If it he secondary to vesicular euiphysema or to valvular disease of the left side of the heart, as pronounced niitrnl stenosis, the <levelo|iment of tricuspid regurgitation must 1m? looked upon as an ouien of im^vending disaster. This form of tricuspid disease cannot be regarded as a separate and independ- ent affection, and therefore shotild be classed among the secondary effci'ts of valvular rlisease, %vhich are now to he discussed in their hearing on prognosis.
From the foregoing it is evident that although the nature and seat of vahi^ilar defects influence their [jrognosis, yet it is tlieir inlerhsiii/ to which we must chiefly look when directing our attention to the heart. It has been distinctly stated in previous chapters that in estimating the extent of a valvular defect one must not rely upon the intensity of the murmur, but n|xin the evi- dences of disordered circulation. These are the secondary effects
404 DISEASES OF THE HEART
or signs which are of such vahic oftentimes in making a diagnosis as well as in stating the prognosis.
One reason for the grave outlook in cases of mitral stenosis is the fact that this defect occasions widespread stasis in the ves- sels of the pulmonary and venous systems, while the diminished supply of hlood to the left ventricle leads to shrinkage in the size of this cavity. If the left auriculo-ventricular opening has become greatly reduced in diameter, no amount of vigour of the left auri- cle and right ventricle can maintain the equilibrium of the blood- stream. It is only a matter of time when the pulmonary system and right heart, systemic veins, and abdominal organs are bound to become engorged.
In mitral incompetence, on the other hand, the left auricle and pulmonary veins may be able to bear the brunt of the regurgitat- ing stream for a long time. Moreover, the left ventricle undergoes hypertrophy, and forcibly ejects into the aorta all that portion of the blood that does not escape into the auricle. There is not so marked a tendency to disturbance of general nutrition. Yet, of two typical cases of mitral disease, the one constrictive and the other regurgitant, if the former with its natural tendency to greater stasis actually displays less pronounced secondary effects, it offers a better rather than a graver prognosis, because compensation is complete. Tlie general venous stasis in the regurgitant case evinces either such a freedom of reflux that the parts behind could not long withstand it, and compensation was necessarily lost, or that compensation was not able to take place at all. Even if treatment should succeed in reinstating the circulation, still the fact of compensation having once been lost would render the prog- nosis worse tlian it would be in tlie case of stenosis in which com- pensation had never been impaired.
Again, compare a case of perfectly compensated insufficiency of the aortic valves with one of extreme narrowing of that orifice in which dilatation of the left ventricle is beginning to outbalance the hypertrophy, and signs of stasis are appearing in the pulmo- nary and general venous systems. In one, secondary effects are limited to the lieart and shown by the adjustment of the left ven- tricle to the altered conditions. In the other they have passed beyond the heart and invaded the remainder of the circulatory apparatus. It is plain that here the degree of the lesion has re-
PROGNOSIS OF VALVn.AR HEAErr-I>ISEASH IN tIEXEHAL 405
versed the iisiml order of things as respects the prognosis in these two valvular defets.
The foregoing remarks show how unreliahlo would he a prog- nosis in valmlar heart-disease, whieh was not hnsed on a eareful study of the extent, even more than tlie vnUnre and hnialion, of the particular defect, and that individual cardiac conditions deter- mine the relative gravity of each case. Nevertheless, I must re- peat that my experience leads me to agree with Broadhent in the opinion that, generally speaking, aortic regurgitation is the most serious ami mitral regurgitation the most favnurahle of the four valvular diseases of the left heart. The two stenoses occupy an intermediate positicm, and of these, mitral constriction is ihe graver. This snlijeet is still further ei^mjdieated hy the consid- eration that there are still other factors that uuist he reckoned with. For the most part these are of minor importance, and yet some of them make strongly for or against an encouraging forecast.
Complicatiotts.— ^The gravity of any valvular defect is neces- sarily enhanced by the existence of complications, although to what extent is determined in great measure hy the nature of the complication. Intercurrent acute disorders, which act as enrnpli- cations while they last, are considered by themselves. Here are discussed only snch chronic local alterations and diseases of other viscera as must of a necessity imfavourably affect the course of valvular lesions. Pericardial adhesions, whether strictly internal or such as hind the heart to some of the surrounding parts, cer- tainly exercise a malign infiiience, since they interfere more or less seriously eitlier with the estahlishment or the maintenance of ade* quate compensation. Their effect is specially detrimental if hy fixation of a chamber in the state of tlilatation they prevent its reduction and ethcient hypertrophy, I have seen this more tlian once exhildted in a case of mitral inccvm|>etence in whicli tixatiun of the left heart threw extra strain uix»n the riirht ventricle, as evinced hy its ready dilatahility. Wljen a chronic adhesive modi- astinitis holds the right heart adherent back-pressure on the two cava? and liver is increased. The pseudrvcirrhosis of the liver leads in time to obstinate ascites, and patients succumb to the hepatic conqdication long before they would Im? likely to die from cardiac inadequacy alone. Moreover, an adherent pericardium
406 DISEASES OP THE HEART
not infrequently renders futile therapeutic eiforts which prove highly efficacious in cases without such complication.
The association of two or more valve-lesions aifects prognosis, not by shortening life necessarily, although such is likely to be the effect, but by rendering impossible the development of perfect compensation and compelling extraordinary carefulness, lest what small measure of compensation already exists be broken down alto- gether. The reader will find more on this subject in the chapter on Combined Valvular Ix^sions.
It goes without saying that chronic nephritts is a very grave complication. Xot only does the renal act badly on the cardiac affection, but this latter, by lowering blood-pressure in the renal arteries, intensifies the insufficiency of the kidneys. The evils of unemia are then likely to be added to those of defective circula- tion. The chronic nephritis renders it unlikely that the patient will live out the term of years that would naturally be granted him by his valvular defect alone. The kidney complication also ren- ders less availing all attempts to remove dropsy whenever it appears.
Pulmonary tuberculosis is not often seen in combination with valvular disease, excepting of course pulmonary stenosis. When it occurs, however, I believe it enhances the gravity of prognosis, for I cannot see liow thoy can fail to react injuriously on each other. Anything which, like valvular disease, impairs nutrition must nec- essarily lessen the likelihood of successful resistance to tubercu- losis, while the destruction of hmg-tissue must seriously affect the already damaged heart.
Harmful blood-states, as chlorosis and ancvmla, affect progno- sis in proportion to their severity and their amenability to treat- ment.
Eheumatic Diathesis. — Some individuals display a marked tendency to rlieuniatic attacks, either acute or subacute, and every now and then suffer from pains in shoulder, wrist, or other joints. In such the outlook is not bright, for the reason that any one or all of these mild attacks may be attended by fresh endocardial inflam- mation either of the same or other valves, or that pericarditis may develop. Even if an active endocarditis is not excited, the changes already set up in the valves may be rendered ])rogressive. Conse- quently, a case furnishing favourable prognosis originally may be
PROGNOSIS OF VALVULAR IIKART-DISKABE IX (lEXEKAL 407
converted into one of a most serious nature. In a word, therefore, r€*exirrenees of rheiinmtisni, no matter how niihl, are to be regarded as iiffurding a ghjomy prognosis in any case of valvular disease.
Digestive and Bronchial DiBorders — These, like rhenniatism, jet in a diifereut way, are capable of unfavourably affeeting prog- nosis. Disturbance of the digestive function is not infrequently observed in victims of valvular disease in whom careful examina- tion fails to detect signs of secondary etfeets in other organs. The chylfipoietic viscera umy have their function impaired by lack of arterial IdiHid of good quality, cunliopaths being tjften anivmicj or in aortic cases by a defective flushing with arterial blood, or in mitral patients by passive congestion, this last being too slight to be rt'cognised by ordinary means of examination, Whetlier the indigestion is owing to such causes or is the result of improj>er food or faulty habits in eatings it is likely to impair general, and hence cardiac nutrition, and thus render prognosis less encour- aging.
A tendency to acute bronchial catarrhs in mitral patients not only evinces greater pulmonary congestion than is otherwise appar- ent, hut also renders them liable to an attack of bronchitis, which may at any time severely strain eompensation. In them, there- fore, prognosis cannot be looked ufx^n as so favourable as if they were less sensitive to atmospheric changes and did not so easily get up a cough, for the severe expiratory etTort of coughing sub- jects the right ventricle to added strain.
Age. — The prognosis of valvular disease is more serious at either extreme of life and most favouralde in young adults. In elderly individuals the myocardium is apt to be more or less degen- erated, and although, as Leyden Ix^lieves, conrixmsation is often as perfect as in the young, it is more easily destroyed. Further- more, the sclerotic process, which is usually responsible for the valvular defer-t, is progressive, and one possesses no means of fore- casting whether these changes will progress slowly or rapidly, I recall the instance of a gentleman of sixty- four in whom 1 detected signs of aortic sclerosis and probable coronary sclerosis in explana- tion of his attacks of angina without any evidence of valvular in- competence or of stenosis. Vet at his death, less than three years subsequently, the autopsy disclosed, I have been infonned, well- marked insutticiency of the atherouiatous aortic valves, signs of
408 DISEASES OF THE HEART
the lesion having developed and been detected by his physician some months prior to his death.
The gravity of the prognosis in childhood is attributable to a .variety of causes. In the first place, the heart-muscle, although free from degenerations, is easily exhausted. The chest is small and affords scant room for the often enormous hearts observed in children with long-standing valvular disease. Any one who has seen much of vahoilar disease in children must have observed that they are strikingly unconscious of symptoms which in adults occa- sion complaint. They are highly sensitive to pain, yet appear to .pay no attention to palpitation and shortness of breath during play; although the onlooker may observe tumultuous action of the lieart, hurried breathing, and cyanosis. Children are therefore very likely to overstrain their already damaged hearts ; and that this does not occur more frequently is quite remarkable. These little ones are excitable and emotional, and therefore unable to exert the self-control so often necessary for the preservation of compensation. They often display astonishingly vigorous appe- tites and overload their stomachs with the sweetmeats and dainties they crave, and are permitted by indulgent parents to have. These ferment with the formation of gas, which, distending the digestive organs, causes them to crowd upward upon and still further em- barrass the heart in its action. Lastly, rheumatism in childhood is so insidious and atypical that it is very frequently overlooked. Prompt and efficient treatment is not instituted, and this disease being frequent in early years of life excites fresh attacks of endo- carditis, lights up a pericarditis, or renders existing valve-lesions progressive. Mitral stenosis in young children is particularly un- favourable. It may be briefly stated that valvular disease at this jx^riod of life is very likely to end fatally before the patient reaches adult age either directly or through complications.
Temperament. — This possesses a not unimportant relation to the prognosis of the diseases now under consideration. The pa- tient who is impulsive, impetuous, and thoughtless is like a child unaccustomed to self-control, and if required to exercise self-re- straint frets and chafes in spirit. Such a person will he forever rcommitting indiscreet acts, and will only acquire with difficulty , that patience and equipoise of spirit which serve as ballast to damaged hearts. Individuals given to outbursts of anger, to
PROGNOSIS OF VALVrLAH UEART-DISEASK IN GENERAL 409
worrv, to fretting over tritles, and who appear never to become reooiicileJ to tkeir physical disability, can never l>e expected to retain their compensation so well or so long as will those who always have themselves well in hantL Verily^ all cardiopaths shoiihl hear in niind tliat Bibte utterance, ** lie that ruleth his own spirit is greater than lie that taketh a city/*
Sex* — Mitral disease, and in particular mitral stenosis, is more frequent in the fair sex, while men are more subject to aortic in- snftieiency. In a sense, therefore, sex may \ye said to exert a gen- eral influence npou prognosis. The inquiry ihnt now concerns us is how does sex affect the prognosis of a given valvular lesion after it luis once been established, without reference to its nature. In other Words, what is the relative prognosis, seten^ pari h us j of the same defect in the two sexes. This is a very difficult matter for decision, since it involves questions of habits, occupation, et<^ Females are expt»sed to certain perils of prepianey and child- bearing, while, on the other hand, men have to encounter even greater dangers incident to occupations that often produce cardiac overstrain. The reader will find these influences discussed at some lengtli in the ehiipter on Treatment of Valvular Disease in Gen- erah One resjRx*t wherein women usually furnish a more favour- able prognosis tliau do males is that of habits^ — that is, a greater frecHhim from the injurious efTects of excess in tobacco, alcohol, and venery. Women are generally held to be more emotional and excitable than men, yet in the matter of self-control they seem to me ro jwssess an advantage over their brothers. The most marked instfint'cs I liave ever sec*n of apprehension — nay, of alarm anr! nervous agitation — lest the examination result in the discovery of a heart-lesion, have been in young men. The female sex is more prone to ansi'niia and chlorosis, and the injurious influence of these blood-states is too well known to require more than tliis passing referenet*. In most other respects I think the question of sex re- solves itstdf into that of the individuah
OocupatioE. — This exerts a pc»werful influence upon prognosis. The day labonrer who earns bis daily bread by the sweat of his brow cannot be expected to keep his compensation intact for so long as w*ill he whose %^ocation does not subject his heart to the possibility of uverstraiTK AH authors are agreed in the declaration that nothing in the daily life of tliese patients affects their hearts,
410 DISEASES OP THE HEART
and hence the prognosis, more disastrously than does severe and prolonged or too oft-repeated physical exertion. This is particu- larly true of mitral narrowing, even in the stage of compensation. Patients with well-compensated insufficiency of the aortic valves may endure overstrain for a time without apparent injury ; but so soon as dilatation of the left ventricle has begim to gain the as- cendency over hypertrophy, a continuance of the strain will in- evitably result in a breakdown, and that too at no very distant date in most instances.
Habits.— ^These are matters of utmost importance if the lives of patients with vahnilar disease are to be prolonged. They should be minutely inquired into, therefore, by the medical at- tendant. The daily life of these sufferers should be ordered on the principle of moderation in all things, ^^^lateve^ is injurious to a healthy person is doubly so to one w4th an unsound heart. Consequently a prognosis which, as regards everything else, may be good, may be rendered very uncertain, if not actually bad, by the discovery of evil practices. By these are meant particularly excess in tobacco, alcohol, or other narcotics, and in sexual in- dulgence. But patients may also increase the gravity of prog- nosis by gluttony, loss of sleep, exciting novel reading, gaming, etc. — in short, by whatever promotes ner\'ous and cardiac ex- citement.
Home Surroundings. — These include all those matters of sanita- tion, as dampness, sunshine, ventilation, drainage, the ability to obtain suitable food and clothing, freedom or not from domestic worry and annoyances, oj)portnnity for recreation, etc. — in a word, the residential and social conditions which in all of us make for happy, contented lives.
The prognosis in the case of the poor man cannot be expected to be as good as that of him who is able to command everything that can minister to his comfort and well-being. If, e. g., a pa- tient with mitral stenosis or a failing aortic insufficiency is com- pelled by the exigencies of his purse or environment to labour or to ascend wearisome flights of stairs or steep acclivities upon re- turning to his home, no matter how often this may be, he can hardly be expected to keep this up without eventually suffering injury. These and many other matters may seem too obvious to require mention, and yet they are details which the physician
PROGNOSIS OF VALVULArt nKAKT-DISKASK IN GKNKHAL 411
liiiist take into consideration if he would form a reliable prog- nosis.
The Probable Effect on the Patient of the Knowledge of his Lesioti. — This is a matter, in my opinion^ having a decided bearing on prognosis, and whiebj therefore, shou!<l Ix* discussed. Phjsi- eians and the laity generally believe a eardiopatli nmst not be informed of the fact when he is fonnd to have a cardiac defeet, lest he be alarmed and become morbid and introspective. Doubtless there are many nervmiSj apprelieiisive persons who woald be harm- fully affected by i^ueh knowledge. When sneh is the case I believe it renders prognosis less favourable, because if kept in ignorance of his true condition he is not prepared to avoid whatever may be harmfnL If detrimental intlnenees are to be shunned, patients must have explained to them how and why these are injurioua to them, since the doctor's dictum in this regard is not enough for an intelligent ]Tersim. Kept in ignorance or put utf with an evasive answer, he may be set to i)ondering and conjecturiug, and hence to fancying his condition is worse than it really is. I be- lieve, therefore, that it is a positive gain to a cardiopath to acquaint him with at least a part if iK^t all of the truth. Of course he does not need to be informed with brutal aluniptness, but gently and in a manner calculated not to frighten him unduly. The individual who cannot hear even a part of the truth without detriment will assuredly furnish a less favourable prognosis than he who, know* ing the rruth, aeeepts it philosophically, and determines to make the best of a bad bargain.
The Effect of Digitalis on the Patient.— Tt goes without saying that when valvuliir tlisease lias readied such a stage as to necessi- tate the administration of digitnlis the prognosis is not good even at the best. Thus much any one knows, but only a few, if any, are able to prognosticate liow much hunger tlie heart is going to bear up, even sustained by such a prop. In such a case, as ]X)inted out by Leyden, a certain degree of information may be derived from a study of the eflFect of the remedy.
If the beneficial action of digitalis is cjuickly lost after its administration has been discontinued, and the heart manifest its need of this tonic by a s]>eedy return of symptoms, the prognosis is serious, for it indicates myocardial inadequacy. It is a still more unfavourable indication if from time to time the dose of
412 DISEASES OP THE HEART
digitalis has to be increased to maintain its effect, for it points to the not distant arrival of a time when the heart will cease to respond to the remedy, and the end will not be far to seek.
The Relation of FrognosiB to Life Insurance. — There was a time when an individual with vahnilar disease was rejected indiscrimi- nately by all insurance companies. In England, and by some com- panies now in this country, some of these patients are accepted as '* defective risks," and therefore it is in order to discuss this sub- ject in this place. There are two classes of persons with valve- lesions whom I would reject except possibly for a very limited term of years, and only then at so high a premium as to make it almost prohibitive. These are cases of pronounced mitral steno- sis and insufficiency of the aortic leaflets. Even when the latter appears compensated there is always the i)ossibility of sudden and unexpected death, which, as already stated, renders prognosis very uncertain. Stenosis of the left auriculo-ventricular orifice is pro- gressive, and how rapidly this tendency will declare itself no one can foresee. On the contrary, mitral regurgitation, and to a some- what less degree aortic stenosis, may sometimes be considered rea- sonably safe risks as defectives. It will be noted that I say some- times. This is because, no matter how excellently the lesion may be compensated, there are circumstances of individuality or en- vironment which determine prognosis adversely. Therefore the examiner should consider oxliaustively and intelligently all those factors which have a bearing dirwtly or remotely on the prospect of the patient living as long as tlic cliaracters of his disease might be expected to allow. J^aborious occupations and bad habits are, in my opinion, a bar to safe insurance of these risks. On the other hand, a robust young nuin who knows that his mitral valves leak, and who is detennined to order his daily conduct in a manner cal- culated to afford his heart the very l)ost chance of carrying him through to middle or advanced age, may often prove a safer risk than many another sound man who banks on his fine health and splendid physique.
CHAPTER XVI
THE TREATMENT OF VALVULAR HEART DISEASE
From a therapeutic standpoint^ cases of valvular disease are to be divided into three chtsses, according to the state of eorapensa- tiuiK (1 ) Those in which the lesion is compensated, (2) in which compensation is incomplete, and (3) in which cardiac inade- quacy is so pronounced that compensation is wholly wanting. We call a valvular defect compensiited when the cardiac pump, in spite of its defect, is able to maintain the circulation in nearly or quite its normal state, and there are no symptoms to make the patient aware of his malady. Under such circumstances laborious occupations, athletic exercises, and games or outdoor sports re- quiring considerable strengtli and agility are endured without more breathlessness or palpitation than are \m\m\ with jiersons having sound liearts. In the secoixl class, patients arc still able to perform their daily duties and engage in some of the less severe sports, but it is with more or less distress and evident signs of heart- strain* There are different degrees of imperfect compensation in this class, and henee it is one of wide limits. In the third class, in which compensation is wholly lost, patients are not onlj^ inca- pacitated for physical exercise, but the circulatory disturbance is slio^m by stasis, generally by rrdenia, and by subjective symptoms that are present even wdien the patient is at rest. Wlien coni[»en- sation is perfect, examination of the heart discloses the existence of a lesion J but no secondary effects in tlie general circulation. In the second clas signs of mta^' or less visceral and venous conges- tion are detected, altliough subjective symptoms may be insignifi- cant, and in the tliird these reach their severest grade. It is evi- dent, therefore, that treatment appropriate to the last stage is not indicated in the first. Neither do patients wiiose compensation is still maintained intact require the same strict management as do those who are beginning to manifest failing heart-power* Conse-
413
414 DISEASES OP THE HEART
queiitly, in dealing with the management of valvular heart-disease, I shall consider it with reference to the three divisions just made.
I. COMPEXSATION BEING STILL PERFECT
The object of management in this stage is the maintenance of cardiac power. Occasionally a patient w^ith valvular disease seeks medical advice for the pur|X)se of learning how he can preserve his heart in statu quo. As a rule, however, such a compensated lesion is discovered accidentally by the physician, who is then confronted by the query w^hether in case the patient is ignorant of his heart- disease he should be informed of it or not. I hold that in such a case the answ^er must dei^nd upon the circumstances of the case, such as the temperament of the individual, his habits, and the nature of his employment and manner of life. If the knowledge that he has heart-disease is likely to frighten him and render him introspective, then the knowledge would better be withheld, unless, of course, he is leading a kind of existence calculated to break down his compensation. Under such circumstances it may be nec- essary, and the part of wisdom, to inform him that his heart is not sound, and is likely to be damaged by his manner of living. In such an instance, however, the information should be imparted in a manner not calculated to create nee<llesa alarm. If the individ- ual is reasonable and cool-headed, ])articularly if his pursuits are active, I believe he should be plainly told of the existence of his valvular defect, for, other things being equal, the knowledge by a person that he has a locus minor is resistcnticv is likely to make for a longer lease of life.
Since, then, the aim of management in this stage is to preserve compensation, t\w. i)hvsician must concern himself with the minut- est details of the patient's daily life. He would take a narrow view of a case indeed who contented himself with the question of medicinal treatment. Compcnsafrd ral re-defects require not drufjs, hut instruction upon the following points:
Exercise. — It may be laid down as a general j)roposition suit- able to all forms of com])ensated valve-defects that when any kind of exercise does not ])roduce symj>toms of cardiac strain it may be permitted. Indeed, as will l)e seen later on, judicious exercise promotes compensatory hyi)ertropliy in some forms of valvular dis- ease. There are other lesions, however, which by their very nature
TTIK TREATMENT OF VALVULAE HEART-DISEASE
415
ore tlieoreticiilly likely to ami often actuallj do suffer injury in time from severe bodily exertion. This statement applies particu- larly to cases of mitral stenosis. If the left auriculo-ventricular opening is but slightly const rietedj considerable, even severe physi- cal effort may be endured without symptoms, but as a rule some shortness of breath is experienced, and patients should be expUc* itiy warned against persisting in their exertion when dyspnoea is felt. The effect of museuhir contraction aud deepened respiration incident to exercise is acceleration of the tlow of venous blood to the right heart aiui lungs. If the i^lood cannot readily pass the mitral ring, it becomes dammed back in the left auricle and pul- monic veins, engorging and overstraining the right ventricle. This may resist the stress for a time, but if the strain is too iirolonged or too frequently repeated the cardiac walk finally yield and the hypertntphy, upon which adequate cumj^ensation depends, is su- perseded by dilatation. Therefore^ patients with pronounced mitral stenosis, even when compensated, should be cautioned against violent, prolonged, or too tift-ref>eated exercise of a severe kind. I lurrying u]j stairs or hills, running, and even very rapid walking, fast bicyt*le-ridiiig, sports and games that necessitate run- ning and springing without frequent pauses to }>ermit recovery of breath — e. g,, furious sparring, wrestling and fencing, la^vn-tennis, basketball, and the like — are among the kinds of exercise partieu- hirly likely to harm patients with mitral i^tenosis, even when com- pensated. On the other hand, if they indulge moderately^ they may enjoy rowing, paddling, aiul bowling. Billiards, golf, and croquet are specially suited to them, while some may be permitted to liunt, and nearly all to iish. When the constriction is not pro- nounced, gentle horseback riding, slow bicycling, and even the lighter kinds of gyiimasium work are permissible. In specifying the kind of exercise and sport to Ije allowed, the physician should always bear in mind the personal equation. The degree of tlie lesion and the gravity of its secondary effects, even more than the nature of the lesion, determine the patient^s ability to endure exer- cise without harm. The individual temperament, judgment, and power of self-restraint are also of great importance. The physi- cian must endeavour to infonn himself as accurately as possible regarding the effect of any given kind of exercise on the particu- lar patient before coming to a decision.
416 DISEASES OF THE HEART
What has been said of mitral stenosis applies also to cases of aortic obstruction when this is pronounced. Slight narrowing of this orifice is often compatible with great muscular exertion and active exercise. When, however, compensation is once broken in these cases, it is repaired with difficulty, if indeed at all, and there- fore good judgment and careful study of each case are essential to a wise decision. In these cases exercise should not be carried to the production of palpitation, particularly prolonged palpitation. The wall of the left ventricle is susceptible of far greater hyper- trophy than is that of the right; besides the effect of an aortic stenosis is confined for a time at least to the ventricle, and does not embrace the thin-\7alled auricle, and consequently exercise is likely to be better endured than when the obstruction is at the mitral opening.
The next in order on an ascending scale, as regards its ability to withstand the effects of exercise, is mitral regurgitation. In this disease, owing to the circumstance that during diastole there is no impediment to the filling of the ventricle, and notwithstanding that a portion of the blood gushes back during systole into the auri- cle, there is not the same degree of engorgement in the parts back of the seat of lesion as in mitral constriction. Of course the meas- ure of the heart's resistance is governed by the degree of the incom- petence and, as in all valve-lesions, by the state of the heart-muscle. If the leak is very free, compensation is not so apt to be complete as when the regurgitation is insignificant. In cases of well-com- pensated insufficiency of the mitral valve continued and severe exercise may often be indulged in without the j>roduction of an- noying symptoms. This statement applies to the rheumatic rather than the atheromatous form of the lesion. I know an attorney who, fifteen years ago, when a growing lad, had a j)ronounced though perfectly compensated mitral insufficiency, and who played lawn-tennis enthusiastically without any other discomfort on the part of his heart than the consciousness of raj)id, strong beating of the organ. Despite frequent injunctions to the contrary, he con- tinued to indulge In this sport during several years, and is now reported to be so well that he does not know he has a heart. An- other of my patients, a merchant past thirty, with a mitral incom- petence in a state of admirable compensation, is much given to sparring and broadsword practice, which, he declares, never gave
THE TKEATMEN'T OF VAL\ULAR llEAKT-UISEASE
417
liim iiii;v' stiortiiess of breiitli and only a rapid heart-action, that subsided so soon as the exertion c'eased. Suoh instances are not rare, and yet severe physical effortd are not without danger to these patients.
Such as are fond of manly sports should he. advised of the pos- sibility of cardiac overstrain^ and told to desist when excessive J ml pit at ion or pronounced dyspna-^a is exi>erienced. They feel the better for a certain amount of outdoor exercise, and when young and vigorous in other respects their heart-muscle, like their skele- tal muscles, is likely to grow soft and weak if debarred from atl'i- letic sports altogether. Other things being equal, the state of the voluntary niusclei:^ is r. fair index to the condition of the cardiac muscle. Of two individuals with well-compensated mitral leakage, one with well-knit muscles trained to exercise, the other unaccus- tomed to outdoor sports because of sedentary pursuits, the latter may break down his compensation by some effort which would be no more than child^s play to the former. It is probable that per- sons with mitral regurgitation would be more likely to suffer injury from long running than by games that necessitate intermit- tent and Bhort spurts of speed or strength. Mouutain-climhing» boat-racing, and other forms of contest or strength, which experi- ence has shown cause dilatation of healthy hearts, will bring about overstrain of diseased ones more readily and surelv.
As a general rule cases of aortic regurgitation should be placed at the top of the list as regards endurance of exercise without injury. This statement does not apply to persons who have ac- quired their aortic incomj>eteuce after the age of forty, and there- fore probably as a part oi" manife.^tation of a sclerotic process that may have invaded the myocardium also. In such, even when com- pensation is still maintained, exepcise should always be moderate. The salvation of patients with this lesion depends on hypertrophy of the left ventricle. The great Stokes recognised this fact, and accordingly used to r(?commend active physical exercise to patients with this form of valve-disease. Von Ziemssen has stated that upon one occasion, when visiting Stokes in Dublin, the latter directed his attention to a man running along the street behind his wagon, and said that he was one of his patients with aortic insuffi- ciency who was carrying out this kind of exercise at his (Stokes's) advice, for the purpose of developing left ventricle hypertrophy. 587
418 DISEASES OP THE HEART
Another of Stokes's patients with the same lesion was a farmer who was able to do a day's ploughing as well as if his heart were sound, and in fact declared he felt the better for the exercise. This patient died of acute pericarditis soon after von Ziemssen learned the facts of his case, and his heart was given to von Ziems- sen, who declared it weighed several pounds and was the most marked example of cor bovinum he had ever seen.
A well-compensated aortic regurgitation will endure arduous physical labour and the most energetic kinds of exercise so long as the myocardium is healthy. Therefore it is young or compara- tively young patients whose aortic-valve disease is of rheumatic origin who are able to endure great physical exertion for many years without a breakdown. Such patients are far more likely to be unconscious of the existence of their cardiac mischief than are the subjects of mitral disease. In the former cardiac stress is manifested not so much by dyspnoea as by palpitation, and if their valve-defect dates from an attack of rheumatic endocarditis in childhood, as is often the case, they have grown up so accustomed to these palpitations that they are apt to speak of them as but a manifestation of strong action of the heart. While such patients can be quite safely permitted considerable latitude in the matter of exercise, they should nevertheless be closely watched for the first evidence of failing compensation. For so soon as the heart begins to waver in its worl:, bounds must be set to their activity.
Whatever is the nature of the valvular disease, the physician should always remember that after the fourth decade of life arte- rial degeneration is frequent, and the myocardium is likely to have suffered changes depending thereon. Consequently, liberty in ex- ercise is more hazardous after than before this period of life, even in the case of old-standing lesions that have not previously inter- fered with active habits. From this time onward increasing cau- tion must be observed, and heed given to what may appear to be but trivial symptoms of heart-strain. Should a valve become de- fective at this period of life, either as a result of endocarditis or atheroma, severe exercise and incautious efforts of all sorts are to be forbidden, even though good compensation seems to have been established. Every physician of experience is aware of the readi- ness with which compensation fails after middle age. Fortunately for such persons they have arrived at years of discretion, and find
THE TREATMENT OP VALVULAR HE ART-DISEASE
419
less diffitniUy In restrain iiig tlieir impulses to overdo than is the cai^e with the young. Exercise niiist now be had by walking, driv- ing, easy riding, billiards, and golf, Ptilley weights, the Whitley exerciser, clubs, dumb-bells, etc., if permitted at all, are to be used under tlie supervision of the medical attendant or of a nurse capa- ble of detecting signs of danger. Moderation in all things must now be the motto of these patients.
Occupation. — The princijiles underlying the matter of exercise should also determine the selection of a suitable occupation or the decision whether or not the patient's vocation is to be continued. The following employments are suitable for persons with mitral stenosis: Book-keeping, stenography, banking in any capacity, or other forms of dcsk-work^^ telegraphy, clerking, engraving, watch- making, tailoring, shoemaking, harness-making, saddlery, etc*, and for females the various kinds of needlework, typewTiting, stenography, and desk-work. Employments that necessitate heavy lifting and the carrying of heavy parcels, as porterage^ running np and diwn stairs, swinging of heavy hammers, etc., are injuri- ous, since they put added strain on the right ventricle. Dusty occupations induce catarrhs and coughs, and in this respect favour hronchial congestion, to which mitral patients are predisposed already. For the same reason they should not follow occupations which expose them to vicissitudes of weather and sudden changes of temperature. Of the professions, journalism, dentistry, archi- tecture, designing, and the various branches of art work, are all suitable — while theology, law, and such other vocations as require public siRniking put a strain on the right heart and are less eligi- ble. Teaching is not so bad, whereas the [irofeasion of medicine, especially a general practice, is too arduous and involves too much exposure for persons with pronounced although coni{K*nsated mitral narrowing, A specialty permitting office practice is not so objci'tiunable, and yet any one with this lesion should be discour- aged froiu studying medicine, or becoming a trained nurse or mas- seur.
Work with light tools, as carpentering, joinery, housepaint- ing and decorating, and even light gardening, may answer for some cases of aortic disease, when not admissible for severe mitral ste- nosis. Most of the occupations foHowed by females are not too severe fur mHral patients win. luu-e good compensation, excepting
420 DISEASES OP THE HEART
such work as requires the carrying of trays heavily loaded with dishes and the frequent running upstairs. A general classification or division of occupations may be made as follows. Those that are indoors and require the use of the mental faculties rather than the muscles are suitable to mitral patients and persons with serious aortic lesions. Outdoor employments and work performed by the muscles rather than the brain may be endured by subjects with compensated aortic regurgitation and the slighter forms of aortic stenosis and some cases of mitral insufficiency. Finally, vocations attended with much excitement or nerve-strain, as locomotive driv- ing, operating on the stock-exchange, detective and police work (these last two for other reasons as well), sea-faring, and soldier- ing, are unsuited to any form of valve-disease, no matter how excel- lent the compensation. The medical attendant can do much good by directing the choice of occupations for the young, and in the case of those who have developed disease after their work in life has been fixed by pointing out how the evils of the occupation may bo minimized.
Habits. — It has already been stated that moderation should be the governing principle in the lives of cardiac patients. Excess of every kind, particularly in sexual indulgence, is to them most injurious. It not only occasions a harmful degree of cardiac ex- citement, but it saps the strength and lowers the tone of the nerv- ous system. The medical attendant who has charge of a young man with valvular disease neglects his duty if he does not instruct his patient concerning the evils of sexual excess. I have known young married people of both sexes have their compensation seri- ously threatened after a few months of unbridled license in this regard. Although males are the chief sufferers in this respect, women with valve-lesions are often made to suflFer through the inconsiderate demands of their husbands.
The tobacco habit has become so well-nigh universal, and youths are so often addicted to cigarette-smoking, that a few words regarding this habit are also indispensable. Young men who are just learning the seductive pleasures of tobacco should be strenuously urged not to form the habit, while those cardiac patients who are already addicted to smoking should be advised to discontinue it, or if unwilling to do that, to keep the use of tobacco well within the limits of harmful excess. Just how many
THE TREATMENT OF VALV^'LAR HEAirr^DlSF.ASIC
421
mild cigars or pipef^ils of mild tobacco a patient with compen- sated valvular disease may be safelj allowed to smoke daily is a question im])ossible of general answer. The degree of indulgence IKTmissible will vary in different eases, ami must be determined by careful observation of the effect produced in each instHnee. The inhalation of tobacco smoke is most pernicious, particularly to individuals with mitral disease, since it will surely increase the already existing tendency to bronchial irritation. If it he true that smoking produces anicmia, then those persons whose com- j^>ensatiou dei>ends upon adequate nourishment of the hciirt-musele cannot afford to have their red blood-cells impaired. It is well known that the immoderate use of tobacco occasions functional cardiac disorders, and, according to French authorities, raises arterial tension. Since, then, a healthy heart may suffer from tobacco intoxication, surely an unhealthy heart will experience the ill effects even more certainly and powerfully. When tobacco deranges digestion and causes insomnia, as it is well known to do in some individuals, its use should be peremptorily forbidden, I have heard it stated, with how much truth I know not, that Sir Morell Mackenzie was wont to say that tlie injurious effect of tobacco could be measure<l liy its influence upon salivary secretion. In other words, when smoking causes salivation and frequent expectoration, it is an indication that the individual is too auscei>- tible to its influence to safely persist in its use.
As regards the liquor habit, T do not propose to enter into a discussion concerning the ftKxl value of alcohol and its effect on the animal economy. Whatever be our views respecting the mod- erate use of liquor in its various forms, we all agree as to the evils of its excessive employment. What has been said already regarding the baneful effect of cardiac excitation in cases of com- pensated valve-lesions applies with added force to the immoder- ate consumption of alcohol. It goes without saying, that the possi- bility of destroying compensation is always present when a pa- tient gives himself over to a debauch. I am a firm believer in the medicinal virtues of alcohol, but in the com|x^usated stage of valvular disease the heart requires no medicinal treatment, and the only indication I can see for an alcoholic beverage ia to pro- mote the aiqietite and improve dic:estion of those individuals who habitually take too little nourishment for the requirements of
422 DISEASES OF THE HEART
their damaged hearts. The conclusion to which I hare arrived, and which governs my actions respecting the matter under dis- cussion, is that the young and vigorous with satisfactory compen- sation do not need alcohol in any form. Moreover, the danger of their becoming slaves to the habit is so real that the circumstances have to be very exceptional which make me incur the responsibil- ity of recommending the use of even beer or wine to such patients. If one has been accustomed to a stimulant with his dinner then I do not interfere with his habit, contenting myself with a caution against its immoderate use. The habit of taking a hot toddy before retiring for the night is certainly not a good one, since, as pointed out by Fothergill, it accelerates cardiac action, and thereby robs the heart of some of its rest that ought to be obtained through the slowing of its contractions during sleep.
Marriage. — The baneful effects of one phase of married life have already been considered under the head of habits. There is another aspect of the subject which I propose to consider here. For the male who has been warned against and will avoid the dangers of a too ardent love, marriage is certainly advisable, since it conduces to regularity of living, and provides him with tlic comforts of a home that cannot be obtained in a boarding-house or hotel. In the case of a woman also it is better to be a happy wife witli a comfortable home and a kind, considerate husband to minister to her needs than to be left alone, and possibly heart hungry. It is quite another thing if she is to become a domestic drudge, obliged to cook and wash for the family and to bear off- spring. It is as regards the dangers of pregnancy and child- bearing for women with valvular disease, even when compensated, that I wish to discuss marriage. Should a girl who has a valve- lesion become a wife ? is the question often asked of the medical attendant. It is a most serious one to answer, and puts an enor- mous responsibility on the medical adviser. There are many cases of even comi^ensated valvular defects in which })regnaney and childbirth are fraught with considerable risk. Yet every physi- cian of experience can probably recall numerous instances of mothers who have successfully carried their oflFspring through to birth, in spite of serious heart-disease. Let us take up the valve- defects of the left heart separately.
Mitral disease, and of this mitral stenosis is the form most
THE TI
fT OF VALVULAR HEART-DISEASE
423
frequently met with in women. ThcoretieaUj% this is the lesion which should be the moat seriously afTeeted during the latter months of pregnancy and the expulsive stage of labour. As the gravid uterus rises in the abdominal cavity and when in the last two months its fundus interferes with tlie proper descent of the diaphragm, and crowds the viscera aside^ dyspnii^a and cyanosis appear, and walking often occasions serious distress. The right heart becomes embarrassed in consequence of mechanical interfer- ence with the circulation. The pregnant uterus impedes the de- scent of the diaphragm, so that the flow of blood out of the great veins and through the right heart into the lungs is deprived of the aid resulting from full and regular respiration. Moreover^ the pressure upon the intra-abdominal veins retards the return flow from the inferior extremities, and blood-pressure in the capillaries is increased. Tbis raises pu!s<:>tensionj and by thus increasing peripheral resistance throws greater work upon the left ventricle. Under the most fav«:turable conditions ibis chamber discharges but a small volume of blood into the arterial system, and w^hen its out- flow is still further impeded by abnormal i>eripheral resistance, it results in augmented stasis within the left auricle, pulmonary system, and right lieart. The vicious circle already existing by reason of the mitral stenosis and the strain upon the right ven- tricle are intensified. If this is not too severe, the woman may be able to endure ber pregnancy to full term.
When at length labour comes on, and the expulsive stage is reached, there is inuninent danger of the right ventricle giving way under the added stress of violent straining efforts.
The same condition obtains in mitral regurgitation, but the enlargement of the left ventricle^ which if compensation is pres- ent is liypertropliiod as well as dilated, is a factor for good by enabling the heart to withstand increased peripheral resistance. The augmentation of arterial tension would by raising intra- cardiac blood-pressure increase the regurgitation into the left auri- cle were it not counteracted Iry the left-ventricle hypertrophy. The danger is that the ventricle may not be able to resist the strain, in which event the evils of the mitral incompetence become intensified, and the right ventricle at length suffers from over- strain. Even if the injurious tendencies of pregnancy are suc- cessfully withstood, the woman w^ith mitral regurgitation is sub-
424 DISEASES OP THE HEART
jected to the same danger during the second stage of labour as is one with stenosis. Whether the explanation just given is correct or not, the danger to mitral patients during this trying period lies in pulmonary engorgement and failure of the right ventricle. With this peril kept constantly in mind the attentive accoucheur can often conduct the pregnancy and gestation to a successful issue.
Capillary and venous stasis are to be lessened by saline or other not drastic cathartics and by keeping the patient at rest. WTien the expulsive efforts of labour endanger the integrity of the right ventricle or when stasis in the lungs leads to pulmonary oedema, instrumental delivery becomes imperatively indicated, and must not be delayed. In these cases chloroform is not at- tended with more than ordinary danger.
In cases of aortic-valve disease the strain of childbearing is on the left ventricle. Regurgitation through the aortic orifice is likely to be increased, and in aortic stenosis the augmented peripheral resistance hinders the output from the left ventricle in the same manner as if the orifice were for the time being still further contracted. Nevertheless, if compensatory hypertrophy is sufiicient, the left ventricle alone, or chiefly, bears the brunt of the struggle. The patients as a matter of fact endure the ordeal of childbearing often without dangerous cardiac embarrassment and better than do mitral sufferers. According to Davis's state- ments, more than 50 per cent of mitral and 23 per cent of aortic cases succumb to the dangers of pregnancy and gestation.
Only yesterday I saw a woman in the seventh month of preg- nancy who prior thereto presented well-marked evidence of mitral regurgitati(m with stenosis, considerable enlargement of the right ventricle, and dyspncra of effort. Except upon walking for a considerable distance and in ascending stairs, this patient yester- day evinced no pronounced signs of cardiac embarrassment, and declared she was not specially inconvenienced by her pregnancy. Iler pulse was only moderately accelerated, appreciably tense and strong, and the apex-beat was powerful, indicating adequate hypertrophy of the left ventricle. There was increased dulness to the right, but it was not excessive, and the right ventricle gave no sign of being dangerously overburdened. If this patient re- ceives proper management during the remaining two months, and
TnK TREATMENT OF VALVUIJ^E HEART-DISEASE
425
IS not permitted to overBtrain herself during labour, I believe her heart will not suffer damage from this, her eighth pregnancy* Her husbandj who is a physician, states that she had heart-disease at the time of her marriage, fourteen years ago.
The following conclusions may be stated: (1) Pregnancy is a condition of gravity, but not necessarily of peril, to women with compensated valvular disease. (2) Labour is a time of real dan- ger, the extent of which depends ujxin the nature of the legion and the degree of compensation, but is often endured without catastrophe. (3) Mitral disease is more liable to disastrous con- secjuences from both pregnancy and gestation than are aortic de- fects, (4) Even in mitral disease the degree of danger depends uptm the state of compensation, (5) Pregnant women with valv- ular disease require special watching as labour approaches, and during the expulsive stage should be <lelivcred iustrumentally at the earliest indication of dangerous heart-strain. ((J) The perils of marriage should be clearly stated to bi»th of the contracting parties, and when comjiensation is imperfect or is maintained with difficulty they should be advised not to wed. (7) Interfer- ence with pregnancy is justitiable only when the nature and sever- ity of the lesion render the umiiiteuance of compensation imposai- ble or when serious symptoms have already 8ui>ervened.
Clotliing.^— The physician who would instruct his patient in matters ui importance in maintaining compensation must have regard for what sometimes apf)€'ar to he things of trifling moment* Among sucli details is to be inchide<l the clothing. All who have much experience in the management of cardiopathies come in time to reuiize the influence exerted by \!iirying conditions of blood-pressure. The reason of one man's success, as contrasted with another's failure, in the treatment of heart-disease is often found in the close attention he pays to undue rise of blood-prea^ sure. Take, for example, an ordinary case of mitral stenosis. Without any recognisable change in the cardiac condition or in his daily conduct, a patient will l>e conscious that bis breathing becomes embarrassed by efforts usually put forth without any such effect. He consults his medical adviser, who, familiar with the case, discovers by stiulying the pulse and state of the venous circuhitton (hat there is unwonted tension in the arterial system. He finds, furthermore, that there is constipation [jerhaps, and
426 DISEASES OF THE HEART
knowing the influence of this condition over blood-pressure through the splanchnics, he administers a mercurial pill ; tension within the abdomen and arterial system is lowered, and the patient's breathing returns to its usual state. A tendency to pal- pitation in a case of aortic regurgitation may be wholly due to increased capillary resistance and be relieved by the administra- tion of a vaso-dilator.
It is because of the effect on blood-pressure produced by a patient's manner of dress that the matter of clothing becomes important, and may make for or against the establishment or preservation of compensation. Cardiac sufferers are often very sensitive to the cold and to sudden changes of weather, partly on account of a rheumatic diathesis and partly because of sluggish cutaneous circulation, as in mitral stenosis, or of relative arterial anaemia in aortic disease. Wool should therefore be worn next to the skin, and during seasons of low temperature the hands and feet must be kept warm by heavy not too tightly fitting gloves and shoes. It is well to have the latter constructed with cork soles, and in very cold weather overshoes may be a necessity. Outer garments should not only be warm, but they must not be so heavy as to tire the wearer. It is very important that the clothing does not constrict the vessels. This applies to shoes, gloves, col- lars, belts, and waistbands in the case of males, and to garters, corsets, and tight dresses on the part of females. Constriction of the extremities tends to raise blood-pressure as well as to mechan- ically impede circulation, and should be corrected in every case of valvular disease. Harm is chiefly done, however, by garments that constrict the chest and abdomen. A woollen undervest that has become shrunken until uncomfortably tight, an overcoat that is outgrown, and can be buttoned only with difficulty, is in a measure at least injurious in the same way as is a too tight corset. Xot only are respiratory movements hampered and venous circu- lation retarded in consequence, but the hypertrophied and there- fore compensated heart is more or less compressed and restricted in its movments; abdominal viscera are engorged and displaced; the play of the diaphragm is limited, and the evil consequences of the valvular lesion itself are intensified. These effects are evinced by increase of cyanosis and shortness of breath, both of which disappear or lessen when the clothing has been removed.
THE TREATMENT OF VALVULAR HEART-DLSEASE 427
Instead, tberefort', of 8ns|)en(liii^ the skirts from the liipSj to eifect which they have to be fastened J^niigly ahout the waist, it is preferable that women, partieidurlv slender ones, wear gar- ments of one piece, so that the weight may be borne by the shoul- ders; or they sbonhl replaee the ordinary corset by a corset-waist, to which ibe skirt** can be bnttoned, thus avoiding constriction of the waist* Kot many months ago I was consulted by a lady on account of attacks of dyspnoea and cyanosis, whicli at times amounted even to partial syncope. She presented signs of pro- nonneed mitral stenoi^is with considerable seeondary enlargement of the heart and hepatic congestion. She was inclined to cor- pnlence, and to preserve her figure wore a long, stiff corset, which, in response to my inquiry^ she dechired was loose and conifyriahle. Not convinced on tlie point, I measnred her waist both on the bare skin and ontside of the corset, and thus demonstrated that when her corset was liooked she actually measnred 4 inches less than she did next to the skin, I then explained at some length the harm she was doing herstdf, and succeeded in getting her to re- form her mode of dressing, nnich to her relief, as she subsequently acknowledged. In this instance I am convinced that the s^^np- toms of cardiac stress under conditions of exercise were due largely To the additional impediment to circulation and respira- tion ix'casioned by the tightness of her clothing.
Baths, — I have found in numerous instances that ladies with valvular disease were in the babi* of taking a semiweekly hot bath, and some of them confessed to lying in the water for twenty minutes m' more. Inquiry generally elieiteJ the fact that the bath was followed by a feeling of languor^ even amounting in some instances to prostration. It is w^ell known that such hot baths are weakening to the heart and lower vascular tone. They should be forbidden fberefore, and the patients advised to content themselves with a rapid sponge-bath daily if strength permits, and once a week a tub-bath of short duration, and of a temperature closely approximating that of the human l)ody. Mitral patients endure bathing less well than do those with aortic lesions. Yet in all cases the degree of latitude iK»rniissible in the matter of baths is to be determined by their effect. If they are followed by a healthy reaction — that is, by warmth of the skin and a sense of rest or well-being — they are beneficial; but if a cardiac patient
A
428 DISEASES OP THE HEART
finds his bath leaves him with cold extremities and a feeling of fatigue, and that the exertion of briskly rubbing his body into a glow occasions breathlessness or palpitation, frequent bathing is likely to do him harm.
Swimming, whether in salt or fresh water, is to be considered not alone with reference to the temperature of the water; there is the shock of the sudden plunge or inunersion, and also the exertion of propelling the body while at the same time sustaining the weight or pressure of the surrounding liquid. For these vari- ous reasons this form of bathing is apt to put a good deal of strain on the heart, and persons wnth mitral lesions, or those whose de- fects, of whatever nature, are maintaining compensation with difficulty, should either indulge in this sport not at all or only under great restriction, both of frequency and duration. It is probable that many of the cases of supposed death from cramp in the water are in reality instances of heart-failure or asystolism.
The Turkish and Russian baths and the various modifications of the shower-bath or douche found at health-resorts affect the heart and vascular system powerfully, and should not be taken by cardiac sufferers without the advice of a physician who is familiar with their effects and competent to decide on the advisa- bility of such baths in each instance.
The saline and carbonated baths employed for therapeutic purposes at Bad Xauheim may be left out of consideration at this time, since they are not indicated for individuals whose valvular defects are in the stage of compensation.
Food. — Of all matters concerning our patients none is so essen- tial as that of nourishment, and yet there is nothing, I venture to say, about which physicians of more than average intelligence and experience are so unable to give precise and suitable instruc- tions. In works on diet are to be found tables of various food- stuffs compiled with regard to the needs of the human organism under conditions of work and repose, and from which one may construct dietaries suitable to the requirements of cardiac patients. In this chapter I shall only make certain general statements that apply to the regimen of persons whose lesions have not greatly deranged circulatory equipoise.
Adequate compensation in any given case implies, nay, neces- sitates, the supposition that the circulation of the digestive appa-
THE TREATMENT OF VALVLtLAR nEART-rHSEASE
429
rat us is iitit apprerialily (listiirbt'd. The eonehision is warranted, therefore, that there is no lUgestive disorder secondary to the car- diac mischief and necessitating a corresponding modification of the diet. It is only essential that the food be of good quality, well- cooked, and sufficient. The proportion of proteids suitable to each case will be governed by the amount of exercise taken, the kind of work, and the tendency or not to obesity. The same consid- erations apply to the (Quantity as well as the quality. The proper preparation of the food is essential if digestive disorders are to be avoided. It is of importance also that meals he taken at reguhir hours ; gluttony is injurious, and the amount of fluids taken with meals should be definitely stated, 10 ounces being ordinarily sutMcient, Patients wlio are aiMcjuic must be given a lil>eral allow- ance of beef, eggSj rnilk, and such vegetables and fniits as are rich ill iron-forming compounds; those who incline to constipa- tion are to get a dietary calculated to correct the tendency. Tea and coffee in moderation may be allowed. In a word, so long as comj)en8ation is complete there is no indication for special rules to govern the dietary further than what would be required for the preservation of health in the same individual were he not afflicted w^ith an incurable muladv.
Illneises.— Among so many items of importance in the preser- vation of compensation it is difficult to specify one as greater than another, and perhaps it is not wise to attempt to do so. Yet I wish to lay particular em|)hasis on this point — namely, no illness or indisposition, apparently trivial in itself, should ever be so regarded in a person who has suffered injury frou* end<x;arditi8. This is specially true of children. In them rheumatism is so apt to he masked that an infection of the throat, a persistent pain in an extremity, a rise of temperature without obvious cause, should always receive careful medical attention. The intestinal tract afffirds so ready and freque^nt a portal of infection that no devia- tion from the standard of health is to Im neglected as of no C4>nse- quenre. Far better is it to bear the imputation of being over- careful and fussy than to some day aw*ake to the consciousness that your neglect has permitted injury to visit one of your pa- tients, whose compensated valvular lesion might otherwise have gone on years longer. Tell your patients emphatically and clearly that a tonsillitis, yes, or even an acute ^oryza, is never to be neg-
430 DISEASES OP THE HEART
lected. In a case of mitral disease, particularly of stenosis, an attack of simple bronchitis may break down utterly the integrity of the right ventricle. Be always suspicious of slight fevers, which to those living in a malarial region may appear to be of that nature; such a trivial yet persistent run of fever has only too often turned out to be an endocarditis. In cases of pneu- monia and other serious affections cardiac sufferers merit more than ordinary care and watchfulness, if they are to come through undamaged. This is particularly true of persons with mitral de- fects not only because of the possible lighting up of a fresh endo- carditis, but because the strain to which the right ventricle is subjected by reason of the valvular mischief is enormously aug- mented by the pneumonic consolidation — while at the same time cardiac endurance is impaired through the effect of the pneumonic toxines on the myocardium. If in such a case paralysis of the vaso-motor centres leads to cyanosis, the outlook is serious indeed. The gravity of jmeumonia, la grippe, and other acute infections, gonorrha'a, diphtheria, scarlatina, measles, puerperal septicaemia, etc., in all cases of comi)ensated valvular disease, is so obvious, particularly as respects the liability to fresh endocarditis, that further connnent is unnecessary. Considerations of prophy- laxis require, therefore, that our cardiopaths be properly in- structed on these points. If it be objected that this is likely to render them introspective, and even hypochondriac, or if the patients are children, then the requisite information may be inij)arted to the family, friends, or parents. Xo one need fear that his motives will be misunderstood. Indeed, I am convinced that the American public likes to be talked to by physicians as if they were intelligent and reasonable beings, and that nothing con- duces more to the establishment of confidence in the medical prac- titioner than frankness and })lain dealing in all matters that con- cern the health of his patients.
Use of Drugs. — It is an error to suppose that every individual presenting signs of valvular mischief requires medicinal treat- ment. Digitalis or some other heart-tonic is not to he ordered in every case in tvhich an endocardial murmur is heard. Inexpe- rienced practitioners fresh from a medical college are very apt to commit this mistake, and consequently the foregoing injunction is not out of place. When a perscm with valvular disease presents
THE TREATMENT OF VALVULAR HEART-DLSEASE
431
himself in your office, iiiqiiirG iiiiuutely into the matter of symp- toms, and if he does not acknowledge any indicative of cardiac stress, remedies influencing the heart directly are not indicated. If you beh>ng to tliat chiss who believe no person should be allowed to leave the physician's ofticc without a prescription or a drug of some kind J lest fursuoth tlie patient fancy he has nut received his money's worth, then let it be a placebo. As a matter of fact, there are few^ persons who cannot he satisfied under such circumstances witli an expression of opinion coupled with sound advice on the points under discussion in this chapter. Careful inquiry will usually bring out some pernicious habit, faulty digestion, consti- pat ion, some iuipairment »if appetite^ etc. ; or there may he more or less anaemia, bronchial irritation perhaps, menorrhagia, some deviation from perfect health, which permitted to go on, will in time exert malign influence on oom|X"nsation. Any such condition calls for corrt*ction, and to this end medicinal treatment may be indicated. What medicaments are suitable in each instance is, of course, to be left to the judgment of the medical adviser.
Although slight disturbances demanding attention are often dependent uikiu scarcely detectable disorders of circulation, they are not necessarily so in perfectly couii>c^nsatcd cases, and hence these patients may generally be treated, so far as regards medi- cines, as tliey woukl be were they wdiolly free from endocardial defects.
Two conditinns likely to iu*ovg more injuriotis to individuals with a valve-lesion, although compensated^ than would be the case if his valves had not been damaged, arc crmstipation and flatulent distention ai the Iniweh In both there is sphinehnic irritation and consequent alteration of blood-pressure, but in the latter the effect of mechanical encroachment upon the contents of the tho- racic cavity must he reckoned %vith. I7ncf>rrected it may con- tribute materially to the destruction of heart adequacy, to say nothing about the patient's discomfort in the w^ay of postprandial breathlessness in mitral and tendency to palpitation in aortic dis- ease. Both disorders of digestive function tend to impair the appetite, give rise to neuralgias, antemia, coldness of the extrera- itiea, and many other phenomena of auto-infection. Moreover, flatulent indigestion, pn^bahly through the absorption of toxines, is a frequent cause of deranged cardiac rhythm. This not only
432 DISEASES OF THE HEART
annoys or even alarms the patient, but it may even lead to the development of dilatation. It is for the relief of such disturbing factors as these, therefore, that drugs find their legitimate use in the management of compensated cardiopathies. In most cases the speediest and surest relief is likely to be afforded by a mercurial, a grain of calomel in divided doses, or 5 grains of blue mass, fol- lowed next morning by a Seidlitz powder or a glassful of some laxative water. Cascara, aloes, rhubarb, podophyllum, etc., pan- creatin, ox-gall, nitrohydrochloric acid, subgallate of bismuth, salol or salophen, naphthol preparations, etc., alone or in various combinations and with which the reader is duly familiar, are serviceable, and will generally afford relief.
Only when gastro-intestinal disorders occasion persistent de- rangement of cardiac action are digitalis, strophanthus, caffeine, convallaria, and sparteine to be prescribed in this class of cases ; even then the remedy is to be withdrawn so soon as the arrhyth- mia or acceleration of the pulse has been corrected. Tomjwrary palpitation or vertigo on the part of aortic patients may generally be removed by minute doses of glonoin, t^^ to yj^ of a grain at intervals of two, three, or four hours, either alone or in conjunc- tion with 3 to 5 drops of digitalis. \Vhen compensation has been seriously threatened by cardiac overstrain or some other disturb- ing factor, digitalis and strychnine may be needed in addition to rest and restricted diet; but in all such instances rest in bed for a few days is unquestionably the agency of greatest value, and should be rigidly enforced until the period of danger is past ; not until then is the patient to be permitted to resume his usual mode of life and to return to his wonted exercise. In this class of cases " eternal vigilance is the price of safety."
Change of Climate, with Special Keference to High Altitude. — The question is so often asked whether a patient with heart-dis- ease should go to Colorado or make the journey over the moun- tains to California, that it seems best to discuss this subject here when considering those conditions that make for the preservation of compensation. It is quite generally the opinion among medi- cal men that the existence of a valvular lesion contra-indicates residence in elevated climates. This is too sweeping, as shown by clinical observation. My medical friends in Colorado assure me that their patients with valvular disease, of whatever kind, suffer
THE TREATMENT OF VALVULAR HEART-DISEASE
433
no more iiifODveiiience from their heart-lesions in Denver or Colorado Springs titan do persons simikriy affected at the sea level. Moreover, Regnard, in an elaborate work on the effect of bi^h altitude on the heart and circulation, expresses the opinion tliitt c^ardiac lesions per se do not coutra-indicate residence in the monn tains when this is necessary^ and that aside from the discom- fort of hcHjoming accustomed to the high altitude individuals afflicted with heart-disease do not experience permanent harm. Nevertheless J he would not advise residence in such a climate for a eardiopath, since there is nothing in his disease calling for such a climatic treatment. This opinion impresses me as too broad^ judging from the experience of some of my cardiac patients. I havt' known jK^rsons with mitral and aortic regurgitation to visit Cidorado, ajid therCj at an elevation of 0,000 feet, to take consid- erahle exercise without discomfort, and apparently without barm. Others with vascular and cardiac degeneration have found the same to be true witli them, and in fact one gentleman was actu- ally able to walk with nuo-e ease at 7,000 feet than in Chicago, On the other hand, my patients who were not able to endure high altitude were sutTerers from mitral stenosis, aortic stenosis, and mitral incompetence, when complicated by pericardial or pleu- ritic adhesions. These eases were all re|K)rted and discussed by me in a paper before the American Climatolngical Association in 1899, and will be found in the Transactions of that year. Singu- larly enotigh, Dr. Sewall, of Denver, in discussing my paper, stated that at that very time he had under observation in Denver a female with pronounced mitral stenosis, who liad formerly been under my care in diicago, and who was able to endure the eleva- tion, not only of Denver, but also of Cripple Creek sit\iated at an altitude of about 12,000 feet. She died a year subsequently, I understand, and I have often woii<lered if her resi<lence at that elevation did not aid materially in shortcming her life.
As the discussion of theories is foreign to the spirit of this work, T shall not discuss at length the considerations which make me conclude that residence in hi^li altitudes is likely to prove injurious to persons liaving stenosis or regurgitant lesions com- plicated by pericardial or pleural adhesions. Suffice it to say that the effect of a rarefietl atmosphere is acceleration and small- ness of the pulse, -together with increase in the depth and fre-
434 DISEASES OP THE HEART
qiicncy of the respirations, the degree of this effect depending of course upon the degree of the altitude. The blood flows to the heart more rapidly, and if there is an obstruction at one of the orifices, this acts as a barrier to the rapid and easy passage of the blood, which tends to accumulate back of the hindrance. In mitral or aortic stenosis this would be in the lungs and right heart, and hence symptoms due to this engorgement are likely to result. If adhesions exist, they interfere more or less with the expansion of the thorax, which takes place in high climates, and consequently they ought to hinder that adjustment to altered conditions, which is essential if one is to become accustomed to a high altitude. Further reflection and observation since the publication of my paper on this subject have led me to the belief that probably all or nearly all individuals with valvular diseases can endure an altitude of 6,000 to 10,000 feet without injury, provided they do not take much exercise. Until they have grown accustomed to the rarefied air they should not walk at all, but remain in bed. At least such is the opinion and advice I give when consulted on this important question. Finally, it is probable that much of the dyspnoea and palpitation complained of by some at high alti- tudes is due in part, perhaps largely, to the fact that in the moun- tains the walks are not level. Hill-climbing is trying for cardio- paths, even at the sea level, and at an elevation where the air is thin such an exertion could readily prove doubly injurious. The phenomena of mountain-sickness — that is, rush of blood to the head, with vertigo, and even nausea, or in extreme cases bleeding from the nose and ears — are liable to attack healthy persons at too high an altitude, particularly during physical exertion. In their milder degrees they may affect cardiopaths in transit to and from the Pacific coast, but apart from these unpleasant symptoms patients who remain at rest in the car need not apprehend serious results even in passing the loftiest points. When vertigo or a tendency to syncope is experienced, relief usually follows the ad- ministration of a diffusible stimulant and the assumption of the recumbent position. Xevertheless, caution would suggest the tak- ing of the less lofty routes.
CHAPTER XYII
THE TREATMENT OF VALVULAR HEART-DISEASE
{Continued}
II. COMPENSATION BEING IMPERFECT
A WANT of perfect compensation may have either one of two expliinations. It may have never been adequately developed after the subsidence of the acute proeeas that led to the valvular mis- chief ^ or having been once established it may be destroyed in con- sequence of a variety of causes. In the first instance the develop- ment of complete compensation may be impossible, owing to the extent of the damage sustained by the valves, in consequence of de- generation uf the myocardium J or of the coexistence of complica- tions or conditions residing in the patient's temperament, environ- nientj etc. In such a case the course of the disease is generally tcm short to admit of its l>eing brought into the category of chronic valvular affections. For the same reasons a long-continued main- tenance of compensation may be impossible after it has once be- come established. In many casesj however^ it is possible to arrest the downward tendency and restore heart-power when the injuri- ous infiuc^nccs are discovered and removed. If these cannot be removed, then their baneful effects must be counteracted by all those therapeutic measures which are at our disposal.
In the numagement of compensated valvidar disease the physi- cian conducts a defensive campaign, so to speak, whereas when compensation has failed, he is called on to wage an active offensive warfare against all those forces that are striving to destroy his patient. His success depends not only upon the skill with which his therapeutic weapons are wielded, but also upon the precision of bis orders, and the faithfidness with which these are executed. The treatment of valvular disease in this stage requires also atten- tion to details of daily life, no matter how trivial they may appear to be, and the recognition of complications. Moreover, there are
ISO
436 DISEASES OF THE HEART
few patients in whose environment influences do not exist which, if permitted to go on, will not act unfavourably and retard the restoration of adequate compensation. For this reason these must be ascertained and removed so far as is possible. It is plain, therefore, that the proper management of these cases consists in much more than the mere administration of heart-tonics or other medicinal remedies. That highly gratifying results follow such strict and careful management is shown by the narration of the next three cases.
Miss X., referred by Dr. Minor, of Asheville, N. C, was first seen by me in July, 1898. She had spent the preceding winter in Asheville, and had there sought medical advice in the early part of summer because of increasing difficulty of breathing in walking, the altitude being 2,200 feet and the nature of the ground hilly. The winter immediately previous had also been passed in Asheville, but without her having noticed the same shortness of breath. She gave a history of inflammatory rheu- matism three years before, and a year and a half before of an ill- ness which, judging from her account, must have been an inflam- mation of a serous membrane within the thorax. Iler age was twenty-two. Her pulse was much accelerated, 120 or more, regu- lar, and equal. The ankles were (rdematous, and the abdomen was distended by the greatly engorged liver. The broad, fairly powerful apex-beat was found immovably fixed in the sixth inter- costal space, near the anterior axillary line, and superficial car- diac dulness extended somewhat beyond the right sternal margin, upward to the third costal cartilage and at the left, almost to the mamillary line. There was an intense blowing systolic apex-mur- mur transmitted to the left and accompanying, not replacing, the first sound, the pulmonic second sound being very accentuated. Upon auscultation, fine crackling rales were detected during in- spiration along the upper and left border of pra^cordial dulness, and upon the arms being raised and lowered a creaking sound could be plainly heard at the superior boundary of dulness on the sternum.
In this case it was manifestly not so much the mitral leak that was serious, as it was the fixation of the left ventricle that was preventing the maintenance of compensation. Jkforeover, it was foreseen that digitalis and similar remedies could exercise but
The treatment op valvular nEART-DISBASE
43T
limited coBtrol over the hearty since only slight if any reduction in the dilatntioii of the left vent riele was possible by reason of the restraining adhesions. Efforts had to he direetedj therefore, to lessening tlie resistance residing in the congested pK>rtal system and at strengthening the right ventricle. The former was to be aecomplislied by purgatives, tonic doses of digitalis, and the re- moval of all constricting clothing ; the latter by those same means, re-enforeed hy abstaining from too miu-h jdiysical exertion, and if need be by rest from all exercise. Aceivrdingly the patient w^as told to give up her corset, which she did^ to take an aperient water daily before breakfast, and thrice daily 15 drops of tincture of digitalis. Stair-climbing w^as forbidden. Directions regarding the quantity and kind of food and the amount of fluids wera added. The degree of improvement was so insignificant during the next few* weeks that at length absolute rest in l>ed was advised and acted upon. Then benefit became at once apparent in slowing of the pulse and diminutitm of dulness over the right heart. The liver also began to shrink, urine grew Tuore abnmlant, and ccdema disappeared. After five weeks of enforced rest the patient w*a9 permitted to gradually resume her ordinary mode of life, except- ing that she was not allowed to go out. All this time digitalis or strophanthus was continued in about the same dose {15 drops) of the one and 1(1 drops of the latter thrice daily, with excep- tion of every sixth day, when it w^as omitted. Apex-imjnilse grew somewhat stronger, Init never altered its jiosition in the least; the marked (*bange was in the right ventricle and liver.
After a few^ weeks longer of such management it was decided to try the effect of a course of Xaubeim baths. They were given in her iuuue an<l not at my rcMuns, as was then the rule w^itli pa- tients w^liom I subjected to this treatment. Whether because I could not watch their pflect as closely in this way, or on account of the hampering effect of the adhesions (I believe it was the latter), the baths did not prfn^luce a Wneficial effect* Heart-rate increased and shmved a tendency to unsteadiness, dulness to the right be- came increased, and the amount of urine diminished. They were discontinned^ tlierefore^ and no permanent harm resulted. Considerable difliculty was experienced in getting this patient to give up her candy and obey instructions as to diet; but the habit of making her furnish me w*ith an account of what she ate and
438 DISEASES OF THE HEART
drank finally convinced her that I was in earnest, and now her obedience to orders is all that can be desired. In this case men- struation is too profuse and somewhat irregular; so that she has been instructed to remain in bed during her menses, and hydras- tin hydrochlorate is sometimes administered. During the summer of 1899 her health was quite satisfactory, and she was able to enjoy a number of outings with friends without very irksome re- striction on her pleasures. She has been very subject to annoying pains in her shoulders, but especially in her chest beneath the ster- num, and upon several such occasions there has been a circum- scribed, faint, yet distinct friction directly above the superior line of cardiac dulness, which was taken to indicate a fresh lighting up of mediastinitis. These attacks have generally yielded to coimter-irritation and antirheumatic remedies.
Towards spring of 1900 her condition began to run down slowly but surely, and complaint of " rheumatic pains " was fre- quent; the pulse quickened, and her flesh grew flabby and cold. She consented to enter a hospital, where her temperature could be carefully watched, as the possibility of endocarditis was enter- tained. Temperature remained subnormal, however, rather than febrile. Her urine was collected and examined, with the follow- ing result: Total amount in twenty-four hours, 660 cubic centi- metres; specific gravity, 1.028; urea, 3 per cent; 2 J per cent of albumin; numerous hyaline and granular casts. Animal food was withheld, copious draughts of water insisted upon, and citrate of potash was administered, together with moderate doses of fox- glove in tincture. A week later the urine amounted to 2,500 cubic centimetres, had a specific gravity of 1.013, urea 1.3 per cent, neither albumin nor casts. This must have been a mild nephritis and not merely congestion, since the kidneys responded so well to the free intake of fluids. As was to be expected, the patient's condition improved rapidly, the pulse-rate decreased strikingly; and two weeks afterward she returned home. It is now four months later, and albumin has not again been found in the urine. She has been allowed animal food but sparingly, and has been required to drink water freely between meals, with the result of her feeling unusually well, and being able to enjoy a moderate amount of walking again. This lady is an invalid, to be sure, who has to lead a restricted existence ; but she is able to
THE TREATMENT OP VALVULAR HEART-DISEASE
439
attend matinees and stxiial functions of a quiet kind, in fine, to get a good deal of enjoyment out of life. She cannot entertain the hope of becoming a wife and motlier, and lias been so informed.
In this ease digitalis has been taken most of the time, because it has been rei^eutedly jiroved by trial that when discarded en- tirely its need is sliown after a few days by increased breathless- nes3 and snbjective as well as objective rapidity of the heart's action, to 120 or more. The tincture has generally been pre- scribed, sometimes 10 drops once daily, and at other times 5, 7, or 10 drops two ur three times a day. Upon a few occasions scantiness of the nrim^ and trdenia, shown by pitting of the ankles, has necessitated the administration vi the fresh infusion of English leaves, a tablespoonfnl three or four times daily, Now and then citrate of potassium has been added. Sulphate of strych- nine has also been taken much of the time, and whenever she has felt more than nsmil weakness she has protited nmeh from the compound syrup of hypopbosphites*
She has been dejjendent on medicinal remedies, but no doubt a large part of her really good condition is owing to the excellent care she has taken of herself. She has dressed sensibly, wearing a loosely fitting corset-waist, and so far as |KissibIe suspending her skirts from her shoulders. Walking has bc^en done at a slow pace and for short distances, care being taken not to walk against a strong wind, and to stop for rest whenever shortness of breath or palpitation has been experienced. Ascending stairs has been avoided, or when that was impossible they have been mounted a few stairs at a time, with freqnc^nt pauses to let her heart tiuiet down or to recover breath. iJuring stormy weather she has either remained indoors or has driven in a closed carriage to her destina- tion. Any indisposition, however trivial, has received prompt attention, and a day of unwonted fatigue or exertion has been generally followed by rest in bid ur on a euuch. Her dietary has been simple and nutritious, and she luas not been f^ermitted to be in the least eonstifrnted. On the contrary, she took an aperient water every morning for a year at least, with a dose of calomel whenever her liver showed more than ordinary congestion or she felt a sense of fulness about the waist. Latterly the laxative water has l>een taken only every other day* Finally, she has been required to see me at regular intervals, generally two or thre^
440 DISEASES OF THE HEART
times a month, that thereby she might be kept under control. In her case certainly eternal vigilance has been the price of safety.
Master W. B., aged eight, was examined by me in June, 1896, at request of Dr. John Streeter. He was a frail, undersized, pale boy, whose whole life had been one of many illnesses; broncho- pneumonia five times in early childhood, innumerable attacks of fever, with coated tongue, pain in the right hypochondrium, nau- sea, and irritable stomach, which had generally yielded to calo- mel and milk diet, and had been considered " storms of uric acid." For a year prior to my visit patient had been under treat- ment by Dr. M. Allen Starr, of New York, who, it was stated, had administered bromide of soda every night during the year. The mother had first learned of her boy's heart-disease in April, 1896. Patient was very subject to attacks of acute tonsillitis, having but just recovered from one, and at the time of my examination had an acute coryza. He had the facial appearance indicative of adenoids, breathed through the mouth, and beneath the angle of the left inferior maxilla the neck was tumefied by enlarged cervical glands. His chest was long, narrow, sunken below the clavicles, prominent in the pnecordium, and expanded poorly on inspira- tion; the finger-ends were noticeably bulbous, but there was no cyanosis. The heart was greatly enlarged, there was a loud, harsh systolic apex-murniur of wide propagation, and both liver and spleen were palpable with much corroborative increase of dulness. The little fellow suffered from dyspna^a and occasionally palpi- tation on ascending stairs or hurried walking. Urine was scanty and of high specific gravity, otherwise negative. His appetite was capricious, digestion weak, and bowel movements irregular.
It was my opinion that, if much improvement was to be at- tained, three things would have to be done — the removal of the nasal obstruction, the development of the chest, and the improve- ment of the blood condition. The adenoids could have been safely removed under ether and even chloroform skilfully ad- ministered, and thus the first step taken towards proper expansion of the chest. I have notes of a similar condition in a boy of five or six, which was successfully operated on without the slightest untoward effects as regarded his mitral insufficiency and with ultimate benefit to the child. In the present case the mother wanted the treatment of the nasal obstruction postponed, and I
THK TREATMENT OF VALVULAR II HA HT-DISKASK
441
have never leiirned wlielljer it lias been done or noL It was evi- dent that if the already enlarged heart was to have room in the thorax for further increase of its compensatory hypertrophy the capacity of the chest would have to be augmented. Accordingly, his attendant, an intelli»reiit train<Ml rnirse, was instrncted liow to give resistance gymnast les and breathing exercises. These w^ere intended not alone to strengthen his heart and develop his thorax^ but also to facilitate blood-flow hy better aspiration up out of the congested liver and abdominal vessels. A bighly gratifying expe- rience in other cases had already shown huw effective and bene- ficial such exercises are in sueb a condition.
In addition, improved mitrition was songbt to be achieved through a dietary suited to his blew id-state and to his feeble digest- ive and assimilative pro(*esseB. Starches antl sugars were greatly though not entirely cut off, such as were allowed being carefully selecte<l — -zw^ieback, toast, a little baked pcjfato, etc. Jleat and eggs were allowed in inodernte amounts, and certain fresh vege- tables and fruits were adfled to the diet list. Such medicinal remedies as would aid digestion, keep down fennentalionj and unload the portal vessels were prescribed. To the last end calo- mel was the drug selected, care l>eing taken not to produce a too powerful purgative effect. Cardiac tonics, digitalis and strych- nine, were a minor part of the treatment, bcnng administered in such doses only as would gra^lually tone up the heart, Some im- provement began to be apparent almost directly, but tbe family remove*! to tbe East before time was affonled to observe the ulti- mate results. Informatiou came to me, however, some weeks sub- sequently that the plan of management detailed was bringing about improvement. I have not seen the patient since that time,
W. IL W,, aged thirty-nine years, male, physician, consulted me in August, 18l>n, on account of an attack of mild articular rheumatism, one week previously, iii right knee and both hips. He gave a history of inHammatory rheumatism at age of nine or ten, at fifteen remembers be had shortness of bi'eath, and thinks he had interniittence. In IS.Sf) valvular disease was diagnosti- cated. During 1S1>5 he bad an aftenuKm tem|jerature from 9?)° to 100^ F., but the cause wms not discovered. In Ilecemher, 1805, had a fe%*er of in,3^ F. that lasted three days, and yielded to rest in bed and milk diet. Afterward felt better than before. Hia
Ui
DISEASES OF THE HEART
eorHlitiim wn» good the following winter, and initil Iiis recent in- llrtiHiiuilury atUirk he hfts atteiideJ quite constatitly to an exact- ing gonernl |>ractit:e. At tlie date of my examination there was slight dizzinefls on walking, temperature at 3 p. m. w^as 99.8*^ F., pube was i}8, sitting, falling to IH on assuming the dorsal decu- bitus, and was collapsing; cnpillarv pidsc was present, and there was a systolic snap in the femoral artery. The broad, strong ajH*x-k*at was in llie sixth left interspace, 3^ inches to left of s^tertuini, and there was a diffused systolic impulse over the body of heart to left of the breastbone. First sound at ai)ex was pro- longed and impure, su^resting a presystolic murmur, while the aortic second was muffleih In Uie aortic area was a soft, faint diiatolie tiiunnnr, tmnsmitteii downw*ard and to the left The 4iigMsi$ was^ plainly an aortic insufficiency of rheumatic origin, HH^ « slill per^ming mikl rh<^mattsm<
Hf 'a*aii a^fised 1o giiEie ap mctive exercise so long as any trace
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V uary, IIHK), he entered my office one momtnjp
^^ W Ktii juat had « quite profuae hicmoptyeiii without the
:.ai of unusmal phy«ical effort. Tbe heart was hurried
.iotuilly tnremilttent ; ita left border was much outside of
|ip|]le, ita npex rather too rounded, and iu impuli
90
442 DISEASES OF THE HEART
condition was good the following winter, and until his recent in- flammatory attack he has attended quite constantly to an exact- ing general practice. At the date of my examination there was slight dizziness on walking, temperature at 3 p. m. was 99.8° F., pulse was 98, sitting, falling to 94 on assuming the dorsal decu- bitus, and was collapsing; capillary pulse was present, and there was a systolic snap in the femoral artery. The broad, strong apex-beat was in the sixth left interspace, 3^ inches to left of sternum, and there was a diffused systolic impulse over the body of heart to left of the breastbone. First sound at apex was pro- longed and impure, suggesting a presystolic murmur, while the aortic second was muffled. In the aortic area was a soft, faint diastolic murmur, transmitted downward and to the left. The diagnosis was plainly an aortic insufficiency of rheumatic origin, and a still persisting mild rheumatism.
He was advised to give up active exercise so long as any trace of joint inflammation persisted, and to take salicylate of soda with small not frequent doses of digitalis. The patient subse- quently reported his recovery and return to practice. During the ensuing three years he abandoned general practice and limited himself to office work; he moved his residence a short distance out of the city, which necessitated travelling to and fro on an ele- vated road, and the ascending of long, steep stairs to the stations. He consulted nie several times, and on one occasion reported an attack of luvmoptysis following some exertion. After that attack I confined him to bed for a week or so, and put him on digitalis, strychnine, and a vaso-dilator. He quite frequently experienced intermittence of the pulse for days together, and as he had some digestive disturbance at those times, it was thought the intermis- sions were due to that cause. On one occasion, in the latter part of 1898 or the beginning of 1899, he was suddenly seized with partial syncope while at work over a patient in his office, which, however, was recovered from after a few days rest at home, with the use of digitalis and nitroglycerin.
At length, in January, 1900, he entered my office one morning saying he had just had a quite profuse hicmoptysis without the provocation of unusual physical effort. The heart was hurried and occasionally intermittent ; its left border was much outside of the left nipple, its apex rather too rounded, and its impulse
THE TREAT.MENT OF VAI.VrLAft JIEAKT-DISEASE
443
not well defineiL It was also noted thai a rough systolic murmur liad developed in the aortic area, wbieli had not existed a year or two previotialy. The condition was considered very threatening, as the htciuoptysis pointed to pulmonary congestion in conse- quence of temporary imulequacy of the left ventricle, TIjc em- phatic admonition was given him to return home at once and go to bed for an indefinite time^ probably many months. The advice was acted on, and he l>egan the regular employment of small, thrice daily, doses of tincture of digitalis, with S grains of potas- sium iodide t i. d., and strychnine; glonoin was substituted now and then for the iodide.
His dietary was light yet nutritions, and the bowels were lept free by calomel and othir laxatives, as occasion required. For a short period he had a light run of fever, with vague joint pains, which yielded to salicylates. His cardiac action was invariably irregular after breakfast, hut subsequently grew less annoying or disappeared entirely after his morning glass of milk w^as aban- doned, and his early meal was made more substantial. This patient remained in bed for four munths, at the end of which time his heart was found to have retracted somewhat in size, gained in the force and concentration of its apex-beat, and had become noticeably steadier in action. He was then permitted to resume exercise very gradually, at first about bis room, and thus by slow degrees to accustom himself to his ordinary habits of life. When at length he iiad grown able to get about as before his illness, he went into the country^ and there, driving abotit with a medical friend, so<m got to feeling as well as usual. Small doses of digitalis and strychnine were continued after he left his bed and resumed walking, for the purpose of maintaining what the heart had gained by the prolonged rest. Considering the age of this patient (now forty -three) and his history of repeated stibacute rheumatism and prolndde aggravation of the endocarditic changes, tlie results secured were highly gratifying, and illustrate the immense value of physical inaction in the recuud>ent posture in cases of aortic regurgitation with breaking compensation. This patient has had no return of his symptoms, so far as I have learned, up to the present writing. Nevertheless, the prognosis is not encouraging, for unless the drictor is very careful a final and irretrievable breakdown is likely to occur at any time.
444 DISEASES OP THE HEART
Medicinal Agents. — From the narration of the foregoing cases it becomes apparent that the principle of management applicable to the stage of compensation does not obtain when heart-power shows signs of failure. In this stage digitalis or one of its con- geners is generally of great service, and is often indispensable for the remainder of the patient's life. Foxglove is incomparably superior to all cardiac tonics of its class, and should always be preferred so long as vascular changes are not present and when it does not disagree with the stomach. The former objection does not exist in the young and in some persons at or past middle age. When the arteries are stiff and the vaso-constrictor eifect of digi- talis is likely to occasion injurious rise of blood-pressure, this effect can be overcome by the administration of -j^u of nitroglyc- erin every two or three hours in the form of a tablet of required strength or a minim of the official solution. Two or three grains of an iodide salt are said to accomplish the same purpose, and may be administered three times a day. If strophanthus is em- ployed instead of digitalis, a vaso-dilator may or may not be neces- sary, according to the degree of vascular tension. The unpleasant effect of digitalis on the stomach is said to reside in a free-fat and certain narcotic principles, the irritating qualities of the drug in free acids, all of which can be removed without impairing its effi- ciency. The method of removing these objectionable constituents was announced in ISUO by Dr. England, the chemist of the Phila- delphia Hospital. Accordingly, such a fat-free tincture of digi- talis is now prepared by several manufacturers of pharmaceutical preparations, which has been found to possess equal if not greater potency than the tinctures ordinarily in use. In most cases of the kind now under consideration digitalis is needed for its tonic effect, not as a diuretic, and therefore the dose may be a moderate one — 5, 10, or 15 drops of the tincture once, twice, or thrice daily, as the case may l)e. The length of time during which digitalis is to be administered is also variable. Usually, however, it Avill be required for many weeks or even months; in grave cases it may even be continued for the rest of the patient's life. I am con- vinced that a digitalis-habit may be acquired, yet see no objec- tion to this so long as the continued use of the remedy prevents a total loss of compensation.
Another medicinal agent of generally recognised value as a
THE TREATMENT OP VALVULAR HEART-DISEASE
U5
cardiac tonic is strvchniiie. It stiioulatcs the heart through its action on the canliue motor ganglia. The slight retardation of the pulse-rate, which is produced by its stimulation of the inhibitory apparatus, is transient, and therefore not to be reckoned with in considering its the ra pent ie induenee. The increase of arterial tt^iision, said to residt from its stimulation of the vaso-motor cen- tres, is so slight that opinions are at variance on this point. This effect is certainly tiM> triding to prove an objection to its employ nicnt, even in eases showing pronounced vascular degeneration and consequent high and sustained pulse-tension. The question of prime importance is, In what dose is strychnine to be admin- istered i Believing that if it stimidates cardiac contractions in small doses through its action on the motor ganglia, it ought to do this still more powerfully in large ones, I have been in the habit uf ordering doses that to many seem dangerous — that is, I have many tiuu^s preseribi^d ^ of a grain hyijoderinically every tliree, and even every two, hours, until seven or even eight injections have been given in a day, and have continued these doses for days, and even weeks together without ill effects, so far as I could dis- cover. On the contrary, they have seemed to 1k^ of positive bene- tit. ludeetl, I may say it never occurred to me that the remedy, even in these doses, could do more harm tliau occasion the primary phenomena of its ]vhysiological effect. As I have but rarely observed twitehings to result, and in these cases have proiuptly discontinued the drug, 1 have not thought to question its beneficial action. In a recent conversation witli Dr. R. G. (Airtin, of Phila- delfdiia, I was surprised to fin<l that he strenuously objects to such hirge doses on the ground that it is likely to protlucc short aud irritable systoles instead of long and strong contractions of the ventriele, suf-h as are required to drive the Idood onward ener- getically. He thinks that the neurility of the cardiac nerves and ganglia become exhausted. He stated, moreover, that he was gratified to find, during a recent visit abroad, that such experi- enced clinicians as Ernest Sansora and Lauder-Erunton do not exhibit the agent in large doses, contenting themselves in fact with 3^0 of a grain three or four times daily. Such opinions are worthy of consideration, and are here given in the hope of stimulating original observation on this point. It is difficult to abandon notions that have dominated one for many years and
446 DISEASES OF THE HEART
seem to have the support of favourable experience. I feel sure that under the influence of such large and frequently repeated doses I have seen a weak heart rally and evince signs of aug- mented power. I have certainly known a dying heart to be kept beating for hours and days by the combined use of strychnine and nitroglycerin after speedy death seemed inevitable. There can be no doubt of patients becoming so dependent upon this medi- cine, when taken for a long period, that they develop a strychnine habit, the same as a morphine habit. Only the former is not so harmful nor so diflicult of abandonment.
Whatever may be the answer to this question of large or small dosage in cases of dire urgency, I would not wish to be thought to advise them when cardiac power is only beginning to fail or cannot be said to be entirely competent. In the stage now con- sidered it would probably suflice to prescribe ^ or at most ^ thrice daily. The length of time during which this agent is to be continued must depend upon the circumstances of each case, and therefore is to be left to the judgment of the medical attendant.
The value of the nitrite compounds has already been stated in speaking of the vaso-constrictor effect of digitalis. It may be said in addition that these agents are often highly beneficial in the treatment of aortic regurgitation even when digitalis is not indi- cated. The earliest premonition of failing heart-power in these cases is sometimes shown by attacks of vertigo, and occasionally by syncope, in other instances by a " pounding action of the heart," to quote the language of the patients. These symptoms are an indication that arterial tension is outstripping the contract- ing force of the left ventricle, which is consequently unable to suc- cessfully cope with the heightened peripheral resistance. Digi- talis augments the vigour of cardiac systole, but it also still fur- ther raises arterial tension, and hence may increase rather than lessen the tendency to palpitation. It is better, therefore, to try the effect of ^-Ju, or it may be less of nitroglycerin three to four times daily for the removal or reduction of undue vascular ten- sion, in the hope that the symptoms will disappear without re- course to digitalis or strophanthus. Glonoin stimulates the heart only indirectly by causing vaso-dilatation, and thus removing ob- stacles in its path, so to speak. Excepting, therefore, as a vaso-
THE TREATMENT OP VALVULAR HEART-DISEASE 44r7
dilator, nitroglycerin ia rarely to be employed in this stage of valvular atTcc*tioii3,
A perusal of the cases narrated in this chapter will impress the reader with tlie groat benefit often derived from cathartic remedies, and the important role played by them in the nianage- inent of patients. Their utility was first really impressed upon me by the writings of English authors, and to their teachings I owe much of my success in the management of cardiopathies, I shall have more to say on t)iis subject farther on. It will suffice at tliis time to direct attention to the tendency of most valvular lesions, especially mitral and those of the right heart, to conges- tion of the veins of the abdominal viscera even before signs of compensatory disturbance grow pronounced. These congestions cannot be so surely and (piickly relieved by any other means; often they cannot Ik* removed at all without recourse to purga- tives.
If all that was needed was to increase the driving force of the left ventricle, and thus to push the venous blood onw^ard, then digitalis would be the remedy par excellence. In these valvular diseaseSj however, there is an impediment to the tlow ut venous — i. 0., of the return blood through the lungs and heart. Behind this impediment the circulation becomes dammed up. The surest mode of preventing an inundation is to jirovide an outlet, and this is done by carrying off some of the water of the blood through the intestines. When this has once been accomplished, tlien a heart 'tonic or Btinuilant may be able to reinstate a satisfactory degree of circulator}* equilibrium. In some cases it is impossible to do more, or even hope to do more, than keep the stasis w^ithin bounds and render the heart's labour somewhat easier. Aloes, cascara, etc., which unload the colon relieve constipation when it exists, biit they do not occasion free watery stools, such us are needed to deplete the engorged portal ami tributary veins. To this end, saline preparations or such other drugs as are not too drastic are required. Of these, nothing is more efficient than sulphate of magnesia in saturated solution or dissolved in hot water and taken half an hour before breakfast. Its taste ia very objcHi't ion able to some persons, and it is sometimes rejected by a sensitive stomach. In such an event it is better tolerated if to it are added half a dozen minims of the ordinary essence of ginger
448 DISEASES OF THE HEART
kept in every household. Four ounces of the compound infusion of senna, the familiar " black draught " of the English, make a very potent and not especially disagreeable hydragogue cathartic Pulvis jalapi compositus is also highly efficient, and by me greatly esteemed. A teaspoonful may be taken by the average individ- ual, whose venous stasis is pronounced, without his being unduly weakened thereby. There are many other remedies having a simi- lar action, of which space forbids mention.
Of all, however, there is nothing which will ordinarily pro- duce such happy results as calomel or blue pill. That they power- fully affect the circulation and promote excretion is shown by the diuresis they promote even before they have emptied the bowel. It is generally well to administer the mercurial at bed- time, and have it followed next morning by a saline. The fre- quency with which such cathartic medication is to be employed will have to be determined by the degree of stasis and the diminu- tion that ensues.
Patients with valvular disease are often ana:»mic, either be- cause the liver is unable to utilize nucleo-albumins in the manu- facture of iron, or in consequence of the destruction of hsemo- globin by some ferment generated in the intestines. The so-called hivmatics, iron, arsenic, and the hypophosphites, would appear to be indicated, therefore, and certainly do act as a tonic, but to my mind it is doubtful whether tlieir beneficial effect is not due to their improving ai)})etite and digestion rather than to their directly increasing the percentage of lurnioglobin.
^fedicines that always appear to me to be of positive utility are all those that facilitate the better digestion of food and lessen the likelihood of gastro-intcstinal fermentation. These are pep- sin, pancreatin, taka-<liastase, dilute hydrochloric acid, the sim- ple bitters, and the various antiseptic remedies, salol, salophen, benzonaphthol, etc. The use of these agents, together with the improved function of the digestive organs incident to the re- lief of stasis by catharsis, has always seemed to me to do more towards the lessening of the spanapmia than do iron and arsenic.
Best. — Leaving now the consideration of medicinal remedies, we come to certain other factors that are of utmost importance in the restoration of compensation, and of those rest takes the first place. It is universally recognised by practitioners that for weak-
TIIK TREATMENT OF VALVULAR HEAUT-DLSEASE
449
ened hearts no measure is so bonetieial as physical repose in the reeiiiiiljeiit position. Not so with tlie laity, and putients fre- quently persevere with some form of exercise in the mistaken notion that therehy they will regjiin strength. So soon as a heart that is damaged by endocardial disease exhibits signs of being sorely overtaxed, physical exertion shoiihJ be interdicted and the patient pnt at entire rest until conditions are improved. The rea- sons for this are not far to seek, being fonnd in the mechanical effect on the circulation and in the resulting improvement to eiir- diae nutrition.
When in valvular disease couipensiation is imperfect, absolute physical rest for several weeks seldom fails to prove highly ttenefi* ciah The heart is not compensating, because it is being overtuxetl by having to receive and discharge more blood than it can handle easily. If in such a case the patient is put to rest, active muscular moveuieiiis are aI>olisbed anti respiration is less ra|dil and more shallow. W'uous bh:>od is deli%'eretj to the right auricle less rap- idly and the right ventricle is given less work to do. Cardiac contractions become less frequent, but more efficient, and its cham- bers are better able to empty themselves. Thus the decreased inflow and the increased fjiittlow tend t<i dimiuisb tlibitatinn and prouiote tlie re-establishment of that preponderating hypertrophy essential to compensation. Improvement of circulation is shown by the better quality and rhythm of the pulse, by the reduction of signs of stasis, and l>y augmented excretion of urine. There is improved visceral function in general, and there is better nutri- tion of the whole Imily as well as of the heart-muscle. This tatter, which is of great iiniKtrtance if cardiac jjower is to be maintained, also results directly from the fact that physical repose favours a b€*tter coronary circulation.
With the slower action induced by physical inactivity ihe heart tends to gain in |>ovver, and tlie left ventricle to discbarge a pater blood-wave into the aorta. The coronary arteries are bet- ter tilled, and the heart-muscle receives a supply of blood more adequate to its nee<ls. This, however, is but a part of the benefit to the heart prcK^eeding from enforced rest, particularly in cases of mitral and aortic obstruction. It has been explained how this treatment lessens cardiac dilatation. It is the right heart chiefly that profits in this way, the ventricle emptying its contents more 29
450 DISEASES OP THE HEART
completely, and stasis in the auricle being diminished. This now acts favourably on the circulation in the coronary veins. With lessened intra-auricular blood-pressure resistance to the outflow from them is less, owing to the fact that they empty into this auricle. Stasis within them tends to subside, and with a better circulation the products of cardiac metabolism are more fully removed.
Let us now consider the benefit resulting from rest in the indi- vidual valve-lesions of the left heart. In mitral stenosis there is practically a dam built across the blood-stream at the point where the blood coming from the lungs is poured into the left ventricle. So long as compensation exists the hypertrophied left auricle and right ventricle are able to discharge over this pathological dam — that is, through the narrowed mitral ojiening — so large a portion of the blood sent through the lungs that serious congestion within the pulmonary vessels does not take place. When compensation begins to fail, and cardiac contractions to grow more rapid, the diastolic pause, during which the left ventricle is expected to fill, is shortened, and time is not allowed for the left auricle to empty its contents.
Stasis begins in the parts back of the stenosis, and grows ever greater with the progressing loss of compensation. Something must be done to diminish the rapidity and volume of the stream pouring into the left auricle. This is precisely what is accom- plished by rest. Diastoles are lengthened, more time is given for the filling of the left ventricle, which consequently throws a larger quantity of blood into the arterial system, and there is a tendency to restoration of the proper balance between the aortic and pul- monic systems, on the one hand, and the great arterial and venous systems on the other.
In mitral inconipetonce there is a systolic reflux into the left auricle, and the stream entering this chamber from the hmgs is momentarily checked, to be the next instant unimjKjded as diastole succeds systole and the blood gushes into the ventricle. Yet, while there is a momentary checking of the flow in the pulmonic vessels and an inevitable tendency to back-pressure, the column of .blood into the left auricle and pulmonary veins, together with the walls of these vessels and of the auricle, serves to resist the regurgitant rush from the ventricle. So long, therefore, as this resistance is
THE TREATMENT OF VALVl'LAR IlKART-raSEASP:
451
effectual (*ardiac adequacy is uu impaired, and evidences of stasis are wanting.
When this corupeiisation begins to fail, it is necessary to re- lie%'e the walls of the left auricle, the pulmonary vessels, and the ri^iht ventricle fruin overstrain l>y lessening tlie frequency of re- gur|*;itution and by retarding the tltjw from the systemic veins into I he heart, and lungs. Rest accomplishes this, and thus proves a p+>werful factor in tlie resumption of Ixeart-power and the renioval of stasis.
In the same way also as in mitral stenosis the coronary veins are hetter ejnptieil nud the coronary arteries are better flushed, nutrition of the lieart-nmscie is improved, the aortic system re- ceives m«jre b]oo4l with each systole, and an improv^ed general nutrition results.
When in anrtic obstruction com{>ensatory hy|>ertrophy of the left ventricle begins to yield tn dilataliun, the contents of the ven- tricle are no longer adequately driven through the stenosed oritiee. Signs of stasis appear and increase in proportion to loss of com- pensation.
Two things are now required if the threatening breakdown is to b(^ averted: (1) More forcible contracti«tns on the part of the left voniricle, and (2) the delivery of less blood to the ventricle. Rest slows the heart by lengthening its <liastoles, and but little if at all its systoles; while if it affects the vigour of the latter^ it does so only indirectly hy relieving it of strain and improving its nutri- tiuu. It can do very little, therefore, towards enabling the left ventricle u* drive blood through the narrowed aortic orifice, and, moreover, exjierienee has taught that when in this disease the left ventricle begins to weaken, it is an indication that the stenosis has overpowered the ventricle. All that is left is to spare this chain- her as far as jKissible. It is by accomplishing this, or the second requirement mentioned above, that rest is of scrvire in aortic ste- nosis. It serves to retard the flow of blood into the left ventricle, and thus to lessen the amount which this chamber is reijuired to dischargp past the point of constriction. Therefore, although this therapeutic measure is of service in conserving heart-i>ower in this affection, it cannot accomplish such brilliant results as in mitral disease.
In aortic regurgitation failing compensation means impaired
452 DISEASES OP THE HEART
resistance on the part of the left ventricle to the distending force of the regurgitant stream, a still more imi)erfectly sustained blood-pressure in the arterial system, and after a time secondary overfilling of the veins, right heart, and hmgs. The danger lies in sudden diastolic arrest of the left ventricle while the mitral valve is still competent, or in such a dilatation of the ventricle that relative mitral insufficiency with all its consecutive evils is pro- duced. The yielding left ventricle must therefore be relieved of dangerous overstrain. Inasmuch as physical exertion and the erect position are thought to raise intra-aortic blood-pressure and intensify the regurgitation, the removal of these injurious, even dangerous, influences becomes imi>erative. This can only be ac- complished by a rigid, and often prolonged, confinement in the re- cuml>ent position.
There are also two other reasons for insisting upon rest in these cases: (1) Physical inaction slows the flow of blood in the systemic veins, and thus tends to check the discharge into the ven- tricle from the left auricle. With this stream, as well as the re- gurgitant one reduced, the disabled ventricle is called on to handle less blood and finds its lalx)urs diminished. (2) Rest of body means also rest to the heart, since by slowing down its contractions its diastole or poriotl of repose is lengthened, while the actual amount of work re<|uired of it is reduced.
It limy be argued that the lengthening of diastole favours a better filling of the ventricle, and therefore compels it to put forth greater eiTort in order to discharge this larger amount of blood. This would be so if the flow to tlie left auricle were not retarded ; but this latter being the ca^^e, there is not so much likelihood of overfilling the ventricle as when the patient is up and active. This consideration, however, renders it probable that the chief benefit of rest lies in tli(» rest to the heart-walls and in the less forcible reflux from tin* aorta.
The mechanical conditions existing in this lesion, and the nature of the pathological changes that take ])lace in the myocar- dium, HMider prognosis excefnlingly grave whenever a case of aortic incompetence shows signs of failing compensation. The ])robability of restoring heart-])ower is so slight that any means, however unpromising, should be made the most of. Accordingly, rest of body and mind must be enforced with greatest rigour and
THK TR?:aTMKNT of VALVrr.AR IIEART-PISKASE
453
for an iiRlofinite length of time, not merely for weeks, InU. for many months. As a matter of faet, tlje prospect of rc;[jaining car- diac power in serious loss of cyiypensation is poor, and rest is of service mainly in jirolonging life.
Since, then, rest is so valiialde a means of treatment in onr attempt to preserve or restore cardiac adei]iiacy in uncompensated valvular disease, the physician must not content himself with par- tial obedience. If the case is urgent, he must see that his orders are carried out faitlifnlly, Wien a patient is told that rest in hcd is needed, he must l)c made to understand that hy it is meant nut rest for a few hoiirs each day, hut rest hoth day and night, ^[iireciver, it does not mean that he can get up as often as he pleases tn fetch some article he wants or to walk to the tcdlet, that is situated |>erl)ajis a short distance duwn the ludL It means that he is til nnnaiu in hed, and is to have the attention of a nurse who can spure him all avoidalde effort.
Patients sutlering witJi aortic insufficiency require more rigid euforcement of ahsf>!ute rest than do most persons with mitral disease. A single indiscreet ri!urt may undo nU that has heen gained hy weeks of iuaetiuii, "riieri'tV>re, such a patient who is struggling to |>reserve his left ventricle from complete destruction must lie as quiet as possihle, njaking use of the l>ed-pan and urinal hotth\ and taking liis meals in the dorsal decubitus. If this is impossilde, as is Sitmetiiues tin- case with nervuus individuals, then fln\v may he lifted a Ittrte higher hy the nurse, and, sup- portc^d hy ]ullnws, may take their riieals in this position. Better yet is tiie adjustahle hed, which [tt^rmits every fwissilde position, without the slightest exertion on (he part of the patient*
Of course eacli case luis to he treated on its own merits and according to its own exigencies. One [>alieiU may he permitted partial I'est, and yet fhi well, while annihi^r nuiy rei[nire the strict- est tvtifurcement of lids principle of management. In some cases, also, the attempt to carry out rigi<l confinement to bed for tnonths, no matter how important it may be, is sure to create snch a spirit of restlessness and discontent as will counteract all that is gained by physical repose. It is evirlent, therefore, that judgment and tact are often recjiiired in the enforcement of this therapeutic agency.
Finally, when asked, as he is sure to be, how long rest is neces-
454 DISEASES OF THE HEART
sary, the physician should not bind himself to any definite time, but should let it be determined by results.
Exercise. — When at length under the influence of enforced rest secondary congestions have been lessened or removed and the heart has regained a sutHcient degree of strength, the patient may be permitted to gradually resume exercise. At first he may walk slowly and for a brief jK^riod about his room, care always being observed to avoid such a length of walk as causes fatigue, or such sudden eflForts as produce shortness of breath and palpi- tation. By degret^s the walks may be extended until the patient is able to leave the house and stroll leisurely in the o]>en air. He must not, however, ascend stairs or hills until by proper exercise on the level his heart has gro^\^l equal to the eflFort. Aproi)os of hill-climbing, a word may be said of the Terrain Cure, or Oertel's plan of having patients with weak hearts develop cardiac power by ascending gentle acclivities. It consists in having a patient walk slowly up a gentle incline at such a pace as does not occasion dyspnu^a or consciousness of a laboured and rapid action of the heart — infallible signs of cardiac strain. Then, when an ascent of a certain grade has been mastered, a slightly more diffi- cult slo])e 13 to be attempted and overcome in the same careful manner as before, and thus paths of greater and greater steepness are surmounted. It must always be enjoined uiK)n the patient that he is to make these ascents with great deliberation, not i)er- mitting himself to talk during such efforts, and stop])ing to rest whenever his breathing grows short or his heart begins to pound. It is possible in this nuinner for weakened hearts to attain much greater endurance, even to develop hypertrophy. Experience has demonstrated, however, that it is particularly suited to cases of myocardial weakni^ss rather than of valvular disease. When a mechanical impediment to the circulation exists, as in stenosis or regurgitation, hill-climbing is dangerous, and ])atients are very apt to ovenlo. Furthermore, Oertel's method has to be v(»rv care- fully supervised if it is to bring about good and not ill results. Consecpiently, it is but little employed as compared with other modes of treatment, and for cases of u n com i>en sated valvular lesions is rarely advocated.
The one system involving physical exertion which gives the best results, and is adapted even to most instances of uncompen-
THE TUEATMENT OP VALVULAR HEART-DISEASE
455
sated valvular disease, is that forming a part of Nauteim treat- ment, und which will now be deseribed.
Resistance Exercises. — These consist of voluntary moveraeuts by the patient of tlexioii, extension, and rotation of the extreTnl- ties and tnnik, wlneli efforts are carefully resisted by an attendant trained to the work. Xnt only nmst the attendant understand huvv to resist the patient's iu<ivriiients without constricting the part to which he ai>plies resistance, hut he must so adjust his comiter-pressure ti» the patient*s strength as to not oeeasion res- piratory or circulatory end^arrassinent, lie nnist therefore be suffi- ciently skilled to deti^ct signs of distress and to judge whether to^i) great nr ttK» slight resistance is being offered.
The indications of respinitory and circulatory embarrassment, ft)r which the attendant is to watch, are dilatation of the nostrils and sighing or irregtdar hreathingj increasing duskiness or pallor of the comitenance, a drawn look about the month, yawning, per- 8j)iration, iind palpitation. So soon as any of these signs are de- tected the movement is to he stopped and the patient's extremity slowly allowed to assume a position of rest. Then, after a suffi- cient iH?riod for repose, the exercises may l>e resumed* Patients are very apt to hold the hreiitli while executing these mo^'ements or to hold the boily rigid, thus putting forth effort with more than the lind) thrit is being resisted. The attendant should tlierefore remind the patient from time to time to continue breathing, and should see to it that his pose is easy and unconstrained. Atten- tion to these points will enable a patient to go through the aeries of movements without fatigue or strain. Furthermore, the same movement is never to he made hvive in suevession^ and each one is to be folhfwed liy a brief pause. It is also wtU in some cases to allow the individual to sit and rest oc*casionally during the treat- nient. As liis endurance grows, such prec»autions bt^xane less and less necessary, although the atteindant must ne%'er allow himself to be thrown off his guard and forget to maintain close w^atch of the patient's condition, ilany persons of considerable muscular strength are inclined to regard the exercises as too easy and to think no benefit can accrue from such gentle exertions. They consequently want to have more resistance offered ; but to all such requests the attendant must turn a deaf ear.
The last injunction tp be observed is to have the movements
,466
DISEASES OF TOE HEART
made slowhj and without jerkiness. Unsteadiness of movement is certain to be produced if a slow niovenient, particuliirly uf the arms, is too strongly resisted* Tlie objeet or purpose (»f these exercises is not to devehjp the uiuseles, but to influenee the heart und circu- lation ; all of which is only aeeumplisheJ when the various move- ments are executed slowly and steadily, and the eounter-resistanee is accurately adjusted Uj the patient's strength- — that is, his car- diac not his muscular strength.
Finally, the operator imist not grasp the patient's arni^ wrist, or leg, as the ease may be» for this woidd hinder the free play of the musch»s, but lie is to exert counter-pressure or resistance by placing the palmar surface of his hand or fingers against that side of the patient*s liudi which htoks in the direction tovvanls which
the extremity is to be moved. It iiften conduces to steadiness of movt*nient for the assistant to place his otiier hand against some uther part uf the lind> tn* trunk than that to which resistance is a^iplied. The following deserip tittu gives the exercises in the Hrder in wliicli they are usually executed :
(1) The arms are extended
in front f4 the hrMly on a level
with the shoulders and with the
]ialms of the hands touching.
They are then slowly aud slt*adily
moved outward until at a line
with the front of the t*hest, while
at the sauje time the attendant
gently resists this horizontal
movement. The attendant now
changes his hands, so as to insert
pressure against the palmar surface of the wrists, and the patient
slowly and steadily brings his arms back to the position whence tlie
original movement started (Fig. 84).
(2) The right arm hanging at the si(k% with the palm of the hand forward, the forearm is slowly flexed against counter- resist-
THE TREATMENT uF VALVrLAlL IIEART-DLSKASE
«nce bv the attcmliuit until the fingers tuiieli tlie front of tlie sliouldor. The attendant llien eliauges his point of pressure to the back of the ami, and the extremity is slowly returned to its former i>osition at the side (Fig. 85).
(IV) Tliis consists of preeisely the same movement^ but exo- ented by tlie left arm.
(4) Both anus, depending at the side, are slowly raised lat- erally until the tlnunl)« meet above the head, and are then brongbt down to their original position, these movements being eare fully rei^istetl throngboul.
(5) The patient clinehes his hands in the form of a fist, but with the thnnjbs extended npon the ulnar surface of ibe index ti uge rs. The tips c»f the thiiujbs are tlien gently pressed tfigether in front of the alt<h»men, iind, a ]irf»iK*i' ilegree of resistance Inking offered, they are thus slowly raised until the bands rest on the top of the head, after wbieb tli(\v are slowly lowered tu the original pfisitiun ( Figs. Si\ and H7).
(♦1) Hie arms, depending n\ the sides, are then elevated for- ward and u|»war(l without brnil- ing lliem urjtil fhey are lield ahdt on a line with the [lerpendienlar axis of the body. They are next slowly a 111* wed to resume their jKisition at tlie side in I lie same eareful uninner in wlueli they were raised. To properly resist this nioveinent requires nuu'b praetiee ami skill, ff»r the reasnu
that the hand f>f tlie attendant nmst lie cuntinnally slipiH^l around the patient's wrist to suit the changing attitude, first to the liorizou* tal and then the vertieal (Figs. SS and 89).
(7) Starting with the arms hanging at the side, the right arm is slowly rotated forward, upward^ backward* and downward arotmd the shonlder-joint as the jnvot, and then in the reverse
Fio. 85.
Fla. ti^
Fiii. b*J,
458
THE TREATMENT OF VALVULAR OEART-DISEASE
459
direction until the circle is couiiileted, counter-pressure being all the time exerted by the attendant.
(8) This consists of a simihir iimvement, cxeented by the left arm. These two movements are difficult both for the patient and the attendant, and should not i^e given to patients who are very weak or whuse hearts are ineapable of withstanding much exer- cise. Resistance to this movement is likewise extremely diHicult, for the reason that the attendant has to change hands during the progress of the movement, yet without causing jerkiness oi too much inferference.
(iM Tbe jTatiiiit ln'iid.s his IhkIv forward at the hijis with- out flexing his knees, and then brings it back to tlie erect position, while the attendant, standing at his side, resists the forward movement by one hand aiiainst tlie upper part of the sternum and the other in the middle of the back, and the return movement of the trunk by one hand against the upper dorsal region and the other upon the epigastrium (Figs. 00 and 91).
(10) Standing with the feet firmly planted upon the floor, the patient rotates his trunk around its vertical axis, at first to the left, next to the right j and then back, so as to face forward, aa before starting. The attendant resists this movcTiient by placing one liand against the advancing shoulder and the otlier in the opposite axilla, and then changing his hands as the Ixnly is rotated in the opposite direction (Fig, 1l>2).
(11) In this movement the trunk is bent laterally, first in one direction, tlten in the other, nnd histly is brought at rest in the upright posture. To resist this flexion the attendant places one hand on the hip and the other against the side of the chest towards which the Wdy is to be bent (Fig, fJ3).
(12) Both arn>s hanging at the sides, with the palms facing towards the thighs, are simnltaneonsly moved backward an<l n|jwiir<l as far as |X)ssible without bending the bo<ly, and are then brought down to the sides, resistance meanwhile being carefully exerted by the attendant (Fig. 94).
(13) The patient supports himself by resting one hand on a chair, and then raises the opposite leg as far as possible in a lat- eral direction, w^hlle ihe attendant resists both the upward and the return movement (Figs. 93 and 96).
Fio. m
Fig. y^.
Flu. s*a.
4G0
flO. i»6.
402
THK TREATMENT OF VALVULAR IIEABT-DISEASE 4**3
(14) This is the same movement, hut rlone with the opposite extremitv.
(15) Resting one hund on a duiir, as before, tlie patient extends his opjwsite leg and thigh, hut without bending his knee, as far forward and npwartl n^ passible, sifter which the extreuiity is skm'ly returned to its original position, resistance to hotli movements being offernl
by the attendant (Figs, 1*7 and t»S ).
( IH) This is a simihir effort pnt forth by the oppusite ex- treniily.
(17) Both hands ^supported on the back of a ebair, one leg is flexed at the knee while re- tsistanee h otfered by the attend- int'ti baml pbieed at tlie heeb The return is resiste<l by the band against the ankle jnst above the instep (Figs. IH* and 100).
(IS) This is a corresponding movement by the other leg. re- sisted in the same manner.
(Ill) Supporting liimself by the back of a ehair the patient flexes his thigh at the hip, the
leg banging limp and flexed, while the attendant resists first the upward and then the downward movement (Figs. 101 and 102).
(20) This IS a similar movement l)y the opposite thigh.
If desired, adilitional movements of flexion, extension, and rotation of the bands and feet roay be devised. In carrying out these exercises care should be taken that movements involving the use of the same groups of muscles do not succeed each other directly, but are interrupted by exercises made by diiferent sets of muscles. The purpose of this precaution is the avoidance of undue muscnhir fatigue of weak patients. Given with requisite deliberation, and with sutEcient pauses for rest l^tween move- ments, such a series of resistance gymnastics ordinarily takes about
Fio. ioa>
464 DISEASES OP THE HEART
half an hour. If after a rest of ten to fifteen minutes the patient does not feel or evince fatigue, he may then rei>eat the series. They are generally given daily, an hour or more after a meal. Patients whose condition is fairly good may he allowed to per- form them iwice a day — that is, in the forenoon and again in the afternoon.
These exceedingly simple exercises are a powerful agent for good or a means of great harm, depending on the manner in which they are given and the condition of the heart. I do not believe they should be given to patients whose comjKjnsation is wholly gone. In this opinion I differ, I think, with Schott and Bezly Thome, who have written so much in praise of them. If there is pronounced stenosis of an orifice, wnth great dilatation of the chambers back of the lesion, harm may follow^ their emplojTnent, the same as with digitalis incautiously given. This was sadly illustrated in one of my cases. First lessen the cardiac inade- quacy by rest and other treatment, and then these movements are likely to prove highly beneficial. In more than one patient, whose enormously congested liver had refused to subside imder the free and prolonged use of cathartics and heart-tonics, I have seen the organ diminish rapidly in size during the administration of re- sistance together w-ith breathing exercises. It seemed as though they served to bring about an aspiration of the blood out of the engorged liver. They arc far superior to massage, which seems to me to ])roduce just the opposite effect. Massage promotes a more rapid and ampler flow of blood to the heart, while resist- ance movements are thought to exert their sahitjiry effect by dilat- ing the arterioles, and thus unloading the overburdened heart.
Nauheim Baths. — TIkj balneological treatment of heart-disease has not received as much attention in this country as in Europe, and yet it has been growing in j)opularity even here. Large num- bers of wealthy Americans and Englishmen annually make pil- grimages to Germany for treatment at the little resort known as Bad Xanlieim, where the employment of cool saline and efferves- cing baths was first introduced in this class of affections. Patients of moderate means cannot afford so expensive a journey, and must either forego this treatment altogether or content themselves with the use of artificially prepared waters. For the consolation of such it may be stated that ample experience all over the world, but
THE TKE^TMEXT OP VALVULAR IIEAUT-DISEASE
465
partieularlv in Englaiid, has sliowTi that oqimlly efficient results may be obtaiiieil in this way as at Bad Nauheini. I myself took a course of haths at that resort in the summer of 181*3, and ever since mv return have been employing this plan of treatment in sui table cases, and can justly claim priority in this regard over all others in this country, I have nut desired to make a fad of this treatment, and therefore have not subjected as many patients to it as might have been donCj hut it is within hounds to say that considerably over one hundred have thus been treated by me. Some of my patients have taken the baths in GennanVj generally after a course in Chicago, although one has just finished here who hag previonsly treid the baths at Tlad Xauheim, All agree in the statement that the effects with artificial waters are the same as with the natural, the chief and perhaps striking difference consisting in the more powerful effervescence of the latter, par- ticularly in the form of the Spmdel-Strom-Bad (flowing effer- vescing bath). Another advantage in favour of the latter lies in the consideration that when a patient goes to Germany he leaves his cares behind him, and while there abandons himself to the one purpose of getting welL On the other hand, I have been assured that, owing to the immense numlx^r of invalids who frequent the place, patients are apt to miss the watchful care and oversight which many of them require and receive at home.
The waters of Bad Xauheim are impregnated with various chloride salts, the two to which particular virtue ia attributed in their effect upon the circubition being the chlorides of sodium and calcium. In addition, the springs used for the preparation of the baths are highly charged with carlionic acid, which makes them very stimulating, particularly when used in tlie form of the flow- ing bath — that is, with a steady stream of effervescing water flowing over the body of the bather in the tub. This is compara- tively rarely prescribed, being considered too exhilarating for any except those in fairly robust healtli. It is the rule in the emplnyment of this balneological treatment to begin with water of a temperature of 9'V^ to 05*^ F., according to the ability of the patient to react, and with water containing 1 per cent of Sfxlium chloride and ^ per cent of calcium chloride, but no carbonic acid, this latter being added at the end of the second week, or w^hen a temi>erature of 91- to 90^ F. has been attained. The duration of SO
4:66 DISEASES OP THE HEART
the first bath is from five to eight minutes, depending upon the strength and reaction of the individual. One treatment is taken daily for two or three successive days, and then comes a day of rest. This is to prevent undue depression, as is likely to be expe- rienced when no interruption in the course of treatments occurs. The patient is required to rest, by preference lying down, after each bath, and if reaction is not good and prompt to take a warm drink of some kind and to cover up warmly. He is also required to see his medical attendant daily, or as often as the latter may elect, that the eflFect of the treatment may be judged of and the baths modified as his progress requires. The principle underlying the ordering of these is that the percentage of the ingredients is to be increased, the temperature lowered, and the duration length- ened until finally the chloride of sodium reaches 3 per cent, chlo- ride of calcium 1 per cent, the temperature 87° or 85° F., and the time twenty minutes.
The rapidity Avith which this change can be effected depends upon the degree of objective and subjective improvement ob- served, but as a rule this maximum is not attained under three or it may be four weeks. In the more serious cases, or such as ex- hibit considerable ansemia and sluggish reaction, it is not always wise to bring the temperature below 89° or even 90° F., although the maximum in strength and duration may be the same as when lower temperatures are prescribed. It is not well to reduce the temperature more than a degree at a time, and whenever this is done the proportion of the salts is usually increased. For the most part effervescing baths are ordered at the end of ten days or two weeks, or when the higher percentages of salts have been reached; but if the patient is inclined to chilliness at a temperature that ought to produce at least a tolerable feeling of warmth, or if afterward the extremities are cold and the skin does not get into a good glow, it may be well to add the gas at an earlier period. The warmer saline baths, 95° to 92° F., are con- sidered soothing, while the cooler effervescing ones, 89° to 85° F., are stimulating, and hence are not applicable to very w^eak hearts.
The direct effect of each bath should be to render the pulse slower, of better quality, and more regular if previously irregular. The area of deep-seated cardiac dulness diminishes and the heart- sounds grow stronger. Endocardial murmurs intensified by dila-
TIIE TREATMENT QF VALVULAR HEART-DISEASE
467
aiion may lieeome less loud, or if weak from canliac asthenia, may after the batli Le foimd to be more intense. The degree of henofit is to be determined cliietlv by the size of the heart and by the character of its action. As a role, also, the patient is con- scious of a sense of well-being and of some lessening of whatever symptoms have annoyed hiuL
If the treatment has been judiciously ordered and overseen j tlie heart is found to gain in strength week by weekj visceral con- gestions diminishj as evinced by increased diuresis, the colour of the skin grows more like that of health, and the patient gradually gains in vigour and ability to exercise without discomfort.
Just how this balneological treatment brings about improve- ment is still a matter of speculation and discussion, l>eing by Schott explained on the hypothesis of increased tissue change together with a reflex stimulation of the heart which causes its slower and more powerful contractions^ and w^ith a physiological stimuhition uf the arterioles and capillaries by the passage of the gas and salts through the skin. By others, in particular Broad- bent, the beneiicial action of the baths is attributed to dilatation of the cutaneous caiiillariesj in consequence of which resistance to the work of the left ventricle is lessened and the transfer of blood from the venous to the arterial system is promoted. The olijcction urged against this explanation is, that the rate of the pulse should be increased rather than decreased, so that there must be some additional influence at work. The following is the view of Mcdicinalrat Groedel of Bad Nauheim: *^ The incon- testable success which our baths have on the heart's function and the entire circulation is only to be explained if we believe in a direct action by w^ay of the end-organs of the cutaneous nerves on the central vascular and cardiac nerv^ous system, both trophic and motor.-- It may also be stated that so far as concerns the demon- strable effect of the two means of treatment, the resistance gym- nastics and the baths, the results if not the action are identical in diminished size of the dilated heart and improved energy and steadiness of its contractions. Consequently it is customary at Bad Nauheim to have the patient receive both forms of treatment each day. Finally, it is usual to send the patient away at the close of a course of baths for a rest of a month to six weeks, after which he returns for another course known as the after-cure.
468
DISEASES OF THE HEART
Inasmuch as the effect on the heart and circulation of the arti* ficial and natural waters is iJeoticalj 1 will now describe how the former are prepared* The ingredients required are common salt (chloride of sodium) and chloride of calcium, hicarhonate of so- dium, and eomiJressed tablets of acid sulphate of lime. Instead of these latter, commercial hydrochloric acid may be used. The first is to he had as ordinary ** butter salt *■ of the trade, while the calcium salt comes in irnn drums holding from 600 to 800 pounds. This latter is, moreorer, deliiiucsccnt, and, being corro- sive, is most conveniently kept in a strong solution of definite strengtlh I have it kept on hand by one of the Chicago druggists, who dispenses it to my patients on my prescriptions. To begin with, the haths contain only these two ingredients, and are there- fore simple brine baths. It takes from 50 to 60 gallons of water in an ordinary-sized bath-tub to inmierse a person of average size up to his neck when lying in a semi- recumbent position. Wl^en the amount of water is known it is an easy matter to determine tbe number of pounds of salt and the number of pints of calcium- chloride solution to be added. When at length the water is to be charged with carlxuiic acid in addition, it is done by dissolving bicarbonate of sotia, 2 poimds to each bath, and the same number of ounces of commercial muriatic acid or the compressed tablets already mentioned. The acid is so corrosive and ditlicult to keep w^ithout its fumes injuring the furniture of the bath-nK>m that I now order tlie packages of '^* effervescing bath salts " manufac- tured for the pur]iose by two firms in New York city, and whicli are likewise kept in stock by the Chicago druggists. Each pack- age contains 2 pounds of soda and 8 tablets and printed direc- tions for their use. One such package is required for a single bath. These effervescing tablets possess this additinnal advantage over the acid, that the evohition of gas is steady and continuous. They are also, however, corrosive, and the bottom of the tub should be protected by a rubber shee:.
It is my custom to prescribe the baths in groups of three with the rest dav between — that is» on everv fourth dav — and a course tisually extends over a period of six weeks. In most cases the resistance exercises are also taken, but some hours prior to or after the bath, that the effect on the heart may be maintained* I alw^ays strive to impress patients with the importance of living
TBSIATMENT OF VALVULAR HEART-DISEASE
as quiet and routine a life as possible, and in particular to strenu- ously avoid undue cardiac strain that tliey may not destroy the benefit expected to be derived from the treatment.
I can recall only 5 cases in which this plan of treatment seemed to do harm rather than good* Two Mere instances of chronic mytx!arditis, the hearts being very dilated and their action arrhythnjic. One was a mitral lesion with uiMleioa and other signs of rather a badly destroyed compensation ; but as this patient was compelled to journey some distance each day to get his bath, it may be that the exertion thus required, and not the treatment, was responsible for the %vant of improvement. The reuuuning two were cases of serious vah^ilar disease complicated by pericardial adhesions. In both, the engorgement of the liver iH^eame mani- festly greater towards the termination than at the conimencoment of the coursej and the treatment Avas discontinued. All other patients have exhibited more or less improvement, w^hile in some instances this has been most gratifying both to the patient and myself.
I am very positive in my belief that this treatment should not be given to persons whose compensation is wholly hist, or indeed seriously broken, and therefore the consideration of this measure has been introduced in this portion of the present chapter. I have just finished giving a course of 30 baths to a lady with a pure mitral stenosis who, when she began, gave indications of fniling^ or at least threatened, compensation. The second sound at the heart's apex was wanting, tliere being only a presystolic murmur and sharp first sound. She complained c»f much ill-defined dis- comfort at tlie heart, and the pnlse was rapid and exceedingly feeble. Before the course was completed the second sound had returned at the apex, the area of cardiac dnlness was distinctly smaller, and the pnlse was slower and of greater volume. She declared she felt perfectly well. Tn this instance, as is often my habit, I ordered the fretjnent use of a laxative water, and for a time 5-drop doses of fat-free tincture of digitalis thrice, then twice, and at last but once daily. I do this because it has seemed to me that in this way I have secured more lasting results.
Contra-indications to the employment of this balneological treatment are tlie following; Aortic aneurysm, pronounced and extensive arteriosclerosis, and, in my opinion, all eases manifest-
4:70 DISEASES OP THE HEART
ing marked signs of cardiac inadequacy, such as ascites and con- siderable dropsy with a greatly distended and feeble heart, and cases complicated by extensive mediastinopericardial adhesions. Chronic renal disease does not contra-indicate the treatment unless, of course, it has led to too pronounced a degree of car- diac incompetence. Lastly, it may be stated that if the pulse does not grow of better quality after the bath, but, on the contrary, is observed to become less full and strong, the treatment will not produce beneficial results and would better be discontinued.
Diet. — This is a matter requiring in this stage of valvular heart-disease very careful attention, yet concerning which notions are for the most part woefully vague and inaccurate. Physiologi- cal chemistry has not yet worked out the changes taking place in the digestive process as a result of disease. We know that the passive congestion of the abdominal organs produced by un- compensated cardiac disease leads to a chronic catarrh of the stomach (Einhorn), with diminution and even disappearance of the hydrochloric acid (Uiifler and Jorn), which, with its im- paired motility, may seriously derange its function. Reasoning by analogy, we may also assume that the pancreatic and hepatic secretions are likewise altered in quantity and quality, or that if not secreted in less amounts they are poured into the duodenum in diminished quantity in consequence of catarrhal obstruction to thoir outflow. Just what modification in tlie character of the pancreatic juice takes place we do not know, yet clinical obser- vation seems to warrant the inference that the amylopsin and fat-splitting ferment are more unfavourably influenced than is the proteolytic ferment.
Furthermore, in consequence of sluggish circulation in the veins that carry blood to the portal system, the bile is absorbed slowly from tlie intestine, and when secreted is watery and poor in mineral constituents. Although the secretion of bile is but a minor function of the liver, still a deterioration in its quality and diminution in its quantity must exert a baneful influence upon intestinal digestion. These theoretic considerations are borne out by clinical observations, for cardiac patients are very prone to gaseous distention of the stomach and intestines and to eructa- tions and other indications of fermentation of the ingesta. The fatty acids thus engendered occasion still further irritation of the
TUK THKATMENT OF VALVULAR IIEAKT-DISEiiSE
471
stomaeli and establish a vicious circle which augments the evils primarily attributable to dialurbed circulation.
This is uut the only aspect of the case. There is alteration in the metabolic processes inciJent to derangement in the blood-sup- ply to the digestive and other viscera, while toxines are locally devtdojicd which either must he destroyed in the engorged and functionally impaired liver or must pass through into the general blood-stream and exert their noxious eifects upon the heart and nervous system. The investigations of llusche appear to show that the excretion of urea and uric acid is altered. The retention of the former is variable, while the excretion of the latter is hin- dered during disturbance of compensation and increased after this has been restonMb
It is not strange, in the light of the foregoing considerations, that some patients are greatly disturbed by fermentative indiges- tion after the taking of the simplest and most easily digested food. Dyspncca is intensified or developed, or they arc distressed by paliiitation. Others are not conscious of local disturbance, but complain of pains and aches, muscular stiffness and cramps, nerv- ous symptoniSj such as despondency, insomnia, and frightful dreams, fidget iiiet^s of the legs, and sundry other sensations that are so commonly attributed to uric-acid retention. It may be re- marked here, hovve%^er, that Dr. Weaener^s researches appear to show that these constitutional symptoms, as well as many others, are due not to uric acid, but to indicanuria and oxahiria. One of my patients was greatly troubled by headache, insomnia, and other nervous phenomenaj and Wesener's analysis of her urine col- lected at the time showed an enormous excess of indican and oxalic acid. Thereupon an attempt was made to stop proteids and administer cark^hyd rates in the hope of relieving her dis- tress. It was found » however, that at once she began to have so much flatulent distention of the stoma eh and b^jwels with aggrava- tion of her dyspncea that the non-nitrogen on a diet had to be aban- doned for a return to meats, etc., with all their evil consequences.
The problem of how^ to meet the food requirements of cardiac sufferers is a complex one and most difficult of solution when we have to do with the stage of imperfect compensation. It is quite generally agrcf^d that in cases of heart-disearG uncomplicated by retial lesions the myo<*ardium should be supplied with a relatively
472 DISEASES OP THE HEART
large proportion of proteids. The main reason for this lies in the fact that the nitrogenous principles are tissue-forming, and hence reparative elements of the dietary, and should be in excess when- ever there is a demand for increased muscular work, as is the case in cardiac affections. Moreover, meats and other foods rich in proteids do not undergo the same sort of fermentation and gen- erate so much gas as do carbohydrates, and do not so injuriously distend the hollow abdominal viscera. They are not so bulky, and therefore, relatively to the quantity ingested, contain a far larger proportion of nutrient material. For obvious reasons persons with imcompensated valvular lesions should have their dietary definitely ordered and carefully supen'^ised by their medical attendants.
It should be remembered that digestion and assimilation are both slow, and therefore the first rule to be laid down is that food is not to be taken at short intervals^ but ample time allowed for the stomach to empty itself before fresh nourishment is adminis- tered. The fatty acids and other irritating products of fermenta- tion often occasion a feeling of faintness or gnawing at the epi- gastrium which is mistaken for himger and thought to indicate a need for more food. In other cases appetite is poor and patients are unable to eat heartily at the regular meal-hours, and hence the friends and even the physician get the idea that the meals must be re-enforced by milk, egg-nog, etc., midway between. I have thus known nourishment to be administered every two or three hours. Such is undoubtedly a mistake. The congested and per- haps crdematous walls of the stomach cannot by energetic peristal- sis empty the chyme into the duodenum as rapidly as normal, and the conditions for decomposition being favourable, the taking of additional food before the stomach is ready for it results in serious disturbances.
Furthermore, these patients are often tormented by thirst and are permitted to pour down liquids of all kinds into the already distended and irritated viscus at irregular inters^als, so that ab- dominal distention, eructations, flatulence, and increased dysp- noea add to the patient's distress. These considerations have in- duced me to set five or five and a half hours as the proper length of the interval that should elapse between the meals. I do not permit milk to be taken between times, since by being curdled in
THE THKATMENT OF VALVULAR UKAUT-DiSKASE
473
the stonuioh it is practically the :^ame as solid f»x>J. When in Some cased the feeling uf fahitiiess and weakness makes some intermediate nourishment luuivoidahle^ 1 order a clear hruth or bouillon, or weak tea containing a little cream but no sugar, etc. So simple a restriction as this lias often been found to work won- ders in removing the thirst and epigubtric gnawing, A cupful of hot water drunk an liour previon.s to a meal seems to facilitate the expnlsion of the stoniacli conti*nts and to clear the way for the ingestion of fresli food.
The next rule is the restriction of the ijuaiitity (»f linids to be taken with meals. In severe cases liquids should be limited to 6 ounces^ and even in mild ones It) ounces should be tlie maximum. This does not mean ordy water in addition to any other fluids that may have been ordered, but includes nil Itiinids combined and consmned in addition to solid ingesta. The purpose of this restriction is to prevent undue distention of the stomach in those cases in which siieh distention won Id be likely to occasion abort- ness of breath or endmrrassed canliac action.
The rule is thot patients are to be restricted in the amount of their solid food, for it is not rarely observed that they manifest a veritable bulimia, and if j>ermitted to do so w^ill overload their Btomadi and sorely overtax their digestive and assimilative capa- city. A simple and usually sufficient guide as to the amount that may be safely consumed is to be found in the injunction that they finish each nieal feeling they could eat more, A little, well digestedy is worth far more than a good dealy poorly digested. This restriction not only lessens the danger of distending the atonic organs which it has been sliown furthers decomposition, but it tends to prevent the cardiac embarrassment occasioned by repletion. Such a limitation of the patient's food must not be carried to the extent of starvation; and yet if the quality of the nourishment is judicionsly selected it w^ill often be a matter for surprise how small a bulk wuU suffice — nay, how it will minister to the patient's comfort.
In considering the articles of food suitable to this class of suf- ferers I think it best to deal with the subject in a general way rather than to attempt to make up appropriate menus. Tea and coffee should be w^eak and contain such an amount of sugar and cream as depends upon the degree of digestive disturbance. Cocoa
lite
474 DISEASES OP THE HEART
or broma is preferable to chocolate because containing less fat, and when made with milk is nutritious. If wine or liquor is thought advisable, it should be freely diluted with water. But- termilk, kumyss, and malted milk make a valuable addition to the dietary, and generally agree well.
Effervescing beverages are objectionable on account of the distention they occasion ; and for this and other reasons malt bev- erages are not advisable, unless in special cases when they are craved on account of their bitter taste or their stimulating the flagging appetite. Iced drinks and very hot fluids are not well borne, since medium temperatures are better for weak stomachs. The admissibility of soups and broths must be determined by the condition of the kidnevs and the habits of the individual. When chronic nephritis exists, stock soups and meat extracts are to be forbidden, since animal extractives are irritating to the renal epithelium. It should be remembered that beef-tea and the like are stimulants and possess no real food value. Cream soups, or purees as they are called, are not open to the same objection and are highly nutritious. All these are fluids, however, and when taken in connection with solid food should be limited in amount, lest they blunt the appetite for what is to follow and create a feeling of repletion.
Carbohydrates should be allow^ed but sparingly because of the following considerations: In the first place tliey readily undergo fermentation and occasion flatulent distention of tlie stomach and bowels; while in the second place they are so readily oxidized that they appropriate the oxygon necessary for the utilization of the nitrogenous principles of the dietary.
Xevertheless, sugars and starches cannot be withheld entirely, and hence they must be in the least objectionable forms. To diminish their tendency to fermentation the latter should be so thoroughly subjected to heat in cooking that the starch granules become converted into grape-sugar. Toast, zwieback, light crack- ers, and *^ pulled bread " and muflins or tea biscuits made with baking-powder are preferable to bread which has been raised by means of yeast and is often imperfectly baked. If potatoes are allowed, they should he baked and mealy, and even cooked in this way they should not be taken in unlimited amounts. Rice when well boiled may be also permitted in restricted quantity, but sweet
THE TREATMENT OF VALVrr.AR HEART-DISEASE
475
potatoes, cereals, and ilw nuiltifarions coiiibinations of flour, but* tefj and siigarj whether with or witliout eggs and milk, known as cake, griddlc-eekes, etc., arc inadmissible.
Most desserts, and in particular sweetmeats, coti feet ions, pre- served and canned fruits, are to be allowed only to tiiose patients who can dispose of such arficles without annoying thitnlence. Fruits are best in their natural state, and even then should be ripo and fresh* Applet are particularly good l>ccau86 of their rela- tively large percentage of nueleo-allnunin, and when baked are often bettor tolerated than when uncooked. Pineapple has always seemed to me a particuhirly dosirable fruit because containing a natural digestive ferment of great effi<*ieney. As a general thing I regard it as better for eardiopaths to take fruits at the close rather than at the beginning of a mc*al, as they do not bbnit the appetite nor create so much gas.
Most of the fresh vegetaldes are valualde additions to the dietary^ either because rich in proteids and other nutritive prin- ciples, or on account of their serving as relishes and containing various salts essential to the organism. Peas, lentils, string- beans, and spinach are said to be relatively rich in iron-forming principles. Tomatoes, cabbage, cauliilower, turnips, and kindred varieties are apt to disagree, but if well borne may be permitted. Asparagus, when not contra-indicated by renal disease, celery, let- tuce, greens of various kinds, and young onions are allowable, while cneuTubers, tender radishes, and olives may be left to indi- vidual desire and ability to tolerate without distress. Jtush- rooms are very rich in proteids, and for renal patients supply a form of nitrogenous food that is not open to objection as is animal food with its extractives. Begets are rich in sugar, as is corn, and are likely to occasion flatulence.
Of ffM>ds rich in proteids beef and pork bead the list, but perhaps are not so easily digested as jire veal, lamb, and mutton, which are excellent when not too fat All meats should be roasted, broiled, or stewed, not fried ; but however prepared, they should be as free from gra\'y as possible and ought to be so well done as to have destroyed the germs of decomposition through whose action during the time of hanging the meat becomes tender. Fowl and game-birds form a capital ad jiinet to the heavier meats, as also do fish and most kinds of shell-fish, particularly oysters when raw.
476
DISEASES OF THE HEART
Some of the suited tish anJ meats when not too rich provide appe- tizing and nutritious dishes. Canned salmon^ sausages, etc, are too rich in oil and fat, and are apt to cause eructations, whereas fresh tripe is said to be easy of digestion. Cheese is highly nutri- tious, and when known not to oeeasion constipation or distress may be allowed. This is esj>ecially the ease with cottage aiul cream cheese. This article of food should not be taken when cooked. Eggs are very digestible and form a valuable addition to the dietary of this class of invalids.
Years of experience in the feeding of cardiopaths has con- vinced me that their fo<xl should he ]dain and that where more than ordinary indigestion exists the tnfnti should not be elaborate. It has seenu*d to me an excellent plan in some instances to sepa- rate the carbohydrates from the anhmd fix)ds — that is, to give them by themselves. Then at the meals composed chiefly of ani- mal fcw>d onh' vegetables or relishes, sncli as asparagus, lettuce, or celery, are allowed in addition. In tins numner has been pre- vented nmch uf the putrefactive decomposition of meats which engender the distressing symptoms of indieannria and oxaluria.
In conchision, a few words may not be amiss concerning an absolute milk diet in cases of cardiac inadequacy. It has been highly recommended in conjunction with absolute physical rest as an excellent means of restoring compensation when this is threat- ened. It acts probably by lowering arterial tension and lessening or removing the evils of the defective digestion of solid foml, since milk alone acts as an intestinal antiseptic. Furthermore, by virtue of its sugar, milk often exerts a pronounced diuretic at^tinn, and thus aids in the removal of minor degrees of dropsy. When administered as the exclusive article of diet, it is best given blood- warm and in moderate amounts at regular intervals — e. g., a cupful every two hours. It sometimes agrees best when diluted with an alkaline water, as Vichy or Seltzer water. Such a diet should not \)e maintained indefinitely^ and in most instances pa- tients begin to jdead for more substanrial nourishment at the end of two or three days. It should be jrersisted in, however, until the results aimed at have been reached, when a gradual return to solid food is to be made.
Clothing, Habiti, Occnpation.^ — ^Wbat has been said in preced- ing pages under these heads applies with still greater force to
THE TREATMENT OF VALVULAR HEART-DISEASE
4T7
""stibjects of valvular mischief when their coin pensat ion is imper- feeL The influence of these factors is subsidiary to those that have just been considered, and yet these matters are by no means imiiiiportant. A too tight corset or waistcoat may so hamper thoracic inovemeiits and so impinge on tlie distended right or left ventricle as to frustrate all attempts to reinstate eoiiipensation by digitalis, resistance exercises, Laths, etc. Constriction of the chest and abdomen is therefore to be sedulously guarded against.
The immoderate use of tobacco will assurer! ly prove depress- ing to the heart-walls we are striving to strengthen. Alcoholic excess, even though intoxication does not result, injures an un- compensated heart by causing excitation and exliaustiun of the cardiac musele-fibres. Sexual excess, perhajis even very moderate indulgence of this kind, may maiutain or increase the very dila- tation we are endeavouring to overcome. It should therefore be strictly forbidden until such time as the heart-power sliall have been reinstated.
Occupation of all kinds, particularly such as involve even the lightest possible physical effort, and exciting, long-<^ontinued brain work, must be laid aside while compensation is deft^ctive. Unfor- tunately, the eircimistanees of the patient do not always admit of a rigid enforcement of this injunction. When this is the case, the danger of injury from his occupation must l>e explicitly stated, that the work may be perfonned in the easiest possible manner. It is always well to furnish such explanation, together with a warning, that in the event of damage resulting from a con- tinuance of the employment the physician may not be held respon- sible for the failure of treatment. Only by attention to details can tlie medical man hope to turn what threatens to prove a disas- trous defeat into a brilliant and it nuiy even be an unexpected victory. It is precisely in this class of cases that modern cardii> tlierapy obtains its most signal and astonishing triumphs. There is no other class of cases which so amply rewards intelligent and painstaking management.
CHAPTER XVIII
THE TREATMENT OF VALVULAR HEART-DISEASE
(Coneliided)
III. COMPENSATION LOST
In some cases of valvular disease that have reached this stage, restoration of their compensation is impossible and the physician can do no more than mitigate the patient's sufferings or add a few weeks or months to his life. In other cases skilful management may so assist the heart in its struggle that it is able to overcome the obstacles in the way of the circulation and regain a measure of its former adequacy. The weapons with which to aid Nature are at the command of all, but the knowledge how to make them most efTective is possessed by only a few. Digitalis is the weapon on which chief reliance is to be placed. It has its congeners, which are sometimes of greater service because of some differences in their action — e. g., strophanthus, which exerts less constricting effect on the arterioles. It is safe to say, however, that thera- peutists of greatest experience place more reliance on digitalis than any other remedy of its class, and that as a clinician grows in exj)erience in the treati.icnt of this group of lesions he generally comes to employ this drug more and more often, and strophanthus and similar remedies with decreasing frequency.
It is not alone necessary to have knowledge of its mode of action; one must also understand the indications and contra-in- dications for its use. The skilled hunter will procure more game with an expenditure of less ammunition than will an untrained sportsman. So likewise with this great remedy. The experi- enced and skilled clinician will accomplish more oftentimes with small doses than can he who is not trained to recognise the condi- tions that do or do not call for its administration. Inexperienced practitioners are apt to think they must order digitalis so soon as called on to treat a case of valvular disease with ruptured com- 478
THE TUKATMENT OP VALVULAR HEAET-DISEASE
479
peiisatioii, no luattef how great the visceral congestion or extensive the aH^lenia. IiRleed, the presence of dropsy is generally consid- ered the indication for digitaliSj and hence this drug is prescribed as the sovereign remedy ; when this fails, the case is considered hojieless. As a general proposition it is true; but in many cases the giving of digitalis at first is analogous to whipping a horse that cannot draw his load up hilL lie fails, not because of lack of offort, but because his load is beyond his strength. Lighten his load, and the poor beast will surmount the hill w:ithout fahering. The crippled heart fails in its labours, as a rule, because its task has become too great, and not from weakness inherent in its myo- cardium. It has Itecvmie like a jaded horse, exhausted yet willing still, which may respond for a time to whip and spur^ but will die in the attempt.
Overdilatation — that is, overdistention — of the cardiac cavitieB renders the heart incapable of responding to a drug which slows the organ by pndoiiging diastole and thus favouring a l^etter fill- ing of its chanik^ rs. The heart is already filled to its utmost and fails to contract adequately because of abnormal endocardial blood-pressure. Even under the stimulus of digitalis its walls cannot coi>e successfully with its contents. As a matter of fact, the drug only intensifies its embarrassment. The stasis wilhin the organ must first he relieved^ after ivhuh fJujifalis maij he adminis- lercd with satisfactory results. This nuiy he <lone by bloodletting or by catharsis; 12 to 16 ounces of blood may be draw^n from the arm, or wet cups or leeches may be applied to the pra*cordia, I prefer, and have usually employed, bydragogue cathartics, because they lessen directly the hepatic stasis that coexists with the cardiac distention and forms another of the conditions acting as a barrier to the action of digitalis. The following is a case in |x>int:
April 17, 1805, I was asked to treat iliss T., aged forty- four, w^ho had been ill with heart-disease for about six weeks and had been given up by a number of doctors as a hopeless case. In fact, the last physician hnd defdared nothing could be done for her, had acted on this belief, prescribed only some codeine to relieve her cough, and had gone his way* The lady gave a history of articular rheumatism twenty-five years before, since which time she had been short of breath. Her present symptoms, however, dated from about six weeks back, yet could not be traced to any
480 DISEASES OF THE HEART
special exciting cause. A pronounced aggravation of her condi- tion had followed the exertion on the previous Sunday of dress- ing and going dowTistairs to dinner.
I found her sitting up in bed on account of dyspnoea and cough which had prevented sleep for several nights. Her colour was a peculiar bluish-yellow or slightly greenish hue, and anasarca was extreme, extending to the trunk, and including the upper extremi- ties. The radial pulses were so flickering that the heart-rate had to be counted by auscultation. As nearly as I could determine, owing to the great arrhythmia, the heart was beating between 160 and 170 times a minute. There was no cardiac impulse percep- tible. Both absolute and relative dulness was enormously in- creased, the latter reaching from 1^ inch to the right of the right sternal margin very nearly to the left anterior axillary line. Heart-sounds were feeble, the first being partly obscured by a murmur that seemed to possess an indistinct presystolic portion; the pulmonic sound was very accentuated and the corresponding aortic was weak. The bases of both lungs, particularly the right, showed dulness that did not shift, and numerous fine moist rales. The firm rounded border of the liver was palpable three finger- breadths below the costal arch, and the abdomen yielded signs of ascites. The urine showed nothing more than the usual changes of congestion.
The i)atient's distress was pitiful, unable to eat or sleep, hold- ing herself upright in bed without even tlie support of pillows, labouring for air, coughing, and expectorating bloody, frothy mucus. The diagnosis was plain — mitral disease of rheumatic origin, which at last had broken down and led to this enormous dilatation of the heart, hypostatic pulmonary congestion, hepatic engorgement, a^dema, and ascites. There were no serious com- plications, and yet it was very questionable whether or not the heart-walls would ever recover from the enormous strain to which they were subjected. To the family I expressed a guarded opin- ion as to the result of treatment, yet encouraged the sufferer to hope for recovery, that she might summon courage from hope to endure the vigorous onslaughts on her (edema that would have to be made. It seemed to me useless to prescribe digitalis with the heart in that state; so I resolved to sustain it with strychnine, which, owing to the fact that she could not afford a nurse, was
THE TREATMENT OF VALVUI.AB UE ART-DISEASE
481
given l»y niuiith, ^ every tliree Imura diiring the day, wliile each evening I injected the same dose hypodennically, together with J of niorjrhine and j^-^ of atropine, to induce sleep and lessen the cough. Then as a package of symphorol had been given me for trial, 1 decided to try its effect on tlie dropsy. A cathiirtic was also administered, hot not a very powerful one. The diuretic failed absolutely, and Merck's diuretin was tried with the same want of success. Then without changing the strychnine and even* ing dose of morphine it was decided to make use of purgation — good, vigorous purgation of the old-fashioned sort
The patient's strength, l)y the way, had increased appreciably, although the II tlenni had ouly grown somewhat less hard. She was also able to take a little more nourishment, consisting of milk and eggs. Accordingly compound jalap powder in teaspoonful doses was administered until a large number of copious w^atery stools wero secured. Indeed at one of my visits — -the first, I be- lieve, after the powfler luui been ordered— she was found sitting on the night-stool, nm] in response to my queries concerning the effect of treatnieut, stated she had been sitting there for two hours, preferring that to the effort and fatigue of changing from bed to the stool and back again every few minutes. The iuHueuce on the heart tuul circnlafinn was wonderful and gratifying. First her cough and dyspntra subsided and the sj)Utuui lost its bk)ody char- acter; the abdomen softened do^vn^ and the redema left the arms and flanks; the pulse grew a trifle less rapid^ but appreciably more waves reached the wTist; cardiac dulness became rather less extensive also. Then T de<dded to let up a little on the purgation and to atl minister infusion of digitalis carefully prepared from English leaves, strychnine and morphine to be continued as be- forf*. The results were alinost magical ; the heart quieted do^Ti and daily grew^ in regularity and strength; dropsy disappeared entirely, and the patient, free from cough, was able to lie down with ease and enjoy a comfortable night*s sleep. The morphine was discontinued, but the strychnine was left undisturbed,
ilay 1st the patient was turned over to Dr. Houston, who resided in the neighbourhood, and by him reports of her progress were made to me. The hist time I saw the patient, about June 1st, she was sitting dressed on a sofa, without the faintest trace of tedema, the pulse 80, perfectly regular, the heart of nearly 81
482 DISEASES OP THE HEART
normal size, and with a loud systolic ai>ex-niurmur. Compensa- tion had become re-established for the time. A peculiar and inter- esting feature of this case now developed; the patient became quiet, morose, and melancholy, very unlike her cheerful, patient self during the height of her peril. This change of disposition Dr. Houston found was due to digitalis and di8api)eared with cessa- tion of the drug. This patient removed during that same summer to Moline, and there, her old symptoms of asystolism returning, she died in Februarv, 1896.
In this case the treatment, though successful, was severe, and under similar conditions I would now advise removing the ascites by aspiration, which, by more quickly relieving intra-abdominal pressure, would permit the earlier employment of digitalis. In most cases of the kind, moreover, diuretin accomplishes the re- moval of the dropsy. Its failure in this instance was owing prob- ably to the extreme renal stasis, which should first have been lessened. I have seen remarkable results follow its use in cases of cardiac dropsy in which stasis was less pronounced.
A. C, a tall, slender girl of fourteen years, was seen in con- sultation with the late Dr. E. M. Hale, December 14, 1891, be- cause of heart-disease and increasing dropsy. There was a his- tory of chorea at eight years of age and again in August, 1891, since which latter attack she had not been well. CEdema had gradually aj)peared and increased in spite of treatment by her home physician; hence she had been brought to Chicago and placed in charge of Dr. Hale. A urine analysis of December 9th by Dr. C. Mitchell had shown a fourteen-hour quantity of 13 ounces, spec*ific gravity 1.027, acid, urea stated as reduced to 75 per cent of normal, a small amoimt of albumin and hyaline and granular casts. The symptoms were the usual ones of dyspnoea, weakness, and swelling of the lower extremities, anorexia, and constipation.
The patient lay on a couch semi-recumbent, evincing plain signs of venous stasis. The lower extremities were moderately a'dematous, and the external jugulars were distended, but not pulsating. There was noticeable prominence of the pnecordium and great distention of the abdomen, which yielded signs of free fluid, the liver being palpable three finger-breadths below the cos- tal arch. The heart was greatly increased in size, the apex-beat
THE TREATMENT OF VALVULAR llEAHT-DISEASE
483
?Ing in the sixth left interspace outsiJe ibe nipple, an J there wiis a loud mitral svstolic anJ short presystolic murmur- Mj notes do not state the pulse-rate, but mention that the pulse was regular, rapidj and small. Signs of the heart being immovably fixed in position were discovered at a much later period.
In view of the fiiet that digitalis had been taken without favourably influencing the dropsy, it was decided to put her on DO grains of diuretin in twenty-four honrs and administer a moderate dose of calomel. Two days subsequently the urine was reported to be SI ounces and to contain a trace of albumin but no casts. This wilfid little miss then began to be so annoyed by the frequent micturition that she refused any longer to take diuretin, and this was stuppc^d. It was replaced by heart-tonics, first digitalis, and then ^ grain of convallamarin thrice daily. Her improvement was so rapid that after about two weeks she was taken to her Iowa home in care of a trained nurse, by w^om orders as to diet and exercise were strictly enforced. Uninterrupted gain was made until February, when the patient wearied of her restraint and my services were dispensed w^ith. The following October I learned that nhe was riding horseback, playing lawn- tennis, and bicyclings but ^* her lips looked blue.'' Five years now elapsed l>efore I again saw her, bnt I learned meanwhile that she had another breakdown similar to her first one, her recovery being very slo\v, and rc-quiring severe pnrgation.
My next examination of this patient was in the early fall of 1896, at which time she was attending a young ladies' school in one of our snburbs. The heart was very greatly enlarged ; its apex-beat w^as immoval>le in the sixth left interspace well towards the anterior axillary line; and mitral regurgitation appeared to be the prechmiinant lesion. Hepatic engorgement w^as consider- able and cardiac embarrassment was evident ujxin exertion. She was resorting occasionally to a few drops of strophanthus, but no cathartics.
She was induced to take a laxative w^ater at regular intervals, which speedily lessened the visceral congestion. She also con- sented to try the eflicacy of a conrse of baths a la Nauheim sup- plemented by resistance gymnastics. The results were gratifying, the dilatation of the right heart being appreciably reduced and the cardiac tone in general being greatly improved for the next
484 DISEASES OP THE HEART
two years, as she subsequently stated. She passed the winter of 1898-99 at a young ladies' school near Philadelphia, and was in tolerable health until April, 1899, when she had an attack of acute rheumatism. This resulted in an acute pericarditis with effusion, which left her very feeble for the ensuing two months, much of that time being spent in a wheel-chair at Atlantic City. I had the opi)ortunity of examining her in June, when the heart was found enormously enlarged, with an intense systolic apex-mur- mur, and also a loud diastolic one immediately following the sec- ond sound. This murmur was of maximum intensity at and about the ai>ex, and was evidently mitral, produced by the inrush of blood into the dilated left ventricle during the beginning of its diastole. The action of the heart was unsteady, the abdominal organs were much engorged, and the patient was pale and weak. She was put on strophanthus, strychnine, and iron, and went on to her home. Her condition improved during that summer, yet remembering the benefit obtained by the Xauheim treatment in 189G, she returned for another course in October, 1899.
My notes record that the apex-impulse was broad and heaving in the sixth and seventh interspaces 5 inches to left of the ster- num ; absolute and relative dulness greatlj' increased, the latter ex- tending nearly to the left anterior axillary line, and at the right to 1^ inch to the right of the breastbone. The apex was fixed in position, and a double murmur was still present in the mitral area, both very intense. The external jugulars were full and the liver i)alpable. Signs of insufliciency of the aortic valves were diligently sought for, but in vain. Tlie mitral valves alone were involved. The enormous hypertrophy and dilatation of the left ventricle were due to the exo-pericardial adhesions acting in con- junction with the mitral disease. Baths and exercises were begim October 19th, and Xoveniber 1st it was recorded that the left external jugular was turgid. The patient, contrary to instruc- tions, was ascending too many stairs and eating too lieavily. Ca- tharsis and great care in the nuitter of exercising reduced the turgescenee of the veins and liver for a while. On Xovc^nber 23d it was again recorded that the jugulars were full and the lips blue. This was attributed to her having hurried in dressing and having walked against a strong cold wind. The venous con- gestion again diminished, although not entirely. At the close of
THK TREATMENT OF VALVULAR HEART-'DISEASE
485
the course of treatments, whidi haJ extended through six weeks, it was iiutcd that tlie left heart bad not diDiiiiished in size at all The enliirgenient of the right heart wns less, however, the action of the heart less easily disturbed, and the patient felt stronger, having logt the weakness* perspirations, and sensation as if the ** heart was trendjling/' syoiptonis of which she spoke at the date of comnieueing the treatment. The winter fullowing she felt better thim ever before.
Since the abuve was written this patient suffered a final break- down, and died nnder my eare in ^lay, lltOl. Her last syuiptoms have Ix^en described in the chapter on Mitral Regurgitation.
March 18, lSi>0, I was retpiested to see Mrs. F., aged thirty- fonr years, who had been dropsical for several months. The patient had had intlaniniatory rhenniatism at the age of twelve or thirteen and again at thirty, soon after the birth of her second child, hot had not been aware of cardiac symptoms nntil Septem* her 10, }S\)'}, 8!ie had then been aronsed in the night by a violent attack of palpitation ; an<l a few weeks -^nbseipiently hail suddeidy developed headache, paralysis of ihe right side of the face, and partial left heniijdegia. This liad gradually improved, leaving behind a paralysis of the extensors of the left arm and contracture of the fourth and fifth lingers. After this attack dropsy !iad gradually cunie on, and had resisted treatment by several local bomoNijuitliic jthysicians. For six weeks [udor to my seeing her she had U^en nimble to lie d<nvn, and had finly slept by sitting with her arms support od on a table in front of her. An enormous ledenia extended as high as the waist and involved also the left or paralyzed arm. The greatly disl ended abdomen yielded fluctua- tion and percussion evidence of free fluid. The liver was made out as greatly enlarged, and tliere were sigiis also of fluid in the right pleura! cavity. The judse in the right radial was very arrhythmic, snralh and accelerated; the left radial ]ailse was, and it may Ik* rrmarki^'d still is, smaller and feebler than ihe right. The external jugulars were a good deal distended but did not pulsate. The apexdi€^at was in the seventh and eighth intercostal spaces close to the left anterior axillary line. It was at first thought to he pushed over by the right-sided hydrothorax, as the fluid in the jileural cavity was thought tu be. Tlie first heart-sound was audi- ble in spite of a loud systolic murnnir which was tranj^mitted
486 DISEASES OF THE HEART
around to the back; the pulmonic second sound was much inten- sified. With exception of the shifting dulness at the right base, the hmgs were negative. The urine was scanty, but gave no evidence of renal disease apart from congestion.
This case was thought to be merely one of mitral regurgita- tion in the stage of destroyed compensation. A year later, how- ever, well-marked retraction of the tenth and eleventh left inter- costal spaces posteriorly was discovered, Broadbent's sign of ad- herent pericardium, and the apex was immovable. Early in April, after I took charge of the case, a quart of clear serum was withdrawn from the right pleural cavity, after which reso- nance and vesicular respiration returned to that side. This was after treatment had removed the dropsy, and hence this w^as concluded to be an old pleuritic effusion that had escaped previ- ous recognition.
The preliminary treatment in this case, as in that of Miss T., was heroic purgation. It seemed useless to administer digitalis or diuretics until after the excessive stasis had been reduced by catharsis, and hence the patient was assured of relief if she would have the courage to bear some very severe treatment. Her re- sponse was to the effect that she would gladly endure anything that would relieve her of her suffering. Accordingly jf^ oi a grain of elatcrin was prescribed hourly until it began to operate. At my visit next day 1 leanio<l she had taken ten of the elaterin granules and that she had vomited 11 times and purged 20. In- dications of improvement were already appreciable, and as she expressed herself as ready to stand another roimd, the granules were ordered repeated on the following day. Their effect was immense, after which the dropsy diminished still more. To sus- tain her during this ordeal she received full doses of strychnine by mouth, stimulants whenever necessary, and a concentrated nourishing diet consisting largely of eggs and strong broths. By the fifth day the circulation had manifestly improved, but she felt and appeared very weak. The family was much concerned and thought the i)atient was never going to endure the treatment. The sufferer was undaunted, however, and I was obliged on more than one occasion to censure certain members of the family se- verely for talking before the patient in a way to dishearten her. Digitalis was then ordered in tablespoonful doses of the fresh in-
TMH TUEATMENT OF VALVULAR HEART-DISEASE
487
fusion every foitr hours, and tlie vigour of the catharsis was abateJ, from 4 to G Wijtery 9tLM>ls daily being still secured. It WHS not long before tlie patient was able to rest in bed, a thing she had not been aljle to do for nearly two months. The sceptics in tlie family circle were now convinced and ready to assist in any therapentic measure proposed. The oxlema was stubborn, yet wholly subsided in about three weeks. When this had been ac- eonipHshed aspiration of the right pleural cavity was performed with the result previously stated. Digitalis was continued daily fur a year, but in the form nf the tincture and for the most part in doses of 15 drops three to four times a day. The change in the pulse was very gratifying, being in June^ as given in my notes, only 05 and tolerably regular. The liver still remained greatly enlarged and kept showing such a tendency to increase in size and tinnness whenever the bowels were not kept freely open that at length the patient was instructed to keep on hand a satu- rated sohition of Epsom salts, and of this to take every morning such an amount as would secure several fluid evacuations. This onler was strictly olx^yed, and in conjunction w^th llie cardiac tr»T»ies proiluced the happiest results. Before the summer was jiast she was w^alking about the house and enjoying drives* As- rending stairs was strictly forbidden, however^ and w^^s not even attempted for at least a year*
Although this patient never lost her appetite and seldom expe- rienced indigestion, her dietary was made very simple and of a somewhat restricted quantity that there might be no chance of her overloading her stomach to the detriment of her still enor- mously hypertrophied and dilated heart. It consisted in the main of a small dish of cereal and cream, a soft-boiled egg, a little buttered toast, and a cup of cereal coffee for breakfast; for dinner at midday a fair-sized piece of meat, green vegetables, little or no potatoes, some bread and butter, and a simple plain dessert, as plain pudding, or some fresh fruit, water in limited quantity being the beverage; for the evening meal she generally took a little cold meat with Ijread and butter and CiX»ked fruit of some kind. After a considerable time, in consequence of the de- velopment of symptoms that serened to indicate she was getting too much meat for the limited amount i)f exercise, I took away the animal food in the evening and she confined herself to her
488 DISEASES OF THE HEART
favourite cereal at this meal. This patient obeyed instructions to the letter, and, owing largely to this circumstance, gained grad- ually in endurance and improved in colour until at the end of two years was said by friends to no longer look like an invalid. For the past four years she has taken very little medicine and has been able to attend to her household, even doing considerable work at different times. She has been allowed to go upstairs, provided she does not hurry, and has not been injured thereby. I have seen her on the average once every two weeks, yet have not always prescribed medicine, contenting myself with seeing that everything w^as progressing as well as could be expected. There has been very little time w^hen she has not taken a little digitalis, usually a single daily dose of 5 or 10 drops, but now and then, when the heart has showTi a disposition to greater arrhythmia or hurry, this amount has been exceeded. There have been periods of days or a few weeks when I have seen fit to order iron or strychnine, and at a few times, characterized by unusual constriction of the pulse and scantiness of urine, she has been obliged to resort to nitroglycerin, usually to the relief of the condition. In the fall of 1899 this patient contracted a bron- chitis which was attended with such a degree of fever and conges- tion of the right hmg that for a day or two I feared she would get a broncho- pneumonia. It finally yielded, however, to rest in bed, heroin and apomorphine hydrcK*hlorate, the heart being sustained by some extra doses of strychnine and digitalis. This patient has never shown much dyspncua, but did for a number of months suffer a good deal from fugitive pains in the left half of the thorax with areas of intercostal tenderness, while below the right scapula and passing through to the front was at times a wearing dull pain that was only mitigated by lying down. Her liver is still very large and growing, as the months go on, percep- tibly thinner at its border and harder. It droj)s down also, being readily pushed upward. I therefore attributed her right-sided pain to the pulling of the heavy liver on its supports.
As the reader has observed, the foregoing cases are all in- stances of mitral disease, and two of them complicated by peri- cardial adhesions. They were consequently not the most promis- ing, yet responded to treatment in a highly gratifying manner. Such is not so with cases of aortic-valve disease, as proved by
THE TREATMENT OF VALVULAR UKAUT-IH8EASE
489
the cases detailed in the ehapter devoted to Aortic Regurgitation. In 18IJ4 1 luid in charge a young man nineteen years of age afflicted with insulHeieney of the aortic %*alves of rheumatie origin* Compensation was not badly ruptured to judge from his symp* toms. He disjdayed no crdenia or marked venous stasis, ahuost his only subjective consciousness that all was not right being shortness of breath and palpitation upon exertion. Yet the heart was dilated and the pulse notably arrhythmic. It was hoped benefit would result from a course of thera|)eutie baths and exer- cises. As a !uatter of fact some decree of strength iippetired to be impartefl to the heart, fur the impulse beeaine ukore defined, the sounds more distinct, and his subjective sensations less pro- nounced. Nevertheless, nut many weeks had elapsed after the course of treatment when he suddeidy had an attack of partial syncope, on account of which he was confined to bed and cardiac tonics were administered. lie did not im])rnve, and a few days later died suddenly with manifestatiuns tbat strongly suggested end hd ism of one of the uuiin divisions of the pulmonary artery. An autupsy was not obtiuncd.
The Treatment of Drapsy. — When this supervenes in the down- ward cuursi' of valvt^-lesions, it is lujt tv he regunleil merely as an indication of ranliae inadequacy, but as evidence of obstruction to capillary ciivulation, plus aini'iuia and greater permeability of the capillary walls. The pressure of tlie transuded serum still further obstructs eapillary fl*iw and augments cardiac endiarrass- meiit. It must be removed, therefore, brfore the strength of the heart eiin be restored. In this stage of valvular disease the occur- rence of dropsy is very common, and its removal is the problem first requiring sohuion. In some instances this is easy and only necessitates for its accomplishment the invigoration of cardiac contractions by putting the patient af rest and l>y administering cathartics and digitalis.
According to my experience, the infusion of digitalis exerts a more decided diuretie action than does any other preparation or any other remedy excepting diuretin. It should \>e freshly pre- pared from English leaves, as these are more reliable than the German, which are said to contain a considerable proportion of stems. The substitution of a fluid extract for the leaves in the preparation of the infusion is never to be tolerated. The addition
490 DISEASES OF THE HEART
of squills or of a potassium salt, as the citrate or acetate, is thought by some to intensify the diuretic action of the infusion, but is objectionable. Squills is likely to occasion irritation of the gastro-intestinal tract and render the stomach intolerant of the digitalis. If potash is used in conjunction it is better alone, so that either of the drugs may be increased, decreased, or withdrawn without affecting the other.
To procure its action on the kidneys the infusion should be given in full doses, ^ an ounce every four hours, and continued for several days or so long as it continues to augment the flow of urine. Its action should be closely watched, that the remedy may be stopped so soon as signs of its cumulative effect are detected. These are slowing of the heart's contractions to 60 or less, nausea, and a falling off in the amount of urine after this has first been increased. It should be remembered that some persons become nauseated by digitalis even before it has been taken long enough to produce its poisonous effects. The most trustworthy indication that the drug would best be discontinued is found in the excretion of urine. If this does not augment after digitalis has been exhib- ited for two or three days, even though the pulse-rate falls, there is nothing to be gained by further administration of the medicine at this time. If persevered in there is danger of cumulative action. Again, if after having been increased for a while the urine begins to diminish, digitalis is beginning to exert its toxic effect, and ought at once to be stopped. Even if these unfavour- able signs do not aj)pear I make it a rule to withdraw the infu- sion at the end of five days, or after the 8 ounces comprised in the pharniaeojxi'ial formula have been exhausted. The drug contin- ues to be eliminated for a day or so longer, and hence it is not usually necessary to follow it directly by any other similarly acting agent.
It is not uncommon for digitalis to fail to remove dropsy, and when such is the case it is well to try diuretin — Ivnoll. This is often surprising in its action, as in one case in which after the failure of digitalis it increased the urine from a pint in twenty- four hours to 8 quarts. Even this remedy may fail, but if it is fresh and given in large doses of 00 to 120 grains a day it gener- ally proves a powerful diuretic. It is best given in solution, 15 grains every three or four hours, yet in conjunction with digitalis
Freatment op vai
TLAR HEART-DISEASE
491
smaller doses are sometimes efficient. Diiiretin has a disa^eeable soapj taste, and after a time may oceasir>ii nausea and even vom- iting. It also loosens the bowels in some instanees. Its taste and unpleasant effects may be coimleracted by the addition to each dose of a drachm or two of essence of pepsin. For the knowledge of tliis vahiahle therapentic fact I am indeltted to the wife of a former patient wlio was compelled to take large doses of dioretin for a long time.
I have tried numenms otlier highly vannted dinretic reme* dies, hnt none aside from diurefrin has ever fulfilled exix-etations. Sugar of milk and vegetable diiiretieSj as apocynnm cannnbinum and squills, have never yieldeil satisfaetory results. Indeed, I do not see how they ean he expeeted to overcome dropsy when (his is doe to cardiac inadequacy and renal congestion. The indications are to relieve stasis and to stimulate heart action, which they can* not do. I have not employed calomel as a diuretic since I have dreaded a possible ptyalisni. When used for its effect on the kid- neys, it is in duses oi o grains several times daily in conjunction with opium to restrain its action on the bowels. Administered in this manner it is said In* the Germans to prove highly efficient in cases of cardiac dropsy uncomjdieatetl by renal disease. It seems to me, luwever, that one is justified in resorting to so pow- erful an agent *m\y when all other means have failed.
If the dropsy is so extreme that serous transudation in the abdomen or other cavities intensities the patient's distress, it is often found that digitalis, diuretin, or caffeine, even in heroic doses, fail to increase the urine. This is ilue to the imp^iSsibiHty of securing adcH|uate hlood-jiressure in the renal arteries. Stasis in the renal veins must first lie lessened! if one is to induce pro- nounced kidney action. For this reason such enormous anlema must be diminished or removed through the skin, bowels, or by mechanical means. Profuse sweating is not advisable, since hot- air hfitbs and pihx'arpine are too depressing for heart patients. We are restricted consequently to catharsis and operative pro- cedures.
The latter include punctures or incisions of the skin of the ankles to permit the serum to drain away. This is often an effi- cient mode of removing obstinate dropsy, but is likely to be ob- jected to by the patient or his friends. Great cleanliness is re-
492 DISEASES OF THE HEART
quired to prevent inflammation of the integument. A most excel- lent means of securing such drainage, and one not open to the objection of possible infection, is in the use of Soutbey's tubes. These are tiny silver cannulas which by aid of a minute trocar can be inserted beneath the skin of the ankles, and are then secured in place by strips of adhesive plaster or by rubber bands. Hypo- dermic needles can be used in the same manner. The quantity of serum that will trickle away through these tubes is astonishing.
Dropsical accumulation in the serous cavities may he with- drawn by tapping, a procedure which, if slowly done, is devoid of danger of collapse. It occasions pain, and patients generally shrink from being tapped on this account. They also often urge the additional objection that it will have to he repeated, and hence in private practice it is seldom resorted to. WTien consent to this proceeding can be secured, the physician should not content him- self merely with having thus removed the fluid. It will quickly reaccumulate unless the advantage thus gained can be held. Con- sequently the tapping should be followed by the administration of digitalis or diuretin, or both. It may be well also to administer an active purge, for by such measures recourse to aspiration more than once may perhaps be prevented. In the case of most private patients it will be found that they prefer active catharsis. They have liad more or less exj)erienee with purgation in times past, it may be, and they naturally look \\\x>n it as less painful than being tapi)ed.
Cathartics. — Whenever it becomes necessary to remove serous accumulations through the intestinal tract, it should be remem- bered that it can only be accomplished by the production of many copious watery discharges daily. It is not sufficient that the de- jections are semifluid and number two or three daily; Nature often does this much by a ])<)uring out of serum into the intestinal canal, in consequence of which the patient has several loose, even liquid, passages daily. In si)ite of Nature's treatment, the dropsy goes on increasing. Nature thus furnishes the indication for treatment, and fortunately we are able to aid her by the adminis- tration of hydragogue cathartics. This procedure is sometimes objected to on the ground that the cardiac sufferer is too weak to endure the depletion. As a matter of fact the patient's weakness is due to his circulatory embarrassment, and experience teaches
THE TREATMENT OF VALVULAR HEAltT-DISEASE
493
ftcit instead of being enfeebled to tlie degree a bealthv individual \vould be by Uie iiurgatlun, the cardiopatli actually tindd be feela ronger so soon as the primary effect of the catharsis is past. This is particularly true of mitral patients to whom heroic purga- tion is specially beneticiaL Although in the case of Mrs. F. elat- erin was highly successful, still it is so drastic that nowadays I grnierally order a less irritating remedy. The best hydragogue is a saturated solnfinn of sulphate of magnesia, and of this I am accustomed to prescribe a tablcspoonful hourly to an adult until it begins to exert its effect. 1 Lave known patients to take as nmch as 4 and even 0 ounces Ik* fore getting appreciable results. The efficacy of the remedy is enhanced if the patient is not alltAved to follow tlie medicine by more than a swallow of water — just enough lo renntve the bitter taste of the salts. If it is com- ]>lained that the drug produces a bad feeling in the stomach, this can usually be counteracted by the addition to each dose of 5 to 10 drops of essence of Jamaica ginger, which is generally found in the house. Compound jalap powder is likewise very efScient and does not prove so drastic as is supposed. Of this, a heaping teaspoon- ful can bc^ safely given to an adult daily, Tlie old-fashioned ** ten ten/' wliicli is 10 grains each of calomel and jalap« was uurIi employed liy our forefathers, riid is not so severe as it ia thotight to be. It is better, Iiowever, to give .5 grains of calomel with soda, or a blue pill of 5 or 10 grains, either remedy to be followed after eight or ten hours by | an ounce of Epsom or Rochelle salts. Bitartrate of jKjtassium is also a capital drug for the removal of dropii,y, and by some patients is better tolerated tijan is sulpliate of magnesia. Ci lac Iter's salts alone is too disa- greeable^ but may sometimes \w cnmbined with Epsom sails to advantage. It is one of the ingredients of Carlsbad water, by the way. Carlsbad salts are often prescribed to cardiac patients, but, to be very efficient for the removal of cedema, has to be given in large doses dissolved in considerable hot water, being said to be more eflicacious when administered warm. If copinns watery stools are to be secured, it is l>est to |U'escribe rather concentrated remedies and not allow the intake of nmch water.
In case such energetic catharsis is found to w€»aken the patient, his strength may be sustained by strychnine, aromatic spirits of ammonia, whisky, or some other stimulant Furthermore, the
494 DISEASES OF THE HEART
success of such treatment depends not alone upon its vigour, but also upon its persistent continuance, day after day, until the upper-hand has been gained over the dropsy. It requires judg- ment and courage on the part of the physician and fortitude and faith on the part of the patient. But if judiciously persevered with, it generally rewards the sufferer.
The Use of Digitalis. — When at length venous stasis has been diminished, and the cardiac cavities have been relieved, digitalis may be prescribed, and will then be found to complete the good work begun by the cathartics. The beneficial action of this rem- edy is generally attributed to its increasing the force of cardiac systoles, in consequence of which the arterial system becomes bet- ter filled. But, as suggested by Broadbent, a part of its beneficial influence is to be found in the greater tonicity imparted to the vessels through its vaso-constricting action. With improved vas- cular tone, blood-flow is hastened, and with accelerated circula- tion in the capillaries and lymphatics absorption of transuded serum is promoted. In addition digitalis lengthens diastole, and thus favours the emptying of the pulmonic veins, right heart, and great sj^stemic veins, and thus counteracts the impending stagna- tion of the circulation. Blood-flow in the renal vessels is im- proved, and forthwith there is a corresponding improvement in the renal function. Accordingly, as j)reviously stated, it is aug- mented diuresis that furnishes the most reliable token of the bene- ficial action of digitalis.
The occurrence of dropsy is a possibility in all four lesions of the left heart, but is far less often seen in destroyed compensation of disease of the semihmar than of the auriculo-ventricular valve. When, however, a^denia occurs in aortic-valve lesions, it is because dilatation of the ventricle has led to relative incompetence of the mitral leaflets with back pressure in the pulmonic system, disten- tion of the right heart, and the establishment of a condition iden- tical with that of uncompensated primary mitral disease.
In cases, therefore, of aortic defects manifesting dropsy the indication is for the administration of cathartics and digitalis the same as in mitral disorders. I believe, however, that the latter should be administered with judgment. There are some physi- cians who advocate the employment of large doses of digitalis in all cases of aortic regurgitation with broken compensation. My
THE TREATMENT OF VALVrLAR HEART-DISEASE
405
experierK-e leaJa me to agree with Broad bent when lie says that a distinction s^huiiM be made between eases of aortic insiitticiency with u'denia and those witliout. Wiien loss of compensalion is sliowH by symptoms pointing to h' ft- ventricle feebleness rather tlian by riMlenia and liack pressure eonsetjoent upon rebilive mitral regiirgitatioiij then I am emphattcally of the opinion that digi- talis must he given with caution. It is quite possible in such cases for digitalis to increase peripheral resistance to a danger- ous degree througli vascular constriction. Endoventricular blood- pressure is CDrreBiMdidingly raised, and if the ventricular wall iB very feeble, unexpected death is not a very remote contingency. In such eases, therefore, digitalis should be given cautiously, and its effects shouhJ Ite attentively watched.
When, on the other hand^ dropsy is present, the drug may be given more freely, although it is not likely to accomplish such brilliant results as in eases of tiiitral disease. Indeed, it has seemed to me that in some cases of aortic insufficiency w^ith sec- ondary mitral leakage large doses of digitalis actually augmented pulmonary and right heart engorgement by driving more blood backward through the mitral than forward through the aortic ori- fice. Such certainly was the effect observed in the ease narrated at the close of the chapter on Aortic Kegnrgitation. CEdema was not present, yet the state of the heart seemeil to call for heroic doses of digitalis in the forlorn hope of lessening the dilatation of the left ventricle. Instead of doing this^ however, the digitalis appeared to aggravate back pressure, and at last death came sud- denly and nn expect odly.
When the mitral valve has given way in eases of aortic ob- struction there is still less prospect of reinstating the ventricle by large doses of digitalis. The impediment to outflow into the arterial system is likely to cause still freer rethix into the auricle if by large doses of digitalis the jdiysician attempts to force the ventricle l>eyond a certain j)oint.
We now oome to the consideration of the question \vhether digitalis is equally efficient in both forms of mitral disease. Broadbent is of the opinion that foxglove manifests its happiest results in mitral regurgitation, whereas in mitral constriction the medicine is not always well tolerated. This difference is due, he holds, to the fact that the narrownng of the orifice interferes
496 DISEASES OF THE HEART
with the aspiration of blood out of the lungs which follows the better emptying of the ventricle produced by digitalis. This argu- ment applies cogently, no doubt, to cases of extreme stenosis in which the orifice is reduced to a mere buttonhole slit, for it is evi- dent that in such an extreme condition no agent can drive or coax an adequate volume of blood past the barrier. Xevertheless, ex- perience teaches that even in such cases digitalis is useful if prop- erly given. This is in accord \vith the following consideration: Digitalis prolongs diastole, and thus affords more time for the stream pent up in the auricle to flow into the ventricle, and hence to be expelled with the next ensuing systole. Inasmuch, however, as the capacity of the left ventricle is reduced in pronounced ste- nosis of the mitral ring, the blood-wave thrown into the aorta is of a necessity small, and mammoth doses of digitalis are not likely to accomplish more than moderate ones. If the beneficial influence of this remedy were limited to the left ventricle, the usefulness of the drug would be limited indeed in these cases. But it acts also on the right ventricle and left auricle, and by strengthening the vigour of their contractions it enables these chambers to exert greater propulsive force. In the light of these considerations it would be a grave mistake to conclude that this remedy is of no value in mitral stenosis even when broken com- pensation lias led to (pdema and other signs of serious stasis. The conibinod use of depleting measures and digitalis will some- times achieve gratifying results. Fortimately stenosis and regur- gitation are often conjoined at the mitral orifice, and hence such cases are to be treated as if only insufficiency were present.
^Vhen, therefore, digitalis is to be employed for the relief of dropsy due to ruptured compensation in mitral disease, it is to he given in large and, as Balfour says, " cumulating " doses. They must, however, be carefully watched, and the remedy must be stopped so soon as signs of its toxic action are perceived. It is my habit in such cases to administer ^ an ounce of the fresh infusion every four hours for four or five days. If it is employed in this manner, and if it is withdrawn so soon as the increased diu- resis first produced begins to be succeeded by a diminution in the amount of urine, there is ordinarily no danger of serious cumula- tive effects. If for some reason the drug does not exhibit its diuretic action, although slowing of the pulse is obtained, then
THE TREATMENT OF VALVULAR HEART-DISEASE
497
Ihe reniedy should be stopped for a day or two, after whicL it may again be given in smaller doses.
There is no use in administering digitalis for tbe relief of oedema in small doses over a long time. Thus administered it will not aceomplish desired results* 1 have frequently seen it fail when thns given, whereas subsequently prescribed in large doses during several days it has succeeded in accomplishing what it previously failed to do. ' '
Finally, I wish to again emphasize tlie statement that if thi5' unrivalled agent is to be employed for the removal of trdema it ia best given as an infusion of the English leaves. The tincture, the fluid extract, or the powder, digitoxine, and the various digital* ins, whether French or German, will not prove so efficient. The tincture is preferable for prolonged administration in small tonic doses. It will undonbtedly augnient the flow of urine by ener- gizing cardiac contractions, but for the removal of anlema would have to be given in doses that would be dangerous in the hands of the average medical man. This is particularly true of digitoxine and tlie French or crystallized digitalia. Excepting the latter, I have tried all forms of the drug, and I think I can safely assert tiiat all can be accomplished with the reliable tincture and prop- erly prepared effusion that can be with the other less familiarly known preparations. I well rememl)er my experience with digi- toxine. In one case it produced so jujwerful an effect in what was considered a safe dose, that I speedily discontinued it in alarm. In the second case, that of a middle-aged woman with mitral disease and an arrhythmic puke, the remedy was admin- istered cautiously and without appreciable effect one way or the other, when suddenly, almost w^ithout w^arning, the patient died, I could not say her death was due to the digitoxine, and yet I have always had an uncomfortable suspicion that it was. Th^re- fore I would urge inexperienced practitioners or such as prac- tice in the country, w^here they cannot keep their patients under as close scrutiny as if they were near at hand — in a hospital, for instance — to content themselves w^ith safer preparations.
Strophanthus, convallaria niajalis, adonis vernalis, erythro-' phlcin, and barium chloride l»elong to the digitalis group, and therefore possess diuretic proi>erties, convallaria having been particularly lauded by the liussians. None of them is the equal
498 DISEASES OF THE HEART
of digitalis, however, and in serious cases they are not likely to prove so reliable. I have used them as adjuncts or substitutes for foxglove when this had to be discontinued temporarily or could not be tolerated, but I have never ventured to rely on any one of them exclusively when dealing with a critical case of cardiac in- competence from valvular disease. In the young with rheumatic endocardial lesions, or in older persons whose arteries are not appreciably stiff, one need not apprehend ill effects from the vaso- constrictor effect of digitalis, while if the remedy be given in ice-water, or if the fat-free tincture be used, it will rarely disa- gree seriously with the stomach. When the vessels are athero- matous its effect on the arteries must be reckoned with, and then strophanthus may have to be used instead or be combined with digitalis. In these cases the latter can generally be employed successfully even for the treatment of owiema if nitroglycerin be given often enough to counteract the constriction of the arterioles. Before concluding the subject of the administration of digi- talis I wish to direct attention to the possibility of its occasioning mental symptoms that may be misunderstood and attributed to the disease instead of to its right cause. These are hallucinations and delirium. H. O. Hall has recently contributed a paper on this peculiar action of the drug, and quotes from an article thereon by Duroziez, who reported twenty instances of the kind. In this present work I have referred to the fact that in two pa- tients whom I attended in connection with Dr. Houston a peculiar mental and emotional state developed during the prolonged admin- istration of digitalis and disappeared after the discontinuance of the remedy. In Miss T., with mitral disease, there was a singular sort of sullen moroseness with taciturnity, while the other patient, a man with aortic insufficiency, manifested a mild delirium of a harmless kind. Hall suggests that this effect may follow the ad- ministration of even moderate doses for a considerable period, and very pro})erly queries if it does not occur far oftener than is sus- pected. For my part I frankly confess that until my attention was directed to this singular effect of digitalis by Dr. Houston I had no suspicion of its possibility. There may be no danger asso- ciated with this action, but it may indicate an unusual degree of susceptibility to its influence, and that in such persons one should be especially on his guard against the cumulative action of the
TJ[E TREATMENT OF VALVULAR HEART-DISEASE
41>f>
ent. 'Vhh luttcr i^ no fancied mie, and should always^ be kept ttt mind.
It is probable that digitalis poisoning occurs far more fre- quently than IS suspected. 1 am painfully certain that in one instance the i^iiJden death of one of my patients was due to digl* talis, which was being adniinistered in large doses. In this case, however^ the patient disobeyed my emphatic injunction to remain absolntely quiet in bed, and fell dead while walking abont, just as ] liad wanicil liini he might do if he got np. Since that time it has been niy custom to fliscontinne digitalis every fifth or sixth day in all eases in wbich it is being taken in considerable doses or when tlie patients are not under frequent observation. Tn this way time is allowed for the elimination of the drug. Lastly, it is said that there is less danger of a cumulative effect if a daily cathartic is taken, since it may be largely eliminated through the bowels.
Acceaaory Heart-tonics. — Strychnine is a valuable heart-tonic at all times, and when compensation is lost is of great value. It should not he dejxmded on alone, but prescribed as an adjuvant to the cardiac energizers already mentioned. Administered hypo- deruiically it is nndunbtcdly more rajiid and powerful than by the njouth, and would best lie empbiyed in that manner. Its bene- ficial action is not confined to the heart, for it is a respiratory stimulant as well, tending tliereby to lessen the sense of dyspmra. Througli its powerful effect as a tonic to the nervous system it induces a feeling of strength and wxdbbeing very scKJthing to the tired, oft(*n irritalile sufferer. It certainly helps a patic-nt endure the insomnia that so often attends his loss of compensation,
I have always been of the opinion that to display its kindly action strychnine shonld be given in full doses, care being had to avoid its physiological effects in toxic amounts. One thirtieth of a grain hy|>oilermically may usually be administered every four, or in extreme cases every three hours. I have not hesitated to order that dose as often as every two hours, or even hourly in times of great peril. The obJ€*ction to such doses have been previ- ously state<i (See page 445.)
Another remedy of inestimable service when the heart threat- ens to fail altogether or the jmtient is tormented by dyspn^ra, par* ticularly at night (cardiac asthma), is morphine. If adminis*
500 DLr.EASES OF THE HEART
tered hypodeniiically and in small doses this drug proves a pow- erful cardiac nmiiilant. An eighth or a tenth of a grain thrown under the skin will arouse a flagging heart, steadying its action and improving the quality of the pulse in a manner not equalled by any other agent of which I am aware. If yH of atropine is combined it serves to warm up the skin by flushing the capillaries, and by deepening the respirations relieves dyspnoea. Given at bedtime, morphine will generally carry the sufferer through the night without his wonted attack of dyspnoea and depression. In some instances it acts as a hypnotic, but even when it fails of this action it allays restlessness and induces a sense of well-being that is most grateful. Larger doses are more or less depressing, and exhibited by the mouth the stimulating action of the remedy is not the same as by subcutaneous injection. I have known many a patient to tolerate morphine in this manner for weeks, and when it was at length withdra\\Ti not to experience any special discom- fort. It is not to be resorted to indiscriminately, but only in those cases in which it is necessary either to tide over a period of crisis or to promote comfort of body and repose of spirit. Of course for the relief of pain larger doses are necessary, as is like- wise the case when it is desired to produce sleep.
Hypnotics. — The ultimate aim of treatment in the stage we are now considering is the restoration of circulatory equilibrium, and thereby of heart-power, and yet we should never forget that the accomplishment of our aim often depends almost as much upon attention to subordinate or accessory conditions as upon measures addressed to the heart directly. For instance, cardio- paths suffering from ruptured compensation are very apt to com- plain of actual insomnia or of fitful and unrefreshing sleep. This may be due to disturbed cerebral circulation, to retention of waste products, or to the generation of toxines, or to all these factors combined. So long as natural sleep is wanting, the invalid is de- prived of what Shakespeare has so fitly termed " Nature's sweet restorer," and the exhaustion of the nerve-centres following pro- longed wakefulness may throw the balance against recovery. Moreover, the heart itself is robbed of the rest which comes from its slower action during sleep. It is most important, consequently, to combat this distressing condition by such means as will prove harmless.
TOE TREATMKXT OF VALVULAR HEART-DISEASE
501
In some cases sleep follows the measures directed against vis- ceral congestion and a^dema, or is directly induced by the hypo- dermics of morphine administered for relief of ncM?turnal dysp- noea. When such ia not the case, recourse should be had to hyp- notic remedies as aiich*
Chloral hydrate is too powerful a cardiac depressor to be safely enipIoy€*d in uncompensated valvular disease, or indeed in any case in which tbe pulse is not strong and tense. On the other hftnd» chloralauiide- Bayer is said to exert no injurious effect on the circulatory apparatus. If it affects the pulse at all, it is by accel* crating it while at the same time augmenting its tension. Tbo main drawback to this agent is its liability to occasion headache next morning and its unpleasant acrid taste. To obviate the for- mer effect, therefore, an etpuil amount of potassimn bromide may be added to each dose of chloralamide, while its disagreeable taste may be *lisguised by some palatable sirup. The remedy is per- fectly safe in doses of from 15 to 40 grains, and to prove efficient ought to be given in a single full dose. A good fonnula is the following: Chloralamide-B. 2 grammes, spiritus frumeuti 15 cubic centimetres, jxjtassii bromidiuni 2 grammes, and syrupns glycyrrhiza', q. s., ad 30 cubic centimetres. M. et sig. This dose to be taken at bedtime.
Chloralose is a hypnotic highly recommended by Balfour in his capital work The Senile Heart. Its dose is from 2 to 8 grains, best given in capsule, and is said to tend to slowing of the pulse while at the same time low^ering its tension. I formerly pre- scribed it a good deal, but ultimately abandoned it l)i»cause I found that when uiy lady patients took 5 grains at a single dose, or w^re obliged to repeat a capsule containing 2 J to 3 grains, they were apt to complain of nervousness the next nioniing; it is, how- ever, safe and usually prmluces sleep fpiickly, Sulphonal and tri- onal are both safe and efficient hypnotics for tbe class of cases now considered, since although they accelerate the pulse and somewhat raise arterial tension, they do not depress the heart. Paraldehyde in full medicinal doses of a drachm acts similarly to chloral hydrate as a sojK>riiic, but unlike the latter is perfectly safe even for weak hearts, being said to slow and strengthen the pulse. Its action is not so prolonged, however, and patients often object to it on account of its burning taste and persistent odour
502 DISEASES OP THE HEART
in the breath. Thi8 does not by any means complete the list of available hypnotic remedies, but comprises those that are the most eflScient for cardiac sufferers. Should these not occasion sleep, and in uncompensated valvular lesions insomnia is often most intractable, recourse would better be had to morphine or some preparation of opium, of the advantages of which as a heart-tonic I have already spoken.
Best. — Having dwelt at some length on the medicinal manage- ment of this stage of valvular heart-disease, I now desire to add a few remarks concerning the great importance of physical repose. Nothing is more essential when compensation has failed than the strict enforcement of absolute rest. There is no greater mistake, and nothing that will more surely render futile all attempts to re- move dropsy, than to permit the patient to walk about. Even the moderate exertion of visiting the closet in an adjoining room will often be sufficient to maintain the venous congestion and opdema. The patient should be required to remain absolutely in bed or on a couch, and he should make use of a bed-pan. Only in those instances in which patients find it impossible to so empty the bowel or bladder should this rule find an exception. When such is the case, they may be permitted to leave their bed and sit upon a night-stool placed close at hand, or better still use an adjustable bed. The effort of raising themselves in bed will often in cases of extreme dilatation suffice to frustrate all attempts at a reduc- tion in the size of the organ. Therefore, dropsical patients should have the necessity of physical repose clearly explained to them, and should be kept at rest until all traces of oedema have disappeared. In mitral disease this precaution will of itself often do much towards removing sjTnptoms. In cases of uncompensated aortic insufRciency absolute repose is of the utmost importance, since a single injudicious effort may occasion paralysis of the overdistendcd left ventricle in diastole.
Another danger arising from exertion in cases of extreme and long-continued back pressure in the lungs is the establishment of relative pulmonary regurgitation. When this once supervenes, it is in my experience impossible to ever again restore compensa- tion, and the end is not far distant.
Exercise. — Only after the cardiac cavities have become un- loaded, and compensatory hypertrophy has begun to be restored,
THK TREATMENT OF VALVULAR HEAHT-IUSEASE
5113
iliir€^ tlio patient be allowed to indulge in exercise. Even then exertion must \\e very slight iit first, and the medicul attendant shonld observe the effects of effort, and thus form an intelligent opinion of how far cardiac strength has become re^stahlislied. I make it a rule to l>e present the first time walking is attempted, sti lis to note the effect of exertion on the pulse.
Baths. — In this critical stage of cardiac incompetence I lielievo Xanheim baths con Ira- indicated, and even in thr matter <d* biithiii»j; for the sake of cleanliness patients must content tlu^mselves witli the morning spon^c-bath given by the nurse. It involves too mut*h L'xertion for them to bathe themselves, and particularly to get into a tub.
EeceiTing Visitors. — Apparently trivial influences may make for ar against tht* restoration of heart- |>ower. Consequently, when there is a damming back of the blood into the lungs and right heart, this latter chanil>er sIiouM not lie additionally strained by prolonged t'onvcrsation. The reason for this lies in the consid- eration that when words are uttered the breiitb is held, and that with expiratory effort air is driven nut through the partially closed glottis. That this throws additional burden on the heart is plain, and is proved, moreover, by the clinical observation that cardiopaths nearly always exhibit brcalhlessuess while talking. TluM'efore, these invalids e^tiould not Ik* allowed to receive visits from friends, unless perha}>h from a few wlm ran be relied on to niono|Milize the conversation, and who know enough to leave so soon as the patients exhibit signs of weariness.
Diet. — This is a matter of tlie very greatest importance, and must not Ih? left to the whims at the invalid or the zealous but ignorant notions of friends. The considerations and principles which obtain in cases of failing but not yet wholly l6st heart- power a]iply with added etnphasis to these, and hence the reader is referreil to what has I>eeTi already said.
Although tlte Mianagpiuent of this stage of valvular lesions is tiv Ih' fi»nducfed along definite lines, still it is and must of a neces- sity Ik* largely symptomatic. There is a certain routine about it, and yet the physician must be ever alert to detect signs of danger and avert it by prompt action, and equally to take advantage of all circumstances that exert an influence for good. He should not exhaust his patient by unnet'cssary examinations, and yet he
504 DISEASES OF THE HEART
should look over the case daily with suflScient care to detect the earliest signs of any of the many complications to which the patient is liable. It is especially necessary to make frequent and thorough analyses of the urine, and he should insist on a record being kept of the temperature for the detection of some of the terminal infections so frequent in these cases. If he cannot restore cardiac ,energ}% he can at least prolong life and do much to minister to the patient's comfort.
If he be so fortunajte as to aid Nature in re-establishing some degree of cardiac power, the case then becomes one of the second class, and is to be managed along the lines laid down in the second portion of this chapter.
SECTION III DISEASES OF THE MYOOAUDIUIH:
ClIAPTEK XLX ACUTE MYOCARDITIS
It 18 not the desijyrn in tiiis chapter to coDsider acute inflam- niatioii of the myoeanliiim in assfK*iation with acute peri- or endo- canlitis, hut the acute inihimmation ohserved in the eoiirse of s\ye- cific fevers and otlier acute iiiiectious processes, and which usn* iillv exists independently of intlainuiation of those membranes* This form of mjoearflitis is described by authors as acute intersti- tial and acute paren(*hymatouft myocarditis, the latter, as re- marked l»y Osier, lieing regardeil l»y some as a degenerative process.
The history o{ acute myocarditis is not clear until we come to the works of comparatively recent years. Suppurative myocar- ditis has been recognised since the earliest days of medicine, and by Galen was rei^ar<led as the disease of gladiators (Iluehard). Beuiveni, in tlie fifteenth century, discovered an abscess in the wall of the left ventricle, and in 1553 Nicolas Massa found an abscess in the right ventricle with a sinuous tract extending into and jMTforating the auricle,
itorgagni was familiar with myocardial inflammation^ and Senae devoted a chapter to this affection.
Since the lH?^iunin»r <»f the last century the names of innumer- able workers, inchiding Corvisart, IIo|>e, Andral, Laennec, and Stokes are linked with the history^ of myocarditis, but their views were more or less obscure. For the most part the changes were spoken of as a soften iiig of the heart-muscle.
Bouillaud considered this softening as due to inflammation of
505
506 DISEASES OP THE HEART
both the niiiscle-fibres and interstitial connective tissue, and dis- tinguished three varieties : The red, which is acute ; the white or gray, which is purulent ; and the yellow, which is a chronic phleg- masia.
Rokitansky distinguished acute interstitial and acute paren- ch^Tiiatous myocarditis, and gave an excellent description of them as he observed them in cases of typhus fever.
Virchow's studies on parenchymatous myocarditis opened a new era, for in ])lace of the old-time changes in the consistency of the heart-muscle he described definitely recognisable micro- scopic and chemical changes in the structure of the muscle-fibres. He was foUowed, in Germany, by Stein, von Zenker, and others, while in France, Ilayem did noteworthy work along the same lines. The three divisions, which Ilayem made according to the duration of the process, were thought, however, to be too sharply dra\vn.
Among more recent German writers who have made valuable contributions to acute myocarditis as observed particularly in diphtheria, are to he found the names of Birch-IIirschfeld, Ley- den, Rosenbach, and KonilxTg. The last-named is considered by Fraentzel to have added greatly to our knowledge on this subject, and I desire to acknowledge my indebtedness to his lucid and eminently practical ex])ositi(m of the clinical features of acute myocarditis, as set forth in Ebstein's Practice.
Morbid Anatomy. — The myocardium is the muscle layer of the heart, and corresponds to the media of the arteries. It is thick in the walls of the ventricles and thinner in those of the auricles.
The lesions of myocarditis are usually most pronounced in the ventricular walls (m account of the greater work thrown on these portions of the heart-muscle. The fibre of the heart-muscle is structurally between that of voluntary and involuntary muscle. The individual cells are short cylindrical bodies, containing one nucleus each. The greater ])ortion of the })rotoplasm is differen- tiated into contractile fibrilhe which possess the optical character- istics necessary to give the appearance of striation, the fibre being thus striated in both the cross and longitudinal direction.
The myocardium possesses a very rich ca])illary blood-supply which is derived from the coronary arteries, and also from minute
ACUTE MYOCARDITIS
arteries opening directly from the left ventricle. Normally there is but little interstitial tissue in the myocardiuui, which is sepa- rated froui the pericardium by a variable layer of fat, while the endocanliuni lies directly on the muscle layer*
Acute myocarditis is either parenchymatous or interstitial. The imreiichynuUous form includes the various acute degenera- tions of the niyocardiunij which are usually dependent on the presence of irritants in the cireulationj such as the toxines of the inftK*tious fevers. Cloudy swelling and granular degeneration aro the most conimon manifestations of the process. In them the myoc^ardium ajJiwara pale and opaque, and is soft, tlabby, and easily torn.
Microscopically tlie fibres are swollen, their protoplasm moro or less granular, and both the cross and longitudinal striations are obscured. The degeneration induces a more fragile condition of the fibres, so that they are often found ruptured or separated along the cell boundaries — a condition of fragmentation or aeg- mentation. In thest! cases the rupture probably takes place in artictilo mortis. Both these forms of degeneration are usually diffuse and not confined to any special areas.
A form of acute myocarditis which may be classed as paren- chymatous, and which sometimes leads to serious results, is that which follows embolism of the coronary arteries. Infarction of the heart is followed by coagulation necrosis of the tissue involved, and is usually attended by some inflannnatory infiltration of the area. ITltimately the necrotic area is replaced by scar tissue in the manner to be considered under the heading of the chronic form of the disease.
Acute inlerMKial myocardifts may he punilent or siuiph*. The purulent fomi is usually characterized by the formation of ab- 1 scesaes, which may be many or few in number* On section these appear as whitish or grayish areas of softening, which are de- pressed Iielow the plane of the cut. The larger abscesses may con- tain fluid or semi-fluid pus.
Often asscx'iated with acute endfM*arditis, it may lie a direct extension from the disease of the endncardium. In this case the foci of suppuration are larger and less numerous than in the case of suppurative myocarditis dej>endent oti a general pyaemia when the foci are numerous, wndely scattered, and may be so small as to
508 DISEASES OF THE HEART
be barely visible to the unaided eye. Microscopically the smaller foci appear as masses of polymorphonuclear leucocytes surrounded by a zone of degenerating muscle.
Bacteria can often be demonstrated by appropriate methods. The abscesses rarely attain large size on account of the early su- pervention of death. They may rupture into the heart or into the pericardium, or the wall may become so weakened as to produce rupture through the entire thickness of the heart.
The simple form of acute interstitial myocarditis is a rare condition which is found in some of the infectious diseases, nota- bly typhoid fever and diphtheria. In this the chief lesion is the infiltration of the tissue with IjTuphoid and plasma cells. These foci of infiltration are more numerous in the left than in the right ventricle, and are usually situated close beneath the endocardium. In these foci of infiltration there is usually considerable degener- ation of the muscular tissue, which is characterized by swelling and destruction of the nuclei.
Associated with acute myocarditis are the various conditions to which the disease is secondary. Chronic myocarditis may often, though not always, be secondary to the acute form. In abscess of the heart, rupture into the circulation may cause gen- eral pywmia and septic embolism.
Etiology. — Acute inflammation of the heart-muscle is ob- served in connection with such acute infectious diseases as diph- theria, typhoid and typhus fever, small-pox, scarlatina, gonor- rh(ea, and even articular rheumatism.
Freund has described a case of acute diffuse myocarditis of the purulent variety in a forty-eight-yea r-old butcher who fur- nished no evidence either before or after death of any other infec- tion than that of inflammatory rheumatism. lie also cites simi- lar instances collected from the literature. Whether in cases of rheumatic arthritis there is some secondary infection that is re- sponsible for the myocarditis, or it is the rheumatic poison itself that creates the mischief, it is impossible to decide. In the spe- cific fevers it is the specific infection ])robably which gains access to the heart-muscle and there excites inflammation. It may also be that the character of the myocarditis is determined by the viru- lence of the micro-organism. Romberg thinks it is the intensity of the poison and not its continued action which determines the
ACUTE MYOCARDITIS
509
iiUiTJiate course of t!io iiiflaiiniintory j)ro<?ess, for " in many cases the disease uf the heart- utilise le reuehes its liighest point a consid- erable time after the deeline of the infection, and it is not to Im3 assimied lhat all this tLaie the toxic agency continues to increase in activity/*
The process may possibly be eumpareil, lie thinks, to the in- flammatory reaction set up in a part whose function has bt*en destroyed by a burn, or to the tabes dorsalis which develops as an after etFect of syphilitic infection.
In Alay» 11)00, Poyntoii reported a comparative study of the changes in the heart-wall in one case each of diphtheria, rheuma- tism, and chorea. In the tirst-named affection, which c^ccnrred in a child of five ycars^ and proved fatal on the seventeenth day, the changes were those of acute parenchymatous degeneration^ the muscle-fibres showing profound destruction, in some places even to the disappearance of the miLscle-fells witli rctcntiou of only the reticulum. Assriciated therewith was a cellular infiltration of the interstitial connective tisstic*. The endocardium and pericardium were free from disease.
In the heart of the rheiimntie patient, a young man with clini- cal evidence of mitral disease on ailmissioUj and a day or two later of fresh pericarditis, which lesions were found after death, the muscle-fibres showed extensive fatty degeneration, but were not so profoundly disintegrated as in the case of diphtheria. There was also an exudation of cells into the connective tissue here and there around the hlood-vessele.
In the case of chorea, a child (bat had manifested great rapidity of cardiac action, the muscle-fibres of the heart also showed more or less fatty degeneration with scattered areas of cell exudation into the interstitial connective tissue. The changes reseuibled those found in the heart of a rabbit that had been ren- dered pya*mic by the injection into the circulation of streptococci.
In commenting on the microscopic findings in the diphtheritic heart, Poynton pointed out their close similarity to those de- scribed by ilollet and Regaiid, and produced by the injection of diphtheria toxines into lower animals. As to the myocardial changes in the rheumatic case Poynton was of the opinion that they were w^ithout doubt due to the* rheumatic poison, and that they strongly suggested the likelihood of the rheumatic virus
510 DISEASES OP THE HEART
being a toxine of microbic origin ; their clinical significance wa3 very obvious and proved that the cardiac failure in rheumatic pa- tients with valve defects is not always to be attributed to mechan- ical causes.
Whereas these observations of Poynton are not new, they are of value because contrasting and illustrating the effects on the myocardium of these two important diseases, diphtheria and rheumatic fever.
Purulent inflammation of the myocardium is found in connec- tion with pyaemia and ulcerative endocarditis, the bacteria being brought to the heart-muscle in the blood or gaining access directly from the endocarditic affection. Septic emboli may enter a coronary artery and give rise to abscesses. The primary focus of infection may be a suppurating woxmd, or micrococci may effect an entrance into the system without leaving any trace of their port of entry behind.
In rare instances acute myocarditis has appeared to follow trauma, as in a case reported by Rindfleisch of a man who gave no other etiological factor than a fall from a considerable height, and striking on the left side of his chest.
Ssnnptoms. — The observations of Romberg and Schmaltz have shown that in diphtheria the symptoms of acute myocarditis occur in from 10 to 20 per cent of all cases, and in the majority of instances appear in the second or third week of the illness, occasionally towards the end of the first, and rarely as late as the sixth or tenth week. These symptoms are the expression of dimin- ished heart-power, and naturally, as regards intensity, depend upon the degree of the myocardial inflammation. Although for the most part they are so apparent that they cannot escape detec- tion by a careful observer, yet there are eases in which death takes place suddenly without previously recognisable sjnnptoms. On the other hand, according to Romberg, the symptoms of acute myocarditis, when occurring in typhoid fever, scarlatina, small- pox, gonorrhcra, and acute articular rheumatism, are less conspicu- ous than those of diphtheria ; particularly is this true during the stage of fever. Furthermore, it is often impossible without post- mortem inspection of the heart-muscle to determine whether the symptoms are not due merely to functional derangement of the heart's action.
ACUTE MYOCARDITIS
511
In all cases of atnUe tu^tx^arditis wtuoh is not purulent, it is a tsuhject for speculation whether the weakening of cardiac energy is due to destruction of the muscular elements, or to the nieehanieal effect of cell exudation into the interstitial con- nective tirisiie^ or dependa merely upon functional depression (Romberg),
Subjective symptoms are not aw^ays present, and if not wholly lacking are not always pronounced* and therefore close observa- tion on the part of the medical attendaut should never fail. Pal- lor of (he countenance is present, and is often a striking phenonie- nun, Poynton mentions it in Wth of his cases of diphtheria and rheumatic fever » especially the ftirmcr. It is due, according to Romberg, to defective tilling of the cutaneous vessels, since the blood is of normal composition. Vomiiing is another symptom sometimes of great importance^ and has been dwelt on by Villy in connection with the cardiac failure of diphtheria. It may be so i>ersistent as to suggest some abdominal disorder. There is anorexia, and the patient is often strikingly weak and listless, or instead of apathy nuiy display restless anxiety. In a word, the patient conveys the impression of being profoundly ill.
The features of the case, however, that must strongly point to my^x-arditis pertain to the seat of misehief^i. e., the heart. The pulse is more frequent than normal, although as a rule its rate is not greatly accelerated, being 100 or thereabouts. Arrhythmia may or may not be present; often there is only irregularity in force and volume. Its striking characteristics arc feebleness and emi^tiness, and as the disc^ase progresses loss of stability as well as volume, very slight exertion being sufficient to send up the pulse-rate out of all proportion to the degree of effort.
Examination of the heart at this time may disclose some in- crease of dulness, jmrticularly of the relative, to the left and upward, but also to the right. Yet in the beginning, sometimes even throughout the course of the nuilady, uuirked <lilatation is not detected. Cardiac impulse is absent, and the sounds are nota- bly feeble, espe(*ially the first at the apex, which is often so toneless as to be almost inaudible. In a few eases dilatation of the left ven- tricle reaches such a degree as to jienuit muscular incompetence of the mitral valves, which is declared by a soft, it may be feeble systolic apex-murmur. The disturbance of the circulation may
512 DISEASES OF THE HEART
be further shown by hepatic engorgement, and in some cases patients complain of pain in the region of the liver.
The presence or absence of other signs of venous stasis, as oedema and scanty, albuminous urine, is determined by the degree of circulatory embarrassment. In some cases there is much prae- cordial oppression and anxiety that may amount even to pain of a dull and oppressive or poignant character. Freund lays great stress on substernal pain, and thinks it a highly significant symp- tom and far more pronounced than in endocarditis. In his case the patient often -indicated the sternal region as the seat of his dis- comfort, and declared he knew he was going to die.
The course of acute myocarditis is very variable. It may set in abruptly and progress rapidly with severe sjonptoms, leading to death in two or three days or one or two weeks; or it may arise insidiously and be latent throughout, even up to the moment of sudden, unexpected death; or there may be alternation of periods of entire absence of subjective symptoms, with times of alarming weakness and indications of threatening dissolution.
The cases which in one sense are the most dangerous are those in which the myocarditis develops weeks after the (Hsappearance of the diphtheria, at a time when convalescence is thought to be progressing satisfactorily, and the patient has perhaps passed out from under the care of the physician. In such the child, uncon- scious or uncomplaining of symptoms, plays about as usual, and one day making some extra exertion falls to the floor and expires without warning.
Romberg is of the opinion that the circulatory disturbance is not to be explained on the hypothesis of mechanical obstruction merely, the same as in cases of chronic cardiac disease, inasmuch as cyanosis, dyspncva, and cedcma are not prominent s\nnptoms. The pallor and arterial emptiness are rather the effects of the toxines on the vaso-motor centre, of the kind shown by his and Passler's experiments to result from acute infections. It is pos- sible also that splanchnic neuritis, as suggested by Veronese, may be a factor, producing stasis within the great abdominal vessels, paralysis of the vagus being out of the (juestion. Only in some such way can one accoimt for the absence of pulmonary congestion and dyspnopa.
As regards myocarditis from rheumatic fever, it usually
ACUTE MYOCARDITIS
618
attaeks hearts rtlrc*ady the i?oat of iieutt* or obruiiii: endocarditis^ ur is iiissoc^iated with iieriearditis, ahhougli the niiiselc ah>ne may sometimes be affected. For this reason it is not easy to recog- uim or detinitelv determine the myoearditic eomplication. More- over, experienee proves the folly of attributing to myoeardial in* flamiuation the cardiac ustlieiiiaj or even dilatation, so often wit- nessed in acute rheumatism, for it is often but a numifestation of the jKiiifson upon the funetion of the organ. At all events, it is the part of wisdom in such eases to refrain from a positive opinion.
In typhoid and scarlet fever it is not uncommon to observe during the heiglit of the attack symptoms of heart weakness^ which in most instances subside with convaleseeuee, and which are [K*rhapa the result of the action of the infection on the vaso- motor centre in the cord, together with exjianstion of the heart- muscle. Xeverthcless, one should guard against an inclination to look on all such manifestations as not due to myocarditis. The onset of acute inflammation of the heart-wall is often so insidious during the febrile stage, and tlie synijitoms are so latent, that the real nature of the heart disorder is readily overlooked*
On the contrary, when after subsidence of all active symptoma referable to the primary disease au*l during convalescence the pulse begins to assume the characters already descril)ed— i. e., feebleness, emptiness, irregularity, and cons|>icuons instability — one should at once suspect the existence of myocarditis.
We frequently encounter individuals who have successfully weathered a severe tyjdioid fever nniny nifinths^ even two or three years before, and still display undue rapidity and even irritabil- ity of the heart's action, 1 am always inclined to speeidate on the jiossibility of such patients having suffered from unsuspected myrn^ardiliB of luild form, and yet sufficient to have left its traces li€*hind. Should the heart-muFtcle become inflamed during or after the subsidence of acute rheumatic manifestations, the symptoms of circulatory embarrassment will be out of proportion to the clinical evidence of cardiac disease, and yet are very likely to be attributed to such structural alterations as are diiseovered. There is far more feebleness, emptiness, inequality, perhaps intermit- tence, and particularly iustaliility of the pulse, than there is evi- dence of viseeral engorgeuient and mechanical obstruction in the 88
514 DISKASfiS OF THE HEART
(^\t rein i ties, at all events until sufficient time has elapsed for the endocardial mischief to become intensified by the myocarditis.
The symptoms of purulent myocarditis depend somewhat upon the nature and extent of the changes induced, but are essen- tially the same as in malignant endocarditis — i. e., rigors, inter- mittent fever, sweatings, and splenic enlargement. If an abscess of the mvocardium breaks into the blood-stream, there are in- farcts in the skin, kidneys, brain, or other organs, or in event of rupture of the heart-wall, collapse and death. The clinical picture is usually such as to direct attention to the heart as the seat of the disorder. Yet in cases of diffuse myocarditis like that narrated by Freund, symptoms referable to the heart may be few and obscure, wholly out of proportion to the gravity of the malady.
Physical Signs. — Inspection. — Pallor is said to be conspicu- ous, and, associated with either apathy or restlessness, is very suggestive.
Palpation. — The pulse is weak, empty, and strikingly unsta- ble, and the cardiac impulse is feeble or absent. In some instances the liver and spleen may be palpable.
Percussion. — This may or may not disclose an increase in the area of deep-seated cardiac dulness, but if such increase is assoc*iated with the characters of the pulse just mentioned, it greatly strengthens the diagnosis.
Ausculiaiion, — As a general thing the ear detects no more than enfeeblenient and perhaps muffling of the heart-sounds. Murmurs are present only when dilatation leads to muscular valvular incompetence or endocarditis or pericarditis is associated.
Diagnosis. — Unfortunately the diagnosis of acute myocar- ditis is usually a matter of conjecture, and reliance must be placed on the history of some infection that may act as an etiological factor, even more than on the symptoms and physical findings. During the height of an acute infection, as diphtheria, acute rheu- niarthritis, and typhoid fever, it may bo utterly inii)ossible to diagnosticate with certainty the existence of acute myocarditis, whereas the occurrence of the physical signs described during convalescence renders the presence of the disease highly probable. If in a case of susjx»cte<l myocarditis j)lienomona of sej)sis are observed, they point strongly to a suppurative process.
ACUTE MYOCARDITIS
515
Prognosis. — It goes witboiit ^^ajing that the progiiutiis ia alwHvs gruvo, even in simple Dijocarditisj and in the purulent form is absolutely unfavourable. Although there is post-mortem evidence that sniallj scattered abscesses in the heart-wall some- times undergo a process of cure^ still a ease that is sufficiently outspoken to be clinicalh' recognisable is from its nature incura- ble. In acute interstitial myocarditis of diphtheria Romberg computes the fatal terminalion as taking place in about one-third of the rei!Ognised eases.
It is not unlikely that in rheumatism the percentage of recov- ery is larger. This would appear reasonable when we consider that the parenehymatons degeneration is not so intense as in diphtheria. AHbongh all cases do not die, yet the possibility of sudden death should never be forgotten; and, moreover, this pos* sihility is not wanting in any given case simply because the evi- dence of cardiac mischief is slight. It is often precisely in this class of cases that danger is most imminent, since the physician, patient, luul friends are likely to be thrown off their guard, and hence i>ermit or commit indiscreet effort.
When, on the other hand^ symptoms of collapse appear, the danger of death is very imminent. Increasing acceleration of the pulse and marked instability, the heart evincing a degree of fee- bleness out of all proportion to the demand made upon it, are signs of great danger. So also is abnormal retardation of the pulse-rate, as is exceptionally observed. Delirium renders the prognosis more grave; and the occurrence of emboli is an exceed- ingly had omen, since we cannot predict how many are likely to follow or where they wdll h)dge. Favouralde indications are to be found in a gradual return of strength^ volume, and regularity to the pulse,
Ti^eatment,^ — We possess no means of directly influencing the inftammatory process after it has attacked the myocardium, and therefore our efforts must, in the first place, be directed to the prevention of myocarditis, if possible, and secondly, to pro- tecting the heart-wall from all extraneous influences which can intensify the damage it is sustaining from the inflammation. To the former end is the early employment of such measures as may lessen the activity of the primary disease, which in diphtheria involves the earliest possible use of the antitoxine. The harm
516 DISEASES OF THE HEART
that may result from delay in the employment of this remedy becomes at once apparent when we reflect on Romberg's statement that the symptoms of acute myocarditis may arise at a time sub- sequent to the administration of diphtheria antitoxine, which goes to prove that the longer the infection is at work in the system the greater the likelihood of the heart-muscle becoming affected. In streptococcus infection the antistreptococcic serum would cer- tainly be indicated; but in scarlatina, typhoid fever, and rheu- matism we have no specific remedy, unless with the exception of salicylic acid in rheumatic fever; and hence we must endeavour to promote elimination through the kidneys by administering copious and frequent draughts of water, and subcutaneous and rectal injections of physiological- salt solution.
So soon as symptoms of myocarditis are detected the indica- tion is to maintain the patient in absolute repose of mind and body. Physical effort is dangerous, and so long as cardiac weak- ness exists the patient must remain in bed. lie should receive as much highly nutritious and simple food as he can assimilate — milk, eggs, broths, etc. The bowels are to be kept active, though depleting purgatives are to be avoided. Strychnine is highly ser- viceable, and should alcoholic stinmlants or ammonia be thought indicated, they are to be administered.
The character of the pulse would appear to call for digitalis, stroplianthus, etc., but if prescribed, it should l>e cautiously and tentatively, for we are not in i)osition to predicate how much of the niyo(*ardiuui is left uninjured and capable of responding, or whether damage may not accrue to fibres that have undergone extensive degeneration. Pnixiordial pain and restlessness are to be allayed, and fur this purpose there is nothing l)etter than mor- phine.
In conclusion, it may be repeated that the agencies of greatest service are rest, food, strychnine, and stimulants, in the order mentioned. In di]>htheria it is often perilous to allow the patient to even rise up in bed to take a drink or to evacuate bladder or r(?ctum ; he must be kept as motionless as possible. Moreover, it will often be necessary to retain the patient in bed for many weeks or months. A rigid enforcement of this rule, even though it seems hard and cruel, is in fact a display of greatest kindness. When at length such a measure of improvement has been reached that abso-
ACUTE MYOCARDITIS 517
lute rest is no longer needful, the patient is to resume exercise by degrees, and at first with the utmost caution. Under no cir- cumstances is an attempt to ascend stairs to be permitted before weeks perhaps of gentle moving about the bed-chamber have proved that the heart is no longer unduly taxed by such efforts. During this period of convalescence cautious attempts may be made to strengthen the heart by resistance exercises and saline baths. At this time benefit may be derived from iron, arsenic, and other haematics and nerve tonics. It is needless to add that in the case of young children it is often most difficult, yet no less important, to enforce the quiet and other measures necessary.
CHAPTER XX CHRONIC MYOCARDITIS
SYN.: FATTY DEGENERATION —FIBROID DEGENERATION-^ MYOFIBROSIS— WEAKENED HEART— CHRONIC CARDIAC INADEQUACY
By far the largest number of persons who at or after middle age begin to manifest signs of cardio-vaseular disturbance are not victims of valvular disease. Clinically they present evidence of failing circulation with enlargement of the heart (hypertrophy with' dilatation), and with more or less thickening of the arteries. In some instances certain symptoms, as angina pectoris, point unmistakably to coronary sclerosis, with its consequent alteration pf myocardial nutrition, but for the most part there is nothing that serves as a criterion of the nature and extent of the change in the heart-muscle. The microscope has revealed not only a con- siderable variety of pathological changes in these cases, but also a want of imiformity or constancy in the relation of these to the symptoms. In other words, various myocardial alterations seem capable of producing the same clinical picture, and conversely, various clinical pictures appear to result from one and the same pathological change. There is consequently much confusion and uncertainty still regarding the pathogenesis and precise relation- ship of the pathological findings, so that in dealing with this phase of cardiac disease one is at a loss whether to attempt to consider it from the standpoint of the pathologist or of the clinician. In either case one is pretty sure to get himself into trouble. German writers, as Romberg and Rosenbach, group the cases under the head of Chronic Cardiac Insufficiency. The latter maintains that as the various changes in the heart-muscle are but different mani- festations of one process, it is impossible to diagnosticate anything more than heart-weakness, while Romberg classifies the cases ac- cording to their etiological factors. Thus he considers in one 518
CHRONIC MYOCARDITIS
519
grmip tliose due to roronary disease, those to obesity, those to strain, and those to nephritis, those to excessive consumption of beeTy etc. Such a division is in accord with the uncertainty of onr knowledge on many points, and also has the merit of sim- plicity, but it is open to the objet*tion that we cannot always l>e sure of the exact etiology of all cases « * of the precise mode of operation of supposed causes. It also, as he himself admits, necessitates much ref>etition, ami therefore T have decided to deal witli these cases under the heading given to this chapter. I am well aware of the object ions to such a grouping, and know that many times it seems simpler, and non-committal in a sense, to diagnose them aiTording to the gross clinical findings of hyper- trojihy or dilatation or idiopathic enlargement of the heart Still in most eases the microscope shows more or less myocardial de- gen(Tatinn, and tli(*refore I prefer the temi Chronic My^x'arditis.
Morbid Anatomy. — Fnder chronic myocarditis the ana- tomical renditions usually considered are tliose of fibrosis and fatty degeneration. (Conditions interfering with the nutrition of the heart may ivrmlnce either or both of thest^ changes^ or the fibroid may be de]>t^ndent on the fatty change.
Fibroitl degeneration of the heart-muscle, or chronic intersti- tial myocarditis, may represent the tinal or reparative stage of the virions acute forms of the disease. It is then to be regarded as a conservative rather than as a pathologic ]M"(k_h*ss. Hius in the ease of infarction of the heart, or nufomalncla conlm, tlic necrr>ti(* area is invaded by young connective-tissue elements, which finally arc metamorphosed into a firm Shroid cicatrix. Such areas of fibrosis, or scleroses, are large or small according to tlie size of tlie original lesion. Very large areas are rarely found, as the acute disease would have probably proved fatal. Except by the forma- tion of other infarcts this process doc^s not tend to progress. It is only when the ix»clusion of many small arteries has prodnced mul- tiple scleroses that the fnnction of the heart is impaired.
Extreme fatty or parenchviuatous degeneration, leading to de- struction of the muscle tissue, may be the cause of a progressive fibrosis of the myocardium. Often the destructive process preced- ing the interstitial increase is a coagulation necrosia. As a rule this prm*es8 is not strictly iliffuso, and the appearance on section is of numerous scatteretl streaks and sfjots of a grayish or wdiitish
520 ' DISEASES OP THE HEART
colour, which project slightly above the plane of the section. In- terstitial increase is not always dependent on antecedent degen- eration, but progressive atrophy of the muscle and increase of the fibrous interstitial tissue may occur pari passu in such a way as to render it difficult to determine which is the primary and w^hich the secondary process. In this case the fibrosis is more evenly distributed than in either of the above cases.
Scleroses are most frequently observed in the wall of the left ventricle, near the apex, and on the posterior side in the upper two thirds, near the auricle, in the papillary muscles of the left side, and in the interventricular swptum. The fibrous increase may cause a thickening of the wall of the heart — connective-tissue hypertrophy — or the presence of the connective-tissue elements may so reduce the tone of the wall as to cause it to yield to the intracardiac pressure with the formation of bulgings, the so- called partial cardiac aneurysm, or in extreme cases with rupture of the heart.
Fatty degeneration is manifested by a general paleness with streaks and patches of a yellowish-brown colour. The markings of such a heart have been compared to those of a faded leaf. The muscle is softer than normal and easily torn. Fatty degeneration is most common in the wall of the left ventricle near the ai)ex, next in the right ventricle, the interventricular sivptum, and the right and left auricles in the order given. It usually affects the muscle close beneath the endocardium more than that near the pericardium, and the brownish or yellowish mottling is sometimes plainly observable from within the heart. Microscopically the protoplasm of the fibres is seen to be replaced to a greater or less extent by fat droplets. These are arranged in rows, and are said to be situated at the junction of the cross and longitudinal striations. Very advanced fatty degeneration leads to a disinte- gration of the fibres, and their consequent replacement by fibrous tissue.
Fatty overgrowth consists in an increase of the normal subepi- cardial layer of adipose tissue. This is normally noticeable only along the course of the large vessels, but in well-marked cases of fatty overgrowi;h the fat covers the entire organ and no muscle is to be seen. A thick blanket of fat over the heart acts as an effectual impediment to its work, but it is in the nature of an out-
CHRONIC MYOCARDITIS
jn
side force, and not, as is tbe case in fatty degeneration, a disease of the !iHLsele itself. Sonietiniee, however, the adipose tissue invades the siibjaeeut mytx'ardium, first penetrating between the tibreri and later causing the complete atrophy and disappearance of the iiiiiSLde eU^ments. This pnx^ess may penetrate the entire thickness of a ventricular ^vall, and of course greatly impairs its functionating power.
The senile heart presents a varying picture made up of ele- ments from all of these conditions. As a rule the failing nutri- tion of old age induces a mixture of lib runs and fatty degenera- til III. Fatty 0%'ergrowth is common in those elderly persons w^ho intdine to obesity. The senile heart may Ire hypertrophie«l — tliis when associated with chronic nephritis and general arteriosclero* sis- — or atrophied in eonsecpumce of malnutrition and inaction. Very frequently tliis atrophy is combined with the condition of autfX'hthunous pignientalion already descriljcd. This condition uf brown atrophy is almost characteristic of the senile heart.
The nutritional disturbance which is accountable for these degenerations is freipiently the result of the gradual narrowing or occlusion of the coronary arteries or their branches. This uuiy Ik* due to a sclerosis that is part of a general disease of all the arteries^ or it may be due fn obliterating endarteritis or to a local atheroma of the coronaries either at their orifices or branches. This local process is more apt to take place in the descending branch of the left coronary artery, and this accounts for the spe- cial j>redis|)Osition of the apical p)]'tiun of the left ventricular wall to fatty anrl fibroid degeneratiun.
Thr*ind)osis or endiolism of the coronaries induces the condi- tion of myumahicia cordis already considered. The walls of the arteries may become of bony hardness, or atheromatous in patches. The terminal branches may Ix* converted into fibrous cords im- pervious tu tlje circulating fluid. If the obliteration of one artery takes place gradually the circulation iiMiy be established through branches of the other. The re^^nction of tlve blood-supply to the parts affected, and especially the lack of oxygen, induces fatty tlegeijcration, and often subsequent fibrosis. The heart-muscle, probably on accoutit of its constant activity, feels immediately any lack of oxygen, and hence the myocardium is especially prone to fatty degeneration.
522 DISEASES OF THE HEART
Changes in the myocardium are almost always found associ- ated with the various valvular lesions, and "with hypertrophy and dilatation of the heart from any cause.
Etiology. — The changes of the heart-muscle which I have chosen to group under the generic term of chronic myocarditis are of slow development, and presuppose the protracted working of influences injurious to the function of the organ. These influ- ences are for the most part conditions which cause a dispropor- tion between the demands made on the heart and its nutritive supply — in other words, which require the heart to work in ex- cess of its nutrition. The influences which put an abnormal demand on the heart may reside within the organism or may come from without, or there may be a union of both.
Under the first head are degenerative changes of the vascular coats and chronic kidney diseases, conditions which persistently augment peripheral resistance. Conditions residing outside the body are those which produce long-continued overstrain, as manual toil, the hardships of the soldier's or the sailor's life, the toilsome daily exertions of the mountaineer, excessive consumption of beer, etc. In many instances influences from within and without are conjoined. Something more is required, however, than mere in- crease of work, and this is to be found in disorders of cardiac nu- trition. The blood itself may be of poor quality, or it may be viti- ated by toxines of one kind or another, or the blood remaining healthy, its sup])ly to the heart may be curtailed. It is in the first way that fatty degeneration of the heart is brought about by wast- ing diseases, cancer, chronic suppurations, repeated loss of blood, secondary and pernicious anaemia, exhausting discharges, as chronic diarrhcoa, by insufficient food, etc. The blood may be vitiated by the toxines of acute infectious diseases, by chemical poisons, and probably by toxic substances develoj)ed within the gastro-intestinal tract, some of them of bacterial and some of pu- trefactive origin. Typhoid and scarlet fever, diphtheria, acute rheumatism, and influenza are all capable of setting up not only acute myocarditis, but chronic myocardial changes of an allied if not identical, yet of a more slowly acting nature. Phosphonis, arsenical poisoning, and alcohol are well-recognised causes of fatty degeneration of the heart.
The myocardial degeneration of chronic kidney disease may
CHROXIC MYOCARDITIS
523
be due IB part, at least, to chronic toxEpmia acting in conjunc- tion with prolonged high arterial tension. The degenerations de- l>ending uiion coronary sclerosis are instances of the third kind— i, e., of defective blood-supply*
When the two great factors, work and excessive or deficient nutrition out of projwrtion to that required for the work, are combined, then we not only have myocardial degeneration, but in time also inevitable cardiac inadequacy.
The hy[>ertnn>hy which so often de%^elops in association with chronic myocarditis is the expression of an attempt at compensa- tion. It probably evinces an effort on the part of Nature to repair the damages going on in the heart, btit it also results from the necessity on the part of this organ to overcome peripheral re- sistance,
Fraentzers idiopathic enlargement of the heart was thought by him to result from the* consumption of an amount of food in excH^ss of the requirements of the organism and of the individuaFs bodily exercise. Hence it is foimd in its most typical form in persons who are large eaters, and who, in consequence of their particular tine of work, are comj>elled to be sedentary. Accord* ing to Hosenbach, physical inactivity is an important element in this class of cases. When these individuals reach middle age they are usually found to have developed corpulent abdomens, and they generally continue to increase in weight. In many at this time the previously existing high-pulse tension is still further aug- mented by degeneration of the blood-vessels and kidneys, often also of the liver, which retrograde changes are probably to be referred to the same etiological factors. So long as cardiac byper- trojihy enables the organ to meet its demands its functional in* tegrity is intact. At length, ho%vever, eitlier because its nutrition has suffered to such an extent that it cannot meet the ordinary demands made upon it, or because extraordinary work is sud- denly r(Hjuired, as from some undue physical effort, the heart finds itself overpowered, and s>Tnptom8 of myocardial incompe- tence set in.
In the working classes, in soldiers, in sailors, and moimtain- eerSf in persons addicted to the abuse of beer and other alcoholic beverages, who at the same time perform manual toil, influences of various kinds are active. Food defective in quality or quantity^
524 DISEASES OF THE HEART
privations and hardships, and toxic agencies serve to intensify the injurious effects of overstrain. In southern Germany, notably Munich, hypertrophy and degeneration of the heart in its most typical form are attributed to the excessive consumption of beer. Some have thought this due to the great vascular strain incident to the daily intake of many litres of fluid, but Krehl, Rosenbach, and others recognise in addition the etiological influence of toil and the nutritive elements contained in the beer as well as of the strain put upon the circulatory apparatus by the consumption of excessive amounts of the fluid. In soldiers and mountaineers who carry heavy knapsacks strapped upon their shoulders, and thus loaded perform wearisome marches day after day, Rosenbach thinks cardiac function is impaired through respiratory embar- rassment occasioned by constriction of the chest, and through the necessity of overcoming abnormal peripheral resistance. Athletic sports, as well as coffee, tobacco, and alcohol, he considers injuri- ous only in the abuse, not their use.
Myocardial degeneration from coronary sclerosis is an expres- sion of inadequate blood-supply, either circumscribed or general; and that one may understand the diverse appearances encountered I think it well to quote in a general way I^yden's views of the mode of production of the changes in this class of cases.
He divides these into four groups in accordance with the de- gree of coronarv changes and the rapidity with which blood- supply to the heart-muscle is shut off, as follows :
(1) The coronary arteries present more or less evidence of sclerosis, but are still able to supply the heart with sufficient blood to maintain its nutrition. Degeneration does not take place, and the organ performs its functions without symptoms referable to coronary disease. Death results from an intercurrent affection, and knowledge of any alteration of the coronary vessels is but the accidental revelation of an autopsy.
(2) One of the coronary arteries, usually the anterior de- scending branch of the left, which has become thickened, subse- quently undergoes obstruction by thrombosis. When this takes place slowly, or when the circulation is but imperfectly cut off from the area supplied by the affected vessel, the wall of the heart within this space undergoes fatty or fibroid degeneration. If the thrombosis, on the other hand, suddenly and completely deprives
CHRONIC MYOCARDITIS
526
the part of its iiiitritioii, thvu this iircii breakt* Jowii into tlio *' myomalacia mrdis *' ui ZiegltT, Oa*asioually the extravasation of blood into this softened area given it an appearance of a hiem- orrhagic infarot. When rupture of tLe heart occurs, it is gener- ally within sneli a spot of acute softening,
(3) Sclerosis of tlic eoronary arteries is general and has come on gradually, giving rise to correspondingly gradual changes in the heart^i. e., fihroid degeneration either eircumseribed or gen- eral. When this clironic or tibrous myocarditis is diffused, the ventricular walls are apt to be thiu and dilated, whereas circum- scribed areas of induration are frequently associated with hyper- trojihy. In rare instances this develtipinent of new conneetive tissue is attended with atrophy of the muscle-fibres^ and the organ shrinks in size after the fashion of a cirrhotic kidney.
(4) In this group, the coronary sclerosis, althotigh essentially chronic, has been hastened and intensified from time to time by acute exacerbations of the prm^ess, throndxisis, etc. The changes in the heart are therefore twofold; areas of acute softening and fatty degeneration are interspersed among those of chronic nmKcarditis. This groni>, which blends tlie second and third, therefore, is the one most often encountered by the physician,
Tlie causes of coronary sclerosis are obscure, but are probably those of arterioj>clerosis in general. That age is of iutluenee seems attested by the fact that more or less evidence of the change is found post mortem in persons past middle age, while it is rare under forty and wanting in children. Some families seem to pre- sent a renuirkable teudeney to sclenisis of the corouaries and con- sequent myoeanlial disease. This has led to tlie suggestion of a possible hereditary influence in its production. Some individuals appear to be endowed with " arterial tissue or vital rubl>er of poor quality, which cannot be explained in any other way," as is so aptly expressed by Osier, *' than that in the make-u|) of the ma* chine bad material was used for the tubing." In my experience individuals who display this tendency to early sclerosis usually manifest distinct gouty diathesis. They may be said to be suffer- ing for the sins of their ancestors, I have long had the conviction that in some famih'es the»heart is the locits minoris resistenlke^ in some displaying particular vulnerability to the rheumatic poi- son, and in others appearing unable to withstand the wear and
536
DISEASES OF THE HEART
tciir of iiiodern business life. Certainly it is not very imcoramon to elicit from a patient, himself suffuring with myocardial disease, a history of a parent, usually his father, and one or more of his brothers and sisters having died suddenly of heart-disease.
I have in mind now a family in which the father is reported to have died of ** ossification of the heart/' while of three of the seven sons one had attacks of angina pectoris, another had heart- disease, develojied at middle age, and the third died suddenly with a dilated lieart, after having suffered from one or two out- spoken anginal paroxysms.
Males suffer from chronic myocarditis more often than do females, but this is probably owing to their greater exposure to those conditions favouring tlie development of myixrardial ineoui- petence rather than to any inherent tendency residing in the fact of sex alone, Wc^men frequently manifest clinical and post-mor- tem evidence of cardiac dc^generation, and according to Rosen- bach, it 18 particularly those who bear children in rapid succes- sion, and are still further depleted by lactation and insufficient nourishment.
The immediate causes of cardiac incompetence cannot always be ascertained. It not infrequently develops as a direct result of heart-strain through indiscreet physical efforts; but it also may appear without any such determining factor, and is then the end- act of all those factors that have li»d to the degeneration. Worry, grief, excsessive business cares, as in times of financial stress, and even emotional excitement of other kinds, may not only tx^casion loss of power in hearts already the seat of mvfX'ardia] disease, but are said to be an etiological element in the development of the muscle-disease itself.
The cardiac inadequacy of chrouic nephritis is generally the result of the organ^s inability to longer withstand the excessive tension in the vascular system. It may develop shuwiy or may be precipitated by some extra exertion or other source of added heart- strain.
Symptoins. — The cardiac incompetence of myocardial dis- ease displays clinieal pictures of considerable variety in detail, yet which possess the same fiuiflamental characters. It may be seen as FraentzeFs Idiopathic Enlargement of the Heart, as the Senile Ileart so graphically |xirtrayed by Balfour, as a case of angina
CHRONIC MYOCAUDITIS
527
"pectoris from coroJiary sclerosis in nochirnal aHaekiri of dys- [jiiti^aj known as cai'diae astlinui^ and in connection with chronic nephritis or diabetes, or bothj and occasionallv as a mitral or aortic regurgitation dim to relativo insufficiency from dilatation*
Idiopathic cardiac enlargement ocenrs for the most part in middle-aged men of powerful physique^ who are intellectually active, but physically inactive. It is especially frequent, therefore^ in men of affairs, as merchants and railroad magnates, and in ]u*ofessional nu^o, as lawyers and clergyineu, who, in addition to ^sitting for long hours at their desks, generally consume large amounts of food. For years there is in such individuals an abnor- mally high and sustained pulse-tension, which resulting, perhaps in part, from abnornuil blood-pressure within the abdominal cav- ity, increases as the girth of the w*aist increases. This state of things is borne without special disctuufort imtil the man gets well along in his forties, or has even passed his fiftieth year. Then he begins little by little to notice he dt^es not breathe quite so easily as formerly on ascending stairs, walking up a slight hill, or hurry- ing to cat(4i a street -car. At times, particularly after breakfast or a more than ordinarily hearty meal, he finds that walking at his accustomed pace is attended by a feeling of uneasiness, ful- ness, or even dull pain in tlie region of the heart. As the weeks go on he finds these two symptoms become decidedly annoying, and instead of wholly subsiding after he sits down they remain as a vague sense of discomfort in the clu^st. lie also ixirceives, perhaps, that the old exertion or some excitement incident to his occupation prmluces consciousness of his heart's action, a verita- ble thongli not violent paljiitatiou. As a rule this last symptom is not at all pronounced, lieing subordinate to the breathlessness and pr!rc<»rilial fuhiess.
By the time things have reached this pass he concludes to con- sult his physician, who finds a strong, usually regular pulse, no cardiac impulse, an apparently normal heart/s dulness, and clear heart-tones without tmirmur, but the aortic second sound decid- edly accentuated. If the radial arteries are not noticeably stiff, and the urine is negative, the real nature of the case is apt to be overlooked, and the symptoms are attributed to the nian*s increas- ing weight. He is told to exercise more, eat rather less, and not to worry. Perhaps he is advised to go to some springs, wdiere he
628 DISEASES OF THE HEART
can drink laxative waters, or he goes thither on the recomuieuda- tion of some friend. At first the waters and active exercise seem to make him feel better, but after returning home, and having re- simied his former mode of life, his symptoms reassert themselves, this time in greater intensity. lie again seeks his physician, who now finds the pulse is accelerated, the heart a little enlarged, and the liver palpable. The urine is scantier than before, and it maybe contains a trace of albumin. He is put upon digitalis and strych- nine, or he is sent to Bad Xauheim. This treatment improves his condition to a greater or less degree. His symptoms are less- ened or disappear entirely for a number of months. Then, in consequence of return to his old ways and his neglect of his doc- tor's injunctions, he finds his enemy has again attacked him. The former course of treatments is repeated with less brilliant results. He is now permanently crippled, but is still able to attend to a part of his duties. As months go on, however, his shortness of breath and other symptoms of cardiac inadequacy grow more and more pronounced, therapeutic measures are less and less effective, and at length this once powerful and active man of affairs is laid by, a pronounced sufferer from dyspncra, hepatic stasis, increasing oedema, scanty, perhaps albuminous urine, insi>mnia, a dull, con- gestive headache, cough, and frothy, or even blood-tinged sputum, a feeble and often arrhythmic pulse, a dilated and feeble heart — in short, all the signs of advanced cardiac insufficiency.
In other cases the course of the disease from initial breathlcss- ness to complete breakdown of lioart-power is much more rapid. Instead of extending over two, three, or more years, it passes through its several phases in a few months, or even five or six weeks, as I have more than once observed. In some instances the clinical history is merely that of ever-increasing cardiac debility, while in others there are some of the special features, as cardiac asthma, bradycardia, or even the so-called Stokes-Adams symp- toms, which are described in full in a special article. Whatever the variety of colouring, the general picture is that of more or less rapidly progressing loss of heart-power, and the ultimate out- come is always the same.
Cases of chronic myocarditis are conveniently divided into three great groups, according to the predominance of their clin- ical manifestations. These are :
CHRONIC MYOCARDITIS
529
(1) The arrhvthinic form, in which tlie piilse is strikingly irregiihir an<l iiiteniiittent, now slow and strong for a few beatd^ now fKerhaps rapid and feehle, or again made up of a perfect jum- ble of large and small, distinct and iuipereeptihle, slow, rapid, in* termittent waves that seem to fairly tumble over each other in their hnrry, or to lag back until driven hastily onward again by the impetuously rushing waves behind. In a word, the pulse is so laeking in regularity of rhythm^ force, and volume that to count it accurately is impossible.
(2) This is the form characterized by tachycardia and called the tachycardial form. The pulse is persistently accelerated, or in a few instances become so^ in paroxysms which so annoy or even terrify the patient that he comes to stand in mortal dread of his attacks of palpitation.
(Sj The udhmafic form, distinguished by attacks of acute pulmonary (XH-lema, which not only occasion distress and terror to the patient, but throw the friends into a state of scarcely less alarm. I have under observation at the present writing a power- fully built, active business man of sixty-three^ with moderately stiff arteries and a hypertropliied heart, with feeble tones, and a scratching systolic muniiur, wha for the past several months has lived in a state of well-nigh intolerable nervousness and apprehen- sion. As be says, be has completely lost his nerve, because last September, after some weeks of neglected shortness of breath, he was one evening seized with an attack of urgent dyspnoea, during which the pulse was scarcely perceptible, and the chest emitted a multitude of fine crackling sounds. He coughed from time to time and expectorated a frothy w^hite sputum. The attack sub- sided after the hypodermic ailministration of morphine and atro- pine. This gentleman has had one recurrence of the kind, but in the meantime lias scarcely passed a week without hours or even days during which his heart has " thumped and bumped/' to use his expressive words, in a manner w*hich throws him into a state of great alarm. lie never knows when this palpitation is to occur, hut it seems in some way connected with temporary aug- mentation of pulse tension. It is also quite certain to follow excitement over business affairs.
The pulse-rate averages from BS to 95, but often runs up to 120 or even 140, and such is the throbbing that he can at any 34
630 DISEASES OF THE HEART
time count his heart-beats without feeling his radial pulse. There is danger of death during his attacks and he knows it, which of course keeps him in a state of hourly apprehension. The fore- going case shows the occasional blending of the tachycardial and asthmatic types.
Patients of the arrhythmic form are very common and display the greatest tolerance of the really serious cardiac condition. Thus I knew a man of fifty-five who, notwithstanding an enormously dilated heart and exceedingly arrhythmic pulse, managed to drag on for nine years from the beginning of symptoms. These were not very severe; panting respiration on exercise, a feeling of weakness, so that he could not attend to business, and consider- able fermentative indigestion. That was about all, and at last his end came through ascites rather than distinctively cardiac inadequacy.
It must not be supposed that cases of chronic myocarditis can always be clearly separated into the forms just described. Many of them blend the symptoms belonging to each in a way to make a very complex clinical picture. Neither are the disturbances of which these patients complain always strictly cardiac. Tliese lat- ter may be said to be dyspnoea, heart-pain, palpitation, visceral congestions, attacks of pulmonary crdema, cough, and dropsy. Thoy are all present in varying proportion, not perhaps in every catfc, but in many eases. In addition, however, there are very sure to be numerous other complaints which in all likelihood depend more or less remotely upon the disordered circulation and per- verted visceral function arising from disordered blood-flow. Ver- tigo, insomnia, neuralgias and myalgias, nervousness, irritability of temper, indefinite sensations in the region of the heart, numb- ness, and formication — in short, a score of sensations which the patient connects directly with his heart, and calls on the medical attendant to explain and relieve. They are a large part of the daily plaint of these chronic suflFerers when able to be about and in a state of partial compensation. When, however, really serious sjTiiptonis of cardiac insufficiency set in, they are so much worse that they drive away more trifling sensations and dominate the scene.
All cases do not fall distinctly into the class of Idiopathic Cardiac Enlargement or of the Senile Heart, but occupy a sort of
CHROXIC MYOCARDITIS
531
intermediate gToimd, Nevertheless, it is condueive to clearness to try to elassify tbeni, as is essayed to do in this chapter.
The senile heart forms but a part of a general degenerative process* In one case the arteries are markedly stiff and tortuous; in another the urine slunvs evidence of jironauneed interstitial nephritis, but in all the phenomena of cardiac inconipetenee domi- nate the scene. There are breath lessiiess on even slight exertion, feebleness, digestive disorders, sensitiveness to cold and changes of weather, a tendency to bronchitis, and insomnia. In some there are attacks of nocturnal dysi>no a of greater or less intensity, Hnt- terings of the heart, vertigo, or even syncopal attacks.
In other cases the breathing assumes more or less typicallv the Cheyne-Stokes type (see article on Cheyne-Stokes Respiration), witii or without axlema^ pulmonary congestions, arrliythniie feeble pulse, and the usual manifestations of progressing asystolism.
Tlie course is usually slow, the symptoms being sometimes mild, and the patient cut off by some intercurrent affection, as senile pneumonia. In some instances there is history of attacks of angina pectoris for five, ten, or even twenty years, and death at last is sudden and unexpected. There arc other eases, chiefly men, whose cardiac inadeciuacy is shown by acceleration and arrhythmia ot the heart's action, inclination to cough and wheeze, an^l various so-called gouty manifestations rather than by pro^ nounced dyspnoea or venuus stasis; the so-called arrhythmic form, TIjey get rather breathless on exercise, and yet then can walk at a moderate rate of speed without much difficulty. They have times when from some illness, as acute bronchitis, injudicious strain of one kind or another, they are laid up in their room w^itli a trace of (pdema and indications of failing heart-power that look very threatening, and yet under gomi nursing and projjer medical attention they rally, and after weeks or months are again able to be about, a little weaker and thinner, a little more breathless, but on the w^hole capable of getting considerable enjoyment out of their quiet existence*
I recall an old gentleman of eighty with stiff arteries, urine of poor tpudity, and a greatly hyiH:'rtro])!ned heart, the first sound accompanie<l by a lond systolic basic murmur, the aortic second intensely ringing, w^ho jet attended daily to the cares of a large personal property besides many other duties of a public and pri-
632 DISEASES OP THE HEART
vate nature. At length one spring he and his friends noticed that he began to breathe with difficulty upon ascending stairs, and at rest displayed a peculiar sort of breathing which they had never observed before. Notwithstanding this difficulty he came to con- sult me at my office, and seemed surprised when he was told to return home, give up his business, and remain in the house. His pulse was rather unstable, occasionally intermittent, but not nota- bly accelerated. His respiration was only moderately dyspnoeic as he moved about the room, but after he had been sitting still for some time, and particularly when asleep, it became irregular, with short periods of nearly but not quite complete cessation of breathing, which were then succeeded by gradually deepening in- spirations until they grew full and vigorous. They then died away rapidly into apparent apnoea. Close observation detected that at some of these times he yet breathed faintly, while at others he breathed not at all. Some of the dyspnoeic periods were longer and more pronounced than others, and for minutes together others of them presented all the characters of typical Cheyne- Stokes respiration.
During these periods he did not seem subjectively conscious of distress. Under appropriate treatment of a stimulating and elimi- nating kind and prolonged confinement to one floor, afterward to the house, his irregular type of breathing gradually left, the heart grew steadier and stronger in action, and he came to look upon himself as pretty well. He required rather close watching to pre- vent indiscretions, chiefly in way of exercise, but as time went on he was able to transact a little business and to enjoy the visits of his friends. In this manner this gentleman w^as able to live on for two years. When at length the final struggle came, it was in the form of a renewal not of incomplete Cheyne-Stokes respira- tion, but of a most distressing dyspncra, w^hich gave him no peace even when quiet in bed. It was not attended wuth notable signs of cardiac failure, and no particular evidence of renal insuffi- ciency. It may have been due to bulbar sclerosis; but at all events it at length necessitated the hypodermic administration of such heroic and frequent doses of morphine, that he at last ex- pired in a state of complete narcosis.
In the case of a man of seventy-one, who had been a well- known journalist, the initial sjTuptom so far as could be ascer-
CHRONIC MYOCARDITIS
533
tallied was an attack cif dyspmra, wlndi seized him one night after he had retired^ He fell asleep^ and after a few minntes sprang up in betl, clutch ing at his throatj exclaiming he was going to stran- gle. This so terrified him that at length he arose, dressed, and eitmpollcd his vnlct to keej* liim walking up and down in the gar- den for tlie remainder of the night, Wlien I saw him the follow- ing afternoon he was still greatly agitated and suflFering from ehoking si>g11s» A hypodermic of an ^ of morphine, with atropine in tlie onlinary combination, gave six hours' uninterrupted sleep the next nighty although during his repose his breathing was tjpi- cally Cbeyue-Stokes- This patient's pulse %vas very arrhythmicj his arteries sclerotic, his heart dilated, with a blowing apex-oiur- mur and feeble sounds. Uis urine was that of a moderate renal cirrhosis, and he suffered from prostatic enlargement. His stom- ach was dilated, and he had any amount of flatulent distention of the bowels. Altogether it was an unpromising case, yet persistent and vigorous treatment witli cardiac tonics and cathartics, with as strict a control of the dietary as was possible with an irritable, self-willed old gentleman, at length pulled him out of his deplor- able condition. For four years he was an invalid, having times iif profound physical and mental depression, and periods of grave cardio-vascular disturbance, during which t^deraa more than once appeared. These periods of distress were alternated with seasons of comparative immuuity from symptoms, and yet they were in- terspersed with numerous attacks of bronchitis, mild unemic manifestations, and once an acute pleurisy with effusion that even- tual ly n ecess i t a ted pa racen tes i s,
ilore than once he rallied from what it seemed nmst prove his final illness ; and thus actually kept alive by cardiac tonics, he man- aged to drag out four years of chronic cardiac inadequacy* ^Mien at length bis end came, it was quite sudden, although preceded by days of more than usual feebleness that had confined him to his bed. Although this patient displayed marked general debility^ with slowly increasing cardiac asthenia, he never again suffered to any extent from his nocturnal dyspna-a, and never bad an attack of angina {>ectoris. lie fr^uently complainetl of obstinate chest pains, but these were unmistakably an intercostal neuralgia, as shown by numerous hy pe nest bet ic areas.
This ease belonged to what may be styled the arrhythmic
534 DISEASES OF THE HEART
group, in which the cardiac insufficiency is shown by such an irregularity and intermittence of the heart's action that it consti- tutes a veritable delirium cordis.
Radizewsky has shown, conclusively as it seems to me, that when the pulse displays these characters there is extensive fibroid degeneration, chiefly of the auricles, which both clinically and post mortem are found dilated. In his communication upon the subject he quotes Ilampeln's researches, which demonstrated that perfect regularity of the pulse is frequently seen in cases in which subsequent necropsy discloses extensive fatty degeneration of the left ventricle. In other words, the state of the ventricle cannot be determined by the state of the pulse. Radizewsky's findings have always seemed to me to explain the protracted course which so often characterizes cases in which the pulse is strikingly arrhythmic.
Degeneration and dilatation of the auricles impair the func- tional integrity of the heart-muscle, but can never so seriously threaten life as when the wall of the left ventricle is degenerated. I have seen many of these cases with unmistakable cardiac inade- quacy drag along for months and even years after the heart had become so feeble and arrhythmic that it seemed impossible for it to maintain the circulation.
On the other hand, experience has taught me to dread those degenerated and senile hearts, which are apparently not much dilated, yet give rise to dyspnoea of effort, while the pulse remains accelerated, but perfectly regular. Such hearts are usually refrac- tory to treatment, and are apt to surprise one disagreeably by stopping suddenly and unexpectedly. They belong to the tachy- cardial form of chronic myocarditis.
In my experience the clinical picture of the senile heart is very rarely that of great dropsy and extensive visceral congestion with overdistention of the cardiac chambers, as in the terminal stage of Fraentzel's Idiopathic Enlargement of the Heart.
In the heart with coronary sclerosis the consequent interfer- ence witli nutrition of the heart-niuscle leads to changes of a chronic nature in the majority of cases. In others, circulation within the coronary arteries is more or less suddenly shut off, and the heart-muscle suffers with corresponding acuteness.
Conseijuently the symptoms due to coronary disease are di-
CHRONIC MYOCARDITIS
535
verse, and are best divided, as bv Leydco^ into actitej subacute, aDfl chronic.
in the acute form the clinical history is confined to a few days, hours, or even minutes. The symptoms are due to coronary thrombosis with secondary myocardial softening, to sudden rup- ture of the heart in some area of insiJiuus fatty degeneration, or of acute molecular necrosis {myomalacia cordis), or the symptoms consist only of a sudden diastolic arrest of the heart's action.
The symptoms of heart-rnjdare may be a sudden sharp attack of angina pectoris or of vague pra -cordial distress and oppression vfc'ith profound prostration. The action of the heart is feeble and disordered^ and the organ fails to respond to stimulants. The in- tellect is generally clear, but unconsciousness may be present. In some cases there are sym[)toms of gastric disturbance, even vomit- ing, and the case is thought to be one of gastric disorder. If life is prolonged for several days, as very rarely happens, the first vio- lence uf the attack abates, not to be renewed, or the angina and pnecordial distress recur from time to time with steadily increas- ing aaystolism and death. In other cases of cardiac rupture the symptoms are chiefly those of rapidly failing circulation with insensibility and death from acute pulnK>nary adema.
With the onset of 8j^nptom» the nearest pliysieian is hastily summoned, and on arriving at the patient's side finds him mori- bund. Stimulants prove inert, and the doctor signs the death certificate without having been able to accurately diagnose the condition. If he examines the heart he discovers clear feeble sounds without any appreciable increase in the area of dulness. In other cases cardiac duhiess is increased, but unless a slo%v escape of blood into the pericardium produces the outline charac- teristic of pericardial effusion, the augmentation of dulness ia attributed to dilatation, and a diagnosis is nuide of paralysis of the heart (acute asystolisni), which seems borne out by the weak- ness of the sounds and strikingly poor quality of the pulse. In such a case recently narrated to me death supervened in half an hour from supposed acute dilatation, and yet the sac was found ab^dutely distended with bh:Hj^L
In another form of this acute type of coronary sclerosis the patient apjiears as well as ordinary, having made no complaint that led to a suspicion of his having heart-disease, and yet in the
636 DISEASES OP THE HEART
midst of his activities, while at work in his office, on rising from dinner, etc., he suddenly falls dead. He may turn pale, speak of vertigo, give a groan, or in some way attract the attention of his family, who spring to catch him as he sinks to the floor in fatal syncope. The mahogany flushing of the face and few gasping in- spirations suggest death from apoplexy, but in reality it is from sudden diastolic arrest of the heart. In such instances the degen- erative process has invaded some of the vital centres in the heart, probably in the upper portion of the interventricular sa?ptum.
In cases which, according to Leyden's classification, may be called subacute, there are attacks of angina pectoris extending over a period of weeks or months. They differ much in different cases, as regards severity and frequency of occurrence. As a rule, however, they grow more intense and more frequent. The suf- ferer speedily becomes incapacitated for business, keeps in the house, or ventures forth only on mild, still days, grows daily weaker and paler, and is very apt to lose flesh. Death comes at last either from slowly increasing asystolism, or suddenly during an anginal paroxysm. The pulse in such cases is usually regular, and but moderately if at all accelerated, while examination of the heart is generally negative. The arteries may display some stiffness, but aside from the patient's age and his attacks of pain there is little to indicate chronic myocarditis.
Cases coming under the chronic head run a slow course and extend over years, instead of months, five, ten, or even twenty. The individuals are always conscious of their liability to an attack, and hence deport themselves most circumspectly, eating and drinking moderately, walking and exercising carefully, avoid- ing raw cold winds, and shunning excitement and provocation to anger, lest at once their enemy be upon them. Their general health does not suffer greatly at first, although as years go by they look and act like invalids. A few experience some shortness of breath, or may exceptionally suffer from veritable cardiac asthma. As a rule, however, their one symptom is their terrible angina. Their pulse is generally regular, always appreciably tense, and their hearts are negative on examination. Death comes through intercurrent disease or during an attack. For further particulars the reader is referred to the chapter on Angina Pec- toris.
CHRONIC MYOCARDITIS
537
Tn general arteriosclerosis there are often symptoms of circu- latory faihire which are apt to be attrihiited to cardiac itmdeqiiaej ah>ne, when in reality it is the arterial stiffness that is respousihle for the stasis and a^dema. The heart may in such he atrophied or of normal size, but as a rule it iti hvpertrophied. The condi- tion of the myocardium depends uix)n the degree of its nutrition with relation to its work, and as the aorta and eoronaries share to a greater or less extent in the sclerotic process, the heart-muscle is not intact, Xevertheless, its driving power is often adequate for years after the bIoi>d-vesseIs have become rigid and beady. At length it reaches the limit of its compensatory ability, and vas- cular resistance still augmenting, the heart-walls begin gradually to yield to the strain of maintaining arterial circidation, and dila- tation slowly supersedes hypertrophy.
In some cases injudicious physical eifort, suddenly or too often exerted, causes acute overstrain of the already tixi greatly taxed heart, and symptoms of cardiac insufficiency set in rapidly instead of slowly. These are not i>eeiiliar, but possess the ordinary char- acters of retarded circulation, breathlessness, slight (rdenia of the ankles, scanty, perhaps alhuminous urine, pulmonary and hepatic congestion. The siiperticial veins stand forth still more promi- nently, the rigid^ tortuous, uneven arteries show a thready, often flickering pulse, Avhieh is accelerated and often irregular both in force and rliythm. The heart is found more or less increased in size, and its sounds are altered in *|ualitv and proper relative intensity. There may or may not be murmurs at apex or base indicative of atlieromatous changes in the valves, but the aortic second tone is nearly always ringing and metallic.
The patient loses strength, and tinally takes to the house per- manently. Dyspmea grows apace and not infrequontly assmnes the characters of carrliac asthma or of ("heyne-Stokes respiration. Urine grows still scantier, dropsy advances, orthopnam sets in, troublesome cough, and frothy, blood-tinged expectoration, betoken ever-increasing stasis within the pulmonary vessels, and the pa- tient succumbs after weeks or months to general exhaustion, car- diac asthenia, or an attack of acute pulmonary a*dema.
Chronicity is the essential feature of this type of cardio-vascu- lar inadequacy. It is not uncommon for cases of arteriosclerosis to drag on for several years under the picture of senility and gen-
538
DISEASES OF THE HEART
oral decrepitude, and death to coioe at last as a result of acute bronehitis, pueumoiiiaj or eveu of renal inadequacy,
Exenptionally, allhuiigh the total nimiber of sucb cases i;^ not small, the teriuiiiation is through cerebnd thrombosis. Rupture of a blowl- vessel in the brain is not so frequent in senile arterio- sclenisis as in vuunger persons whose renal cirrhosis leads to enor- mous left-ventriele hypertroi>liy.
ChroiHC nephrids leads to very serious changes in the heart- muscle, Clinically, this is shown by liypertropby of the left ven- tricle either idotie or as a part of a general cardiac enlargement. The niyocardiiun mny or may not be seriotisly degenerated, but whether it is or not, it is subjected to an enormous p<n'ipheral resistance to siiccessfully cojje with which it is eomi:)ellerl to un- dergo hypertrophy. I do not intend to discuss the various theories which have l)een advanced to explain this increase; for these the reader is referred to works dealing with kiclney diseases.
The pulse of chronic ne|>britis shuws prolonged high tension, which is primarily of renal, not cardiac* origin. If the kidney changes are of slow development, as in chronic interstitial nephri* lis, or if the patient is not carried off by the sudden onset of renal ina<leqnacy, there surely conies a time when the heart, struggling with abnormally high en4h>eardial lilood-prossure, is able only %vith difficulty to withstand the enormous resistance in the arterial system. Then gradually or suddenly, according to circumstances, the wall of the left ventricle gives way.
If slowly, the volume of urine begins to fall off, and the patient finds his wonted physical efforts are attended Ijv shortness of breath and palpitation, and his pulse-rate is found to be decidedly augmented. Signs of venous congestion and pronounced cardiac dilatation are tisually wanting at this stage. Unless the danger is recognised and means are resorted to of restoring the equilibri- luu between pulse-tension and heart- power, cardiac insufficiency grows daily more apparent, and the patient is at length comjielled to remain inactive. Examined at this time, he is found to twince immistakidile signs of failing circulation. The pulse is rapid and perhaps of jhmjt quality; the liver is palpable and more or less ten- der; tension, and it may l>e pitting of the ankk^s, is detected ; the tongue is coated, breath foul, and the urine is apt to Im? decidedly scanty and allium inous. If the heart is examined, the apex is
CHRONIC MVOCARDITIS
^Jisplaced tiTid lacking in coneoTitration ami force, tlie Becond sound at the right of the sternum is tioinewhnt enfeel>led, and the pul- monic is nearly or quite as intense.
The striking alteration in tlie heart-findings consists in the pei'uliiir rcMhiplication of the sounds at t!ie apex, whieh is known as gaUop rhyrhni (see introductory chapter). Oeeurring in the course of chronic Bright's disease this phenomenon is of very evil portent, for it indicates that the left ventricle is yielding to the abnoruial strain and tottering on tlie verge of an irreparable breakdown. In most cases treatment is unavailing, symptoms of stasis progress, and dyspnu'a liecomes most distressing. It may be of the Cheync-Htokos type^ bnt is more often of a paroxysmal nature, coming in waves, as it wei-e, with evidences of great agita- tion, even alarm, on the part of the patient, yet without corre- sponding signs of more than usual cardiac failure. This form of dyspno-a is proI>ably partly of toxic (unemie) and partly of cardiac origin. Xevertheless, the insufficiency of the heart aug- ments, renal excretion fails correspondingly, and after the lapse of w*eeks or a few months the patient dies w^ith unemic manifesta- tions or from acute pulmonary <rdema.
Tliere are other cases of Bright^s disease in which cardiac in- competence sets in abruptly. This is usually owing to some indis- creet effort or excess which causes rapid dilatation of the left ven- tricle. The symptoms are mneh the same as in the more gradu- ally evolved loss of compensation, but are apt to be of far greater intensity. Examination shows feeble apex-beat, displaced far to the left and jjerhaps downward, enormous increase uf cardiac dulness, and a systolic apex-murmur^ whicli often replaces the first sound, and a feeble second tone except in tlu> pulmonary area, where it is intensified. The liver swells rapidly, is often painful an*l very tender, particuhirly in the epigastrium. Dropsy sets in, extends rapidly upward, and invadcvS the serous cavities. The pa- tient suffers from orthopn<i^a with paroxysmal exacerbations, from severe, tensive headache, insonmia, or it may l>e somnolence, and many other distressing symptoms of combined cardiac and renal inatlequacy. Few clinical pictures are more distressing^ and none are more hopeless.
In many eases in which there are enlarged hearts with stiff- ened arteries and urinary findings of renal sclerosis it is difficult
540 DISEASES OF THE HEART
to say whether the symptoms of failing circulation are due pri- marily to incompetence on the part of the heart or of the kidneys. Some of these patients manifest symptoms of slowly failing heart- power for many months before being compelled to regard them- selves as hopeless invalids. I recall one gentleman of fifty-eight with this combination of cardio-vascular and renal degeneration, who, nearly two years before his death, suffered from paroxysms of dyspnoea which because of his rapid, unsteady pulse was thought cardiac, but seemed to me in reality ursemic. It did not yield until pulse-tension was reduced by frequent doses of nitro- glycerin. Another gentleman of forty-seven with the same asso- ciation of diseases used to complain that he could not breathe " more than an inch deep." This patient's heart manifested clinically the most enormous enlargement I have ever seen. His breakdown was initiated three vears before by a " century run " on his bicycle.
Diabetes mellUus occurring after middle age, and usually con- joined with vascular and renal changes, is often seriously compli- cated by symptoms of cardiac incompetence. The arteries are more or less stiff, the heart is hypertrophied and dilated, and its action is rapid or pounding, sometimes intermittent. Glycosuria is the feature which has especially to be combated, and yet one must never lose sight of the cardio-vascular s^-mptoms. At the present writing I have under observation two ladies who have dia- betes mellitus with atheromatous arteries and hyi)ertrophied hearts. In one, whose age is not far from seventy, the main com- plaint (so long as strict diet keeps down the glycosuria) is of great weakness, palpitation, and shortness of breath upon exertion. The other ])atient, of about sixty, suffers chiefly from dyspncra, attacks of palpitation, and faintness. On two occasions in the early morning hours she has been awakened bv a sense of suffoca- tion, and has nearly died from acute pulmonary cedema. Signs of cardiac inadequacy are present at all times, and yet she shows no traces of dropsy or special venous congestion. In both of these cases hypertrophy still predominates, and is able to endure the high endocardial blood-j)ressure so long as this is not intensified by the strain of physical effort. The nocturnal seizures in the second lady were probably due to the augmentation of blood-pressure in the arteries occasioned by the recumbent position in sleep. This
CHRONIC MYOCARDITIS
oil
at length overpowered the left ventricle, whieh temporiirily be^^anie weaker than the right, and acute pulnionarv aHiema supervened. In some of these cases of chronie mvocarditis such attacks form the principal feature, and the cases are particularly grave on this account.
Vases of Secondaty Valvular Insufficiency, — Lastly, one occa- sionally meets with cases of myocardial degeneration which mas* tjneradc in the guise of a mitral or aortic regurgitation. I Jo not refer to atheromatous valvular disease, but to cases in which the vah'ular incompetence h relative or muscular. Arthur R. Ed- wards has reported a case of relative aortio insufficiency from ex- tensive myocardial degeneration, and T have myself ohservod three cases in which the necro|>sy revealed the same condition. In all of them the clinical history was that of aortic regurgitation.
Mitral incompetence is common and may be relative, but more often is muscular from degeneration of the papillaries or slight ventricular dilatation. I do not now refer to lialfour's Curable Mitral Regurgitation, which is seen in chlorosis and amemia, or to that ftjrm seen in young athletes as an effect of acute strain. These all yield to appropriate treatment. I am now speaking of left-ventricle dilatation and secondary' mitral insufficiency seen in cases of chronic myocarditis. I have under observation a man of sixty-five, a veteran of the late civil war, whose mitral valve leaks in conscHpicnce of great dilatation of the ventricle. There is no history of inflanunatory rheumatism or any other disease to occa- sion endocarditis, but there is history of severe physical effort (climbing a mountain) ten years ago. Previous to that strain he had no cardiac symptoms, i^it ??ince then his mitral nmrmur and dilatation of the ventricle have been present. At times the mur- mur wholly replaces tlie first sound, but as the ventricle retracts under treatment by baths and resistance exercises, the first sound becomes audible and cardiac impulse palpable. I think few would venture to assert that in this case the myocardium is healthy,
I have notes of the case of another gentleman of forty who presented the signs of a typical mitral regurgitation, and who for four years struggled to preser%'e his compensation. He gave a his- tory of mild inflanmiatory rheumatism, of gonorrha^a, and of a thrombophlebitis of the right femoral vein, and therefore his valvular incompetence w^as quite naturally supposed to be of endo-
DISEASES OF THE HEART
canlitic ori^^in, a eoiirlusiun tlxut was streiigtiieneil bv the occiir- renee of t%vo attacks of subacute articular rheumatism during the time he was under observation. He at last died^ after having been confined to his bed for only a week, wntb symptoms of cardiac exhaustion. There was no or'dema, very insignificant venous sta- sis, and at lirtit a profound sense of weakness rather than of short- ness of breath. Towards the close of his illness, however, dyspntea asserted itself, beeoming raiher spasniodic. Ilis temperature grew subnormalj the pulse feebler and slightly more rapid^ and he died apparently of simple cardiac asthenia*
The necropsy made by Dr. W. A. Evans disclosed a perfectly healtliy mitral valve, and on the frieusj>id, changes too insignili- eant to have afTected their function. The myix-ardium was in- tensely fatty, particularly of the right ventricle; the cavities were all more or less dilated. The coronary arteries were healthy, but the aorta was congenitally small throughout. This num had been an athlete in college, an*l subsequent to his death I learned that before his s^ynxiptoms of cardiac inadequacy began he had over- strained his heart by a long, hard bicycle ride. Owing to the apparent integrity of the coronary arteries in this case, I l>elieve there can be only two explanatJmis of his mywardial decay. It was either an expression of chronic myocarditis in the strict sense of toxic origin, or of a flisprojiortion between the work re<]U!red of it imd its nutrition, this latter being restricted by reason of the congenital smallness of the aorta, which also had served to put undue strain upon the mywardium.
Finally, in concluding what I have to i^ay upon the symptoma- tology of myocardial inailequacy^ I desire to add a few words concerning two symptoms which are generally thought indicative of fatty degeneration of the heart. These are yawning and sigh- ing. I have never, however, been able to satisfy myself of the import of these two s\^nptoras. Indeed, I not only have seen many cases of myocardial inadequacy in which they were absent, but T have, on the other hand, observed them in patients who pvv- sented no suspicion of myocardial disease, as in young nenrotic or anaemic women. I should certainly attach no value to yawning and sighing in the absence of other less doubtful sjT^nptoms, and in suspected cases of cardiac degeneration I should esteem them of very minor importance.
CHRONIC MVOCAKDITIS
543
Physical Signs. — Inspeclion, — In most cases insj>eetion is negative. If the v\e delects signs of stasis, tliere is iiulliin^^ in this faet to indicate the underlying condition. The generul ap- pearance of the individual may show to the experienced physi* cian si^ns of premature or senile decay. When hvpertrophy of the left ventricle is present, this may be shown by the displaced apex-beat. But in the class of cases in which it is the most diffi- cult to arrive at a detinite conclusion — that is, middle-aged and well-preserved men with capacious chests, the cardiac impulse is not visible because of the chest-capacity and Inng-vohime, Conse- quently, it may be saiil thitt thr chief value of inspect iiju lies in the fact of its negativcness, for other disorders of the hiart than myocardial degetieratinn are very apt f<t furnish some visilVh^ indi- cation of their nature.
PallffUioH, — This is of value in the determination of tedema and of hepatic engorgement even iin^re thiin in rhe examinatifin of the tieart. Yet by careful palpati<^>n t^{ the pnirnrdinm one is often able to locate an apex-beat which is t*m feeble to be visible. It may enable one also to i^erceive that the cardiac impulse hits the dif- fused jogging character of dil- atation with hypertrophy, or the feeble, slapping shock of dilatation. Palpation is of special value in disclosing th< state of the arterial coats. It these feel thick and resisting, or tortuous and uneven^ like a string of beads, they furnish presumptive evidence that the heart-muscle is not sound. In searching for signs of cardiac incompetence one should always endeavour to palpate the liver. If the lower border *>f this organ can l>e felt below the costal arch, and particularly if it is smoothy rounded, firm, and perhaps tender, there is hepatic con- gestion, probably secondary to more or less cardiac inadequacy*
Fig, 103.— SiKiwiM, Siivi'^; mf KFrMivE Di u insB i» lJvi>i.initi»riiY. Qtiadriloteral with rounfkt^l cviruem.
k
544
DISEASES OP THE HEART
Percussion. — This means of investigation should never be neg- lected, for very much depends upon the size of the heart. Abso- lute dulness may or may not be increased, but as the organ is enlarged in most cases of myocardial degeneration, careful percus- sion usually elicits an augmentation in the area of cardiac dulness. If this is found increased to the left and upward, it indicates left- ventricle hypertrophy; if to the right and downward, enlarge- ment of the right ventricle. In general cardiac hypertrophy the area of deep-seated dulness is of a quadrilateral outline with rounded corners (see Fig. 103).
In estimating the size of the heart it is customary to take the left verticle nipple-line as the normal boundary of deep-seated dulness at the left. But Fraentzel dwells particularly on the lia- bility to error existing in the custom of considering the left nipple as the normal boundary of relative dulness on that side. If the dulness is not found to pass beyond this mark it is taken for granted that the size of the heart is normal. It should be remem-
|
Age, |
WeiflTht. |
HeiflTht. |
Ctrcumfer- cbest. |
Distance from Bternum to left nipple. |
|
|
K. A |
29 24 25 30 28 29 42 24 24 33 23 33 28 23 23 31 ^'a 21 82 29 30 30 25 25 27 24 22 43 |
155 185 130 150 145 157 191 149 185 170 160 125 161 195 158 145 155 140 130 165 164i 135 162 189 204 150 130 145 189 |
FmI. IsckM. 5 7 5 7 5 7 5 9 5 6 5 9 6 1 5 6 5 7 5 8 5 10 5 4 5 9 5 10 5 7i 5 9 5 Qk 5 10 5 7i 6 I 5 lOi 5 4 5 9i 6 0 6 0 5 7i 5 6 5 8i 6 0 |
ladm. 33 84 84 34 34 35i 40i 36 36 36 34 30 35 40 35 34 37 33i 33 35 35i 33 38 39 39i 38 33 35 39 |
ladm. |
|
T.B |
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|
C. B |
8* 3» 3i H 3t 3+ 8* 3* 2f 3* |
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|
E. B |
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|
W. C |
|||||
|
S. D |
|||||
|
H. De V R.E |
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|
E. E |
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|
S. E F.G |
|||||
|
G.G |
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|
c.n |
|||||
|
H..J |
|||||
|
P.J G. L |
9i |
||||
|
L |
|||||
|
F. M J. M |
3 3* 1* |
||||
|
H. M K. S |
|||||
|
J. S. . |
|||||
|
J. s |
H 3i n 3 |
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|
W. V |
|||||
|
J. W |
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|
J. W |
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|
J. W |
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|
C C. H |
8* 3i |
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CHRONIC MYOCARDITIS
545
bered, hmveverj tliat the ilii^tance between Hie niidsterual and kft inainilkry lines is by no uieana always the ca«e. I have not in- frequently foimd the left nipple situated 5 inches from the mid- stern uni. ileasiirements of twenty -nine of my students, taken for the purpose of detenu ining variations in this regard, gave the rerndts shown in the table on the opposite page^ ♦
These figures indicate plainly that the only accurate me^Jis of determining the lionndaries of the heart by percussion lies in mt^atsuring the diKtanee to which the area oi deep-seuteil dulnoss extends to the left of the median line. The size <if flie nonual heart, as shuwn by percussion, lias already boen stated in the in- t rod uctory chapter.
One often obtains valuable information by the sense of in- creased resistance on firm percussion, and hence the value of Ebstein*s palpatory percussion. I am in the habit of verifying the results of f>ercnssiou in the ordinary way, by recourse to aiis- cultatory percussion, and am frequently surprised and gratified to
how closely they correspond.
Aiisculiation, — Here, too, much depends upon the thickness or tliinness of the chest-wall If hypertrophy exists the first sound at the flj)ex is prolonged and of low pitch, while the senmd is usu- ally clear and ringing. Tn some cases the systolic sound is muf- fled and indistinct. At the base of the heart the aortic second is sharjdy accentuated^ ringing, or it may be so intense as to he actually banging. There is also intensification of the pulmonic second sound when the left ventricle logins to fail, and at the base of the heart one sometimes detects reduplication of the see^ ond sound. If the first in the region of the apex is short and sharp, resembling the normal second, it indicates dilatation rather than hyjK^rtrophy.
Occasionally the heart-sounds take on the canter-rhythm de* scribed at length in the introductory chapter. This character- istic rhythm is limited to one or the other ventricle, and there- fore to the neighbourhood of the left nipple. It is especially likely to appear in left-ventricle dilatation consequent u|>on a granular kidney, but, according to Fraentzel^ occurs, although rarely, in enlargement of the heart from other causes* This gallop rhythm most be kept distinct from reduplication of the second sound heard at the base, and from that apparent or simu^
546 DISEASES OP THE HEART
lated doubling of the second sound that is not infrequently dis- covered in the mitral area in cases of stenosis of that orifice.
A full, tense, not accelerated pulse, a dull first sound, and an accentuated aortic second, form a combination of signs highly sug- gestive of hypertrophy of the heart, even though its area of rela- tive dulness cannot be defined with certainty.
. There is no pathognomonic sign of degeneration from coro- nary sclerosis, and often the heart-sounds appear normal. It is highly important, however, and sometimes yields valuable infor- mation, to study the relative pitch and intensity of the several soimds. If, as there is good reason to believe, one of the elements entering into the make-up of the first sound is a muscular ele- ment, imparting to the sound its booming quality, and caused by contraction of the ventricular and papillary muscles, then impair- ment of their contractility through disease should theoretically diminish the intensity of the first heart-sound. Experience shows that this is precisely what takes place in some instances. Over the weakened left ventricle this sound at the apex may be weaker than that over the right ventricle, having a distant or muffled character. The pitch of the sound may be raised also and its dura- tion somewhat shortened. The second sound at the apex is often relatively louder than the systolic, and on moving the stethoscope to the base of the heart this intensification of the second sound is found due to accentuation of the aortic second, which may even possess a ringing character from sclerosis of the aorta. In other cases the second sound at the right of the sternimi is feebler than that in the pulmonary area.
As the aortic second sound should be the louder of the two in persons of the age at which myocardial degeneration usu- ally develops, relative weakening of the second sound in the aortic notch points to diminished vigour in ventricular contrac- tions, and hence furnishes indirect evidence in favour of degen- eration.
Murmurs are accidental findings, and are due either to rela- tive incompetence of the valves or to atheromatous roughening of the orifices. In either event they may afford valuable testimony as to the state of the heart-muscle. A murmur may, of course, in some instances be the result of a rheumatic valvular defect, as will be shown by the history.
CHRONIC MYOCARDITIS
547
Diag;ilOSiB, — Fnun the furrgoin;;, it is eviileiit that in the (liagMo.^ii^ ni di'^^vuvrnlum uf tlie Hiy<x'nniiiim, but liniittHl in- foriTiatiMii is ilcrived fiuiii ii study of iho heart. Thtjre is no iurni of carfliae disease, tlierefore^ in the diagnosis of which so much depends on the judj^nent and experience of the physician. In valvular defects theje arc niurnmrs to serve as giiidt!- posts; in hypertrophy ur ililatation there is obvious alteration of size. In the affection under eonsiderati»>n the volume of the organ may or may not be changed, and therefore great dependence must he placed on age, state of the vessels^ history, and symptoms*
Age is so important an efiologieal factor that the development of cardinc insufficiency in an individual well on in years may be get down to degenerative changes with tolerable certainty. It is quite otherwise when heart- weakness, without obvious signs of disease, develops in a person about the middle period of life. In sncli persons careful search should he made for traces of prema- tnre decay^ for indications of rL*nn! <lisease, or a gouty diathesis, etc. There is an <dtl saying that a man is as old as his arteries^ antl therefore the radials, temporals, and other peripheral vessels should be carefully paljiated for evidences of thickening or for nodnlar deposits of lime-salts.
It may be necessary in some eases to make an ophthalmoscopic examination of the retinal artery for the signs of sclerotic change which are said to tirat manifest themselves in this situation. The physician should note the appearance or not of premature whiten- ing of the hair» and examine the texture of the skin, I have more tlian once observetl tliat |>ersons with a strong suspicion of fatty degeneration of the heart have a skin that has lost its elasticity and feels pet^uliarly soft, as is often the case in the aged*
The examiner should scrutinize the fingers an<l ears for chalky deposits, and the nails for those longitudinal ridges said to be indicative of the gouty state. In tliis way valuable hints may often bi^ obtained.
The urine slum Id be analyzed carefulh% and repeatedly if nec- essary, for evidence of nefdiritis^ since it is well know^n that de- generation of the myocardium is a frequent accompaniment of chronic renal disease, particularly the interstitial form.
Minute inquiry into the patient's history may elicit facts con- cerning family tendencies, jrersonal habits, previous diseases, etc.,
548 DISEASES O^ THE HEART
that may throw light upon the nature of the present malady. It is particularly important to ascertain whether the patient has suf- fered from attacks of angina i)ectoris or cardiac asthma. The significance of the former in individuals past middle age is very different from that of anginoid seizures in adults under forty, especially women.
Even in spite of the most painstaking investigation and atten- tion to all circumstances, however trivial, a positive diagnosis in this class of cases is not always possible without awaiting the results of therapeutic management. If decay of the heart-muscle is present, it will be ultimately showTi by the gradual or more rapid development of symptoms sufficiently characteristic to settle the diagnosis.
Aneurysm of the heart is only possible of diagnosis when it is of sufiicient size to affect the outline of cardiac dulness in a way to suggest localized bulging of the heart-wall. It is stated that cardiac aneurysm may be suspected when there is a striking disproportion between the force of the cardiac impulse at or near the apex and the smallness and feebleness of the pulse. Its exist- ence can probably be determined by fluorescopic examination.
In most cases of cardiac rupture its occurrence can only be suspected but not determined before the death of the patient It may be surmised in cases running the extremely acute course de- scribed in Symptoms. Physical signs pointing to fluid disten- tion of the pericardium, with a pale, anxious countenance, a small, feeble, irregular, it may be intermittent pulse, and other symp- toms of profound shock, furnish strong evidence that rupture of the heart-wall has taken place. If life is sufficiently prolonged a correct diagnosis is often possible, but when death occurs within a few minutes the physician can rarely do more than conjecture the occTirreneo of rupture.
The diagnosis of chronic myocarditis is largely a matter of probabilities, since there are no pathognomonic signs of the con- dition. Physical examination may disclose certain gross changes, as hypertrophy or dilatation, or a combination of both, and pathol- ogy teaches that such hearts are as a rule more or less degenerated, but we possess no means of determining outside the dead-house to what extent the heart-muscle is diseased or the precise nature of its degeneration. The majority of elderly individuals who consult
CHRONIC MYOCARDITIS
549
us lieeause of cardiac syiiiptoius do not suffer from the conse- queiiees of rheiimatie emlm^aniitiB as do the young* They pre- sent evidence of cardiac incompetence; of this we can l>e certain, but concerning the state of the myocardium we must take much for granted.
Prognosis.— This dcpcnda uj>on the cause, the degree of the hypertrophy^ and the state of the heart-imiacle. If the high pulse- tension is due to luxus consumption, and the individual is young and robnstj correction of liis habits may lessen peripheral resiiit- auce, and may retard, if not \vh«dly prevent, dcvelapment of car- diac inade(|uacy. In cases of advanced renal or vascular disease there are two dangers: <.>ccurrence of apoplexy and the breakdown of the heart under conditiuns of unwonted strain. If the cause, whatever its nature, is persistent and not amenable to treatment, the ultimate prognodis is unfavourable, l>ecause there will at length come a limit to the hyiJertrophy iind the heart-wall will give way.
So long as the myocardium is functionally healthy— that is, receives sufficient nourishment — the hyi>ertrophy proves a pre- servative measure ; but when incompetence sets in, the most fa- vourable management can do no more than defer the evil diiy; Palpitation, and particularly intermittence of the pulse, are unfa- vourable signs; they may be the first evidence that the heart is yielding to the untMpial struggle, or by CKX^asioning incomplete emptying, and hence distention of the cardiac chambers^ they may hasten tlie coming on of dilatation.
In forming a pnigiMisis in any given case one must take into consideration also the age and temperament of the patient, and the state of his general nutrition. The younger the patient and the greater his self*eontrol, the better his prosp<*cts of maintaining com|K*nsatory hypertrophy and the less the likelihocKl of injury from excesses, emotional or otherwise. Tbe further one gets l)e- yond middle age the stronger tlje probability of the cardiac in- sutticiency being due to myocardial degeneration, and of the obstacle to circulation proving too much for the weakened heart- walls.
When serious symptoms at length set in there is small pros- pect of medical skill being able to do more than patch up the crip- pled heart. In a word, the prognosis depends upon the relatioD
550 DISKASE8 OF THE HEART
existing between the demands made upon the heart and its ability to respond. It is therefore almost entirely a question of cardiac nutrition. The younger the individual the less the likelihood of serious degenerative changes, but after middle age such changes are usually present and compensatory hypertrophy is rarely re-es- tablished after it has once seriously given way. One should make a careful study, therefore, of the condition of the vascular coats, as they furnish presumable indication of the state of the heart- muscle. Xevertholess, experience teaches that the latter may be extensively diseased while the arteries appear healthy. The de- tection of the gallop-rhythm over one or the other ventricle, most often the left, is of evil import, as it indicates a loss of muscu- lar tone and either incipient or fully developed dilatation. In the cardiac inadequacy of chronic nephritis this symptom may be regarded as indicating a not very distant termination of the case.
In coronary sclerosis the prognosis is most grave. We pos- sess no means of ascertaining the location and extent of degenera- tion, and hence cannot say whether life will persist a single hour. Indeed, a person with fatty degeneration of the heart-muscle can never l)e sure of his life from one moment to another. He may live for years, and he may die suddenly when apparently in the best of health.
The (H'CMirrcnco of angina pectoris makes prognosis doubly bad. In acute and subacute cases death is not likely to be long deferred, and ex('e])t in the most acute forms, which are usually ra])i(lly fatal, no one can venture to ])re(lict the length of life. Chronic forms of coronary sclerosis may ])ersist for many years with ever-recurring attacks of angina. As a rule it may Iw stated that the more easily and fretjuently pain is induced the graver is the ])rognosis.
The arrhythmic form of chronic myocarditis is apt to run a very chronic course, whereas those showing attacks of cardiac asthma or of acute pulmonary (edema are in danger of terminat- ing abruptly in such an attack. The development of Cheyne- Siokes res])iration is in most instances an indication that the end is not far off (see article on this type of breathing). Syncopal attacks are likewise of evil portent, owing to the danger of sudden death from asystolism at such times.
The cardiac insufficiency of Bright's disease and dialxites is of
COKONIC MVOCARLHTIS
551
particularly great gravity, since the abnormally high pulsc-ten- ^mu whic'li is the cause of the eardiao einbarrassiiioiit, cannot lie reinoveil, and prevents the left veiitriele from regaining its lost {>ower, A serioiia breakdown in this class of casc*8, therefore, may 1)0 said to be irreparable.
Finally, the prognosis is idso cietennined by the presence or absence of selerotie changes in the kidneys, Inngs, and liver, sinoe the healthier these organs the lesa the straiTi npon the diseased lieart. Chronic fjastritis^ with it^ flatnlont distention of the hol- low viscera, intlncneci^ prtjgnosis bulb through mechanical pres- snre and the generation of injnrions toxines*
Acute bronchitis or other illnesseSj in particular pneumonia and influenza, must always till the medical attendant with alarm, since it reqnires but little to throw the balance one way or the other in these cases, and acute infections are very liable to prove the immediate cause of death in cases of chronic myocarditis, which, witbuut such an intercurrent affection, might have persisted for years hmgen (Conditions of environment also affect prognosis^ an individual who is able to spend his winters in a mild climate and avail himself of all other means of warding olT injurious in- fluences Itoing, reterLs pftrihuSy likely to live longer than he who is compelled to toil on for bis daily bread.
In conclusion may l>c ipioted Mnchard's emphatic statement concerning cases of myocardial disease: "Their evolution is latcmt, their beginnings insidious, their course paroxysmal, their progress interrupted, their visceral complications various, and their explosions of cardiac insutficieney are sudden."
Treatment. — This must be considered first with regard to preservaiion of cardiac competence, and second with reference to the stage in which heart-ixvwer is either showing signs of failure or has actually been lost — pronounced cardiac insufficiency. Medical aid is n(»t sought so long as the myocardium is adequate, and if the discovery of hypertrophy is made, it is only by accident. When, however, su(*h discovery is made, it should l)e the physi- cian's duty to call the patient's attention to the dangers threaten- ing him in the future, and to show him how his habits of life are likely to affect his heart.
The uianagement is now along the line of prevention; patients who habitually eat or drink too much must have the evils of glut*
6&2 DISEASES OF THE HEART
tony explained to them, and be put upon a diet that will not over- tax kidneys, vessels, and heart. The man who takes little or no exercise, and is too rapidly gaining weight, must be sent to the gymnasium to be put in training, or must be made to walk more and ride less.
If vessels are sound and heart still competent there is noth- ing better for such patients than moderate bicycling, tennis, ball- playing, etc. If such sports are thought too vigorous, there is golf, which is an ideal form of exercise, since it trains the eyes and muscles without subjecting weak organs to undue strain. Those with corpulent, flabby abdomen are much benefited by a course of massage and Swedish movements. The processes of digestion and assimilation are improved, and constipation, if piiesent, is generally corrected.
Gouty individuals or persons suffering from defective excre- tion usually derive benefit from a semi-weekly or a weekly Turk- ish bath. This not only increases elimination, but lessens blood- pressure. This seems especially beneficial to persons addicted to the abuse of alcohol and tobacco. If the cause of the hypertrophy is • not preventable, or if vascular and renal changes are pro- nounced, then patients should be frankly informed of their con- dition, and warned against undue muscular effort, or whatever may serve as an additional and imnecessary strain to the heart- muscle. Arterial and kidney disease call for still greater strict- ness in the matter of diet.
.A highly nitrogenous dietary often serves to intensify the already existing high arterial tension, while a vegetarian diet, or Qi^e bordering thereon, lowers blood-pressure.
Digestive disturbance and constipation must, if possible, be corrected, since they not only increase arterial tension, but may produce palpitation and intennittenee, which, if allowed to go on, may ultimately impair the integrity of the heart-muscle, which in this stage it is our aim to preserve.
Cardiac tonics, especially digitalis, are not needed at this time, and if administered are likely to do harm. Our attention is to be addressed not to the heart itself, but to its protection from all injurious influences.
Unless induced acutely by severe heart-strain, signs of inade- quacy begin to declare themselves slowly and at first very insidi-
CHRONIC MYOCARDITIS
55:3
on sly, so that the nvanagcuient may be said to pass almost imper- ceptibly into the treatiuent of gymptonis directly due to:
Commencing Lo^s of II earl- power*— Among the earliest signs of this second stage are apt to be tachycardia and palpitation. These are not to be looked uiK>n as indications of excessive hypertrophy, for tsneb a thing d(x^s not exist. They are the earliest token that the organ is beginning to find its work too heavy. Therefore, nothing is more jiernieions than to attempt to control these symp- toms by aconite or veratruni viride, which are powerful cardiac depressors.
Digitalis and strophantlms are likewise not to be always pre- scribed for attacks of palpitation or for tachycardia until after an attempt has been made to discover and remove possible sourcea of irritation and increased peripheral resistance.
In my experience a too rapid or violent action of the heart in this stage may be due to digestive disorders^ constipation, r^r faulty excretitm, which augment arterial tension, and hence often subside with the removal of the cause. To this end I find very satisfactory a periodic dose of calomel or a blue pill^ followed next morning by an ajierient water.
It is also nec^f*ssary in these cases to restrict the diet by cut- ting out red meats and limiting the intake of water or other fluids at meahtime. The former raise pulse- tension by means of their extractives, while the latter distend the stomach and abdominal vessels.
Should blood-pressure still be too high, it may be reduced by one of the nitrites or a jKvtash salt. Three grains of potassium iodide nuiy be given after meals in essence of [X'psin without dis- turbing the stomach, or nitroglycerin, -j^^ of a grain, may bo given every tliree hours, Erythrol is said to be more lasting in its effects on the arterioles, Imt this advantage has not seemed to me sufficient to cnmiK*nsate for its greatly increased cost
Should such treatment fail to control cardiac action, then it is well to resort to iligitalis or allied remedies. They may be given in conjunction with iron, arsenious acid^ or strychnine.
Gentle exercise is now very beneficial by its action on the heart and vascular system.
It causes dilatation of the intermtiscnlar arterioles, promotes venous flow, and thus tends to restore circulatory equilibrium, re-
554 DISEASES OP THE HEART
moves waste products from the tissues, and flushes the heart-muscle with freshly oxygenated blood. This explains why patients who feel pra?cordial oppression upon starting out for a walk often ex- perience a sense of relief and well-being after their exercise has " warmed them up," as they say.
Gentle pedestrian exercise is to be recommended, therefore, in this stage of commencing cardiac incomi>etence, but under certain restrictions. Patients must be cautioned to begin their walk at a slow pace, and to increase their speed only as they find exercise and breathing grow easier. Walking against a cold or strong wind is very trying, and on such days they should walk with and not in the face of such wind. The carrying of heavy parcels is to be forbidden, and the restraint of trunk or limbs by tight clothing is inadmissible.
The ascent of stairs and hills is fraught with danger to the failing heart, and should be avoided. Oertel's plan of hill-climb- ing is to be advised only for patients whose hearts still retain a fair measure of their integrity and whose judgment can be relied upon. The principle underlying this mode of treatment consists in the ascent of gentle inclines at a rate of speed that does not cause dyspnona or palpitation. Only when such acclivity can be surmounted with ease is a steeper grade to be allowed. If hill- climbing is done so as not to occasion respiratory or circulatory embarrassment, the heart-walls are gradually strengthened and a tendency to dilatation is overcome. This form of exercise requires excellent judgment on the part of the patient lest he overdo, and on the part of the ])hysician in the selection of suitable cases.
Another kind of cardiac exercise not open to the same objec- tion, and suited to a larger number of cases becauses its effects can be more accurately gauged, are the ** resistance exercises," which were described in d<»tail in the chapter devoted to Treat- ment of Valvular Disease. If golf is permitted to patients in this stage of deficient cardiac power it should be restricted to put- ting, or at most to the playing of a limited number of holes. Whatever the form of outdoor exercise allowed, the following restrictions should be imposed: (1) Patients must not exer- cise immediately after eating, the length of time devoted to rest being determined by the degree of cardiac weakness. In most cases patients should remain quiet for at least an hour, and
cimoxic jiyorARniTis
555
when the heart h feeble Fnientzel does not allo^v exercise before throe or four hours after a meal. (2) Walking or other exercise shouUl not be indulged in to the poiut of fatigue. In some eases indeed it should be for only n short p€*riod^ several times repeated during ihe day. (3) In cases showing decided indications of a threatened loss of adequacy, rest in a recumbent postnrc must be insisted on at the close of exercise.
As our aim at this time is to prevent the heart from becoming still more taxed in its labours, and blnod-pressure is increased by hearty feeding, it is necessary to restrict the diet. It is quantity even more than quality that is harmful^ and hence patients should be told to eat lightly. T(X) much liquid raises bkiod-prcssure in the abdominal vessels^ and therefore it is well to restrict it to 8 or at most 10 ounces with each meal. Alcoholic stimulants, if permitted iit all, must k^ in the form of a light, dry wine, or still better of a modicum of whisky, largely diluted with water. To- bacco is to be allowed in great moderation, a small light cigar or a single pi[)eful of mild tobacco after meals, lluehard, Fraent- zel, Kreiil, and others are wry strenuous in their opposition to strong Havana cigars on the ground that they augment arterial tension, and state that many middle-aged men with weak hearts find out for themselves that they are obhged to substitute mild domestic cigars for the heavy Havana ones to which they have been accustomed.
Excesses of all kinds are injurious, and these patients are to be warned agaius^t the harmful effect of fretpient sexual indul- gence. Indeed, the principle that must govern the daily life of these individuals is moderation in all things. If patients give due heed to the doctor's admonitions they may succc*ed in holding their hearts in staht rpio for a considet*able time. Unfortunately, how- ever, the tendency of mym^ardial decay is downward, and hence we are called on, soon or late, to institute active treatment for the relief of symptoms which mark the arrival of the third stage.
Cardinc Incompetence Pronounced, — Venous and visceral congestion now begins to ujanifest itself, and calls for the more vigorous and fref|uent use of cathartic remedies. It is also gen- erally necessary to resort to cardiac tonics, and of these digitalis heads the list, although strophanthus, spartein, convallaria, adonis vernalis, and caffeine are all useful. Whenever digitalis is admin*
556 DISEASES OP THE HEART
istered to a patient who exhibits high pulse-tension, particularly if this depends on arterial thickening, it should always be given in conjunction with an iodide salt or nitroglycerin to counteract its effect on the arterioles. So long as cardiac weakness is not ex- treme the dose of digitalis may be small, 10 drops of a fat-free tincture thrice daily, or 15 drops every twelve hours. Given in this way it may be continued for weeks or even months without losing its effect or exhibiting its cumulative action. In more than one instance of myocardial inadequacy with stiff arteries I have seen striking results follow the prolonged use of strophanthus. It is sometimes well to combine these two remedies, a few drops of each being taken at a dose. Spartein sulphate is highly recom- mended by the French when the pulse is irregular, but although I have tried it repeatedly I have never been able to satisfy myself of its beneficial effect or advantage over digitalis.
Strychnine is so indispensable a heart-tonic that I believe it should be taken by this class of cardiopaths as regularly as is their food. A fortieth or even a thirtieth of a grain three times a 4ay is not at all too much for the average patient.
The one form of treatment from which I have seen patients with myocardial insufficiency derive most benefit are the natural or artificial Nauheim baths (see page 466). They should be com- bined with resistance exorcises. In my opinion this form of treat- ment is particularly adapted to this class of cardiopaths, and I have rarely seen a case of dilated hypertrophy which has not been improved by its judicious employment. I recall a typical example of this form of heart-disease in a medical man of forty-four, who began to manifest symptoms of threatening dilatation. His area of absolute cardiac dulness was greatly increased, particularly to the left, and anything!; more than moderate exercise occasioned a very considerable degree (»f discoinfort. Six weeks of baths com- pletely restored the heart's power, and although five years have now elapsed, the doctor is still able to attend to the duties of a large and exacting practice. His professional calls have required him to daily climb many flights of stairs, and although unwonted exertion still calls forth some degree of breathlessness, he has, by keeping down his pulse-tension through a somewhat restricted diet and an occasional purgative, never again displayed the same threatening symptoms. The last time I heard from him he had
CHRONIC MYOCARDITIS
557
taken to a bieyclej and l\v rarofiil rifling siic*(*cHHle(l in still fiirtlier streiigt helling his liL'tirt. At tlu^ close of his murse of hut lis ahso hite diilaeiSS had retnrntHl to normal, and the relative become manifestly reduced. He weighed over 200 jxninds, and of course still has a eonsiJerable degree of cardiac hyiN?rtrophj. In the summer of 1899 I treated by means of baths and resistance exer- cises two middle-aged gentlemen, eaeli witli enormous hyper- trophy. The symptom chiefly roniplained of by rme %vas great primordial oppression, amounting almost to what Gairdner would call " angina sine dolore^^^ whenever walking was attempted about an hour after meals. His pnlse was slow^ and tense, and his heart enormonsly enlarged. At the end of treatment the heart was not mnch reduced in size^ but the sonnds were manifestly stronger, and the pulse had become fuller^ stronger, and slightly more rapid. He then passed a month at his summer cottage, where he daily indulged in light carpentering, and was able to ascend the sandy hill on which his home stood without experiencing the former discomfort. A very restricted diet and the daily use of small doses of the tincture of strophanthus and iodide of so<linm have been rewarded by continued improvement. The second patient also derived much benefit from the baths and exercises, although, as in the preceding case, the area of deepseated cardiac dulnesa did not become permanently diminished, I was frequently able to determine a reduction in the size of the heart following a bath> and he always experienced a sense of well-being and lightness in the chest. In this case there was a very obstinate indigestion, and the urine always contained an excess of solids, although it never showed albumin or casts. His pulse was for the most part irregu- lar and intermittent, seeming to be governed in this re8j>ect by the intestinal indigestion, for every time his digestive disturbance bc*came aggravated his pulse grew more irregular. He was subse- quently induced to take a course of massage and Swedish gymnas- tics, with the result that not only did his corpulent abdomen be- come greatly reduced in size, but his rligestion improved, his pulse became regular for days together, and he said he felt as well as he ever did in hia life. The heart, however, still showed great en- largement.
In both these cases a change of habit as to food and exer- cise lo%vered blooj-pressurej treatment of the heart restored ita
558 DISEASES OF THE HEART
competence, and threatening dilatation was averted. I should add that all these three patients continued their professional and busi- ness duties while undergoing treatment.
In most cases that have reached this stage restoration of heart- power is out of the question. The problem confronting the physi- cian is how to relieve symptoms and postpone the final catas- trophe* In such, exercise is likely to do harm instead of good, and yet my experience has convinced me that harm is also likely to result from a too rigid enforcement of rest. If the breakdown is complete, the suflFerer may be forced to remain in bed or his easy chair. If things have not reached this pass, I believe it is better to allow the invalid to move quietly about his room that venous circulation may be aided by muscular contraction and the deepened respiration consequent upon this exercise. In some in- stances venous circulation may be assisted by gentle massage, and carefully conducted resistance exercises may, by dilating the arterioles, and thus flushing the muscles, help to unload the over- distended heart.
Romberg and Fraentzel are both emphatic concerning the in- jury of too strictly enforced rest in chronic myocarditis, and expe- rience has convinced me of the soundness of their advice. In the earlier years of my practice I used to consider prolonged rest indi- cated in all cases of cardiac incompetence from whatever cause, but I ultimately found that elderly individuals, who were not suffering from valvular disease, showed an acceleration of their downward course when they were denied all exercise and kept rig- orously in bed.
The aggravation of symptoms thus resulting is attributed by Romberg to the enervating effects of inaction, the same as is ob- served in the case of the voluntary muscles from disuse. The same thing is observed in previously healthy persons who are obliged to remain in bed a long time, from one cause or another; when again permitted to get up they not only find their legs weak, but the first attempt at walking produces slight shortness of breath and acceleration of the pulse. This explanation is in accordance with that given by Fraentzel, and is doubtless correct so far as it goes. In the case of a degenerative heart, there is another reason which I think holds good. When a patient remains quiet in a recumbent position the venous circulation is deprived of two fac-
THRONIC MYOCARDITIS
SS9
tf»rs of grcut iiniRH'tiHUT in its iiuxiiiteiiauee. Tiiose are miiBculur efToii and dei'pi'iied ivs])iratioiL Alu^t-ular coiitnii'tioii aided by the venous valves exerts a [nmipiiig action on the venous current, and also the flow within the ahsorhents. Abolish the use of the nius(.*le:3 and you remove one of tlie well-known causes of venous t'ireuktion. Furthermore, with rest in bed the patient breathes more slowly and stiperfieially, and hence blood is less rapidly aspi- rated out of the great veins into the right heart, and a second iroportant factor in maintaining venons flow is dinuni.^hed.
The work of maintaining the circulation now devolves npon the heart even more than under normal conditions. It must con- tract more powerfully that its driving force may be felt tlirough- out the entire circle propelling the blood onward in the %'eins. In those cases In which hreathlessness on effort is a pronounced fea- ture absolute rest for a time may be beneficial, hi/t it will not do to let these patients remain quiet for loo long a period.
The heart-muscle is weak, and cannot be left for too long a time to cope unaided with tlie labour of maintaining adequate bhxHl-flow. Instead, therefore, of complete rest, it is better that the physical repose l>e interrupted by short periods of gentle exer- cise. This last, however, is to be strictly controlled. The patient must only be allowed to wmlk about his room, or at the most into the adjoining room. Under no eircumstancc^s is he to be allowed to clin»b stairs nor to walk about soon after a meah lie nuist be impressed with the danger of jumping up suddenly and of hurry- ing across the room. If very weak, and dysputea is considerable, lie had better lean upon the arm of an attendant while taking his exercises.
The patient should also not be allowed to dress himself un- aided, and he must be instructed not to strain at micturition or defecation, since, aceonling to Sommerbrodt, straining during such acts raises blood-pressure reflcxly, and has more than once caused sudden diastolic arrest of the left ventricle.
If massage is employed it must not be applied to the abdomen, unless very eatitiously, since it raises blood-pressure. Also, if re- Btanee exercises form a part of the management at this time, "tbose are not permissible which constrict the abdomen or necessi- tate the elevation of the anns to a lev^el above the patient's head^ as they are likely to occasion dyspnoia and do harm.
560 DISEASES OP THE HEART
In the matter of food, it is well to remember that these patients require a relatively small amount of nourishment on account of the enforced inactivity of their lives. They should consume a lim- ited quantity of fluids, since it is an easy matter to ingest more than can be excreted by the kidneys because of congestion, and only such an amoimt is to be allowed as is found by actual trial to promote the renal function. Special care is to be had in order- ing such foods as do not induce flatulent distention of the stomach and bowels, and when this occurs it must be relieved by carmina- tives and medicines that assist feeble digestion.
Of equal importance with the prevention of fermentative indi- gestion is the correction of constipation. This is injurious not only because it necessitates straining at stool, but also on account of its raising arterial blood-pressure, and thereby increasing dys- pnoea, and the liability to attacks of angina pectoris and cardiac asthma. The patient should therefore take a laxative pill at bed- time, containing some of the well-known combinations of aloes, cascara, podophyllin, rhubarb, and colocynth, or a morning draught of some aperient water. It will not do to purge these patients repeatedly and violently, since there is danger of aug- menting the already existing debility, and yet a considerable degree of hepatic engorgement may render necessary an occasional sharp purge.
Having in this way endeavoured to remove or lessen the vari- ous conditions which may embarrass heart-action, the medical adviser should next turn his attention to those therapeutic meas- ures which usually afford a prospect of strengthening the heart- muscle. Digitalis is the agent usually employed in this as well as other forms of cardiac debility. It should be prescribed, however, with care and judgment. If the heart-muscle is greatly damaged, it is not likely to respond to the remedy, which will then exert itself chiefly on the arterioles. Through contraction of the latter blood-pressure is raised, so that instead of strengthening the heart digitalis may actually increase its labour. If given in such a case, the remedy should be prescribed in moderate doses, 5 or 10 drops pf the tincture, twice or thrice daily, and its constricting effects on the vessels should be counteracted by nitroglycerin. ,i In coronary sclerosis the nature of the degenerative changes that take place in the heart precludes the possibility of doing any-
CHHONIC MYUCAKUITIS
561
'tiling more than to relieve symptoms. In the most acute mhnifes- tatioDS of the disease, the physician, who has been has^tily sum- moned, is usually able to do no more than attest the fact of death* In the somewhat leas acutely fatal cases with manifestations of profound shtK^k stimulation is urgently indicated. Time should not be lost by sending for some favonrite stimulant, but use should be made of whatever is at hand. A tablet of nitroglycerin, with wiiich every phyaician is usually provided, may be placed upon the tongue; ami while an attendant follows this with i an ounce of whisky or brandy, the physician shuuld inject under the skin ^ of a grain of morphine. Twenty drops of spirits of cam- phor, or ^ a draehin of aromatic spirits of ammonia, pn>perly diluted, is also an etficient stimulant, and may be repeated at inter- vals of twenty minutes. Meanwhile, members of the family should fill bottles with hot water and place them about the body and limbs of the patient, w^ho is then to be wrapped in blankets. A hot bag or bottle should also be placed at the pra'cordium.
By these and other means every attempt is to be made to restore the failing circulation. In some cases^ unfortunately, all efforts are imavailing, but should the patient rally somewhat, stimulation is to be continued in stieh doses and at such intervals as will main- tain the beart's action. If after the lapse of a few hours it be thought best to administer fcK>d to the patient, this should be liquid and hot, as a cupful of soup or hot milk, to which the am- monia, wdilsky, or brandy may be added. It may now be well to order strychnine hyjxxlermically, in doses of t'tr o^ i^ of a grain every two or three hours; but digitalis, strophanthus, and the like are contra- indicated or are to be given cautiously.
If the initial symptom ia an attack of angina pectoris, nitro- glycerin, 1 minim, and ^ of a grain of morphine under the skin, will probably afford relief, and may he followed by hot whisky, and hot applications to the extremities and priccordium, the subse- quent use of stimulants being left to the judgment of the attend- ing physician.
In suhacuie cases^ which run their course in a few weeks, or at the most in a few^ months, the serious changes which the heart- muscle has undergone place the restoration of eompensation out of the question. Both the pliysician and patient must concern themselves with such measures as tend to make the downward 36
562 DISEASES OP THE HEART
career as slow as possible. What strength the heart still retains must be carefully preserved, and all unnecessary demands upon it studiously avoided.
The management of chronic cases of coronary sclerosis is also largely preventive and symptomatic, but there is often enough re- serve power left in the organ for considerable improvement fol- lowing measures calculated to reinstate the heart-muscle to a lim- ited degree. Exercise and diet must be governed by the same rules that apply to the more severe cases, although as time progresses and the heart appears to gain strength these restrictions do not need to be so rigorously enforced. The patient should be made to understand, however, that upon his obedience to the physician's in- structions, and his care in avoiding unwise eflFort as well as ex- cesses in eating or any other kind, depends his hope of prolonging life. In such cases more depends upon habit and daily routine than upon remedies. It is often interesting to observe how true it is that these patients can only learn by personal experience the wisdom which their physician has vainly tried to teach them. Tliey may be repeatedly and emphatically warned against infrac- of rules of diet and exercise, lest they thereby bring on a
Dxysm of angina pectoris, or aggravate the already existing 4y8pn<ra, and yet so soon as symptoms that serve as a monitor have become lessened, they think they can allow themselves more latitude and connnit some indiscretion.
A siKJcdy return of angina or cardiac asthma brings them to their senses, and they are again ready to submit to any restriction. The going and coming of these patients must be ordered by their medical adviser, who therefore should keep them under surveil- lance that he may discover early signs of impending trouble, and take prompt action accordingly.
Attacks of cardiac asthma are most surely and quickly allevi- ated by hypodermic injections of ^ of a grain of morphine combined with ^^ of atropine. A prompt effect is more surely obtained by throwing the medicine into the arm instead of the leg. The relief thus afforded is sometimes almost miraculous within a few minutes, the patient being able to lie do\vn and fall into a refreshing slumber. In the less severe forms of cardiac asthma the administration of the morphine at 10 or 11 p. m. will often carry the sufferer through the night without one of his
CHRONIC MYOCARDITIS
ses
clreiulrfl attacks. The reine<ly is never so efficiently adioiiiistered ill a II J other wav n& under the skio, and the dose should he as small as will produce the desired effect. This will rarely be less than I of a grain, wliich do^e should be administered nightly with- out increase. Should it he thought best for any reason to with- hold this remedy, then insomnia may he overcome by paralde- hyde, chloralamide, and bromide together, or by sulphonal.
The treatuient of cardiac asthiua is of a necessity that of the piiroxysm and the protection of the patient against influences which imiy precipitate an attack. If Cobnheim's explanation of its motle of production is correct — namely, tliat it is the result of i(*nipcirary increase of left-ventricle weakness, in consequence of which its systoles are relatively feebler than those of the right^ — then efforts must be directed to the protection of the degenerated left heart against conditions which by raising arterial tension tend to overpower the left ventricle. Blood-pressure may be in- juriously raised by the horizontal jmsition of sleep without other factors, and thr augmentation af peripheral resistance thus in- duced serves to overstrain tliis relatively too weak portion of the heart. We cannot abolish tlie need for sleep, nor can the patient be required to pass his nights in an easy chaiTj but we can guard him against other hannful influences, as constipation and flatulent distention of the Iwwek. The former raises blood-pressure in the aortic system ; and the latter exerts injurious pressure upon the weakened heart.
Dropsy is to be combated in the usual way, by an infusion of digitalis or dinretin-Knoll, as laid dowTi in the treatment of tederua from valvular disease.
The physician is not infrequently called to see a patient suf- fering from excessive distention of the right heart, consequent it may be upon the rapid giving way of hypertrophy. Two lines of treatuu^nt are open to him: a resort of free catharsis by some one of the drastic purgatives, as elaterimn, or to venesection. Tliere is no donbt of the speedy relief often following the abstraction of 16 to 20 ounces of blood from the ann, and if the urgency of the symptoms or the patient's exhaustion make the medical man hesitate to administer a drastic cathartic, no objection can be urged against the opening of a vein and the letting of blood. The relief thus afforded is justification enough for the procedure.
564 DISEASES OP THE HEART
Moreover, this operation can then be followed by the administra- tion of elateriuni, jalap, or any other hydragogue cathartic.
In a case of extreme dilatation of the heart, seen for the first time it may be, in this dire condition, the administration of large doses of digitalis, before having depleted the heart and venous system by venesection or hydragogue catharsis, is bad practice. Thus overdistended, the heart cannot respond to the drug and only struggles vainly to perform its work, like the jxwr horse that in response to blows strives in vain to draw the too heavy load up hill. So it is with the overburdened heart. It may be better in some cases to administer diffusible stimulants, as ammonia, cam- phor, ether, and the like, before prescribing digitalis, and only order the latter after the pulse has been improved in strength and volume by ammonia, etc.
Dropsical accumulation in the serous cavities may be with- drawn by aspiration, often to the relief of the sufferer. Such a procedure is of course not calculated to help permanently; it may, however, by lessening pressure for a short time, enable the heart to respond to stimulation. When at length all measures, have been tried and found of no permanent benefit, the medical attendant may then resort to opium in some one of its many forms to lessen the patient's sufferings. If we cannot promote restora- tion to health, we are justified in producing euthanasia. It is a physician's duty to prolong life, 1 presume; but I have seen pa- tients kept alive for days by drugs when it seemed to me it would have been far kinder not to prolong the struggle after it became manifest that the end was not far off.
CHAPTER XXI
HYPERTROPHY OF THE HEART
I
Morbid Anatomy. — In Lypertrophv the heart-nniscle is in- creasetl in thickne:?^ lunl weiglit. llypertrophv of the organ as a whole is judged by its weight, while that of a single chamber is better estimated by a measurement of the thickness of its walls. This increase in size seems, according to the latest investigations, to he dependent on an increase in the size of the individual mns- ele-fibres. According to Gntch, th(* increase in breadth of the fibres is insufficient to account for the total increase in weight of the organ. Ho thinks, thcrctV»n\ that the discrepancy can be ex- plained by taking into consideration the increase in interstitial fibrous tissue that is almost always present in hypertrophied hearts, and aW) by the supposition that there is, with the increase in width of the fibre, a corresponding increase in length. These two factors he considers sufficient to account for the increase with- out supposing any numerical increase in the fibres, and indeed evidence of the latter is wanting. The question can, however, hardly be considered settled as yet.
The hypertrophied muscle is firm, cuts with increased resist- ance, and is usually of a deep-red colour. Increase of muscular tissue without any corresponding increase in the blood-supply causes retrograde changes to bo common in hypertrophied hearts^ and in consequence yellowish streaks of fatty degeneration, or gray or whitish areas of local fibrosis, are not uncommon. This is seen especially in the hypertrophy accompanying arteriosclero- sis and renal disease, in w^bich aflFections the blood-supply to the myocardium may be reduced by reason of narrowing of the coro- nary vessels*
The normal heart weighs al>out 300 grammes (10 ounces) in the male and 250 granunes (8.5 ounces) in the female. These
565
HYPERTROPHY OF THE HEART 567
figures are for iiidividiial.s of the average siz*^, btit of course the Lfart weight varies witii that of tlic whole iKuly, In hypertrophy the weight may l>e doubled or even tripled. Stokes is said to have reported a heart weighing ^6 ounces, but one weighing more than GOO grammes; (20 ounces) is u %*ery large organ. According to Eiehhorst, a geni^nilly enlarged heart may attain such dimen- sions as to extend from the right mamillary to the left midaxil- lary liTie. When the left ventricle is chiefly involved the organ i*^ conical and its apex bhmt and broad (Fig. 104). When the right <'hamlj4?r is also enlarged it assumes a more quadrangular form, and the apex is formed wholly by the right ventricle (Plate III),
The papillary muscles and columnie carne^e share in tlie gen- eral hyiH^rtropliVj the latter especially in tlie right chamber (Osier), irypertrophy may be circumscribed, however, and then the traliecuke, j^jipilhiry muscles^ either conns, or one of the au- ricular apptrndices, may be the seat of the change. Such local hyjiertrophy is not common and prohably is due to trophic changes rather than to any circulatory disturbances.
Post-mortem rigidity of the heart-nuiscle may simulate hyper- trophy by causing the lieart-wall to be thicker than normalj and hence increase in weight is the only trustworthy sign.
(Vmcentric hypertrophy, or thickening of the wall of a cham- ber without increase in its capacity, is but rarely met with (Fig. 10). It is usually the result of stenosis. Hypertrophy combined with more or less dilatation of the chamber — i. e., eccentric hyper^ tn*phy — is by far the more usual condition. When such a heart ciimcs to autopsy, the dilatation ba.^, as a rule, broken do^vn the hypertrophy and is the predominating feature.
For the purposes of comparisHm, I give the following figures, quoted by Eiehhorst, from Thoina-s tables:
Weight of Heart
Until tlie end of the first ymr 87 granimea,
Seconct to fifth YOAF 50 to 70 **
Sixth tt^ tenth year .,., 70 10 115 "
Etev^nth to fiftcpnth year, * 180 to 205 *•
Sixtc^vnth to twentieth year 218 to 2M "
Twenty-fif^r to thirtieth year 2<I0 to 204 "
Thirty^flr^t to fiftieth year 207 to 808 •*
Fiftic*th to sixty-fifth year 808 to 883 *•
Sixty-flfth to eighty-fifth yi^ar _,.,,.. 88310806 **
568 DISEASES OF THE HEART
Eichhorst also furnishes the following table from Bizot:
I
In males. In females.
Length of the heart ' 85 to 90
Width of the heart ! 92 to 105
Thickness of the heart 80 to 85
Thickness of the left ventricle at the base ! 10.1
Thickness of the left ventricle at the middle < 11.6
Thickness of the right ventricle at the base 4.5
Thickness of the right ventricle at the middle \ 8.1
Thickness of the right ventricle at the apex 2.5
Thick ness of the sieptum ven triculonim at the middle. .1 11.0
80 to 85
85 to 92
80 to 85
9.8
10.8
8.7
2.8
2.1
9.0
Etiology. — Hypertrophy of the heart is rarely met with clinically except as secondary to some other condition. Thus we have seen that it is a part of the process styled chronic myocar- ditis, and is present also in valvular disease and adherent peri- cardium. It is often, though not necessarily, associated with arteriosclerosis. These affections may all be ranked among its etiological factors, but, as it is not of hypertrophy thus occasioned that I intend now to speak, they may be dismissed with this bare mention.
Hypertrophy of the whole heart, but chiefly of the left ventri- cle, is an almost invariable sequel to chronic disease of the kidneys, especially of interstitial nephritis, although also of the chronic parenchymatous variety and, according to Fraentzel, of long- standing pyelonephritis. There is persistently high pulse-tension in these cases, but there is probably some additional influence at work in the production of the hypertrophy — toxa^nia, it may be, or atheroma. Cardiac hypertrophy of this origin becomes a clini- cal entity only as it is incidentally discovered in connection with the nephritis or after indications of myocardial inadequacy have declared themselves.
A much less frequent but by no means unimportant cause of hypertrophy of the left ventricle is congenital smallness of the aorta or of the entire arterial system. There is usually some other abnormality, as persistence of Botalli's duct, whenever the narrowing is limited to the isthmus of the aorta or is extreme; but in minor degrees of narrowing an increase in the thickness of the heart-wall is the only result. This condition is not unimportant, for, according to German authors, it leads to cardiac incompe-
HYPERTROPHY OF THE HEART
569
tence and dilatation in young soldiers who are subjected to the Btrain of long, toilsome marches.
In chronic Bright'ts disease and congenital smallnesa of the aorta^ hypertrophy develops in consequence of abnormal periph- eral resistaijcc, wliich forces the heart-muscle to jierforHi extra work. It therefore becomes increased in size (see Morbid Anat- omy), the same as does a skeletal muscle under like conditions. Yet the muscular fibres could not grow in thickness and length if they did not receive sufficient nourishmentj and hence aug- meiited nutritive supply is indispensable. It is this consideration which leads German i^Titers to regard the consumption of inordi- nate quantities of beer as an undoubted cause of the enormous hearts seen among excessive beer-drinkers of Bavaria. The intake f>f large anifnints of fluid alone wouM nut be cajjable of prmlucing cardiac hyj>ertropljy, no matter how greatly they increase periph- eral resistance^ but containing no incoiisirlera1)le iimjKirtion of nutritive elenients, as it does, the excessive consumption of beer furnishes all the requisites for the causation of hypertrophy.
It is believed that contestants for athletic honours, particu- larly oarsmen and |n"ofessional bicyclists^ develop tliis form of hearted i sea se, and doubtless some of them do. The hypertrophy is thought to result from the heart having to overcome abnormal pe- ripheral resistance created by severe muscular effort. This is not the corn*ct explanation, since the initial rise of bhw id-pressure oc- casioned by muscular contraction is later on followed by a fall as the intermuscular arterioles become dilated. Therefore some other factor is rt^sjwnsible for the hyjiertrophy. This may lie in some unrecognised abnornuility of the vascular system, but in the case of professional wheelmen and rowers is probably due to the constrained position they take during their exertions. As seen in the next chapter, the heart-strain of athletic contests is nuich more likely to result in dilatation*
In the case of soldiers, mountaineers, |>eddlers, labourers, or others who carry heavy packs strapped on their shoulders, the in- jurious effect on the heart is to be attributed to the combined influ- ence of respiratory embarrassment and arduous physical exertion, even granting that there are no such influences at work as abuse of alcohol, atheroma, etc.
Rapid and violent action of the heart of a psychical origin is
570 DISEASES OF THE HEART
also thought to produce hypertrophy, but it is likely that tachy- cardia and palpitation alone are incapable of such a result The hypertrophy and dilatation of the heart observed in exophthalmic goitre is to be attributed not to tachycardia but to the underlying condition, whatever that may be.
Hypertrophy of the right ventricle is a sequel of various tho- racic disorders — i. e., pulmonary emphysema, cirrhosis of the lungs, pleuropericardial adhesions and chest deformity, as kyphoscoliosis. In these conditions there is excessive peripheral resistance in the lesser circulation from compression or even oblit- eration of pulmonary capillaries. In time, as the nutrition of tho heart suffers, its undue strain leads to dilatation and even to de- generation.
A so-called physiological hypertrophy of the left ventricle is said, especially by the French, to take place during pregnancy. There probably does develop an increased weight of the heart, a true hypertrophy of the muscle-fibres, but it is never so consider- able as to become of clinical importance.
To sum up : As remarked by Krehl, the development of hyper- trophy has to do essentially with the propulsion of an increaseil volume of blood, with the overcoming of abnormal resistance, or with a union of both these factors, and each one of them may depend upon a variety of causes.
Ssrmptonis. — iryj)ertrophy of the heart is to be regarded as a wise provision on the part of Nature by which the organ is enabled not alone to perform increased work but to accommodate itself to those conditions which render increased work necessary. The normal heart can perform increased labour by putting forth extra exertion, but its ability in this direction is limited. If, therefore, the heart did not rosjwnd to demands for extra effort by the development of hypertrophy, its accommodative power to diseased conditions would soon reach its limit. Consequently car- diac hypertrophy may be regarded as a conservative process.
These considerations make it apparent that there are no symp- toms directly referable to hypertrophy of the heart as such. If tachycardia, attacks of palpitation, and irregular or intermittent action of tlie organ disturb the patient, they are not due to the increase in its size but to disturbing conditions without, or are to be regarded as an indication of beginning inadequacy. In other
nYPKRTROPIiy OF THE IlKAItT
571
words, the extra labour retjuired of the heart ia heginning to tell on it, and if the undue strain is continued, its reserve strength will becuiiR^ cxhaiisitecl. The hypertrophy is discovered either accidentally or because a supervening dilatation occasions Bub- jertive :^erLsa!ion8 wliich bring the indiviiliial to the phyairian.
Physical SigHB. — Inspection. — The amount of information derived from ins|)eetion of the patient depends upon the degree of hypertrophy and conditions residing in the thoracic walk and lungs. If the chest is eapacioun and the hmgs are interposed between the chest- wall and heart, there may be no visible impulse. When, on the contraryj the parietes are thin and the organ is con- siderably enlarged, it protluees visible shock wdiich is exaggerate<i both in force and extent, while the apex-beat is displaced outward and in sunie instances downward^ aeeording to the degree of li_v]R>rtrophy. In hyj>ertrophy of the right ventricle there is apt to be visible pulsation in llie epigastrinni,
Palpalion. — Confirmation of the facts perceived by the eye is obtained by the hand, and for the most part nothing more. In some instances careful palpation enables one to locate the position of the apex-beat when this is not visible, and to judge of the force and extent of cardiac contractions. In women with large mam- mary development in whom inspection and percussion are futile, ]>alpation is often of great aid in estimating the size of the organ* The pulse of left-ventricle hypertrophy is full, strong, and in- clined to be slow rather than aectderated. Increase in its rate comes on, as a rule, only w!ien dilatation begins to gain ascend- ency and cardiac insuthciency to declare itself. It is a pulse of high and sustained tension, as shown by pressure of the finger on the artery and by Gaertncr's tonometer or the sphygmograph. This is not due to stiffness of the vascular coats, but to the in- creased force with which the blood-wave is propelIe<l by the power- fully contracting ventricle. 8ucli a pulse is difficult to compress, but when the artery has been thus collapsed, the wave of blood is ftdt to strike the palpating finger strongly, while below the point of pressure the vessel is empty and its coats cannot be rolled be- neath the finger, showing that they are not thickened and the in- crease of tension is not due to atheroma.
Pfrcussiot}, — This forms our best and most reliable means of determining increase in the size of the heart. Absolute dulness
572 DISEASES OF THE HEART
may not be greater than normal^ but the relative is, as shown by some one of the various modes of percussion described in the introductory chapter. Increase of deep-seated dulness to the left and upward is indicative of left-ventricle hypertrophy, pro- vided, of course, the organ is not displaced.
The measurements given in the article on chronic myocarditis show that the distance between the midsternum and left nipple is not constant in all persons, but varies within considerable limits. It is not safe, therefore, to conclude that because relative dulness does not pass outside the nipple the heart is of normal size, yet, if dulness is found to extend beyond the vertical nipple-line, it is pretty sure evidence that hypertrophy exists. Likewise an in- crease of relative dulness to the right and do^vnward betokens hypertrophy of the right ventricle. The measurements for the normal heart may be found in the introductory chapter.
Auscultation. — As one of the elements entering into the pro- duction of the first heart-sound is the muscular element, or that produced by the contraction of the wall and papillary muscles, the first sound is generally loud and booming. It is also apt to be rather prolonged. A more reliable criterion is obtained, however, by the study of the second soimd at the base. Owing to the high pulse tension present in left-ventricle hypertrophy, the aortic second tone is accentuated, and this intensification is generally put down as one of the signs of hypertrophy. It is only of value, however, in connection with other signs. Similarly accentuation of the pulmonic second sound is an auscultatory sign of hyper- trophy of the right ventricle. It should he remembered, however, that in children and young adults this tone is normally louder than the aortic. Auscultation is a much less reliable means of judging of the size of the heart than is percussion, since various conditions may temporarily alter the relative intensity of the sounds.
Diagnosis. — The recognition of cardiac hypertrophy de- pends not alone upon its degree, but also upon various conditions on the part of the lungs and thoracic parietes. Minor degrees may be assumed but cannot always be made out with certainty. On the other hand, a heart may be greatly hypertrophied and yet may escajHj our recognition because it is covered over by a volumi- nous or emphysematous lung, or the chest-wall may be so thick
HVPERTHOPflY OP THE HEART
578
frniii fat and miisrle as to rendor onliimrv methods of diagnosis fiitila
The clinical findings generally thought tu warrant a diagnosis of cardiac hypcrtru|>hv are: (1) A full, tense pulse which is either slow or of normal rate, not accelerated; (2) a powerful, broad apex-heat which is displaced outward and perhaps downward; (3) increased cardiac dulness to the left and upward or, it may be, in all diameters; (4) a booniing, low-pi tclied first sound and an ac- centuated aortic second sound, llypertruphy of tht? right ventri- cle is shown by: (1) Epigastric pulsation, (2) increase of cardiac dulness to the right and downw^ard, and (3) intensification of the pulmonic second tone. Should the condition of the lungs or tln>racic walls not enable one to rely on the evidence furnished by the usual means of physical examination, then one may have re- course to the tluoroscope, which ought to settle the diagnosis beyond further question.
Dilfereniial l)l(ujnosis, — It is hardly necessary to remind the reader that displacement of the heart towards either side may simulate Iiy|>ertrophy, aufl therefore uuist be excluded. The most frequent source of errcu" in this direction, however, lies iu the fact that scoliosis, or that forward curvature of the spinal coluum, may cause the heart to lie close against the anterior chest-wall and to pulsate so fcuTibly and widely as to give an appearance of marked hypertrophy. In all cases, therefore, the shape and depth of the thorax ought to be carefully scrutinized.
In addition, I wish to refer to wliat Italian writers term *^ pseudo-cardiac hypertrophy," by wdiich is meant a condition sometirues observed in young persons who are neurotic and have thin chest-walls with broad intercostal spaces. In siich, owing to excitability, the at^tion of the heart is apt to Ix* rapid and unduly forcible. The apex of the organ strikes in the broad and thin intercostal space with what appears to Ije exaggerated force and abnormal breadth, or the entire cardiac area may heave strongly with each systole. The heart-soimds are infensified and ringing, and altogether the organ convoys the impression of abnormal strength. Consequently, unless the examiner makes careful meas- urements of deejvseated dulness, he is very liable to erroneously conclude that he has to do with a bypertrophied heart.
In all cases in which hypertrophy is susijected and physical
674 DISEASES OP THE HEART
signs are not convincing, a positive diagnosis of the affection should not be made until some condition has been discovered which is capable of inducing hypertrophy. In the absence of such predisposing conditions hypertrophy is not likely to occur, and hence one should be conservative in relying on physical signs if they are not very conclusive.
The liability to error was forcibly impressed upon me by the case of a young coloured man who was an applicant for life insur- ance and who was likely to be rejected by the examiner because of a supposed enlargement of the right ventricle. Absolute cardiac dulness was manifestly increased transversely, whereas relative dulness as shown by careful measurement was not augmented. It was then noted that he stood in a very faulty attitude with his shoulders thrown strongly backward and the scapulae pressed closely against each other. In this position the spinal column was forced strongly forward to such an extent that it shortened the antero-posterior diameter of the thorax, and consequently pressed the heart against the anterior chest-wall so as to crowd the lung- borders aside and produce an apparent enlargement of the heart.
In some instances the diagnosis of cardiac hypertrophy is made almost at a glance, but in minor degrees its determination is only possible after one has carefully considered the degree of blood-pressure.
For the diflFcrential diagnosis of hypertrophy from dilatation the reader is referred to the succeeding chapter.
Prognosis. — The prognosis of the condition we are now con- sidering may be said to be that of its cause. If this is of a pro- gressive nature so that it is only a question of time when periph- eral resistance will outstrip the accommodative ability of the heart, prognosis is ultimately unfavourable. It should be borne in mind, moreover, that the hypertrophied heart-muscle is likely to suffer degeneration ; and when this sets in cardiac inadequacy is ultimately inevitable. If hypertrophy of the left ventricle is asso- ciated with a granular kidney and vascular changes, prognosis is influenced by the possibility of rupture of a brittle cerebral artery.
If hypertrophy has resulted from the abuse of athletic sports and the individual is still young, with healthy vessels, the condi- tion may not prove serious i)r()viding the exciting cause is re-
HYl'ERTROPHY OF THE HEART
575
inov^ed. lii sui*li [lersims^ liowevcr, one; sliuiild not ignore the pos- sibility of congenital siiialhiess of the arterial system.
Treatment. — llyjiertrophv of the heart does not require tlierapentie interference, and hence one should not attempt to lessen the vigour of cardiac contractions, as I have known at- tenii^ted, by the itse of aconite. The increased thickness of the heart-wall is a conservative measure. The aim should rather be to |>re8crve hypertrophy and protect the heart from the inadequacy of overstrain. The underlying condition is the object of our solici- tude. Valvular lesions, pericardial adhesions, chronic nephritis^ congenital smaUness of the aorta — these and many other causes cannot be removed. When detected, tluM*r existence should be stated to the patient and he ahonid lie warned against the danger of breaking down his hypertrophy by unwise physical eflForts or any other injurious influences. If the cause lies in the excessive consnniptiyu of beer, in gluttony, in faulty athletic exercise, the patient should l)o plaiidy informed of his injurious practices and urged to desist before they lead to cardiac insufficiency.
If disordert^d lictiun of the heart seems to call for digitalis, this remedy should he administered with great caution. As a matter of fact, sneli an In vigor ator of cardiac systole is not indi- cated unless signs of myocardial incompetence are actually pres- ent. When tills is the case it is no longer the hypertrophy hut it is the dilatation which calls for treatment. This will be found detailed in the appropriate place.
CHAPTER XXII
DILATATION OF THE HEART-RELATIVE MITRAL INSUFFICIENCY
I. DILATATION OP THE HEART
Except in cases of acute overdistention, dilatation of the heart is rarely primary, but secondary to some affection of an acute or chronic nature, as pericarditis, acute and chronic myo- carditis, and valvular disease, and the diagnosis should not be made merely of dilatation, but, if possible, of the underlying pathological etiological condition. These have been already con- sidered in previous chapters, and to them the reader is referred for particulars. More or less dilatation of the heart is recognis- able whenever there is cardiac incompetence from whatever cause, but in this chapter the endeavour will be made to portray what may be considered as overstrain of the heart-walls, whether grad- ually or acutely induced, and independent of previous recognis- able myocardial or endocardial disease.
Morbid Anatomy. — Ih*- dilatation of the heart is meant an increase in the capacity of its chambers due to rapid or gradual stretching of its walls. In most cases hy|>ertroj)liy is combined with dilatation and has preceded the development of the latter. A dilated heart is as largo or larger than one imly hypertrophied, but the muscle is flabby, and the orirnu does not keep its shape when laid on the table. Extreme instances have been described in which the heart held up by the great vessels collapsed over the hand so as to cover it like a mushroom. This flabbiness is not characteristic of dilatation as such, but of all conditions of the myocardiimi in which the muscle has lost its tone and which have predisposed the organ to stretching. These are cloudy swelling, fatty degeneration, etc. Slight degnn'S of dihitation, as well as acute overstrain, are not attended bv these mvcHnirdial changes — 676
PLATE III
N.B.H^oi^^
EXTERIOR OF HEART OF FIG. 42, SHOWING HYPEBTBOPHY AND DILATATION OF BOTH VENTRICLES.
DILATATION OF THE HEART
577
they are often a part of the L*(Hiij»ciisafory prricess attending valvu- hir lesions. WheUj however, compensation breaks down and dila- tation heeomes extreme, the walls are found degenerated and flabhy. The muscle is usually paler than normal and may be cloudy or of a brownish tint, due to the deposit of pigment.
As dilatation usually results from the further action of the causes that jiroduce hypertrophy, it has much the same distribu- tion. It may aflFeet but one chamljcr or the heart as a whole* The trabecuhe and papillary muscles are naturally not concerned iu the process of dilatation except in so far as the latter may stretch or lengthen in order to fnnctionate properly within the enlarged chambers. Relative insufficiency of the valves is gener- ally present and may be caused by stretching of their ostia or of the cardiac walls.
Etiology. — Cardiac dilatation may be said to he the result of a disproportiitu Ijctwecn the work the heart has to do and its abil- ity to do it. This undue demand upon its energies may have ex* isted for years in the form of prolonged high arterial tension, and only at length become disproixn'tioned through degeneration and gradual waning of the lieart-ijower. Not infrequently it is ftome unexpected call for extra effort that overpowers the heart, when witliont it the organ might have been able to perform ita work successfully for years longer. It is in this way that dilata- tion so often succeeds cnnipcnsatnry hyi>ertrophy in vaU^ular dis- ease. In many Imt not nil such cases the integrity of the heart- nmself^ luiri been slowly undermined by the development of degen- erative changes.
Such an exciting cause of dilatation may he a hasty run, a spurt on a Idcycle, the lifting or carrying of a heavy weight, a prolonged debauch, etc. Anxiety, grief, and even frightj through their action on the inhibitory nerve of the heart, are capable of inducing a stretching of the cardiac walls through stasis in the cavities they inclose — the ^^ stauungs^- dilatation of the Germans.
Romberg lays stress on the deleterious influence in this re- sfK^ct of acute infectious diseases, and cites instances in which he has observed cardiac dilatation and ultimately fatal insufficiency follow an attack of influenza, I have notes of the case of a gentle- man of fifty-seven whose dilatation and eventual death from pro- gressive cardiac asthenia were attributable to his having carried
578 DISEAStlS OF THE HEART
a heavy travelling bag several bloeks in Denver at an altitude of 5,280 feet. As this patient was moderately corpulent, weighing 192 pounds, his heart was probably not sound at the time of his exertion, and yet it had been adequate to all demands made on it previously.
We sometimes observe dilatation of the heart when we have no reason to assume that the organ is the seat of wide-spread structural disease and there may be no extensive post-mortem al- terations that can be recognised. The heart-walls are soft and flabby, and that is all that can be said of them. In such a case the individual may have been anaemic, or his heart-muscle as well as his skeletal muscles has been weakened by years of close applica- tion to business or intellectual pursuits. Without any preparation such an individual takes to bicycling and at once indulges in long tours at a scorching pace up hill and down, over rough sandy roads and against heavy winds. Under the absurd impression that such exercise is good for his weak muscles, he heeds not his panting respirations and rapid heart-beats. But outraged Nature avenges the insult by permitting the gradual if not sudden development of cardiac dilatation.
I once had under treatment for a time a clergyman of mid- dle age who had left-ventricle dilatation with relative mitral incompetence as the result of a single injudicious eflFort of this kind. As he expressed it, " he had pumped up " the steepest road on the banks of the Hudson River a thousand feet up the face of the Palisades — a road so steep that very few were ever able to make the ascent on their wheels. Although not aware of injury at the time, he not long thereafter began to suflFer from alarming fainting si)ells, the first of which seized him while delivering a sermon. Fortunately for him his heart-muscle was sound and ultimately recovered its tone.
It is rather singular that I have been called on to treat for car- diac incomjx^tence due to dilatation from strain three men whose occupations required them to inspect buildings in the process of construction. Failing to discover any satisfactory cause for their dilatation, I was led to inquire minutely concerning possible heart- strain, and found they were in the habit of climbing ladders or ascending many flights of stairs in order to reach the diflFerent parts of their buildings. It has seemed to me very reasonable to
DILATATION OF THE HEAHT
;}i\
be likelihotxl o£ heart-strain Uy such exertion, and in the ease of one of these itien interiniltenee persisted in spite of treat- ment until he exdianged his work as building inspector for a sedentary o<>cupation in an office.
In not a few instances the resistance of the myi>cardinm is diminished by the inordinate nse of tobacco or by sexual excesses, late hours and social dissipation, dancing, etc* In one case the young man breaks down in his nervous system, a second develops a cough, wliile still auuther manifests ai^wA of cardiac dilatation that may have been suddenly or gradually induced. In most of such cases complete restoration of heart-power follows removal of the cause and appropriate treatment. In some the heart remains permanently imiiairecl, and in others every fresh excess is followed by renewed dilatation until at length irreparable cardiac stretch- ing and insufficiency remain. Such examples are not confined to the male sex.
Anaemia and chlorosis predispose to this form of heart-disease, and more than one society belle pays for the season's round of dancing and other gaiety by slowly or acutely induced incompe- tence of the dilated heart, llimy a jaded uuitron who declares she is " w^orn out " by the demands uf society is really suffering from serious though perhaps not extensive stretching of the heart-cham- bers. Her heart-muscle has grown flabby and is not always capa- ble of entire restoration.
Fortunately the heart-muscle is susceptible of development the same as are the voluntary muscles. Were it not so, the athlete would be incapable of cou^peting for the laurel wreath of victory. If, however, he is overtrained or if his training prove inadequate, the heart may be the part that suffers. Under such circumstances acute dilatation may result from a single contest. It usually affects the right ventricle, and stretching of the right an riculo- ven- tricular ring permits the *' safety-valve action of the tricuspid '* to come into play. (See the chapter on Tricuspid Regurgitation.) It is possible, however, for the left ventricle also to become acutely 0%'erdistendedj as w^as shown by cases reported by Harold Wil- liams.
If muscular incompetence of these valves is set up, then the strain is lifted somewhat from the walls of the left ventricle and shared by those of the left auricle and pulmonary veins. This is
5S0 DISEASES OP THE HEART
likewise a compensatory provision on the part of Nature, for with- out it there wouKl be positive danger of diastolic arrest of the overtaxed left ventricle. In carefully trained athletes, or in the young with a robust myocardium, such a degree of cardiac strain is usually recovered from speedily and permanently. If the walls are not perfectly sound, or if there is sustained high blood-pres- sure in the aortic system because of vascular or renal disease, or if the heart is too frequently subjected to overstrain, permanent dilatation may result with all its consequences.
Finally I desire here to dwell on the harm in this regard that is likely to accrue to young children from the immoderate use of the bicycle and from games that necessitate long, hard running. There is actual^ not fancied^ danger of cardiac dilatation. If their hearts are sound no permanent injury may ensue, unless, of course, the strain be too oft repeated. In many cases the children have suffered from undetected rheumatism and latent pericarditis or endocarditis, and in such, unrestrained indulgence w^U surely result disastrously through the development of dilatation of the heart with possible coincident inflammation of some of its struc- tures.
The heart of a growing boy endures a degree of strain disas- trous in a man of forty, and yet if overstrain be too frequently rei>cated duriufi: one of the " fatigue periods " of childhood, it may, I am convinced, ultimately enfeeble the heart's resistance even in a boy. The overdistention of the heart is due probably to ineffectual systoles, which allow a residue of blood to remain in the distended cavities, while with the continuance of muscular effort and deepened respirations blood is passed on to the heart more rai)idly and in larger amoimts than can be expelled.
Another factor that should not be ignored in considering the question of cardiac strain are those unknown ** fatigue products " develojH'd during severe exercise and to which particular attention has been called by Clifford Allbutt.
Symptoms. — The symptoms of cardiac dilatation develop slowly or rapidly according to the development of the dilatation. The stretching and often thinning of the heart-walls impair their contractility, and there is a tendency to stasis within the organ which leads to loss of equilibrium between the arterial and venous streams. As the heart-|)ower begins to fail the pulse grows more
DILATATION OF TIIK HEART
§81
rapid, often irrogiilar in force imd volume, iiml in many cases in- termittent. CarditH' iinpulrio becoities weaker, its area of diilness inereased^ and its sounds fcc^ble.
The patient Iw^ins to notice more or less breatlilessness on exertion and a feeling of unwonted lassitude that niay amount to aetind weakness. His eoluiir changes from the reddish hue of Ijealth to the hliiish gray tint of increasing capillary stasis. As cardiac inadequacy advances, syinptoms of visceral congestion ap- pear. The urine lessens in amount ami Ix'comes of high specific gravity, often containing a trace of albumin. The liver increases in size, which may cause a feeling of fulness in the right hypi> chondrium or of dull pain in tlie back below the shoulder. Its inferior margin becouies more or less distinctly palpable, being smooth, firm, and rounded^ and palpation of the organ may be somewhat painful.
Congestion within the gastro- intestinal veins is shown by im- pairment of appetite and more or less flatulent indigestion, so that tlie patient feels bloated after meals and complains of windy con- stipated bowel movement. Piles may develop, sexual |)ower be- come deficient, and women are apt to suffer from leucorrh<pa and derangement of menstrual functiun. Congestion within the lower extremities leads at first to puffiness of the ankles, which by night feel tense and uncomfortable. When the shoes are removed the ^kin is found creased, auil a ridge indicates where the upper edge of the shoe pressed. After a night's rest this swelling of the feet and ankles may have subsided, hut as cardiac incompetence pro- gresses, (edema remains |x*ru laneut. Pitting on pressure 16 now pronounced and found to gradually extend upward.
Thus gradually but steadily grow the symptoms of failing cir- culation, and at length, if the condition is not arrested by treat- ment, the patient is compelled to keep his room. Pulmonary con- gestion is no longer shown mrrcly by dyspua-a on effort, but by cough with frothy, perhaps bloody expectoration, and by orthop- ncea. Talking causes breathlessness and so much fatigue that the patient dreads or even shuns the effort. Examination of the lungs discloses more or less dulness at the bases Whind w^ith fine crack- ling rales — in short, the signs of hypostatic congestion.
The apex-lw^at is now impc^reeptible or is but a feeble tap much outside the left nipple. Absolute and relative cardiac dul-
582 DISEASES OF THE HEART
ness are greatly increased, of a quadrangular outline, and in ex- treme cases may extend from close to the right nipple on the one hand nearly to the anterior axillary line on the other.
The heart-sounds are almost inaudible and there is very apt to be a systolic murmur denoting relative mitral or tricuspid in- sufficiency or both. The leak through the tricuspid valves is shown by the positive venous pulse in the external jugulars and liver. The veins of the neck stand out like blue cords, and if pul- sation in them is not apparent at all times, becomes plainly visible 80 soon as the patient coughs or makes a forcible expiratory eflFort. The pulse is now rapid, feeble, and often arrhythmic.
The state of things has now become pitiable, and if not re- lieved grows steadily worse, with the development of general dropsy, transudation into the serous cavities, somnolence, even low muttering delirium and death. This last may occupy hours, appearing to come from gradual exhaustion, or it may be ushered in by pulmonary oniema. In such a case fine crackling rales de- velop, spread throughout the lungs, and at last become plainly heard at a distance with every laboured respiration. In other in- stances pulmonary infarction occurs, as showTi by cough and the e^cpectoration of bright-red blood. In some the heart stops ab- ruptly and unexpectedly, while the patient is at rest or making some slight exertion, although this sudden cessation of the heart's action has Ix^en preceded for several days by signs of such increas- ing weakness that its final arrest is scarcely a matter for surprise.
In some cases symptoms of cardiac dilatation, even extreme, persist for many months or even two or three years. I recall a man of fifty odd whom I treated in 1893 and who was a striking example of this chronicity. For more than a year he had been incai)acitated for attention to business and yet had managed to keep about in spite of very apparent shortness of breath, a rapid, exceedingly arrhythmic pulse, enormously increased cardiac dul- ness, and feeble heart-sounds. The liver could be felt thin-bor- dered and hard, and this patient eventually died apparently from the pressure-effects of ascites rather than from independent asys- tolism. This man's heart was undoubtedly degenerated and very thin-walled. It might be reckoned as an example of cardiac in- adequacy from chronic myocarditis, but it was a typical picture of chronic dilatation of the heart.
IMLATATIUX OF TIIK IlHAltT
583
I hnvo recent l_v treated with highly gratifviii^ resiihs, by rjieaiis i»f baths uml resistaiice exercises^ a powerfully biiik man *if thirty-eiglit \v\ui \\n& suffering froni the effeets of heart 'Strain four years before. When in apparently |)erfect health he endured a day of terrible fatigue fruui the exertion of journeying in a severe snow-stunu at tlie altitude of 18,000 feet. By night he was completely exhausted^ looked blue, felt eold, ha<i a ft^eliug of great pnreordial oppression, and eonhl not get his breath. After a few days* rest be felt better antl returned to the East, lie remained at business, but when suuimrr eaiiu- on^ went abroad for a rest, !Uh1 in Lfitidnu eonsnlteil a well-known inedieal authority. By bini be was tobl he had suffered a heart-strain and was advised to give up business. He did not do so, however, with the result that he gradually deveIopt*d Hviuptoms of ehronie heart-disease* For some months l>efore I saw biiti be suffered from dyspna^a of efft^rt, a feeling by niglit of profnund exhaustion, and the eonvic- tion that be was liable to die suddenly at any time. He neverthe- less remained at business.
When T first saw him he presented the signs of mitral regurgi- tation witli seeouda ry enlargement of tbe heart, ehietly of the left V(*ntriele. Lungs were negative, but the liver was palpabk\ There was no pitting, but the tissues everywhere felt tense and hard, and the |>atient said he ** felt swollen." Preliminary treat- ment by rest in btHb cathartics, and a milk diet for two days re- (hiced eajdllary stasis, improved the quality of tbe pulse, and re- luoved the patient s sense of air-huiiger. There was 2 per cent of albumin in tbe urine, l>ut although re|ieated search was made for casts, tbey were never found.
At tbe end of less than four months this patient declared he felt |>erfeetly well and desirc^d to return to business. The heart was manifestly sniaih'r and its action greatly improved, but the uiitrat systolic murnuir still remained. It was less loud and less harsh, however, and the first sound, originally inaudible, could 1)0 beard distinctly. Tbe liver could not Ix^ felt, but albuminuria persisted. This man had never ha<l articular rheumatism or any disease to lead to endocarditis, and prior to his arduous mountain climbing had never had even the slightest symptoms of heart weakness. I have no doubt that bis heart-muscle has suffered in its integrity, but I look uj>on this as an instance of chronic left-
684 DISEASES OF THE HEART
ventricle dilatation due primarily to strain and leading to relative mitral incompetence.
Acute dilatation of the heart from strain most commonly affects the right ventricle, but it may also take place in the left This was shown in the cases of the young men who were examined by Harold Williams inmiediately before and after a run of twenty- five miles. Cardiac dilatation was shown by exhaustion, cyanosis, a rapid thready pulse, manifest increase in heart's dulness both to right and left, and by a systolic murmur having the characters of a mitral bruit. The safety-valve action of tricuspid regurgita- tion may be rather quickly induced as compared to the time it would take to set up such a left-ventricle dilatation as would pro- duce relative mitral incompetence. In a run of twenty-five miles requiring three or four hours, time would be given for the safety- valve action of mitral insuflSciency to occur. Were this not so, the left ventricle would be subjected to a degree of strain that might prove dangerous and even fatal.
The symptoms of acute heart-strain are those of deficient arte- rial circulation (relative arterial anaemia), a rapid, weak, and it may be irregular or intermittent pulse with signs of an overloaded venous and pulmonary system, dyspnoea, exhaustion, praxsordial discomfort, perhaps pain, and cyanosis, congestion of the liver, and positive venous pulse of tricuspid regurgitation.
Within the last year I have seen two instances of acutely in- duced dilatation of the right ventricle in powerfully built young men belonging to college foot-ball teams. One of them walked off the field after the contest was over, but he looked blue in the face, complained of dull pain behind the lower end of the sternum, and the physician having charge of the team detected increase of abso- lute dulness to the right. Symptoms did not disappear for a num- ber of days, and it was months before the heart's action regained its wonted steadiness.
When the heart-muscle is healthy, acute dilatation from over- strain may be recovered from, yet if too frequently repeated may without doubt result in pennanent cardiac incompetence. I be- lieve this is a very positive danger attending college athletics, par- ticularly in foot-ball and rowing matches.
When the heart-muscle is not healthy, and therefore when per- sons have passed their forty-fifth year and have arrived at a time
DILATATION OF THE HEART
585
of life in which the state of the niytxrardium is questioBahle, acute cardiac dilatation from overstrain Ijecojiies a very serious matter. The first symptoms of heart-strain may be recovered from, but more or less inadequacy is likely to remain. In time, as a result of renewed but less severe strain, evidence of weakness sets in and the patient ultimately presents a clinical picture of gradually increasing dilatation of the heart.
Physical Signs. — Inspection. — The nuiltiplieity of condi- tions which atTeet the results of inspection renders this means of investigiitioii of cooiparativelj smiill value. The eye may per- ceive the well-known manifestations of (*ardiae weakness, but it cannot furnish infornuition as to the actual state of the heart. There is usually an absence of visible cardiac impulse, but this alone is of no value, since it is nonnal to many individuals to have no visible apex-beat on account of the volume of the lungs or tlie tlu'ckness of the chest- walk In emphysema, which so com- monly lends to ultimate dilatation of the right heart, visihle im- pulse is also likely to be wanting. In all cases in which the apex- beat is not plainly visible the patient should be placed in a strong light and inspection made across the front of the chest from the side or from tib<»ve downward. If dilatation exists a feeble apex- shock may thus be sometimes perceived outside of and below the nipjile or in the epigastric notch.
Palpation. — Aside from the knowledge which this affords con- cerning the pulse and hepatic congestion, palpation is of service in the estimation of the feebleness or strength of cardiac contractions, Tbin-walled and dilated hearts may give no |>erceptible shock to tlie chest-wall, or they may occasionally produce a sudden quick tap whenever the organ gathers itself, as it were, for an extra effort. When the apex-beat jcrsists, it is not like the broad heav- ing impulse of hypertrophy, but is a circumscribed feeble stroke of a slapping chanicten This is particularly the case in long- standing dilatation with still some degree of efficiency.
Percussion. — ^This is, as a rule, our most valuable means of determining if dilatation of the heart is present, but it may afford very unreliable evidence in cases of pulmonary emphysema. If the state of the lungs and of the thoracic parietes renders percns- sion available and if dilatation exists, the area of deep-seated if not of superficial dulness is found increased in accordance with the
586 DISEASES OP THE HEART
degree of dilatation and the chambers affected. In dilatation of the left ventricle relative dulness is increased towards the left and upward, while in stretcliing of the right heart it is augmented to the right and downward. When general dilatation of the heart exists the area of dulness is found to have assumed a quadrangular outline with broadly rounded comers and sides.
Auscultation. — The heart-sounds are feeble, altered in intensity and rhythm, and are frequently accompanied or obscured by mur- murs of relative or muscular mitral or tricuspid incompetence. The systolic tone becomes shortened and valvular like the second, and with lessening of the long pause the rhjthm of the sounds tends to assume that of the ticking of a small clock or watch. In cases of great weakness and rapidity of heart-action the tones follow each other in quick succession, or but a single sound may be detected. The aortic second tone is usually diminished, while the pulmonic second is accentuated. If munnurs exist, they are, as already stated, those of relative or muscular incompetence of one or both auriculo- ventricular valves depending on the degree of dilatation. The auscultator should not forget, however, that it is possible for bruits of pre-existing valvular disease to be present, and therefore he must not hastily conclude that the murmur is necessarily due to dilatation alone. In many cases he must await the result of treat- ment before deciding definitely on its real nature.
Diagnosis. — The recognition of cardiac dilatation is ordi- narily not difficult, es{)ecially if it has been acutely induced or has progressed to the production of considerable inadequacy. Minor degrees of stretching are not always easy of detection and require minute inquiry into the history and symptoms, as well as pains- taking physical examination. In slowly induced dilatation there is history of gradual onset and progressive increase of symptoms of cardiac incompetence, while there are clinical findings of (1) a more or less rapid and feeble, it may 1k» irregular or intermittent, pulse; (2) feeble, tapping, or even imperceptible cardiac impulse; (3) increase of relative and perha})s superficial dulness in one or more directions according to the chamber affected ; (4) feeble tick- ing soimds and perhaps systolic mummrs of relative or muscular mitral or tricuspid insufficiency.
In acute overstrain the })henomena of cardiac embarrassment follow some unusual exertion and are easily recognised, while the
DILATATION OF THE HEART
887
patient IS apt to display more or less cyanosis and other evidence of iiiipeiiding stasis.
Differential Diagnosu. — Acute dilatation of the heart can scarcely be iiiistaken or confounded with any other condition pro- vided due attention is paid to history and objective symptoms. Distention of the cardiac cavities that has developed more slowly and has grown extreme may, however, be mistaken for pericar* dial effusion. The differential points are fully dealt with in that chapter, but speeial emphasis may here be laid on the necessity of determining the relation of the outer and inferior margin of deep-seated dulness to the position of the apex-beat In car- diac dilatation dulness does not pass beyond the limits of car- diac impulse, whereas in pericardial distention the apex-im- pnlse is situated w^ithin the outer border of dulness. This, and this alone, is the trustworthy criterion of difference between the two affections. In other respects there is often a striking similarity.
Dilatation and hypertrophy can scarcely be confounded if due attention is paid to the characters of the pulse, to the nature of the impulse, and to the greater feebleness and rapidity of the sounds in dilatation. A simply dilated and yet not specially de- generated heart cannot often be distinguished from a degenerated and hence secondarily dilated organ, and it is not always prudent to attempt Bueh distinction,
Prognosis. — Dilatation of the heart should never be regarded as a trivial matter, and yet the degree of its gravity depends upon the state of the heart-muscle, the extent of the dilatation, and the length of time it has existed. It is the integrity of the myocar- dium in the young and in trained athletes which in them makes the lieart recover so quickly and well from the overdistention caused by strain. On the other hand, it is the likelihood of the heart-walls being not cpiite sound which renders prognosis serious when dilatation supplants hypertrophy or when elderly individ- uals suffer heart-strain. Stiffened arteries do not necessarily mean that the heart-w^alls are seriously degenerated, and experi- ence abnndantly proves that in some cases proper treatment may restore a dilated heart even when the vascular coats are thickened. Xeverthelcss, under such conditions stretching of the cardiac chambers is always a grave affair, and only too often there is but
588 DISEASES OF THE HEART
little prospect of the heart- walls again becoming as sound as before the injury.
Cardiac dilatation associated with a granular kidney may al- ways be said to furnish a very grave prognosis, for the resistance in the arterial system is so great that in all likelihood the heart has been gradually yielding, and having once given way, cannot re- gain its lost adequacy. In such a case the prognosis depends both upon the state of the heart-muscle and the possibility of lessening the high pulse-tension by treatment.
In the face of both arteriosclerosis and interstitial nephritis a seriously dilated heart is likely never again to recover its former compensatory hypertrophy.
It is so evident a fact as to scarcely require statement that the more extensive the dilatation the more serious the prognosis. With care and proper management minor degrees of the condition may endure for a long time — even years — yet in such a case the tenure of life is always imcertain, for the reason that some addi- tional and unexpected strain may at any time convert a not alto- gether unfavourable into a most serious prognosis.
Stretching of the auricles or of the right ventricle is not so grave a matter as is left-ventricle dilatation. Owing to the thin- ness of their walls they may not be so amenable to treatment — that is, not so likely to have their hypertrophy restored ; but on the other hand, the right ventricle is more likely to be relieved by stretching of its auriculo-ventricular rinp^ and therefore is less liable to paralytic ovordistcntion and diastolic arrest. This con- sideration leads me to the belief that in cases of left-ventricle dila- taticm the devolopnient of a systolic murmur at the apex is a favourable rather than an unfavourable provost ic indication. Such a murmur is usually held to indicate relative mitral insuffi- ciency, and bv th(* giving way of the mitral valve a part of the excessive endocardial blood-pressure becomes transferred to the auricle and pulmonary veins, and thus the wall of the left ventri- cle is relieved, in a measure at least. T can recall more than one instance of sudden and unexpected death in men whose hearts were seriously dilated and in whom such a systolic apex-murmur did not exist. On the other hand, T have more than once observed that when the mitral valve gave way the progress to asystolism was gradual, and death was usually preceded by the symptoms and
DILATATION OF THE HEART
589
signs of venous stasis, extend itig thnnigli a period of weeks or munthii.
It is also evident that prognosis is largely governed by the length of time the dilatation has existed. If the myocardium is still liealthy, as in the young, a chronic dilatation may yet be recovered from. In persons past middle age the condition is likely to resist treatment if it has become chronic^ and if in such the pulse is persistently arrhythmic, it is to be looked upon as an in- dication that the heart-musele is not sound or that the auricles are greatly dilated. According to Radizevvsky, habitual irregularity of the pulse points to preponderating degeneration of the walls of one or both auricles. If this be correct, tlien arrhythmia in con- nection with chronic dilatation of the heart is a better prognostic sign as reganls length of life than is tachycardia with jx^rfect regularity of rhythm due to a dilated ventricle. In acute dilatation from overstrain, as in fo<>t-ball or mountain cliiiilung^ the progno- sis is as a rule good, for with rest and proper treatment the heart is likely to return to its former healthy condition. Repetitions of its abuse may, however, eventually induce permanent inadequacy.
Another element that enters into the question of prognosis is the degree of snhjcc^tive symptoms ]vrodu{^ed by the dilatation. If dysjmtra be less than one would be led to expect from the appar- ent gravity of the condition, the case is likely to pursue a chronic course; if, on the other hand^ the shortness of breath be out of pn>portion to the apparent size of the organ, or to the amount of exertion performed by the patient, or if the dyspnoea assumes the form of cardiac asthnui, then the prognosis is had, unless the urgency of this symptom can be accounted for by an associated em]>hysenm or bronchitis.
If skilful treatment succeeds in producing only temporary ira- provcmcTit, and the heart drops back to its former state so soon as treatment is discontinued, or less vigorouSj it is an indication that the heart-muscle is either too weak to be regenerated, or the peripheral resistance is too great to be permanently overcome, A steady though gradual loss of ground, in spite of treatment, proves that very little is to be expected from any management, no matter how skilful.
Except in cardiac strain of effort in the young, one should never venture to prognosticate the length of time it wull take for
590
DISEASES OF THE HEART
the heart fo be restored to health, or in those in which this is raani- festlv inipossihlej to predict how long the disease is likely to last. If the left heart is the one chiefly affected, the end may come sud- denly and unexpectedly, hut in thoae cases in which the right heart 18 the one chiefly at fault, and particularly when the right auricle is much dilated, pulmonary infarcts are very likely to occur and to be the immediately determining cause of death.
Two states of mind on the part of the patient, if they come on after the disease has existed for some time, and serious symptoms of stasis are present, always make me apprehensive of the near approach of the end. These are, great restlessness and an ill- defined nervousness that keep the patient constantly moving about, and on the other hand a sudden lull in the patient's sense of distress. After days or perhaps weeks of severe suffering he suddenly has a day in which he feels remarkably well and free from distress. This is often like the calm that precedes the stonn. I have more than once seen death speedily succeed such a day of apparent welM)eing. Aproi^os of the former state I recall a large middle-aged man presenting all the symptoms and signs of ex- treme cardiac dilatation whom I examined in consultation wnth Dr, Harrison late one afternoon and in whom I saw no evidence that the end was imminent; he had been in that condition for a week, and, although very dyspntpie, walke<l into an adjoining room. He displayed, however, an indescribable restlessness^ and less than three hours after we left him he died suddenlv.
Treatment. — In dilatation of the heart suddenly induced through strain the first indication is to place the patient at rest in the recumbent or semi-reeumbent position for the purpose of lessening the heart's work so far as that is possible. Mnscnlar in- action and a more tranquil respiration bring the venous blood to the right heart less rapidly, and if the circulatory apparatus is healthy, as in the youthful athletej Nature alone, under favourable conditions, will speedily effect a restoration of the blood-stream to its former equilibrium.
If, on the contrary, the patient's age or state of general nutri- tion justifies the inference that the heart cannot return to normal without further aid^ then a mercurial pill and digitalis should be prescribed. By unloadinp: the portal system the cafhnrtic tends to restore balance within the abdominal vessels and secondarily
DILATATION OF TUE HEART
:>9i
m the sy&tcm at larg<\ Five gnilns of 1>liie in jibs followed by J ounce of Epsom salts eight hours thereafter^ or a grain or two of calomel at bedtime and a glassfiil of the solution of citrate of magnesia next morning, or any one of the numerous aperient waters in the market, will prove highly efficient to that end.
The purpose of the digitalis i& to slow down the heart and en- able it to empty its distended cavities effectively* This may be accomplished by the admin ifttrat ion of 10 to 15 minims of the tincture t-vcry six hours for four or five days. Improvement will he shown by a reduction in the rate and corresponding gain in the force and strength of the pulse, by disappearance of cyanosis and other signs of venous congestion, by increased diuresis, ami a gradual return to nornuil in the size and sounds of the heart. Strychnine and nitroglycerin will probably not I>e required. It is well, however, to insist on light yet nutritious diet until the normal state of the circulation has been regained.
When permanetd eardiac ittsaffiCiency is threatened from re- peated heart-strain or from the gradual giving w^ay of hypertrophy in the face of relatively too great peripheral resistance, the prin- ciples of treatment must be the same as in any other form of heart- weakness. The first indication is to relieve the overtaxed heart. Therefore the patient must be put at physical rest for a length of time which is to Ik? determined by results. To the pa- tient^s query, '^ How long must I stay in bed i '' do not permit vourself to make a definite answer, but tell him that is to be de- terra ined by the rapidity and degrt^e of improvement. In other respects the same general plan of action previously detailed for cases of lost compensation is to be followed^ but varied to meet the peculiarities of each case.
Most cases of cardiac dilatation which the physician is called on to treat are not instances of acute strain^ hut of chronic cardiac insufficiency. They are to be managed, therefore, in accordance with the principles laid down for the treatment of inadequacy from chronic myocarditis, and the reader is referred to that chap- ter for details.
There are three measures, however, of which it may be well to speak with special relation to cardiac dilatation:
(1) Bioodleiiing,' — Occasionally a patient is encountered who from one cause or another is suffering from great overdistention of
692 DISEASES OF THE HEART
the right heart. The action is extremely feeble and disordered, the face is congested, the veins are turgid, dyspna^a is profound, the lungs are filled with rales of pulmonary a*dema, there is cough and bloody, frothy expectoration, there is no a^dema, but the ex- tremities are cold and cyanosed. Percussion shows enormous dilatation of the heart, and, so well as can be determined, the heart-tones are very weak and impure. Dissolution appears immi- nent. Under such circumstances the physician realizes that what- ever is to bring relief must be done quickly.
There is not time for digitalis and cathartics to be tried ; they are too slow. In such an extremity there is nothing that usually affords such prompt relief as venesection. Twenty or more ounces of blood taken from the arm are generally followed by diminution of cyanosis, noticeable improvement in the quality of the pulse, and increased clearness and strength of the heart-sounds. Of course such improvement will be only temporary if nothing else is done. This treatment must be followed up, therefore, by the judicious use of digitalis, strychnine, and cathartics, to secure what is gained by the abstraction of blood, since this latter is of course only a temporary measure resorted to for the dire emer- gency. Many a patient's life has been saved by such treatment, but, unfortunately, it will not save all.
(2) Nauheim Baths, — By some authors who seem to make a fad of this mode of treatment those saline and effervescing baths are advised even in cases of extreme and long-standing dilatation. Judging from my experience, such treatment is a mistake in cases in which, from the arrhythmic pulse, enormous area of cardiac dulness, and feeble tumultuous heart-sounds, it is clear that the cardiac walls are too thin to ever regain their old-time power. The- oretically these baths should unload the cardiac cavities and thus assist the heart in its labours. As a matttn* of fact, I believe in these cases they do not accomplish this result. Such persons can- not be materially benefited hv anything, yet if any remedy can help them it should be digitalis, strychnine, and cathartics judi- ciously administered for an indefinite time.
(3) licsisiance Exercises. — If given hv an attendant who thoroughly imderstands how to apply the proper degree of resist- ance to a feeble heart, these exercises nuiy j)rove of real benefit even to a seriously dilated heart. They are supposed to relieve
DILATATION OF TflE HEART
593
the cardiac cavities by diverting a part of their contents to the |)eri]>l)eral vessels^ and as a m otter of fact they arc followed by a demonstrable decrease in the area of cardiac diilness. Neverthe- less I do not believe it is possible to create so remarkable a decrease as is claimed by Tbeodor Scliott, who finds in this effect a mcan*^ of differential diagnosis between a dilated organ and a pericardial effusion. When employed in the condition now considered they must be given with very great geiitlenesSj and movements are to be omitted which necessitate the elevation of the arms above tlie head as well as bemliitg of the trunk at the hipSj which are capable of augmenting dyspmea and aggravating the dilatation. Even when pernuinent improvement in the patient's condition does not resnlt it is generally found that for a time at least there is a less- ening of his distress and an iaiproveinent in his colour. I therefore reeonunend their trial in all cases of chronic cardiac dihitation.
Shonhl eases of chronic cardiac incompetence be not improved by the measures just spoken of, then it is reasonable to infer that the case has passed beyond the stage in wdiieh anything more is to be hoped from treatment than the amelioration of s^'mp- turns. One may yet do what be can ^vith digitalis, strychnine, nitroglycerin, diffusible stimulants, and cathartics. In the ma- jority of cases morphine will no^v have to be given^ and if admin* istered hypodermically to secure comfortable nights, the remedy is generally of the greatest service. In many instances mor- j^biuf thus given wdll prolong life and ease the sufferer's path to tlio grave.
Only a few months ago Dr, George F, Roberts, of Minneapo- lis, called me to see a gentleman of nearly sixty who presented a typical picture of a dilated heart. The myocardium was probably degenerated, l>ut his arteries were soft and urine w*as negative, so lljat one cmdd not say there was more than cardiac incompetence from ililatatiom He was in bed and dyspn^eic, but his suffering arose from vertigo, wdiich catne every few^ minutes and lasted from a few seconds to a minute or more. During the vertigo his radial pulse w^holly disappeared and the heart-sounds t)ecame exceedingly rapid and feeble but i>erfectly regular; the cavities were not being emptied. Suddenly the action of the heart w^onld change, becom^ ing slow, strong, but irregular; the pulse w^ould return and the 88
594 DISEASES OF THE HEART
]»atient would exclaim, " There! it is gone! " iiieaniug, of course, his dizziness.
The cervical veins were distended, liver was palpable, urine scanty, but no oedema and no turgescence of the superficial veins over the trunk and limbs. Cardiac impulse was absent and the area of dulness enormously increased and of a quadrangular out- line. It seemed as if the large vessels of the abdominal and portal systems were holding the most of the blood.
Venesection was indicated and might have afforded temporary relief, but for certain reasons it was not performed. Instead, nitroglycerin, camphor, and valerianate of caffeine were injected subcutaneously at short intervals and the bowels were opened by calomel and a saline. Vertigo was relieved by this means, but circulation was not materially improved. The heart-walls were too greatly stretched and probably degenerated to regain their ade- quacy, and the patient died about ten days subsequently.
II. RELATIVE AND MUSCULAR MITRAL INSUFFICIENCY
Relative. — By this term is meant that variety of incompetence which results from over-distention of the left ventricle and is en- countered in its most typical form in the acute heart-strain just described. When so produced the insufficiency is sometimes spoken of as primary, to distinguish it from the subdivision known as secondary. It is the latter, or secondary, that not infrequently develops in tho late stage of aortic stenosis and regurgitation and has so often been referred to in the foregoing pages.
Balfour's term, Curable Mitral Regurgitation, was intended to cover cases of primary relative mitral incompetence, particularly as seen in chlorotic girls, since it is very amenable to treatment. The term was based on the supposition of such a stretching of the mitral ostium as precluded the adequate closure of the valve-flaps. In the light of more recent knowledge, however, it is likely that the insufficiency described by that distinguished author is in reality the form now to he considered.
Muscular. — This term, which may be applied to incompetence whether of the mitral or tricuspid valve, denotes a form of in- sufficiency depending not on over-distention of the ventricle with corresponding dilatation of the ring, but on a functional defect of the muscular mechanism bv which normally the valve is enabled
KELATIVE AND MUSCULAR 3MTRAL INSUFFICIENCY 5d5
to close. For our knowledge of the facts imderlying this sub- division of mitral incompetence we are indebted to the Leipzig School J whose viewy it must be confessed have been very tardily accepted by English and iVjuerican authors.
Pathology,— The morbid anatomical condition nnderlying trial iie iitsufficienci/ of tlie aiiricnio-ventricular valves is dilatation (if the ventricle. This dilatation must reach such an extreme grade, liHwever, as to carry with it more or less stretching of the mitral ring, as shown l>y its admitting more than three fingers. The valve itself is structurally intact, or in cases of long standing the cusps may be longer and broader than normal and the papillary muscles be flattened and elongated as a result of the pressure to which they have been subjected. In brief, the organ presents the changes pre%^iousIy dt-scribcd imder Dilatation of tlie Heart, either with or without stnictural disease at the aortic orifice.
In muscular mitral tnsufficlFncy the left ventricle may or may not present evidence of dilalatitm, but if tliis condition existed dur- ing life it was not of so high a grade as is the case wdien relative incompetence occurs. In many instances the pathologist is sur- prised by finding nothing at first sight to explain the mummr heard before death. The mitral ostium is not dilated and the valves are intact.
Closer examination^ however, discdiTses changes in the muscula- ture which interfereil with the perfect coaptation of the valve-flaps. These are the changes of acute or chi"onic myot/arditisj which favtmr the occurrence u{ Uiore or less dilatation and defective action on the part of the ring muscle or i>npillarics, or lx>th.
Three factors are concerned in the closurt:' of the auriculo- ventricular valves, (1) the prcissure of the blood within the ventri- cle upon their ventricular surface, (2) the contraction of the ring muscle at the base of the ventricle by which the orific(* is nar- rowed to a mere chink, and (.3) the contraction of the papillary iimscdes and consequent tightening of the eordffi tendinea?. The combined effect of all these cdenients is the f)erfect apposition of the valve-flaps throughout practically their entire surface, and not merely at their margins.
If now, in consequence of inflammation or degeneration, the wall of the ventricle dilates sutficiently to prevent the mitral ostium from becoming adequately contracted during systole, or to inter-
596 DISEASES OF THE HEART
fere with the proper pull of the papillaries, then the condition is present which permits more or less regurgitation; the valve is rendered muscularly incomi^tent. Consequently, in any case in which the clinical diagnosis of mitral insufficiency has been made and in which the valves are found intact after death, careful examination must be made of the state of the myocardium, since in degeneration of the wall or of the papillaries may be discovered the pathological cause of the regurgitation.
Etiology. — Primary relative insufficiency of the mitral valve is the result of acute dilatation of the left ventricle from excessive physical exertion, i. e., acute strain. This was well shown by Har- old Williams's observations. He found that of 13 healthy young men examined immediately after a run of 25 miles, 11 presented appreciable dilatation of the left ventricle with a mitral systolic murmur and vascular evidence of stasis. When the myocardium is degenerated and the arteries are stiff, indiscreet physical effort is especially likely to occasion cardiac overstrain, and I have more than once discovered this form of valvular incompetence in elderly men after a business or hunting trip in the Rocky Mountains.
Secondary relative mitral insufficiency may be said to be the result of chronic heart-strain. It is possible, therefore, when the left ventricle has been compelled for a long time to labour against great |K»riphoral resistance, as in cases of aortic stenosis. It is seen not infrcHiucntly in chronic interstitial nephritis when the hyper- troj)liic(l ventricle is no longer able to co|)e with the excessive blood- pressure in the aortic system, or when the ventricle struggling to preserve its adequacy is overjxnvered by the addition of some un- wonted physical (»r mental strain. The same holds true of the mi- tral inconiiH^tence secondary to long-standing aortic regurgitation.
The causes of muscular rnltral insufficiency are identical with those of the sc^condarv relative form. Less dilatation of the left ventricle is reciuired to produce it, however, hence it is a more frequent o<x*urrence. iloreover, degeneration of the papillaries is a condition which often leads to mus^'ular incom})etence, whereas it cannot j)rcKluce the relative form. The muscular incompetence may likewise result from acute heart-strain when this is not car- ried to the point of extreme dilatation.
Acute myocarditis is a cause of the muscular form far more commonly than is recognised. The dilatation may be slight and
RELATIVE AND MUSCULAR MITRAL INSUFFICIENCY 59T
cape ret^ogiiition, and liont'e the apex nniniuir is gem-rally sup- ^ posed to indicate endoc*arditis. Such an tTror is the more likt-ly since the acute myocarditis develops in the course of some acute infection, as rheumatism, diphtheria^ typhoid fever, etc. The ulti- mate suhsideiice of the muniHir pari passti with the return of the ventricle to nonnal siz.e prohahly jiroves the condition to have been muscular and not end<x*arditie.
The Curable ifitral Rcgurgi tat ion of clilorogis and grave ana'mia^ which h probably muscular in the strict sense, is due prob- ably to the bltMtd-.state, which by depriving the heart of rerpiisite nutrition leRseni? its resisting power so that a moderate grade of dilatation supervenes.
SjTBaptoms are those observed in cardiac inadequacy, and need nut be detailed here. Their intensity and, to a certain extent, their character depend upm the freedom of the leak and the rapidity of its dt*velopment. In the slighter grades of muscular mitral incoiniietence syni|)toms may Ijc st* mihl as not t<> draw attention to the real seat nf trnnble, and it may be difficult to fleeide how nuich of the clinical picture is due to the leak ami how much to the underlying cardiac, vascidar, or renal condition.
Relative mitral insufficiency of acute beart-strain produces pronounced symptoms^ viz., pni*cordial distress, dyspna»a, a feel- ing of weakness that nuiy amount almost to sync<»pe, cyanosis t>r an ashen pallor of the cuuntenance. Auicmic or chlorotic girls with ** curable mitral regurgitation " are apt to display breathlessuess, muscular weakness, and sometimes slight ankle putfiness, which is flue tr> thf' state of the bkwd rather than the heart.
Physical signs are essentially the same as in mitral regurgi- tation of endocanlitic origin, but with slight differences. In rela- tive insufficiency jxTcussion is apt to show greater increase of dul- ness to the left, while in muscular incompetence the murmur is more typically blowing and generally accompanies, but does not replace, the first sound at the apex.
Diagnosis* — The re<*Hgoitii»n of the mitral insufficiency is generally easy. The difficulty lies in differentiating the forms we are considering from the incompetence of endocardial inflamma- tion. The main differential jwints are the following:
(A) Age, the individual in most cases being past forty. (B) History of articular rheumatism wanting^ but in tlie primary tela-
598 DISEASES OF THE HEART
live form history of cardiac strain. (C) Habits and occupation that tend to chronic myocarditis and arteriosclerosis. (D) Signs of stiff arteries or interstitial nephritis or both. (E) Chlorosis or anffimia in females without previous rheumatism. (F) The asso- ciation of an acute infection, as dij^theria, tyj^oid fever, influ- enza, etc., during which the characteristic murmur develops.
The recognition of the real nature of the incompetence is often most difficult if not impossible before one has had opportunity to observe the effect of time and treatment. Great distention of the left ventricle may enable one at once to pronounce in favour of a relative incompetence, but muscular insufficiency with little or no recognisable dilatation may readily be mistaken for a valvulitis. An important differential point is to be found in the characters of the murmur.
In muscular mitral incompetence the murmur generally accom- panies, but does not replace, the first tone at the apex. It is not widely propagated, being as a rule circumscribed to the vicinity of the apex. It is not so intense as the mitral regurgitant bruit of chronic endocarditis, and may be most plainly audible between the left nipple and sternum. Given such a systolic murmur with accentuation of the puhnonic second tone in a person having stiff vessels, or an impoverishment of the blood or one of the acute infections which is more likely to produce acute myocarditis than endocarditis, one may with reasonable confidence diagnose muscu- lar mitral rather than relative or endocarditic insufficiency.
Prognosis. — This is determined by the cause, the freedom of the leak and the age of the patient. The relative incompetence of acute heart-strain in the young is likely to be recovered from under proper treatment. The muscular incompetence of the mid- dle-aged or senile may be removed by suitable therapy for a time, but is pretty sure to return. The mitral regurgitation secondary to interstitial nephritis furnishes a very grave prognosis, since the high blood-pressure precludes closure of the valve even under the most approved treatment. The mitral leak in the chlorotic or profoundly ana?mic is removable if the blood-state can be corrected, and hence has been termed " curable."
Treatment. — This is that of the underlying pathological con- dition to which, as well as to Chapters XVII and XVIII, the reader is referred.
CHAPTER XXIII
FATTY HEART
CARDIAC INADEt^UACY UF THE CORPULENT
Fatty heart is the term most conimonly employed to designate, not fatty degeneration of the lieart-nniscle, Init a deposit of fat be- neath the epieurdinni and l>etwoeii the nui«eh?-lihres — a eondition varionsly istyled fatty overgrowth and fatty infiltration.
Morbid Anatomy. — In this disease the subepicardial layer of adipose tissne is strikingly, sonietinies enoriiions1y» inereased. The fat is particularly abundant in the interventrienlar and inter- anrienlar grooves, ea|jccially the latter, and along the branches of the coronary arteries. It is usually thicker over tlie right than over the left ventricle. It is not only de|>osited on the surface of the organ, Init makes its way het%vcHm the hiindles of nmscle- fibres, which, examined microscopically, are seen to be more or less widely separated and to have become attenuated or atrojdiied. In some instances there may even l>e masses of fat beneath the endocardium.
Pathology*— It is generally l)clieved that when cardiac in- sufficiency declares itself in fat people it is owing to an exces.^ive deimsit of adijwse tissue upon the heart or to fatty degeneration of the heart-muscle, Romberg has, however, set forth in so ad- mirable a manner the real pathology of this eondition that I shall avail myself of much of wliat he says.
He agrees with l.eyden in the view that the old conception of fatty heart as an independent affection must bo abandoned, and, instead, makes the term fatty heart include those disturbances of heart action manifested by the obese which either bear a direct relation to their oliesity or have develo]>€*d independently. That their cardiac insufficiency is not rlue to fatty overgrowth is sub- stantiated by the observation that hearts loaded ^lown with adiposa
599
600 DISEASES OP THE HEART
tissue have not always given signs of inadequacy, and on the other hand that such as were manifestly insufficient during life have not always sho^^^l a deposit of fat sufficient to account for the weak- ness.
The cause of the heart difficulty resides, therefore, in some other condition, and this Romberg finds to be relative smallness and weakness of the heart-muscle — i. e., disproportionate to the demands made upon it by the condition of general corpulence. In some fat but muscular individuals the heart is correspondingly large and muscular, and symptoms of cardiac inadequacy do not appear. Other corpulent individuals of indolent habits are anae- mic and have a flabby musculature. In them the heart-muscle, rendered weak and flabby through ansemia and want of exercise, is incapable of responding adequately to the work required of it, by the great exertion of moving the ponderous body-mass, and hence symptoms of heart-weakness appear.
In such, the heart is overtaxed even when the body is in re- ])08e, and manifests its debility at all times. In some instances car- diac symptoms first make their appearance after some unwonted exertion or after an attack of influenza or some other acute in- fectious disease. In a few cases disease of the coronary arteries is responsible for an attack of angina pectoris, or for sudden death, through rupture of the heart-wall. But such conditions are wholly independent of the obesity. This conception of the fatty heart, entertained as it is by two such masters as Leydcn and Romberg, is in strict accordance with daily observation, and makes it clear why one enormously fat person is capable of performing a degree of physical effort wholly impossible to another much less obese. It is evident, also, how fallacious it may be to diag- nose fatty heart merely on the ground of general corpulence.
Etiology. — The causes of an excessive growth of fat on the heart may be said to be those of obesity in general. There seems to be a marked tendency to corpulence in some families, and their members accumulate fat notwithstanding all efforts to the con- trary. Such a predisposition is sometimes witnessed among chil- dren ; but as a rule corpulence does not manifest itself until after puberty or still later, between the ages of thirty and forty. Age itself is a predisjwsing factor, particularly with women, who show a striking tendency to increased weight after the menopause.
FATTY HEART
001
The female sex in general is said to show a greater inclination to eurpuleiicr thuii dues tlie mule sex^ yet fhe difference in this regard is probably to he attributed to differences in occupations and habits, since women generally take less exercise than men. They are, moreover, apt to be chlorotic and anamiic, and it is well knowu that fat and ana'inia often go together, in consetpience probably of the diminished oxidizing power of the blood. People of t?edentary pursuits are esifeeially liable to take on fat, and with family inheritance and ocenpation combined, ubesity becomes in- evitable.
Of all eanses, the one most potent next to inherited tendency is cunsnmjitiuii of fooil rich in carbohydrates cimjoined with an excessive intake af fluids. Gluttony (luxns eonsnmption) con- duces to obesity even though there is not a relative disproportion in carboliydrates. This is esjiecially injurions when added to in- adetpuite exercise. The too free drinking of fluids is another |K»tent factor, and when in the form of midt liquors^ fat may be taken mi vltv nipidiy. The excessive use of alcohol in any form, moreover, is saitl to favour the develo])nient not only of fat in general, but in particular of the deposit of adipose tissue upon the ht'art.
The foregoing are the lending causes of fatty overgrowth, but it must he reniemberetl that tlie modern eoneeption of fatty heart is not necessarily a surjdns neciumilatiuii of a<Iipose tissue be- neath the epieardium and between the bundles of niuscle-fibres, but a manifestation of cardiac insutticiency attributable primarily to general obesity, ronsetpiently, in studying the etiology of the heart-weakness exliiliited by corpulent people, we must bear in Uiiiid what was said above rnncerning the pathology of the fatty heart. Whatever temls to undermine muscnlar strength in gen- eral produces a weak heart-nnisele, and in the obese such influences are specially deleterious.
Luxurious living, indolent habits, excesses of all kinds (in- eluding the abuse of tobacco), anaemia, and chlorosis-^all tend to prmliice a flahliy heart-muscle. Such a heart is incapable of that driving pow*er nec^essary to force the bh>od through the extensive system of capillaries created for the supply of new adipose tissue^ in addition to those rauiifving in the organs, muscles, bones, etc. Under the demands of a quiet existence such a heart may show no
602 DISEASES OP THE HEART
incompetence severe enough to attract the person's attention. When, however, cardiac inadequacy makes its appearance^ it is gradual and insidious, or abrupt in consequence of unwonted exertion or of acute illness. In such cases the obesity is the predis- posing cause, and the conditions that bring about heart-strain the exciting cause.
Finally, Romberg includes among the causes of cardiac insuf- ficiency a too strenuous anti-fat diet which is practically a starva- tion diet, and too rigorous depleting measures acting through the skin and bowels. If, in addition, vigorous exercise is taken, the undernourished heart-muscle can readily become overstrained.
SjrmptomB. — There is nothing in the symptoms peculiar to the disease under consideration. Shortness of breath is usually the first symptom to make its appearance, but such persons are so accustomed to quickening of respiration during exertion that they give no heed to it until it has reached a degree of considerable or continuous dyspna^a. At first, embarrassment of breathing is only noticed during hurry or the effort of ascending stairs, but subsequently it is called forth by the mere act of rising from a chair and walking across the room. Stooping or bending forward is apt to cause great dyspna»a; and as cardiac feebleness pro- gresses, distressing shortness of breath declares itself during the taking of fmnl, and there is panting respiration even during con- versation. At loufrtli in this, as in other forms of heart-disease, a stage of orthopncra is reached when dyspncea becomes habitual, even while the patient is at rest.
Another early symptom in some cases is lightness of the head or vertigo, especially likely to appear when the patient gets on to his feet or chan^ros the rocunibent for the upright position. In some instances there are attacks of veritable syncope, the feeble heart failing temporarily to maintain cerebral circulation. It sometimes happens that a patient dies in such a syncopal attack under appearances which caused Stokes to term it ** apoplecti- form."
Another symptom also observed in the early stage of the dis- ease is acceleration of the pulse. Stokes, Walshe, and other early English writers laid particular stress on slowness of the pulse as a sign of fatty heart, but as a matter of fact it is more common for the pulse to exhibit an increase in frequency. It is also apt to be
FATTY HEART
003
small and foelilo, altLoiigli associated arterial sclerosis or clironic nephritis may gi%'e it uiidiie tension, Anotlier not infrequent fea* tvire of the pnlse is inatabiJity — i, e., a lack of steadiness in its rhythm — fluctuations taking phiee in its rate without apparent cause. Irregularity in force and volume and intermittenee, how- eve r, are not eunimini.
In some instances the earliest symptoms are referable chiefly to the digestive organs. The patient finds that his usually small appetite has lieeume still more dimintshed^ or that so soi>n as he has eaten a little he is oppressed by an uncomfortable sense of fulness and shortness of breath* Unquenchable thirst impels him to drink large amounts of water or tea, which but increase his oppression, and he is annoy etl by frequent eructations of gas. His bowels are sluggish and constipated, and his urine becomes scanty and high-coloured. He is apt to fall asleep in the chair, particu- larly after meals, while at night lie is wakeful, or if he sleeps, is harassed by nightmare and dreams. Headaches, usually dull and heavy, but sometimes of a neuralgic character, are not nn- common.
If the circulation has not l^econie too seriously embarrassed, and particularly if the heart-uuiscle is intact^ the syniptoms being due to a disparity between the size nf the body and the power of the heart, then measures calculated to reduce the obesity and thus restore the proper relation between body weight and heart power may reinstate the patient's health. In very many cases, unfortu- nately, this is impossible; the heart-muscle has become seriously danmged through atrophy or degeneration or coronary sclerosis, or srrious dilatation has been set up in consequence of long years of «»verstrain, or as the result of some single indiscreet effort, Symptoms fif failing circulation now appear and progress steadily, it may be rapidly. Cnugh and frothy mucous expectoration, at- tacks of asthma and cardiac pain of an auginoid character, or even of true angina pertoris, are added to the j>reviously existing dyspno\T. Hepatic congestion and tenderness, scanty albuminous urine, and o'dema of the ankles are discovered, and before long the patient presents the w^ell-known picture of the final stage of heart-disease which has been so often described in these pages. It scarcely requires physical examination of the chest to convince one that the heart is dilated and overburdened. Orthopncea com-
604 DISEASES OF THE HEART
pels the patient to remain in his easy chair, and in the hope of obtaining still greater ease, or of lessening the dropsy, the swollen, tense, and shiny legs are supported upon another chair or stool. Nurses stand by his side to administer stimulants, or by fanning him, to mitigate his attacks of dyspnoea. Sleep visits him but fitfully, if at all, and neither day nor night brings him relief from his torment.
In this manner one week merges into another, and he is to be accounted fortunate when pulmonary oedema ends his suffering, or the heart stops suddenly and unexpectedly. It is the same old story over and over, varied only by the greater prominence of some symptoms in one case and of others in another, or by the longer or shorter duration of the struggle.
Physical Signs. — Inspection. — Obesity renders examina- tion of the thoracic and abdominal organs diflScult and unsatisfac- tory. If close scrutiny fails to detect cardiac impulse, this must not necessarily be attributed to feebleness of the impulse ; it may be due to the intervening layer of adipose tissue.
Palpation. — For the same reason the hand laid upon the chest fails to locate the apex-beat, or indeed to perceive any cardiac shock whatever. The real value of palpation, therefore, is in the study of the pulse, which should be carefully studied for any in- formation it may afford. If it is of good strength and volume and in rate is stable and not unduly accelerated, it points to a fairly healthy heart-muscle. If, on the contrary, the peripheral arteries are thick — a matter which the corpulence often renders by no means easy of determination — if the pulse is unsteady and per- haps intermittent, then it is likely that chronic myocarditis is present or that the muscle-fibres have suffered atrophy from possi- ble encroachment upon them by the excessive deposit of fat. Pal- pation of the liver with a view to ascertaining if this organ is en- larged, is also a matter of great difficulty and even impossibility, in consequence of the size and resistance of the corpulent abdomen. Even if the liver is palpable, this may be due to its being fatty, and not to a state of passive congestion.
Percussion. — This means of investigation, upon which so much reliance is ordinarily placed for the detection of cardiac enlargement, is of but small aid in the obese, for reasons that lie in their corpulence. There is often a development of fat within the
FATTY HEART
niediastiniim which gives an area of dulness that may be tliought to ht'!i»ug to rhe heartj yet in it^ality dm^s not, Furtlieniiorej the mass of fat within the omentum and upon the abdominal walls im- pedes the descent of the diaphragm^ if it does not actually crowd it upward J and thus cause the heart to assume an abnormally high and horizontal position. When this is the case the area of cardiac dulness is inereased trauBversely and upward, giving a false ap* pearance of increased size of the organ. Consequently extreme eare is neeessary in drawing any conclusion from an increase of pneeordial dulness. If, however, by percussion in the various ways described in the introductory chapter one becomes satisfied that such an increase diies not existj it affords presumptive evi* dence that the symptoms arc due to potential, not structural in- competence.
Aiiscidfation.~Thi^ is likely to afford the best evidence of the real state of the heart, and yet we know that the muscle may be seriously diseased without any apprcciuble change in the heart- sounds. If these are found to be only rather distant and feeble but still clear, and the aortic second sound of good relative strength, it is in favour of the integrity of the heart-musele being still preserved. If, on the contrary, the first sound is disproportion- ately feeble, perhaps impure or even obscured by a systolic apex- mnrmur, if the aortic second sound is weak and the pulmonic sec- ond nnduly loud, there is reason to believe the heart is enlarged. This may be a simple hypertrophy with dilatation, or there may be in addition myocardial degeneratiom Physical examination alone does not enable us to decide; we must endeavour to deter- mine this pcdnt by the stmly of all those factors outside of the heart which make for or against cardio-vascular decay.
Dlagnosie.— It is not a difficult matter to diag^iose cardiac inudecpiacy. The real problem to solve is whether the heart is only potentially une^jual to its work or is incompetent in conse- quence of fatty overgrowth or of myocardial disease. If the pulse is normal in rate and quality, and if subjective symptoms are felt only upon exertion, are slight and quickly subside after cessation of effort, the heart-walls are presumably intact. This conclusion is strengthenetl if minute inquiry fails to elicit history of cardiac strain, acute infectious disease, bad habits, or any otber influenc© that may serve to impair the integrity of the myocardium. On the
606 DISEASES OP THE HEART
other hand, degenerative changes are probable if the patient is past middle age, if the pulse shows notable alteration in quality and rhythm, and if symptoms of inadequacy are present even when the patient is at rest or not making unwonted demands on his heart If the individual belongs to the category of fat and anae- mic, the heart-muscle is likely to be flabby and its incompetence to be due to dilatation. If, on the contrary, symptoms of inadequacy develop in the fat and plethoric, whose skeletal muscles are firm and large and whose weight is due to the great specific gravity of their muscles, bones, organs, etc., and not to adipose tissue, it may reasonably be concluded that the heart is overstrained, perhaps dilated, but not hampered by deposit upon it of fat.
Finally, if symptoms of cardiac incompetence develop in any corpulent person it is the part of wisdom to make a diagnosis of cardiac inadequacy and not of fatty heart, for we possess no means of determining during life whether there is or is not an excessive deposit of fat within the heart-muscle.
PrognofidB. — This depends upon the condition which is re- sponsible for the embarrassment of circulation. If the patient is young and muscular and the cause of the heart-weakness is found to lie in potential, not structural disability, or if the symp- toms date from some recent cardiac strain, the heart-muscle having been previously competent, the prognosis is comparatively favour- able, since appropriate treatment may restore compensation. If, on the other hand, the patient's musculature is flabby, he is anje- mic, and gives a history of indolent habits ; if his s^^nptoms have steadily increased, and especially if their gravity indicates a seri- ous breakdown of the heart — then there is but small hope of rein- stating compensation, and death is only a question of time. An- gina pectoris, attacks of asthma, thickened arteries with high sustained pulse-tension, likewise furnish a hopeless prognosis as regards recovery. The probable duration of the malady cannot be stated with any accuracy, but the course is likely to be a short one. In other respects, prognosis is governed by the same conditions as in other forms of heart-disease.
Treatment. — It is essential, in the correct management of any disease, that the physician have a clear knowledge of its pa- thology and of the object to be attained by treatment. If by the term " fatty heart " were meant simply a heart overgrown and
PATTV HEART
OUT
iiitilt rated with adipose tissiu/, iheii tlie plain iiiJieatioii of treat- ment would be tilt' aljst>rptioii of excessive fat, and the object would be aeeoniplishcd by putting the patient upon a regime cal- t'ulated to reduce his obesity. In this chapter, however, the dis- ease has been eou.^idered from a different standpoint It has Ix^en IcKjkeil upun as a conditiuu uf putential weakness, the heart becoming relatively inadequate to the requirements of the circula- titm, rendered necessary by the size of the lx>dy. There may or may not be an undue <leposit of fat upon the heart itself. This iMung the pathology of the disease^ the indication is to restore or establish a proper relation between cardiac power and body weight, lliis is to be aeeomplished by measures that will either invigorate the heart-muscle withnut reduction of the obesity, or w-ill bring about the latter without the former, or w^ill do both. By the pa- tient, it is generally thought that the reduction of his corpulence is all that is necessary ; but Romberg repeatedly utters an em- phatic warning against such an idea. lie states again and again that harm rather than benefit is likely to follow the indiscriminate emploxTuent of the ordinary anti-fat cures, since they increase the already existing heart-weakness. The need of such a warning was forcibly Iin])rcsscd ni>yn me only this past winter.
A corpulent man of fifty-iive» who had yet been able to exer- cise without s])et^ial discomfort, concluded he would try a reduc- tion-cure at Marienbad, CJermany. By vigorous use of the waters and an unreasonable amount of walking he reduced his weight 45 [Kiunds in a few weeks and returned home feeling, as he said, '* fine/' Xevcrtheless, he had not been home long w^hen, on at- tempting to walk to his jilace of business one luorning as usual, he was seized with great shortness of breath, that compelled him to return to the house. This was the beginniug of the end, for he failed steadily in spite of the most approved treatment, and died in less than six months.
Depleting measures should be confined to cases in which circu- latory disturbance is attributable to oliesity and not to cardiac insufficiency. Such cases are found for the most part in persons wdio are still young, or have not yet passed the age of forty. It is often a matter of great difficulty to defermine whether the trouble resides in the heart or not, and therefore an anti-obesity plan of treatment should not Ik* decided on hastily or without thoughtful
608 DISEASES OP THE HEART
study of all those considerations bearing on this point. Should this plan of management be at length decided upon, the effect on the heart should be carefully watched and the treatment dis- continued altogether, or the weight reduction carried on less vigor- ously, so soon as debility, nervousness, and other signs of cardiac or general asthenia make their appearance.
It is of importance also what system of dietary is selected. There are several well-known anti-fat dietaries, such as Banting's, Ebstein's, Oertel's, and Sweninger's, but they all have the one fea- ture in common, that they greatly restrict the consumption of car- bohydrates. Their chief differences are in the amount of albumin and fat allowed. Ebstein permits much less albumin and far more fat than do the others, while the Oertel system allows considerably more albumin and far less fat, and again more carbohydrates. They all restrict the consimiption of fluids. Whatever differences they possess, they all attain their end by causing an absorption of fat, both by the taking away of fat-forming food and, with the exception of Ebstein's, by the administration of a relatively large proportion of albumin, which is thus said to stimulate the absorp- tion of fat. In addition to restricting the diet, exercise is insisted upon and saline cathartic waters are administered.
The great objection to the employment of such a regime in cases of so-called fatty heart lies in the fact that unless the indi- vidual is capable of considerable exercise, whereby adipose tissue may be oxidized, the obesity will only yield when the diet is so strict as to become practically a starvation diet. It is a well- known principle underlying the dietary of heart-disease, that in- asmuch as the heart-muscle performs an enormous amount of work, it should receive a relatively large proportion of proteid — i. e., tissue-forming food — and must under no circumstances be deprived of adequate nourishment. Consequently, if an attempt is to be made to diminish the corpulence of a person with cardiac insufficiency, a dietary must be selected that will most nearly meet the demands of the heart. This is undoubtedly the one se- lected by Oertel, while the Ebstein and Banting systems are clearly inadmissible. The daily allowance of the several elements permit- ted by Oertel are as follows: Albumin, 5i ounces; fats, 1 to 1\ ounces; carbohydrates, 2 J to 3^ ounces. For particulars the reader is referred to OerteFs original work, or to treatises on dietetics.
FATTY HEAUT
009
In carrying out a diet for the reduction of obesity in the class of cases now under condderationj it m very unsafe to produce a too rapid loss of weight. In my opinion this should not exceed 2, or at the very outside 3 pounds a week, and in many cases 1 pound is better. Consequently the physician should keep an accu- rate record of the weight, and many times will have to modify the diet given above by increasing the albumin or starches, or both. If the physician is in doubt concerning the actmd state of the heart-musclCj or if the patient finds he is unable to take adequate exercise, then massage will often he found of great service by promoting oxidation of adipose tissue. It also aids the circu- lation.
The daily use of laxative waters is essential, and Germain See recommends the administration in moderate doses (5 to 10 grains) of iodide of potassium three times a day.
For the past few years the public and profession have heard ranch concerning the efficacy of reducing fat^ of the alternate daily use of Vichy and Kissingen waters. From my rather lim- ited observation of their effects, I am inclined to the opinion that if these waters are to prove eflicient they must be combined Avith exercise and at least a moderate restriction in the consmnption of carbuhydratcs.
In elderly people, or those with feeble muscular development, or in such as already display pronounced symptoms of cardiac inadequacy, energetic treatment for the reduction of corpulence is hazardous, to say tlie least. In many instances the weakness of the heart will be intensified. Romberg is of the opiuion that such persons should not be suhjeeteJ to the possible dangers of such treatment ; while to make a routine practice of depleting all fat patients certainly cannot be too strongly condemned. Xever- theless, I believe in most cases, even when the heart is primarily at fault, some modification of the diet wiU usually prove bene- ficial. Some of these patients are ansemic as well as corpulent — some because they have been light feeders for years, others be- cause they have habitually taken too little albumin and too much starch and sugar, while still others have consimied altogether too much fluid, particularly at raeal-tinie.
In the first class, attempt should he made to secure more ade- quate nourishment through medicinal or other measures calcu-
CIO DISEASES OP THE HEART
lated to improve the appetite and assimilation. To this end sim- ple bitters and tonics — as quassia^ gentian, iron, nux vomica, arsenic, or the hypophosphites — may be tried, together with acids, pepsin, pancreatin, and kindred preparations. A cupful of hot water half an hour before each meal often improves both appetite and digestion. In quality the meals should be highly nutritious, so that in quantity they may be light. This may be accomplished by the addition of the expressed juice of fresh beef, or by some one of the prepared foods rich in nitrogen and fat but poor in carbohydrates.
For the second class it can do but little harm to reduce starches and sugar and increase the animal food, without, however, con- forming strictly to the amount and proportion laid down in rigid anti-fat dietaries. In the last class it may be sufficient to dimin- ish the ingestion of fluids without otherwise curtailing or modify- ing the food allowance.
In all individuals who display more or less heart-weakness the important point in the management must be the attempt to re- invigorate the heart. If its load cannot be lightened — that is, if the corpulence cannot be reduced — efforts to strengthen the heart are likely to prove futile. The physican will then have to choose one or the other alternative; either to persevere in his futile attempt to rehabilitate the heart, or to run the risk of reducing the body weight. The wise thing will be to try to accomplish both. It may be that the loss of half a pound or a pound a week will not materially weaken the patient, and yet may be sufficient to greatly aid the doctor's efforts towards re-establishing cardiac power.
By all odds, the best means to this end is exercise. This should be limited to two kinds — easy walking and resistance gymnastics. Rules for the latter have already been given (see page 455). The conditions that are to control the daily walk should be carefully laid down by the physician. (1) Walking should be done from one to four hours after meals, according to the degree of cardiac debility. (2) The walk should not be so prolonged as to occa- sion fatigue, and of course must vary greatly in individual cases. The medical adviser will have to determine its length by observ- ing the immediate effect of exercise, or by a searching inquiry as to symptoms. (3) The pace must not be fast enough to cause
FATTY HEART
611
snortness of broalli or palj^itutioiij and it is alwfijs best to l)egin very slowlv, the gait to be quickened only as the exercise produces a feeling of well-being or lightness in the chetit. (4) The patient must not Wiilk against a strong wind, and must confine his exercise to level ground. Attempts to carry out the Oertel system of as- cending an incline are not to be permitted until a considerable degree of compensation has been established. If the patient is exceptionally intelligent and his judgment can be relied upon, it may be safe to allow him a little hititude in this regard; but patients are more likely to do theiuselvt^s harm by essaying paths that are too Bteep, than they are to derive benefit from accustoming themselves to ascending gentle acelivifies. Therefore in a hirge majority of instances the fourth rule shrmld be strictly insisted upon.
When heart-weakness has reached such a degree that walking even about the room tK-casioiis decided dys]>no^a, there is no pros- pect of improvenient from exercise, and life will probably be pro- longed by keeping the patient quiet and relying on skilful massage or very carefully conducted gymnastics. Another highly useful and often very promising measure for restoration of heart-po^ver is the balneological treatment — i. e., saline baths as given at Bad Nauheim and already dcscribetl. In the hands of one experi- enced in their use thene Imths are rarely likely to do harm, except in tliose eases in whicli dilatation has become extreme, or other contra-indications are present.
Among therai>cutic measures are included also the ordi- nary heart-tonics, such as digitalis, strophanthus, and their con- geners, as well as strychnine and cardiac stimulants, nitroglyc- erin, ammonia, camphor, and valerian. The same rules govern their administration in these as in other cases of cardiac insuffi- ciency from whatever cause. Romberg is of the opinion that but little gixjd is to be exi>ected from digitalis; but in my opinion, if its vaso-constrictor effects can be counteracted by nitroglycerin or iodide of iiotassium, the remedy should theoretically support the failing heart in cases of obesity, as well as in any other non- valvular disease. If pulse-tension is persistently high, strophan- thus may be of use, either alone or combined with digitalis and strychnine. The last-named heart-tonic should never be omitted.
In all cases of obesity blood-pressure is high within the ab-
G12 DISEASES OP THE HEART
(loiiiiual vessels, and therefore I finnly believe that if any results are to be attained from the use of heart-tonics, or indeed from other measures, as exercise and baths, tension within the abdomen must be lessened by the persistent use of cathartic remedies. Both because of the tendency of alkalies to reduce weight, and on account of their non-irritating properties, the cathartic selected should be a saline aperient water — Hunyadi, Rubinat-Condal, Concentrated Pluto, Apenta, Franz Josef, Carlsbad, or any other of the well-known aperient waters on the market. Care should be had not to produce weakness by a strongly purgative effect each day, but only to keep the stools semi-liquid and copious.
It is usually well to introduce a dose of calomel or blue pill occasionally at bedtime. The compound infusion of senna, which is only the old English " Black Draught," 4 ounces of which may be taken at a time, forms a capital purgative for occasional use.
Special management is required by complications, as, for ex- ample, the use of iodide of potash or soda in chronic arteriosclero- sis, sometimes observed in obese patients, nitroglycerin and mor- phine in cases of angina pectoris or cardiac asthma. When at last cardiac power is utterly lost, diuretin-KnoU may be of service in reducing dropsy, or at least holding it in check. Overdisten- tion of the cardiac cavities, particularly the right chamber, may be temporarily relieved and the patient's suffering ameliorated by venesection. Owing to the associated anaemia, the amount of blood thus abstracted should be small, 6 to 12 ounces being usually suflieient to render the pulse soft and full. Other measures for the relief of the patient must be left to the physician's judgment and to the special indication of each case.
CHAPTER XXIV
CARDIAC ASTH MA-CHE YNE-STOKES RESPIRATION- BRADYCARDIA-STOKES-ADAMS SYNDROME
In this and tlie succeeding chapter are considered certtiin
phenomena that are sometimes encountered in the course of
myocardial disease, and in the opinion of tlie author may not
inappropriately be discussed in connection with disorders of the
myocardium,
1. CARDIAC ASTHMA
No one symptom i& bo frequently a feature of cardiac disease as dyspnoeaj and with the possible exception of prsecordial pain there is no snbjective dii?turbance so distressing. In many in- stances, moreover, it occasions »ucb obvious suffenng as to be actually harrowing to the spectator. True cardiac dyspncea is due to the swelling and rigidity of the lungs caused by stasis within them, and consequently forms an important part of the clinical picture in most cases of cardiac inadequacy.
It would be a mistake, however, to attribute the dyspnoea of cardiopaths solely to circulatory end(arrassnient. Thus it may be duo to pain^ in consequence of which the individual fears to breathe with his customary depth and slowness. In other cases it may result from nervousness or apprehension, as e, g., during <n examination of the heart. In all such instances, however, it is usually easy, by giving due consideration to the state of the circu- latory apparatus, to recognise the true cause of the breathlessness.
Cardiac dyspmea is par exeellenee a dyspnoea of etfort — i. e., it is either evoked by exertion or intensified by the same. This breathlessness of effort may be regarded as the earliest manifes- tation of failing heart-power, and so long as cardiac incompe- tence is of minor degree, is confined to periods of physical exer- tion. There nearly always comes a time, however, when dysp- nt^a becomes more or less constant even during rest and when apparently trivial conditions intensify the shortness of breath even to the point of positive air-hunger. This has been repeatedly
613
614 DISEASES OF THE HEART
dwelt upon in foregoing pages in considering the manifestations of valvular disease.
Persons suffering from myocardial inadequacy of whatever cause also display dyspnoea of effort quite like that of other cardio- pathsy and likewise due to circulatory embarrassment.
There is a form of dyspnoea displayed by these patients^ how- ever, which is so intense and paroxysmal that it has not inaptly been termed cardiac asthma. As implied by the name, it closely resembles an attack of bronchial asthma. In most cases it is not a growing intensification of already existing dyspnoea, but is a more or less sudden attack of such distressing shortness of breath as to constitute veritable orthopnoea for the time.
The attack may be induced by effort, but in its most typical form it comes on at night. It is therefore a nocturnal dyspnoea. The attack may seize the individual so soon as he lies down at night, but frequently it does not appear until after he has been asleep for a few hours. The patient is then aroused by a sense of oppression or want of sufficient air, which obliges him to sit up or arise and walk slowly about his apartment.
In its mildest manifestations this is all, but generally the dyspnoea is far more severe. The shortness of breath increases until in a few minutes, occasionally from the very start, the suf- ferer is forced to breathe with great rapidity and difficulty. His chest emits a multitude of fine or coarse moist rales due to intense pulmonary congestion and transudation of serum into the air- tubes, and the consequent cough is attended with the expectora- tion of frothy or even bloody mucus.
The patient's distress is now terrible both to himself and friends, his face becomes cyanosed and bedewed with perspira- tion, while his pulse is rapid, extremely feeble, and even irregular or intermittent. If the heart is now examined it is found to be dilated, while its sounds are extremely faint, partly in conse- quence of the rales of pulmonary oedema, but mainly because of cardiac weakness.
Such an attack may last for minutes or even hours, yet with scarcely the initial severity. As a rule it abates in from fifteen to thirty minutes. With cessation of the terrific dyspnoea the sufferer is left exhausted and usually in a state of great mental agitation.
CHEYNE-STOKES IIESPIHATION
615
rhe cause of this cardiac asthma is believed to be temporary weakness of the left ventricle and disproportionate strength of the right ventricle. This eondition on the part of the two ventricles leads to congest ion of the lungs and consequent dyspnoDa. As the stasis increases and pulmonary cedema occurs, dyspna^a becomes increased in consequence of mechanical interference with oxy- genation of the blood. Certainly such an explanation fits the clin- ical manifestations of an attack.
The predisposition to cardiac asthma is furnished by degener- ation and enfeehleuient of the left ventricle, while the immediate or exciting cause Jtiay be found in whatever temporarily overpow- ers the ventricle — -i, e,, imdne physical effort, (^oitns, by reason of the union of lx»th effort and exeitcTuent, seems particularly apt to excite an attack. The occurrence of tlte attack after some hours of sleep is thought to be explained by the augmentation of Wood- pressure said to be incident to the recumhont posture, lluchard states tluit hlood pressure is increased by the reeumlwnt position^ while Gaertner, on the other hand, claims that his tonometer shows an actual though slight decrease of pressure. If this is bo, some «*ther explanation is ret pi i rod for the ix^cnrrence of cardiac asthma during sleep. This may Ik^ found in the aclded work put upon tlic left ventricle in maintaining blood-flow by muscular inaction, and the more rpiiet respiration incident to sleep.
Tt IS !ieedless to remark that such attacks are highly dangerous and call for prompt and energetic treatment. To this end stimu- lants arc indicated, and nothing is so efficient as the hypodermic injpi^ion of ^ of a grain of uuirphine combined with the atropine found in the ordinary hypodermic tablet.
II, CHEYXE-STOKES KESPIRATTON
This is a rhythmical form of dyspna'a, first carefully described liy the two eminent physicians wliose names are now inseparably linked with this distressing symptom. Tt is characterized by alter- nating periods of dyspn<Tn and apntra, which recur at regular in- tervals and supplant normal breathing.
The phenomena of this type of respiration may be described as follows: After a period of susfiended breathing or apncra, res- pirations return^ at first slowly and superficially, each succeeding one quicker and deeper, until at lengtli the inspirations become
614
mSEASEii UF THE HEART
dwelt upon in foregoing pages in considering the iimnifestations of valviiliir disease.
Persons suffering from myocardial inadequacy of whatever cause also display dyspna-a of effort tpiite like that of other cardio- paths, and likewise due to circulatory embarrassment
There is a form of dyspnira displayed by these patients, how- ever^ which is so intense and paroxysmal that it has not inaptly been termed cardiac asthma. As implied by the name, it closely resembles an attack of bronchial asthma. In most eases it is not a growing intensitication of already existing dyspna^a, but is a more or less sudden attack of such distressing shortness of breath as to constitute veritable orthopntra fr^r the time.
The attack may be induced by effort, but in its most tyiucal form it comes on at night. It is therefore a nocturnal dyspnoea. The attack may seize the individual so soon as he lies down at night, but frequently it does not ap|K?ar until after he has been asleep for a few hours. The patient is then aroused by a sense of oppression or want of sufficient air, which obliges him to sit up or arise and walk slowly alxiut his apartment.
In its mildest manifestations this is all, but generally the dyspn<ra is far more severe. The shortness of breath increases until in a few minutes, occasionally from the very start, tlie suf- ferer is forced to breathe with great rapidity and difficully. His chest emits a multitude of tine or coarse moist rales due to intense pulmonary congestion and transudation of serum into the air- tubes, and the conscipient cough is attended with the expectora- tion of frothy or even bloody mucus.
The patient's distress is now terrible both to himself and friends, his face becomes cyanosed and bedewetl with perspira- tion, while his pulse is rapid, extremely feeble, and even irrcgidar or intrnnittent. If the heart is now examined it is found to Ixi dilated, while its sounds ore extremely faint, partly in conse- quence of the rales of pulmonary cedema, but mainly because of cardiac weakness.
Such an attack may last for minutes or even hours, yet with 8cart*ely the initial severity. As a rule it abates in from fifte^en to tliirty minutes. With cessation of the terrific dyspna^a the snffcrer is left exhausted and usually in a state of great mental agitation.
CITEyNF^STOKKS RESPIRATION
61T
the ptilse-rafc during both periods of the cycle, while Little^ (plotted by SansoMij witnessed 15 heart-beats during an apiia3al period of ten seconds, and only G in a like period in the dyspnceal stage. Others have reported retardation of the pulse during apntea, and a relative acceleration during the period of dyspnoea. Aside from changes in rhythm, the tension of the pulse is said to be raised, the pulse feeling harder and tinuer than normal.
Diseases in which Chvyne-^Slokes Bretifhiutj is Observed.-^ The following list is taken from Sansom's work on the Diagnosis of the Diseases of the Ifenrt and Thoracic Aorta, and shows that the eases in which this form of dyspnoea is observed are by no means exclusively tliose of cardiac disease. (1) Cases attended with cerebral affec^tions — viz., cerebral ha-morrhage, tumours, tul)ercuhir meningitis, epilepsy, shock from surgical injury with unemia, alcohol intoxication, opium poisoning, and insanity, (2) Cases attended with lesions of the Iieart and great vt^ssels — vi^,, fatty degeneration of tlie heart, pericarditis, atheromatous disease of the aorta, aortic aneurysm, valvular disease (double aortic, with mitral insufficiency, mitral stenosis, dibitation of aorta coex- isting^ aortic regurgitation and obstruction), and chronic Bright's disease. It U with diseases of the aorta and its valves that it is most frequently associated, but it may occur, in the absence of valvular disease, when the coronary arteries are obstructed. In any of these comlitious it is most probable that the arteries at tlie l)nse of the bniin are atheromatous, and the concurring af- fectiiins of the beart and brain speedily lead to death. (3) Cases of certain acute febrile diseases— viz., difjbtberia (Hutterhren- ner), typhoid fever (Wbarry), puerperal septicaemia, scarlet fever, pneumonia, pertussis (with inanition), and influenza.
Theories lo E.r plain Vheijne-Shkes Respimtion. — Before giv- ing a brief statement of the leading theories which have been advanced to explain the rhythmical alteration of breathing, it may be well to state certain physiological facts concerning respira- tion. (1) Inspiration is a result of the contraction of the in- spiratory musf*les in response to a nervous impulse sent out from the respiratory centre in the upper portion of the medulla oblon- gata, close to file calamus scriptorins, but extending to the upper pc^rtion of the spinal cord. (2) Expiration is for the most part a passive act due to the elastic resilience of the lungs. (3) The
618
DISEASES OF THE HEART
action of the respiratory centre is aiitomarir an<l rhythmical. (4) The activity and energy' of the re&piratory cetitre dcfiend in great mcftHnre upon the amount of oxygen contained in the bloody and upon the anionnt of blood aiipftlied to the centre. It is not ditKcult to nnderstand why there may be dyspncra in any given case, but it in ditticuh to explain why the dyspnijea should be rhythmical in the way characteristic of ( 'heyne-Stokes breathing.
The first attempt to exphiin it was made by Traube, and is known ad Traubes theory. This assumes that the nonnal excita- bility of the respiratory centre is diminished in consequence of tho supply to it of imperfectly oxygenated blood, Ihiring the stage of apn<T*a earlwmic acid aceunnilates in the bl(X>d, and when it baa l»c*come exeesaive begins to stimulate the respiratory centre to discharge its impnlses. In response to these discharges^ w^hich are at first alow^ and imperfect, contraction of inspiratory muscles takes place, grows ever deeper and more rapid imtil at length the maximum stage of dyspnn-a is attained. The centre now ceases to bo stimulated, or becomes exhausted, and inspiratory efforts gradual ly decline until they fin ally terminate in the stage of res- piratory pause or apnoa. Carbonic acid in the bhx>d is again accumulated, the respiratory centre is again stimulated, and thus the cycle is rejieated in ever-recurring paroxysms,
ifany objections have been urged against Traube*s theory, but the one that Bramwell thinks is fatal to it is that a defieient supply of properly oxygenated l>lfMxl to the respiratory centre would stimulate it into action rather than imjinir its irritability, since it ift not so much an accumulation of carlxuiic acid as a wuuit of oxy- gen in the bkuxl which stimulates the respiratory centre*
To explain the lowered irritability of the respiratory centre, wdiich is assumed in Trauhc's theory, Sansom has advanced the propositicni that the centre is in a state of paresis or partial paraly- sis in consequence of some cerebral disease, and with a satisfactory explanation of the ilinnnished excitability of the respiratory cen- tre Traube's theory WTiuld then tfrocomc coni]>lete,
Fifehnr's Theory, — This assumes that Ivoth the vascvniotor and respiratory centres are concermHl in the pro<luction of this form of dyspmra. According to his explanation, the deficiency of oxy- g«»n and exin^ss of cnrlx)nic acid in the blocwj, which result frera the period of apnGea, stimulate the vaso>motor centre, and the
CHEYNI'VSTOKES RESPIRATION
619
terioles of tlie bniiiij as well as those tliroiigboiit the bo<lyj become utracled. This constrict ion of the arterioles diiiiiuishes the supply of blood to the respiratory centre, and in consequence this centre is stimulated tu discharge, imd inspiration begins. So sooUj however, as respiration has become energetic and the blood properly aerated, st in ml at ion of the vasoinotor centre ceases, arte- rial spasm is no longer maintained, the respiratory centre receives a projier supply of arterialized blooil, and dyspncea is no longer experienced. The respiratory acts gradualh* die away and tlie ])eriod of apna>a is again reached. There again occurs stimulation of the vaso-motor cejitre, and another cycle is repeated. Bram- weO is of tlie opinion that if Filehne's theory is correct, then ( 'heyne-Slokes breathing should occur much more frequently than it really does. He says: ** I am disjwsedj therefore, to think with Dr. Sansom that something more is necessary, and that there must be some alteration of the respiratory ceiitre itself in addition to the condition which Filehne's theory sKi>plie9. A state of irri- table weakness would, in my opinion, account for this condition," BramipeU'is iheory in explanation of Cheyne-Stokes breathing is based on the supposition that the respiratory centre consists of two parts: an inspiratory and an expiratory, and that, as sug- gested by Rosenthal, '* the inspiratory centre is the seat of two conflicting forces, one tending to generate inspiratory impulses, (the discharging portion of the inspiratory centre as we may call it), and the other offering resistance to the generation of these iuipulses (the restraining or inhibiting portion of the inspira- tory centre)— the one and the other alternately gaining the vic- tory, and thus leading to rhythmieal discharge/* Bramwell as- sumes that venous blood excites the discharging portion, restrains the inhibiting portion ; while oxygenated blood depresses the for- mer portion, and intensifies the action of the restraining portion. If the discharging portion is in a condition of irritable weakness, and therefore more easily excited to discharge, bnt also more quickly and easily exhausted, or if Iwth portions are in a condi- tion f»f irritable weakness, then there is a condition of things^ Bramwell thinks, which satisfactorily explains the phenomena of Che\Tie-Stokes breathing. At the end of apnnpa the blood is highly venous, and therefore gradually excites a paroxysm of dyspnoea, by stimulating the discharging and restraining the inhibitory
DISEASES OK THE HEART
portion of the centre. In the i?econd phice, the earhonic aou! in the hlood stiiunlates to action the vaao-niutor centre, tlie arterioles l>ecome contracted, and tlie supply of oxygen to the respiratory centre is still further diminished. Fnrtherniore, the irritahle weakness of the discharging centre causes its impulses to become excessive, and the state of dyspna^a results. Moreover, the weak- ness of the discharging portion of the inspiratory centre causes it to t»ecoine quickly overexhanste<l and the dyspmea subsides. In consequence r*f tlie energetic respiratory effort during the stage of dyspncea the blc>od becomes arterialized and the discharging portion of the inspiratory centre is no longer stinudated» hut the reverse takes place as regards the restraining portion, which gains the ascendency over the weakcnied and exhausted disc^-harging por- tion, and the state of apntea is produced. During this period of rest the oxygenated bloud, whi<*h had stimulated the restraining and depressed the discharging powiion of the inspiratory centre be- comes replaced by carbonic dioxide; the discharging centre k aroused into action again, and the inhibiting is restrained ; inspir- atory efforts are renewed and aTiother cycle is rejM^ated.
Uf the foregoing theories, conceived to account for this distress- ing rhythtnic form of dyspiara, Bramweirs is the most satisfac- tory, and yet, as he himself suggests, it is dithcult to explain how this condition of irritable weakness of the respiratory and vaso- motor centres is produced. Brumwen assumes that in those cases of ( 'heyne*Stokes breathing displaying a contracted pulse and pallid cumtenance, tln^re is hK*al anaemia of the centres in conse- quence of arterial spasui» and irritable weakness takes place.
In other cases not showing arterial spasm he suggests that this unstable st^ite of the centres may be due to disease within the medulla or to imprc*ssions received from nervous centres situated higher up or from the periphery, especially froiu the heart or lungs, through the agency of the pneumogastric and superior laryn- geal nerves. Such peripheral stitmdi are particularly likely to be received by the centres in those cases of heart-disease manifesting right-ventricle dilatation with diminished supply of blood to the lungs,
Hosenbaeh's Theory, — After, as he states, a searching analysis of the various ther*ries, Un:^enba(Ji has adopted the following ex- planation. Under the inilncnce of certain anomalies of brain-
CHEYNK-STOKES RESPlKATlUN
021
I
nutrition tlirn; ilcvrlop luailizA'il disturbances in the brain or in individual wntre^^ particularlv in tbat of respiration, which dis- turbances lessen the excitability of the aflfected part and augment the normal exhaust ibility of the same. Thereby are produced remissions in the activity of the respective centres with loss of tone in the vaso-motor and vagus centres, or complete intermissions, such as a pause in the respiratory actj with a kind of paralytic state of the cerebrum, nuinifestcd by a periodic sleep with contrac- tion of the pupils and movements of the eyeballs. So soon as the fatigue and exhaustion of the centre have disappeared in conse- quence of cessation of respiration and an augmented internal ac- tivity, and its excitability retnrns, respirations again set in and con- tinue to increase, because the excitability of the nervous apparatus grows out of proportion or waxes more rapidly than the stimulus to activity wanes in consequence of organic work. So soon now as the abnormal cxhanstibility of the centre again begins to be felt, it supersedes the stinuilus, and therefore the fnncti<inal activity of the centre lessens, and finally ceases altogether when at last the centre has become completely exhausted. Whether or not res- piration takes place is determined by the ability of the centre to respond to stimulus^ and the depth of the respiratory act depends not upon the strength of the impulse, but on the functional capa- bility of the nervous apparatus. He thinks that of the various nervous centres the respiratory is the one that suffers most readily and often alone, while the vaso-motor centre is relatively much less frequently affected, and paralysis of this means death.
He furthermore thinks tbat a regularly intermitting pulse, pulsus bigeminus and alternans^ may be a numifestation of peri- odicity in the function of the vagus and vaso-motor centres in certain cases of nutritional disturbance of the brain, and are analo- gous to the Cheync^Stokes phenomenon. As liosenbach states, this explanation of this abnormal type of breathing differs from others in the assumption, not of a periodic alteration of the stimuhiSy hut in a rhythmic change in the excitability of the centre w^hich pre- sides over respiration, even to a complete abeyance of its function for the time being. He assimies that this rhythmical periodicity as regards excitability is to be referred to some peculiar charac- teristic inherent in the nervous apparatus by virtue of which it is capable of being exhausted and again aroused to activity.
622 DISEASES OF THE HEART
It is needless to add that, however ingeniously the pathology of Gheyne-Stokes respiration may be speculated upon, the subject is still enveloped in great obscurity.
Prognosis. — The development of Cheyne-Stokes breathing is generally held to be of unfavourable significance, by indicating that a fatal termination is not far off. Yet weeks or even months may sometimes intervene between the appearance of this symptom and death. Murri reported a case in which the phenomenon per- sisted for forty days, and Sansom one for one hundred and eight days. In the Lancet of April 5, 1890, is the report of a case of a man of ninety-two who manifested the symptom for several years. This type of dyspnoea has also been known to appear, then cease, and reappear after a lapse of several months. In most of the cases that recover, or in which the symptom is greatly protracted, the disease upon which it depends is either some brain-lesion or an acute affection, as influenza. When Cheyne-Stokes breathing is observed in cardiac patients, the underlying malady is itself of a grave nature, and the occurrence of this symptom usually por- tends a not distant termination of the case. To this rule there are exceptions, however. In April, 1895, I was consulted by an old gentleman of eighty who manifested this symptom. He had pro- nounced thickening of the peripheral arteries, a greatly hypertro- phied and dilated heart, a harsh bruit along the course of the aorta, and a remarkably intense and metallic aortic second sound. In addition to his arteriosclerosis and myocardial degeneration, his liver was cirrhotic and the urine gave evidence of chronic in- terstitial nephritis. Cheyne-Stokes dyspna^a was typical, and in consequence a well-known Chicago consultant had given a sombre prognosis on the ground that he had never known this symptom to endure for more than three weeks in such cases. Yet pari passu with improvement in cardiac tones the dyspncta gradually abated, and after about two weeks was entirely lost, never again to return during the two years that this patient was spared to his family.
Another gentleman of seventy-one displayed this form of breathing, rather irregularly by day but typically by night, dur- ing the time, in which cardiac asthenia was marked, yet recovered from it with gradual improvement in his condition.
It has seemed to me that when Cheyne-Stokes respiration is more pronounced, or perchance is manifested only during sleep,
CHEYNE-STOKES RESPIRATION
G23
it is not of so grave a prognosis a^ when present with equal inten- sity both waking and sleeping, ilnrri, and recently renibrie, have called attention to a physiological Cheyne-Stokes respiration observed in healthy persons during sleep. But the patient of sev- enty-one was not healthy, and therefore the nocturnal manifesta- tion of CLeyne*Stokes dyspnoea during his periods of unconscioug- nem in sleep could not he regarded as physiological Finally, the prognosis must he looked upon as specially grave in those cases whicli alsu niunifest ohseurah'on at the mental faculties.
Treatment, — Wlu^n Cheyne-Stokes dyspncea is a symptom of riirdiac disease the treatment must he essentially thot of the un- derlying condition. Yet we are called on to mitigate the patient's <listrcss so far as this is possible. This is best accomplished by the hypodermic administration of morphine, which, if it does not remove the dyspna'a, blunts the patient*s sensibility. The value of morphine in this class of cases has iK^en the subject of some contention in Germany. At the meeting of the Congress for In- ternal Medicine at Wiesbaden in 1892, Unverrieht read a paper in which he expressed the decided opinion that morphine and atropine are powerless fur the removal of (.'heyne-Stokes breath- ing. Otiier observers have gone so far as to assert that morphine intensifies rather than relieves this symptom. Stadehuann made 25 observations upon the effect of morphine and atropine, alone and combined, upon this type of breathing. The observations were made upon two patients, and the doses were 0.01 to 0.02 (J to i) of a grain of morphine, and 0.001 to 0.0015 (uV to :^) of a grain of atropine. The effects were neither uniform nor constant They sometimes shortened the period of apna?a, sometimes that of dyspnoea, and at other times they lengthened one or the other or both. In 5 experiments morphine lessened or removed the Cheyne-Stokes respiration^ and in 4 it aggravated the symptom.
Although Stadehuann's observations were so inconstant and unreh'able as to the effect of morpliine that they seemed to con- firm Unverricht^a assertion, he nevertheless concluded that on the whole the effect of this agent was to mitigate the severity of the attack. Morpliine certainly seems to exert no injurious effects; and since it undonbtedly blunts tht* patient's sensibility and in- duces sleep, there can he no contra-indication to its employment, even if it seems occasionally to change an irregular or un periodic
624 DISEASES OP THE HEART
form of this dyspn(T?a into the periodic rhythni characteristic of Cheyne-Stokes respiration.
A word of caution should be spoken, however, regarding its use in these cases. This symptom is usually observed in elderly individuals with stiffened arteries and degenerated hearts, and as the kidneys very commonly participate in this pathological pro- cess one should bear in mind the possibility of these patients being more profoundly affected by the morphine than is desirable or even safe. For this, as w^ell as other reasons, one should employ the smallest dose that will render the patient comfortable. In my experience this is generally ^ of a grain, an amount which I have rarely found necessary to exceed. In this dose the remedy is also a powerful cardiac stimulant, and as such beneficial to this class of patients.
III. BRADYCARDIA
Bradycardia and brachycardia are terms applied to an abnor- mally slow pulse-rate — that is, to one of less than 60 beats to the minute. Allbutt in his system of medicine objects strenuously to their employment on the ground that, as slowness of the pulse is but a symptom, they are likely to mislead the student by seem- ing to raise the symptom to the importance of an independent dis- ease. Nevertheless the term bradycardia has come to be so gen- erally used that I have thought best to follow the custom of most writers and give it special consideration. I know by experience that practitioners not only regard it with apprehension, but are often at a loss to account for it, and consequently seek for a state- ment of those conditions in which it occurs and for an explanation of its significance.
Slowness of the pulse may be either physiological or pathologi- cal. A normal pulse-rate of less than GO is occasionally observed, but when it is as slow as 30 or 28, of which instances have been reported, it becomes a truly remarkable phenomenon. Napoleon Bonaparte is often cited as an instance of a physiologically slow pulse, having had only 40 heart-boats to the minute. It has been thought by some that he was a victim of epilepsy, and that his bradycardia was explicable on tliat ground. Physiological brady- cardia is very exceptional, yet when encountered is not to be re- garded as anywise likely to affect the general health.
BBADVrAHDlA
Osier states that slmviR^ss *>£ the pulse sufficient to merit die appellation of bradycardia is sometimes a family peculiarity. Under physiological bratlycardia iimst also be included those in- stances sometimes yet very rarely observed in coimeetion with hunger and cases of transient slowing of the pulse said by Blot to be seen in about 25 per cent of wouien during the jnicrperium. In such cases the rate may sink to 44 or even to 34. Allbutt has noted bradycardia in a healthy man of forty-nine given to excessive sexual indulgence^ and luis likewise seen it in children as a result, he thinks, of masturbation^ In his own case his pulse-rate fell to 48 and to 44 in consequence of exhaustion, for it was restored to its normal rate after a refreshing sleep.
Rombergj in writing on diseases of the heart in Ebstein's Prac- tice, displays characteristic German exactitude by limiting his ftnsideration of bradycardia to cases associated with cardiac dis- ease. This appears to me to be too exact, since slmvue^^s of the pulse may by the ignorant be thought to indicate heart-disease. I have decided, therefore, to enumerate the diseased conditions of whatever kind which, according to Kiegel, may he associated with abnornuil retardation of the pulse. As a basis for his classification he made a study of 1,047 cases in which a pulse-rate of less than 60 was observed. (1) Bradycardia may occur during convales- cence from acute infectious diseases, as pneuuK>nia, diphtheria, typhoid fever, erysipelas, and acute rheumatism. Sansom also includes influenza among the acute disorders capable of producing slowness of the pulse, an observation in which Allbutt concurs. It is believed that exhaustion is the cause in such cases. (2) Riegel observed this symptom in 379 cases of disorders of the digestive organs, as chronic dyspepsia, gastric ulcer, cancer, and icterus. The occurrence of a slow pulse in chola^mia is a matter of frequent observation. Orob is also said to have seen bradycardia in connec- tion with oesophageal cancer and typhlitis. (3) The phenomenon under consideration is sometimes met with in diseases of the respiratory organs, particularly em])hvsema and (4) in diseases of the heart and hhiod-vesscls, specially degenerations of the myo- cardium dei>ending on coronary sclerosis, atheroma of the aorta (Sansom), but is not fref]uent in valvular defects unassociated with other alterations of rhythm. In 1 recorded case embolism of a coronary artery was attended with a pulse-rate of 8 to the 40
626 DISEASES OF THE HEART
minute. (5) Bradycardia is occasionally seen in acute nephritis, in uncmia, and was seen in 1 case of hasmaturia (Sansom). (6) Aside from uraemia, bradycardia may be produced by other poi- sonsy as lead^ tobacco and coffee, alcohol and digitalis. (7) It is sometimes seen in cases of diabetes, chlorosis, and anaemia. (8) Apoplexy, epilepsy, brain timiours, diseases of the medulla and of the cervical portion of the spinal cord, paresis, melancholia, mania, are all said to sometimes be accompanied by slowness of the pulse. (9) It is sometimes seen in skin disease, affections of the geni- talia, insolation and exhaustion from whatever cause.
Finally, with regard to the pathology of bradycardia it may be of interest to give the following summary of Regnard's conclu- sions presented in a doctoral thesis in July, 1890, entitled fitude sur la pathologic du pouls lent permanent lie is of the opinion that every chronic lesion which causes irritation of any portion of the moderator apparatus 9f the heart may suffice to produce permanent slowness of the pulse and give rise to the aggregate of sjTnptoms. Such nervous irritation may have many causes, as local anaemia through the influence of atheroma on the periph- eral circulation and blood-supply to the nerve-centres, deficient blood-supply to the bulbous portion of the pneumogastric, txmiours of the meninges of the bulb, or in the mediastinimi acting on the vagus, morbid excitation of the laryngeal and gastric branches of this nerve, but most frequently some affection of the heart itself, as fatty degeneration or coronary sclerosis.
The predisposing conditions are stated to be arteriosclerosis, whether syphilitic, alcoholic, gouty, or rheumatic in origin.
It is not within the scope of this work to consider the signifi- cance of bradycardia in other conditions than of the circulatory apparatus. In these conditions marked slowing of the pulse is generally regarded as of serious import, because it is most com- monly observed in cases of sclerosis of the aorta or coronary arte- ries, and in such the heart-walls are likely to be degenerated. The lengthening of diastole incident to slow cardiac contractions sub- jects the heart to the possibility of diastolic arrest and the patient to the possibility, therefore, of sudden death in syncope. Moreover, the heart-muscle is extremely feeble in such cases, and hence it may require very little additional strain or depression to bring it to a standstill.
STOKES-ADAMS DISEASE
627
I have notoa of an old man with rigid arteries and ehronic myocarditis in whuin for several years prior to death the pulse- rate was peraistently about 28. In another the heart was actually 8low% but aa only every other systole sent a hliX)d-Avave to the wrist, the pulse-rate was in reality only half as fast. It is essential, thereforcj in every instance of suspected bradycardia that the heart he auscultated to determine whether there may not be apparent instead of actual bradycardia.
IV. STOKKS^ ADAMS SYNDROMS
By this term is designated a very remarkable and obscure com* plcx of symptoms which consists in a paroxysmal intensification of an already existing bradycardiaj together with vertigo or syn- cope and epileptiform seizures. Adams in 1827, and Uiter Stokes, were the first to describe such attacks, and therefore Huehard devised the term now" generally employed in commemoration of these tw^o famous physicians. English and French clinicians were the ones chiefly who for many years paid special attention to this syndrome and repMurted cases. Within comparatively recent years^ however, it has attracted the attention of German and American physicians, by whom numerous valuable contributions to the sub- ject have been added. In America, Prentis and Edes deserve men lion, while in Geniiany the most notable and latest articles with reijorts of cases are by Ilia, Hoffman, and Jaquet, The ex- haustive paper by the last named in Deutsches Arch, fiir klim lied,. Band Ixxii, is particularly worthy of note,
Adams's original case was in a man of sixty-eight, and Stokes's 2 were in men of fifty-sLx and sixty-eight resj>ectively, all 3 of w4om presented clinical and post-mortem evidences of cardiac and vascular degeneration. It was thought, therefore, that the disease was limited to individuals w^ell on in years. For instance, of 21 cases collected by Boyer from the literature there were only 2 whose age fell below fifty years. It is now known, however, that much younger persons may be befallen, and Jaquet states that he has found in literature 15 cases in which the age was below forty, and including his owti, 9 that were below thirty years of age.
The etiology and pathology of this disease, if disease it is to be called, are at ill obscure, and hence a subject for speculation. Thus Stokes and early writers considered the attacks due to degen-
628 DISEASES OF THE HEART
onition of the heart, Charcot to disease of the medulla, while Iluchard and his pupils regarded it as the result of arteriosclero- sis, especially of the coronary arteries. In Ilalberton's ease the symptoms dated from a fall which injured the back of the head, and led, as shown by the autopsy, to great narrowing of the oc- cipital foramen and consequent compression of the medulla. The disease has been attributed to lesions of the vagus and cardiac plexus, and in a few instances such structural lesions have been discovered at the necropsy.
On the other hand, fatal cases have been observed in which searching post-mortem investigation has failed to reveal any lesion capable of causing the symptoms, and indeed any recognisable changes that could be held responsible for the death of the pa- tients. Such, indeed, was the state of things in Jaquet's case.
Hoffman's patient was a woman of twenty-three without clin- ical signs of cardiac or other organic disease, but with a severe anaemia. In her case the symptoms appeared to yield to inhala- tions of oxygen and other treatment appropriate to the blood-state. In other instances the disease has seemed to depend upon syphilis, indiscretions in diet, disorders of digestion, or obstinate constipa- tion, the cure of which has favourably influenced the attacks. Ja- quet's was an example of this kind, with a suspicion of syphilitic infection years before, and suitable treatment was instituted, to- gether with correction of the constipation.
Syphilis a|)])oars to have had an etiological connection with the attacks in 5 eases (Jaquet). Emotional excitement, as a fit of an«ror, has l)een known to call forth a seizure, and did so in Jaquet's patient.
Tri])ier lield that the disease was a genuine epilepsy, a view to which some features of the attacks in certain cases appear to lend su]>port. Tt is now not so regarded, however, by the great majority of writers.
Tt is ])lain therefore that the pathogenesis is uncertain, but that we iiiiist now recognise two great groups, (1) in which the age of the individual is advanced and there are structural changes of the heart or vascular system, or definite lesions in the central or peripheral nervous system; (2) cases occurring in younger persons sometimes with clinical evidence of cardiac disease, some- times without anv demonstrable lesions either before or after
STOKEtv-ADAMS DISEASE
n29
death, aDfl which appear to depend upon S€>uie obscure disturbance of the nervous system, as the brain, or upon an interference with normal cardiac contractions.
The former hypothesis is advanced bj Jaquet, who thinks that tlie pbennniena de])cnd ni>on a eranij>like constriction of the vessels of the brain,
Hoffman, cm the other liand, ascribes the symptoms to an in- terference with the ability of the cardiac njuscle-fibres to respond to irritation or hi conduct the ini pulses to uont ruction from the auricles to the ventricles. In other words, there is a block in tlie iibrcs that carry the impulses to contraction from the auricles to the ventricles.
From the forcu:oing, it is jdain that we nuist enlarge our con- ception of this Stokes-Adams syuilromc and not confine it to cases showing age or signs of cardiac or vascular disease, as was once dfine.
The symptoms which make up this singular clinical picture are, in tlie lU'der of tbcir frequency, (1) bradycardia and other |)henomena ctuinected with the circulatory system, (2) vertigo and syncopal attacks, (3) epileptiform convulsifms, and (4) disorders of respiration. The firs! tbrc*e are by far the most counuon^ and in cases displaying all of them it is not always possible to deter- mine which ushers in the series. It seems to be generally held, however, that the i^'culiarity of the heart's action soon to he de- scril)ed is the first to appear.
The pnlse is habitually slow and usnally regular in individuals displaying the ciniiphisnt, but during the attack it becomes still slow^er, sinking to 20 nr less, or, as in Ilalbcrton's case, to 5 in the minute. It may remain regular, or, as in my case (see page 324), may show marked irregidarity in the intervals between the waves. Another t>€'f*uliarity is its great tension, which in my patient was shown by Oaertner's tonometer to 1»e 105 ujillimetres of mercury. Still another feature which I had observed, and upon which Ja- quet comments, is the obstinacy with which the bra<lycardia is nuiintained in spite of diffusihle stinudants and the effect of exer- cise. This jversistence of the slow pulse-rate is observed of course during the intervals as well as in the attacks. When my patient's pulse is at 2n no amount *>f walking or e%'en of stimulants is able to cause appreciable acceleration. Bax has reported an observa-
630 DISEASES OP THE HEART
tion in a single case which was cited by Regnard — namely, that on one occasion the administration of digitalis sent up the pulse- rate to 60. Singularly enough a similar effect was reported by my patient to have followed his taking the same drug.
If during an attack the attending physician auscultates the p^a^co^dia, he in some cases hears nothing during the pause be- tween the pulse-waves, while in other cases one or more extremely feeble cardiac tones, or possibly a faint systolic murmur, is audible. This peculiarity has been noted by many observers and by myself. These tones are as a rule not accompanied by perceptible impulse in the heart region, and for this and other reasons these feeble tones have been thought to indicate auricular contractions, but not ventricular, and hence are spoken of as abortive cardiac contrac- tions. Such was the view held by Stokes, and recently maintained by Hoffman in his report of an interesting case in which he argues for this explanation at considerable length. Jaquet, on the con- trary, has, for reasons that will be stated further on, come to the conclusion that they are in reality contractions of the ventricles.
Another phenomenon of great interest and singularity is some- times perceived in the neck, and was first described by Stokes. This consists in feeble pulsations in the right internal jugular vein directly above the clavicle, and synchronous with the almost inaudible cardiac sounds. In Stokes's case there were two such " semi-beats,^' as he called them, between every two powerful car- diac systoles which sent a strong large pulse-wave into the caro- tids and peripheral arteries. Such was also the observation made by Jaquet, while in my patient these tiny jugular pulsations num- ber two so long as the heart's action is regular, but, as will be found by reference to my case (page 327), may number many more dur- ing his attacks when the pulse is no longer slow and regular.
Jaquet, by recording a tracing of these jugular pulsations and a cardiogram simultaneously and afterward carefully measur- ing and interpreting the records thus obtained, came to the con- clusion that these jugular waves do not indicate merely frustrated contractions of the right auricle, but are tokens of feeble systoles on the part of the right ventricle. ITe believes that owing to the enormous arterial tension, and hence peripheral resistance, the ventricles are not able to force open the semilunar valves in con- sequence of the feebleness of their (ventricular) contractions.
STOKES-ADAMS DISEASE
681
These are able, liowever^ to drive a portion of the contents back- ward through the two aiiriculo-ventrieiilar openings, and hence these jugular pulsations are venous waves caused by tricuspid insutKciency.
When at length the ventricular rauscle has regained its ability to respond normally to the impulse to contraction discharged from the auricles^ its systole is sufficiently energetic to overcome the re- sistance in the aorta and a blood-wave is sent along the arteries with a resulting puli^e-wave. This either relieves the right ventri- cle and a jugular pulsation does nut occur, or this latter is ob- scured by the massiveness of the pulsation in tlic carotid.
This explanation of Jaquet's is in accordance with what I have repeatedly observed in my patient — namely ^ that the feeble tones audible between every two loud cardiac sounds aro synchronous with weak yet recognisable impulses of the heart against the chest- wall al the exact site of the |X)werful apex-beat. This it seems to me indicates that the ventricles contract feebly at these times^ since I cannot conceive of auricular systoles being pow^erful enough to cause a perceptible though indistinct apex-beat.
It was this synebronisni between the tiny waves in the neck and the fe<*ble cardiac impulsea which at first made me look upon the jugular inilsations as occurring in the common carotids and l>eiug too feeble to be transmitted as an appreciable wave higher up, beneath the angle of the jaw. Closer observation at a later date, however, convinced me that the pulsations were really in the internal jugular vein.
Another peculiarity in ray patient^ and which has been ob- served in other cases also, is that at times when he was wholly fre<; from symptoms his heart l^eat 72 times a minute, and each beat was represented by a wave at the wrist, ^loreovcr, the pulse Avas notably soft and a sphygmographic tracing taken at the time by Dr. E. F. Welles was commented on by this competent obser\"er as showing striking want of capillary constriction, a condition in fact of capillarj' dilatation. Wliereas whenever a sphygmogram was taken during this patient's state of pronounced bradycardia, it invariably manifested abnormal capillary resistance. These observations lx*ar out Jaquct's contention that the attacks are duo to abnoruuil %*aso-niotor constriction, or spasm in fact.
Vertigo is experienced to a greater or less degree in all cases,
632 DISEASES OF THE HEART
and annoyed my patient for over two years before more alarming phenomena set in. The assumption of the dorsal decubitus did not prevent its recurrence or even mitigate its severity. The diz- ziness was evidently a mild manifestation of cerebral ansemia that ultimately declared itself as distinct fainting fits.
Syncope may or may not be experienced, but in most cases is a prominent symptom. It does not last more than a few seconds or a minute as a rule, is ushered in by an ashen pallor, vanishes with a sudden rush of blood to the head, which produces an intense flusli of the countenance and feeling of distention of the cerebrum that leaves a dull headache behind. A patient may have no recol- lection of what has transpired, or, as with mine, he may awake with a clear consciousness of his having fainted. During the moments of syncope the medical attendant perceives no pulse in any of the arteries, and may not even be able to detect any heart- sounds. Consequently, if the intermission persists for five or eight seconds he may be deceived into thinking death has really come.
Mild epileptiform convulsions are apt to be shown during the syncope. These may be no more than a twitching of the mouth, but they are generally obser\'ed in one or more of the extremities. In the case of my patient the convulsive movements are confined to the right arm and corners of the mouth. In most instances there is no foaming at the mouth, wounding of the tongue, or in- voluntary discharge of urine or fa^es. Yet biting of the tongue has been noted, and in a case reported by His there was involun- tary evacuation of the contents of the bladder. Iluchard, I be- lieve, was the first to direct attention to the association of epilep- toid seizures with the bradycardia and vertigo previously noted. In the case observed by me there have never been involuntary dis- charges or any other more pronounced symptoms of epilepsy than the slight muscular contractions already mentioned.
DUiturhonce of respiration has been given as the fourth symp- tom of this singular group. Tt may occur, but is not at all com- mon, and is said to consist of Cheyne-Stokes breathing, that may occur at apparently any time during the attack. It was observed by His, T believe.
Finally, this symptom-complex may occur at long or short in- tervals, but as a rule not daily or many times a day. Yet my
[ES-ABAMS DISEASE
mz
tiont has been known to have attacks as often as every five min- utes for an hour or longer. They would tlien diiiappear for sev- eral hours or a day, after which they recurred with previous sever- ity. This state of things had persisted for three weeks prior to his coming to Hiieago and placing himself under my care.
It will be seen by referring to the more detailed report of his case in the chapter on Aortic Stenosis (page 324), that after this young man had put liiioself on a rigid vegetarian diet and had thereby regidatcd his bowels, he enjoyed imnumity from ]m ver- tigo and intermittent pulse for a period of iive months. He then returned to his former mode of diet, and liad two premonitions of a return of hia former symptoms. It wai^, however, quite a year before his attacks assumed the severity exhibited in ilarch and April of 1902. At the present writing (June, 1902) this patient is enjoying a respite from his attacks, apparently as a result of treatment by which both digestion and the action of his bowels have been improved. His pulse is now running 20 to the minute with two incomplete systoles interposed between every two power- ful cardiac contractions. The heart findings remain essentially as they %vere two years ago.
Notwithstanding the fact that patients who presented a car- diac murmur during life, have yet, after death, in a Stokes- Adams attack, hoeu found entirely free from eviilence of heart -diseasCj it is still my belief that in this ease there is moderate obstruction at the aortic orifice. It is conceivable that this obstruction, acting in conjunct icm with the peripheral resistance of abnormally high hlood-prcssnre, proves too much for the left ventricle, and thus leads to rehitive insufficiency of both sets of anriculo-vcntricidar valveSj with consequent generation of the apex systolic murmur which has puzzled so many competent observers.
The cardiac defect in this case may possess some etiological connection with the attacks, but it has always been my opinion that the relation is an accidental one.
The condition which determines his attacks appears to reside in the intestinal tract^ as shown by the results of diet, treatment, and numerous urine analyses. Urine passed by this young man during the days in which attacks occurred always showed a reduc- tion of solids to below normal, and a quantitative estimation of the indican showed this substance to be within normal limits. So
634 DISEASES OF THE HEART
soon, however, as there came a period of several days entirely free from Stokes-Adams symptoms urinary solids increased, and in particular the indican rose to three and even four times the amount previously obtained. The accuracy of this observation was proved over and over again.
This, as it seems to me, may be taken to indicate a condition of auto-toxaemia which in some way excites the attacks. At all events, it is in line with Jaquet's observation in his case, in which the seizures disappeared for many months after constipation and in- digestion had been removed. As in the case of my patient, they recurred with a return of digestive disorder and proved fatal in the fourth attack.
The diagnosis of Stokes-Adams disease presents diflBculty when the paroxysms are characterized only by vertigo and increase of an already existing bradycardia. I did not recognise the real significance of my patient's symptoms until months had elapsed. There ought not to be any difficulty even in such unpronounced forms, provided one is on the lookout for them. They are not common, and hence the physician is not prepared to recognise them.
When syncope and epileptiform convulsions are also present there ought to be very little difficulty in determining the real nature of the case. The occurrence of brief periods of uncon- sciousness, during which the individual may fall to the ground, and the prcvicaisly slow pulse grows still slower, and the discov- ery in such a person of stiff arteries or signs of cardiac disease, make up a group of symptoms that are sufficient to stamp the attack as one of Stokes- Adams disease.
This is es])ecially true of an individual past middle age: but if this complex of synij)toms is found in a person under forty, or still more below thirty, then the muscular spasms are very likely to arouse a suspicion of epilepsy. Indeed, my patient's attacks are so regarded by one of my colleagues. There is certainly what may be called a symptomatic but not an idiopathic petit mal, but if one will carefully note the action and sounds of the heart during an attack, he will be likely to correctly interpret the phenomena. The pulse-rate of epileptics is commonly slow, hut during their seiz- ures it does not become so slow and disordered in rhythm as is the rule in Stokes-Adams disease. Moreover, it must be remembered
STOKES-ADAMS DISEASE
S3S
'?!i«t these latter patients do not as a rule bite the tongue or have in\'oIiintary discharges uf urine and fa^ceg.
Prog^OBiB ia exceedingly grave and uncertain. Hoffman's patient appears to have recovered, and many other cases have been reported without mention of a fatal issue, hut such instances do not alter the fact of a liability to death when the heart stands still for so long a time as is occasionally ohaerved. The prospect of recovery depends upon the nature of the cause, the possibility of its discovery, and its anienahility to treatment.
The etiology is still veiled in obscurity, and moreover we are not yet sure that there may not be various predisposing if not exciting factors. It is quite possilde also that the flisease in the aged with structural changes of heart, vessels, or central nervous eystemj as the bulb, may not constitute a group separate and dis- tinct fron^ that form occurring in persons below the age of thirty^
Treatment of this affection is unsatisfactory, because in the presenl state of our knuwledge it is mainly symptomatic. If gastro-intestinal derangement is suspected to he an exciting factor, it is of course to be corrected. Hoffman f<>und the daily inhala- tion of oxygen beneficial in his antcmic patient, and together with proper diet this seems to have removed the attacks. The same agent was freely emphDved by my patient and at first appeared to do good, but subsequently was found to exert no influence.
One of Stokes's men was able to mitigate or arrest an impend- ing attack by supporting himself on his hands and knees and allowing liis head to hang low, the position favouring improved cerebral circulation. The device is so simple that it should be tried.
Theoretically, diffusible stimulants, as ammonia, camphor, ether injections, etc., ought to be of lM?nefit by arousing the heart to more rapid action, I found them of no avail in the case under my observation. For the same reason, and because it acts as a vaso-dilator, nitroglycerin thrown under the skin ought to mitigate an attack, but in my hands this remedy has utterly failed. It may be used, however, and should lie given several times if no effect is observed to follow the first injection.
My patient found the greatest comfort from a hypodermic of ^ of a grain of morpbTne administered snlK^utaneously. The rem- ed^^ did not appear to exert any controlling influence over hia
636 DISEASES OP THE HEART
symptoms, but served to steady his nerve and promote sleep, which in his state of dread was c?rtainly a boon. The unexpected effect which followed the avlministration of digitalis in Bax's case, and according to report on one occasion in mine, would seem to justify its trial. Nevertheless I must add that when this rem- edy was ordered by me for my patient it utterly failed of such effect.
In fact I did not find anything that seemed to positively influ- ence the seizures themselves. Maintaining free elimination through kidneys and bowels appeared to keep them off, for so long as such treatment was persisted in this patient enjoyed an immunity from his symptoms. At the present writing he is well, but how long he will remain so is a matter of uncertainty.
CHAPTER XXV
ANGINA PECTORIS
I
Befinition* — Attflcks of intense pain in tlie rc*gion of the heart, with more or letis disturbance of cardiac action, usually aecumpa- nied by a feeling of constriction of the chest and a sense of im- ] lending death.
History. — Although this form of heart-pain was not systematic- ally described until the latter part of the eigliteentli century^ yet a graphic account of his own sufferings from this complaint was given by Seneca, and in 1707 Morgagni gave a clear description of a paroxysm in a ease of aortic aneurysm. In February, 17CS, Rougnon addressed a letter to M* Lorry which contained the de- scription of the death of a certain Captain riiarles, who, from the account given by liongnon, a] spears to have suiTered from at- tacks of angina pectoris. It was Hebcrden, however, who in July, 1768, first systematically described this formidable complaint and who gave it the name by ^diich it is now universally recognised. The names of John Hunter, P^dward Jenner, and Parry are also intimately asscieiated with it.s early liistory^ Hunter having expe- rienced it in his own person, and having ultimately died in an attack.
Jenner in 179 J) pointed out a definite connection between scle- rosis of the coronary arteries and angina pectoris. He is said to have refrained from publishing his views at an earlier date out of consideration for his famous friend, John Hunter, who during his life had held contrary opinions concerning its etiology. Parry gave it the name of " syncope anginosa/' for, although he recog- nised its connection with coronary disease, he considered the at- tacks due to paralysis of the heart.
From this time for%vard the literature of the profession teems with contributions on the subject and with divers theories con-
638 DISEASES OP THE HEART
ceming its pathogenesis. Most of the earlier writers attributed the complaint to morbid anatomical changes in the heart itself. In 1816 Kreysig definitely stated that it was due to ischoemia of the myocardium in consequence of defective blood-supply from sclerosis of the coronary arteries. In 1821 Reeder amplified the theory of cardiac ischemia by asserting that this condition might proceed not only from ossification of the coronaries, but also from any other disease — i. e., as atheroma of the aorta — which might be capable of shutting oflF the blood-supply to the heart-muscle. This same theory was likewise espoused by Tiedemann in 1843, and in 1875 Germain See described the case of an elderly man who had suffered from anginal seizures and in whom after his sudden death the mouths of the coronary arteries were found almost obliterated by atheromatous plaques situated on the intima of the aorta. Throughout the balance of their course the coro- nary vessels were healthy. These few instances are sufficient to show in a general way the trend of opinion on the part of the sup- porters of the so-called anatomical theory.
In 1834, says Iluchard, the theory of the purely nervous mech- anism of the attacks was formally announced by Gintrac, although its neuralgic character had been previously asserted by Baumes in 1808, and others. Gintrac attributed the pain to irritation of the fibres of the cardiac plexus, and in 1863 Lancereaux published 3 cases in which the autopsy revealed inflammatory or other changes of this plexus.
There has been wide variance of oj)inion among French au- thors concerning the nerves inij)lieated. Thus Laennec considered it an affection of the sympathetic system and called it neuralgia cordis. Boiiillaiul regarded it as an affection of the phrenic nerves, and Peter, while accepting this view as applicable to some cases, also believed there was a neuritis of the cardiac nerves. Trousseau termed it an epileptiform neuralgia.
In Germany also the subject was extensively discussed and re- ceived a variety of explanations.
Romberg considers it as a mere neuralgia of the cardiac plexus, a view not unlike that of Friedreich, who thought it due to hyper- a^sthesia of that plexus. The names of 'Bamberger, Traube, Noth- nagel, Landois, Eulenberg, Guttmann, Leyden, Rosenbach, and many others are identified with the literature of this interesting
AXGIXA PECTOUIS
siibjwt. Laiidois, who in 1803 subjc^etcd the (]i!estion to a critical stiuiy from a jihysiokigical staiulpoiut, dividrJ angina pectoris into four groups, as follows: (1) Cases caused by disturbance of the excito-motor or iieeelerator nerves of the heart; (2) those due to irritation of the cardiac branches of the vagns; (3) cases aris- ing from retlex irritation of tlie abdominal viscera — '* angina re- flectoria '' ; (4) such as arise from, vaso-motor disturbance in vari- ous parts of the body — ** angina vaso-motoria/' Eulenberg also contributed an elaborate article on this subject in Ziemssen's Cy- clujucdia of ilediciiiey vol. xiv.
Ley den considers the attack due to degenerative and inflam- matory changes in the heart-niusele depending upon disease of the curonary arteries, wbieb changes lead to impairment of the heart's fi met ion.
According to Rosenbachj some alteration in the contractions of the cardiac muscle takes place, which alteration may, but does nut necessarily, lead to funetiuual weakness. Ln consequence of this change, irritation is imparted to the sensory tract j and this stimulus sets free the various forms of pain and anxiety character- istie of stencH^ardia, in accordance with irritability of the sensory ap|>araturi and the function of the resijective nerves composing it. Painful sensati<»ns are more or less pronouneed according to whether the sensory centres are or are mit accustomed to the irri- tation to which they are subjected.
According to Koseubaeh's view^ this true heart-pain is an indi- cation of the heart-muscle hemg less able than usual to accommo- date itself to sudden change taking fdace in the performance of its work; or, in other wurds, its ability to respond to demands from %vithout for a display of extra effort is impaired. Now and then, also, obstacles residing in the heart itscdf and capable of in- terfering with its perfect action may interrupt the perfornumee of its regidar work and in like nuinner give rise to the phenomena of angina j)ectoris.
During the ceufury just ended many contributions to this in- teresting subject have appeared in England and America, of which the most noteworthy were by Latham, Gairdner, and Osier, The last mentioned, in his Angina Pectoris and Allied States, deals with the affection in a very complete and entertaining man* ner. The most exhaustive discussion of the subject, however, to
640 DISEASES OF THE HEAKT
which 1 have had access is that by Huchard. His historical resume of the various theories is complete and shows painstaking research. His own view of the pathogenesis of this formidable complaint is highly suggestive and wuU be stated in the appropri- ate place.
Pathology and Etiology. — It should be clearly understood at the outset that angina pectoris is but a symptom and not an independent aflFection. It therefore can have no morbid anatom- ical characters peculiar to itself. Its pathology is obscure, and hence there have been, and are still, various theories to explain its nature and mode of production.
It may be stated in a general way that angina pectoris is divisible into two forms: one incurable and likely to terminate in death, the other curable and not likely to end fatally. Some authors, therefore, following Walshe's classification, speak of a true and a false angina. Osier makes this distinction, while Bal- four, Gibson, and others consider such a division irrational and unscientific, on the ground that all pain is real, and that there can be no such thing as true pain and false pain. There can be no great objection to these terms if it is understood that they are employed for the sake of convenience, to distinguish grave cases from those that are not grave.
Huchard also classifies eases of angina which are purely neu- rotic and not likely to terminate fatally under the head of pseudo- angina, which he makes include the reflex and toxic forms. In certain cases, however, he believes that nicotine poisoning is capa- ble of producing the fatal form of angina pectoris.
The confusion and obscurity which so long characterized the consideration of this subject, and which indeed may be said to prevail largely even now, arose from the attemy)t to make the same pathology responsible for all cases of pain that merit the term of angina pectoris. On the other hand, the recognition of tw^o en- tirely diverse groups renders the subject clear and simple, so that we are able to get a tolerably definite notion of its pathology.
The angina which always carries with it the possibility of sud- den death, and which therefore may he called true or grav^e, is usu- ally associated with, and therefore thoufrht to be dependent upon, structural disease of the heart. Various lesions have been found in fatal cases, but they are all of such a kind as to interfere with
ANUIXA PKtTOUlS
G41
till? blood-supply to the he«rt-iiiitsek\ Coronary i^elcrotsis is the moist fre(]ueiit, but iiuisniiich us all maes of tliis disease are not attended with aiigiiui pertoris, it is evident that there must be something more than mere sclerosis of these arteries. According- ly it has been determiued that it is not so much the fact of disease of these vessels as it is that this disease must interfere with cardiac circulation if it is to give rise to attacks of angina jiectoris.
Shutting off of the blood-supply to a limited portion of the mywardinm — i. e., by thrombosis of terminal twigs or even of a branch f4* cousiderable size — does not apiiarently always occasion this [>aiu, if, however, one nuiiti trunk, or, still more, if both tniiiks tiYv iiceluded, or if tht-ir Iniucn is sufficiently narrowed without being actually obstrncted, I hen attacks of angina are very likely to occur. Accordingly, a Cfindition which is specially apt to result iu anginal seizures is narrowing of the mouths of the ciu*onarv arteries by the sclerotic process, as has been repeatedly ju'ovcd at the necropsy in cases of this terrible agony.
It is upon the evidence furnished by such discoveries that the theory has been reared of ischa'mia of the heart-muscle being the essential pathological factor in the causation of the fatal fonu known as true or grave angina pectoris. In this variety pain is usually absent so long as the individual is at rest or is not making exertion that requires unwonted labour <»u the part of the heart lender such conditions the circulation of bltx>d within the myo- cardium is sutficient for its needs, but when some emotion or extra physical effort calls for unusual heart-work, the narrowed coronary arteries are iiu^apable of supplying the organ with an additional volume of blood and the ischaniiia is intensiticd for the time being. Thereu|)on an attack of angina pectoris is evoked. According to this hypothesis, the nerve-filaments or ganglia with which the niy(x*ardinni is so richly supplied become irritated by this depriva- tion of required bloorl and send an impression through the cardiac plexus uji to the centre, w^hieh then responds by discharging a sensation of pain along certain nerve-trunks connected with eer* tain segments of the spinal cord. This will again be considered in greater detail.
The pain thus induced promptly causes a cessation of exertion and consequent lessening of the heart's w^ork. As the organ re- sumes its accustomed tranquility its blood-supply proves again
41
642 DlSKASh^S OP THE IIFJAKT
sutKeieiit for its needs, irritation ceases, and with it at last goes the pain. Whether or not this is the actual modus operandi of the attack, the assumption that it depends upon a diminution of the blood-supply seems borne out by the nature of other cardiac and vascular lesions sometimes discovered in fatal cases of angina — i. e., aneurysm and atheroma of the ascending aorta, insufficiency of the aortic valves, and very rarely extreme degrees of aortic and mitral stenosis. In cases of angina that appear due to aortic scle- rosis the mouths of the coronary arteries are very commonly found extremely reduced in size by reason of calcareous plaques on the surface of the intima or by calcareous thickening of the aortic wall, while the coats of the nutrient arteries are also generally invaded by the same sclerotic process. In cases of aneurysm the coronaries are narrowed either by the direct effect of the aneurysm or by associated atheroma. In the diseases just mentioned the changes must be of a kind to obstruct blood-flow into the coronary arteries if they are to occasion the agonizing symptom under con- sideration.
In aortic regurgitation adequate blood-pressure in the nutrient vessels is not maintained, and under conditions of extra effort rela- tive ischemia of the hypertrophied left ventricle is produced. Mitral and aortic stenosis prevent the discharge of a normal vol- ume of blood into the aorta, and consequently hinder the adequate flushing of the coronary arteries. By some authors the influence of valvular defects in the causation of angina is denied without associated sclerosis of aorta or coronaries, and certainly angina pectoris is exceedingly rare in valvular disease.
Xevertheless, I have observed typical angina |)ectoris in one case of pronounced aortic stenosis that was, from the history and patient's age, presumably of rheumatic origin and in two instances of aortic insufficiency. In the first case no autopsy was obtained, but in one of the patients whose aortic incompetence was associ- ated with angina and whose case was described in the chapter on aortic regurgitation, the pain was found to 1x3 clearly due to scle- rotic narrowing of the coronaries. I am inclined to believe, there- fore, that aortic incompetence of itself is not so likely to lead to angina as is stenosis.
Post-mortem obser^-ation ])roves undeniably that the nutrition of the heart-muscle may suffer seriously in cases of valve-disease
ANGINA PE(TQRIS
MS
without associated coronary scleru^is^ and that such uiyocardiEl degeneration is particularlj likclv to be found in long-standing and extreme stenosis of the aortic oritice. This indicates that dur- ing a long period of time the demands on the energy of the heart untstripjx.^d its nutrition owing to the small supply of blood sent through the atenoised orifice into the aorta and coronary system.
If in -such a state of things the supply of blood to the heart- muscle is still further diniinishedj although hut temporarily, then it is |)08sible for a ]uiroxysm of angina pectoris to occur; The in- fluences capable of determining such a temixjrary increase of car- diac ischannia may he vaso-motor spasm, afflicting the coronaries, as suggested by Powell, or the continuance of undue physical exer- tion after such effort has begun to overtax the lieart. In extreme aortic stenosis cardiac overstrain is shown by still greater feeble- ness of the pulse, and when such is the case the coronaries are still more imperfectly flushed. There is temporarily a relative cardiac ischaemia which makes an attack of angina jiectoris possible. For* timately such attacks are rare, yet on the hypothesis of cardiac ischa^mia as the cause of angina the conditions favourable to its production are present.
Finally, it should be stated that the degenerative changes dis- covered in the myocardium of persons who have died in a parox- ysm of angina pectoris probably bear no direct etiological rela- tionship to tiie pain. Were it not so, this formidable agony would be far more common than it really is. Such degenerations of the heart-muscle are to be looked upon as the result of the pathological condition in the coronaries or aorta w^hiVh have led to the angina.
It now remains to consider how the morbid anatomical condi- tions just mentioned act in the pathogenesis of this obscure com- plaint. They are to be regarded as predisposing factors merely, which to be operative require some additional influence, since, if such were not the case, all per&ons in whose heart such changes are found after death ought to have suffered from angina pec- toris. This we know is not the c^se. It is this consideration which has given rise to the various hy|>otheses propounded in explanation of the symptom-complex. The best know^n of the the- ories have been stated already in the history of the complaint and do not cull for repetition. I would direct attention particularly to Ros€'nbach-s and to that of cardiac ischiemia.
C44 DISEASES OF THE HEART
With reference to the latter, I think one should also bear in mind the suggestion of Sir Douglas Powell that oftentimes we are obliged to assume the jwssibility of relative cardiac ischcemia if we are to understand how some cases originate — i. e., the condi- tions under which they originate, and the beneficial influence of certain lines of medication. According to this hypothesis, vaso- motor spasm may affect the coronary arteries and temporarily seriously diminish the flushing of the heart-muscle with arterial- ized blood. The irritation thus evoked is declared by pain and often by disordered cardiac action. WTien, upon administration of vaso-dilators or on cessation of arterial spasm from other influ- ences, the coronaries become relaxed, and hence better flushed, irritation ceases.
Whatever is the exact condition, however, the generally ac- cepted view is that there is abnormal and excessive cardiac irrita- tion which initiates the paroxysm. This is Iluchard's view at all events, and herein he appears to coincide with Rosenbach.
According to Iluchard, the course of vents in cases of grave angina is as follows: The heart itself is the starting-point of the attack. From here the stimulus ascends by way of the sensory centres and finally reaches the medulla. Thence it is reflected along the intercostal nerves and brachial plexus as a manifestation of pain. Tlic stimulus next reaches the vagus centre, and from here an inhihitorv ini])ulse is sent down to the heart, the original start- ing-place, and declares itself by slowed, and it may be intermittent action of the heart.
Such an inliihitory action explains the sense of constriction and of impending death, as well as the dilatation of the cardiac cavities soniotinies noted.
In ])soud()-an<!;ina, on the contrary, the point of departure of the irritation is an intercostal nerve or some other peripheral or visceral nerve, wlience, as in true angina, it also passes to the medulla. From there an imj)ulse is sent out 7iot along intercostal 7ierves and brachial plexus, but is passed down along the vagus or accelerator nerves of the heart to this organ. According to the route thus selected, the action of the heart becomes either rapid or slow and otherwise disordered.
In these two forms, therefore, the original source of irritation is entirely different and the circuit is traversed in a contrary di-
ANGINA PECTORIS
G45
rectjon* To my iiiinJ tliis is a liiglily satisfactory explanatioTi of the ilifTereiiees in their clinical pheiioaiena* It likewise proves serviceable in making up diagnosis and prognosis and in deciding on the mode of managements
Leaving now the ]jathology of angina pectoris, which, however mnch we may speculate upon it, is nndeniably obscure, we come to the considcratiun of the remaining predisposing causes as well as the influences which directly excite an attack.
Aside from the anatomical conditioim already oivnsidered, wc are at once impressed by the important part played by age* An- gina pectoris of coronary origin is emphatieally a complaint of individnals who have passed middle age ami have entered thcdr sixth or seventh decade. Ttiis is an age in which the etfccts of arteriosclerosis usually declare themselves, and yet angina of this origin is sometimt^s observed before the fiftieth or even the fortieth year, One or two instances are on recor<l <*f its wcnrrcnce in chil- dren. Xeverthtdess such fa(*ts dn ni»t invalidate the correctness of the statements made cuncerning tlie importance of age.
Males are niucVj nmrr frequently affected than are females, and of men who are befallen it is a noteworthy fact that it is espe- cially the well-to-do and well-fed. Regarding the influence of sex, Osier states that out of his 40 cases but 3 ooeurred in women. I have notes of 32 cases, and of tliese, 7 were in the female sex. Of 2 that came to autopsy, 1 was a woman of sixty-six with aortic and mitral stenosis, with sclerosis of the aorta and coronaries ; while in the other, as already stated, there was coronary obstrnc' tion and aortic regurgitation, l>oth of sclerotic origin. Of the re- maining 5 cases, 1 was in an aged woman presenting well-marked signs of arteriosclerosis, a hypertroidiied left ventricle, and a harsh systolic basic limit. Another was a comparattvely young female with aortic regurgitation of uncertain origin, but whose questionable habits always made me suspicious of the likelihood of syphilitic infection. The third was in the lady of forty-four with signs of pure aortic stenosis whose ease has been already de- scribed in the chapter on Aortic Stenosis, and will Ik* again alluded to in this. The fourth was in a woman of fifty with aortic regurgitation, due prnViably to arteriosclerosis, to ju<lge from her history and the arterial thickening. The tiflh case was that of a woman of fifty-six who was corpulent and had thickened arteries
CM DISEASES OF THE HEART
with a greatly hypertrophied and dilated heart. As regards this striking discrepancy between the two sexes^ it may be stated that the greater prevalence of angina pectoris among elderly men is to be referred not so much to sex per se as to those conditions which are responsible for the greater frequency of arteriosclerosis in the male sex.
Heredity is also a predisposing factor, what was said under this head concerning coronary sclerosis and myocardial degenera- tion being also applicable to the symptom now considered. In- stances are on record of this formidable complaint having been passed down through three generations. It is not at all uncom- mon for both father and son to suffer or even die from angina pectoris. The most notable instances of the kind occurred in the persons of Thomas Arnold, of Rugby, and his equally well-known son, Matthew Arnold.
Gout predisposes to arteriosclerosis, and therefore to angina pectoris. Syphilis, alcohol, and, according to Huchard, tobacco, are also predisposing causes. The last named may, however, be an exciting cause.
The exciting causes of true, or coronary angina, as Huchard calls it, are conditions that suddenly raise blood-pressure in the aortic system, or, according to the theory of cardiac ischemia, re- quire more work of the heart than it can perform in consequence of its diminished blood-supply. Foremost among these is muscu- lar effort. The patient may have had no premonition of the mal- ady, when, one day, perchance immediately after breakfast, he starts out for a walk and is arrested by an indescribable attack of praecordial pain. In other instances the first paroxysm is expe- rienced upon the patient attempting to hurry to reach a car, or the like, and thereafter is repeated whenever he quickens his foot- steps beyond his usual pace. Atmospheric conditions imdoubtedly intensify the influence of exertion, for on a day when the wind is easterly and raw these patients find themselves imable to walk at even their accustomed gait; while in warm weather and on still days, or here in Chicago, even in the depth of winter when the air is dry and cold and the sun bright, these patients frequently find themselves able to get about with comparative comfort.
I have kno\\Ti patients who could walk with ease when the
ANGINA PECTORIS
04:
.#omach was emptVj yet who invariably experience J pain^ of greater or less severity, whenever attempting to walk soon after breakfast. This is undoubtedly to be explained by the augmenta- tion of arterial tension, prcKluced by the presence of food in the stomach. Xevertheless the rise of blood-pressure thus occasioned is of iti^elf not sutBcient to evoke an attack, since it requires in addition physical exertion.
Emotional states, as anger, worry, or excitement from what- ever cause, which accelerate and intensify cardiac action, are also capable of evoking an attack of angina f>ectoris. This was illus- trated in the historic case of John Hunter, who w^as wont to say that '* his life was in the hands of any rascal who chose to annoy or tease him/' As a matter of fact, Hunter died during a parox- ysm brought on by a fit of silent rage in consequence of having been flatly contradicted at a meeting of the Board of Governors of St. George's Hospital, Octolier 16, 170.*^. His coronary arteries were found ossified and the aorta dilated. I knew a gentleman of this city, a great sufferer from ferocious attacks of angina for many years, who frequently declared that nothing was so bad for him as a fit of temper.
It is very remarkable bow diverse are the effects of exertion in different persons, or in the same individual at different times. I rtH:*all the instance of a gt'utlt^man of fifty-two, who, by the way^ had been an inveterate smoker of strong Havana cigars, and who cnnld not walk out of an evening without suffering from his an- gina. Vet on one occasion he assisted in carrying a loaded hook- case up a flight of stairs without experiencing the slightest pain. This patient ultimately ilied sudtlenly, I have another gentleman under occasional observation who invariably experiences more or less pain of a true anginal character the first thing in the morning when he goes into the bath-room to dress. The taking of a cool bath is almost sure to evoke one of his seizures. Excitement and exertion combined are jiarticularly apt to call forth an attack. For this reason crdtus is esj>f'(*iHlly injurious to some of tliese pa* tients. The influence of cold in determining a paroxysm has been referred to, and is shown by the inability of patients to face a cold wind, particularly when damp as well as cold, and by the effect of a fold Initli*
Distention of the alwlominal viscera by flatus and the taking
048 DISEASES OP THE HEART
of a full meal are enumerated among the exciting causes by some authors, but in my experience these have been operative only in connection with other determining factors, as exertion. Tobacco is counted by lluchard as both an exciting and a predisposing cause, and he narrates instances of individuals who had abandoned smoking because of the attacks of angina it induced, and who upon returning to their former habit again found it promptly followed by the same impleasant effect.
Gibson likewise speaks of tea and coffee in this connection, say- ing they also claim their victims. Regarding the angina due to tobacco, lluchard recognises three forms: (1) Functional or rela- tively benign form, resulting from spasm of the coronary arteries, without disease of the myocardium, and which is the " Angina spasmo-tabagique," and which is recovered from by giving up the use of tobacco. (2) An organic angina of a grave character, re- sulting from coronary sclerosis and which is not recovered from by the abandonment of the tobacco habit. This is the " Angina sclero-tabagique." (3) The form most benign of all results from digestive troubles produced by the tobacco habit (gastralgia, dila- tation of the stomach, and insensibility of the mucous membrane). This is the ** Angina gastro-tabagique." Strictly speaking, these all, with the possible exceptions of the second form, belong to the pseudo-angina.
In the group of cases known as false angina, and which, ac- cording to lluchard, belong to the peripheral or visceral neuralgias, and which will be considered in connection with cardiac neuroses, the exciting causes are not always easy of recognition, yet, as stated emphatically by lluchard, are never due to effort. Herein, therefore, lies the great distinction between true and false an- gina. Occasionally in true angina, the paroxysms occur at night, arousing the patient from sleep, but, according to lluchard, this does not invalidate the statement that coronary angina is evoked by effort, nor are these cases to be classed as pseudo, because com- ing on at night.
Their advent during sleep is referable to some condition which augments blood-pressure and acts in the same manner as does effort made by these individuals. Some of these conditions may be flatulent distention of the bowels, coldness of the air in the sleeping apartment, an uncomfortable position during sleep, or
ANGINA PECTORIS
640
reriiiTibent iH>stiire itself, wliirh is kiiowB to augment blood- pressure ( lliichanl ).
Clinical History and Features of an Attack. — ^The sufferer from angina of coronary disease is most often an elilerly man of about sixty years of age who has l>een engaged in mercantile, profes- sional, or literary ^nirsnits rather tluin in mannal labour, and who often presents the appearance of well-preserved health, lie not infre<jnently states that j^rior to liis tirst attaek of angina he never ha*l any syniptonis tliat made him tliink his heart was affected, and that were it not for this avmptom he would still think his heart as aoimd aa ever,
Qnestioned eimeerning the syini»tonis for whieh he eonsults the pliysician^ he says he has a pain in the front of the ehest» w^hieh he locates at the ujiper antl middle portion, frequently putting hia hand over tlie manubrinm steriii^ He describes this pain as enniing on snddeidy, usually during a walk, and becoming so intense as to eompil him to stand slill until it goes away, whieh it usually thtes in a few nmments. Further inquiry brings out tlie fact that associated witli tlie pain is a feeling of oppression or weight on the ehest, and in some cases a sense of ini|xniding death. The eastrntial features of an attack, therefore, or the ehar- at'teristic triad of sj'mptoms, as it may be ealledj are (1) a subster- nal pain, that is usually so severe as to be an indescribable agony, (2) a sense of great constriction of the chest, a feeling as if this were being crushed or squeezed togetherj^ and (3) a sense of speedy or impending dissolution.
The dursition of a paroxysm is not long, generally not more than a few minutes, i^rnbably because the violence of the agony necessitates a cessation of the effort occasioning it, and with the removal of its exciting cause the attack subsides. Occasionally it persists for twenty minutes or more, and when it occurs in the middle of the niglit it is apt to last longer than do day attacks. Thus it is seen that the pain may come on eilher by day or by night, but as a rule and particularly in mild eases it is more likely to manifest itself during the waking hours and when the patient is exfiosed to some obviously exciting cause. Nocturnal seizures are apt to be more severe as well as of greater dnration, I>ecau^^e, according to ITnchard, ihe rise of blood -pressure incident to the rccnmbent posture does not subside quickly even after the
050 DISEASES OP THE HEART
patient leaves his bed, whereas that due to effort or emotion yields promptly to the removal of the cause.
The first seizure has been known to prove fatal, and on the other hand attacks have recurred at varying intervals for five, ten, fifteen, and even twenty-five years. A single sharp paroxysm has been followed by years of immunity, and in other instances, after having been absent for a long period, the malady has then assumed a frequently recurring type. Huchard speaks of the paroxysms as sometimes occurring with such frequency as to over- lap each other, and thus become practically continuous with only remissions in severity, a condition which he terms Vetat de mal angineux. Some patients are aware so soon as they arise in the morning that they are going to have a " bad day," as they say, or that they will have to be more than usually cautious lest they pre- cipitate an attack. As a rule, however, anginal seizures come on abruptly without warning and wnth such agonizing intensity that the sufferer is compelled to stop in his tracks and remain standing, scarcely daring to stir or breathe lest he intensify his pain beyond all possibility of endurance.
At other times he leans against a tree or wall for support, or he stands in some peculiar attitude w^hich experience has taught him will somewhat mitigate the severity of the pain. He may lean forward or bend backward, let his arms hang motionless at his side or stretch them above his head in an effort to fix the pectoral muscles so as to thereby increase the expansion of his chest, which seems to him to l)e compressed and too small for its contents. But whatever his attitude, it is, according to Huchard, always an upright rather than a recumbent position, which latter, by augmenting arterial tension, increases the severity of the attack.
Most happily for the patient the angina usually departs as quickly as it comes, and unless the attack has been one of un- usual length or severity tlie victim feels as well immediately after as he did before the seizure. Tie is generally able to resume his walk, although perhaps rather more cautiously than before. Such is the history of a comparatively mild angina pectoris, but in some sad cases the attacks grow more frequent and more agonizing until at length the patient is not able to move in bed or engage in con- versation without frightful suffering, and life becomes a miserable existence.
ANGINA PFXTORIS
651
Tt now becomes neeessarv to consider the features of anginal attacks in detaiL It has been stated that the pjiin is subster- nal; that is, that its seat of maximum intensity or its point of departure is beneath the upper or middle third of the breast- hone. It is for this reason that Bauuies applied to the camplaiot the name of sternalgia. The pain may remain centred beneath the sternum, but in most instances it radiates into the side of the thorax and along the course of the brachial plexus into the left shoulder or dowii the corresponding arm to the elbow or still farther, as far as the wrist, or even into the two fingers .supplied by the ulnar ner^'C. In some eases the pain takes origin in the region of the apex-heat or epigastrium, or^ as in the case of one of my patients, just above the ensiform appen- dix, whence it shoots into the left shoulder and down the left arm.
In rare instances the attack starts in the arm, at the wrist or elhow» and thence passes into the chest to the region of the heart. In one of Trousseau's patients the paroxysm began in the back of the neck, and then darted forward into the tongue and front of the thorax. Very exceptionally the pain mux take origin in the left interscapular region or at the adjacent dorsal spines. But whatever is its point of departure the anguish radiates more or less widely throughout the chest, flashing from the cardiac area into the left, sometimes the right arm, and in some cases into both anus, or upward into the side of the neck or the occiput, or, instead, downward into the left half of the abdomen, and now and then even to the thigh. These latter lines of radiation are, how- ever, very uncommon as compared with its course into the left shoulder and arm.
Very diverse terms are employed by patients in attempts to describe their agony. It is spoken of as crushing, grinding; tear- ing, cutting, burning, scalding, or» in want of appropriate adjec- tives, SLB indescribable, frightful, and the like. One of my pa* tients, a lady with extreme aortic stenosis, depicted her anguish as '* a feeling as if my chest were being crushed beneath the wheels of a passing train,"
The sensation of pain is sometimes lost in the terrible distress occasioned by the sensation of the chest being squeejsed in a vise, or of the walls being forcefl together from l>efore backward.
652 DISEASES OF THE HEART
Balfour describes it as if the heart were being " grasped by a mailed hand."
Then, as if this were not enough, the sensation of impending death is added, to complete this awful suffering. The lady just mentioned, said in reply to a query upon this point : " Oh, yes ! of course I feel as though I were going to die, but I have learned by experience that I do not die, and therefore I no longer speak about it. I always used to declare that I knew I was going to die." Nearly all sufferers from severe angina pectoris agree in the assertion that no other pain can compare with the awfulness of its agony, and if it were not happily of short duration, life could not endure.
The physician is not often a witness of the terrible agony, the attack being over before he arrives, or his attention is so occupied in efforts for the patient's relief that he cannot note the several features. Nevertheless, from such observations as have been re- corded, we possess certain facts concerning objective symptoms. The face is expressive of unspeakable agony; it is anxious and usually pale, and bedewed with perspiration, but it may be con- gested. The patient is usually motionless during the height of the paroxysm, yet it may be ushered in and terminated by restlessness. The extremities are usually cold, and the pulse is variable. It is sometimes stated to be imchanged, but is for the most part small and tense.
It may be regular or irregular and, if accelerated in the be- ginning, is likely to become slower than normal before the cessa- tion of the pain. The size and rate of the pulse have given rise to much discussion, but the consensus of opinion seems to be that it is small, sharing in the condition of spasm, and that its rate is slow, indicating vagus stimulation. The heart sounds are usually clear, but feeble, although in some instances a systolic apex-mur- nmr has been audible.
As already stated, the seizure usually subsides suddenly, leav- ing nothing more than a feeling of weakness behind. The pain in the upper extremities may be accompanied but is more often followed by a feeling of numbness, even by transient paresis. The lady to whom reference has been rej)eate(Uy made, said her left arm was always helpless after cessation of the suffering.
In the case of my aged female patient, already mentioned as
ANGIXA PEPTORIS
053
liaving arteriosclerosis, the face was lluislieJ during the attiiek, initl the eessatiaii of pain was follovveci by voitiitiiig- 1 have stated that patients remain motionless tin ring the paroxysms, yet I have known two instances, both inerij who thought they obtained some relief by walking gently about the room while the pain was on. One of them was a well-known attorney, in whom the necropsy verified the diagnosis of coronary sclerosis and fatty degen- i-ration of the left ventricle. In the other case the age of the patient J the thickened peripheral arteries, and the history of the attacks, left no donbt as to the nature of his angina. Douglas Powell states that when relief is produced by quiet walking it has seemed to him to indicate a fairly sound state of the heart-nmsele. This may he so in some but not all eases. ^Ir. H., the attorney, was found to have extensive myocardial degeneratioHj and hence some other explanation is needed in his case. In my other pa- tient, the gentleman was not only able to endure without jmin certain gymnastic and breathing exercises which produced great jjersp! ration, but he declared that he felt better for them. That they did not call forth bis suffering the same as did walking against a wind, may have been due to the lowering of arterial ten* sion which they induced.
The extremely variable course of the malady and its not in* frequent termination in death during an attack are also note- worthy features. An historic instance is that of the Rev. Dr. Chalmers, who is thought to have died during a paroxysm of angina, since he was found dead in his bed with a bowl be.sitle him into which he had emptied the contents of his stomach. I knew a similar instance of an old gentleman who, after having suffered attacks of angina pectoris for twenty years, was found lifeless in his bed in a hotel with a wash-bowl resting on the bed in front of him and containing von^ited matter. I knew of another elderly gentleman who, while in attendance upon a lawn fete, was seized with a paroxysm of pnecordial pain, vomited, and imme- diately died before assistance could reach him. So far as could be ascertained, it was his first and oidy attack.
Before leaving this subject^ it should be mentioned that Oaird- ner has described what he calls angina sine dolore. What he means by the term is lw?st described in his owti w'ords : "Apart from what has been variously termed cardiac asthma, dyspnoea.
G54 DISEASES OF Til£ UEAUT
or orthopncea^ which in many cases receives its clear explanation from the associated states, either of the pulmonary circulation or of the lungs, bronchi, and' pleurae, as disclosed by physical signs, there is often an element of subjective abnormal sensation present in cardiac diseases, which, when it is not localized through the coincidence of pain, is a specially indefinable and indescrib- able sensation, almost always felt to be such by the patient him- self. I make this remark deliberately, as the result of experience, and well knowing it is liable to be brought into question in par- ticular instances — that, in fact, a large part of what has been de- scribed under the titles given at the commencement of this para- graph has been inextricably confounded by systematic writers with the sensation, or group of sensations, to which I refer.
To this group of sensations, when not distinctly accompanied by local pain, I have, in various instances, given the name of angina sine dolorCj recognising thereby what I believe to be its true diagnostic and pathological significance, and its alliance with the painful angina of Heberden; the pain in which, however, as we have already seen, is an exceedingly variable element, both in degree and in kind."
DiagnOBifl. — Two questions present themselves for answer in the diagnosis of this formidable complaint: First, is the attack of pain angina pectoris ? and second, what is the pathological con- dition underlying the attack? In other words, is the paroxysm to be classed as coronary angina ? or is it a disorder of the nervous system independent of any cardiac or vascular disease? In at- tempting to answer the first query, one should keep clearly in mind the fact that all prapcordial or so-called heart-pains are not attacks of angina pectoris. Many of these pains are simple inter- costal neuralgias, and although variously described as cutting, stabbing, tearing, shooting, darting, burning, smarting, or only as dull, sore, heavy, and the like, they lack two features essential to angina pectoris — namely, the feeling of the chest being crushed, and the sense of the near presence of death.
The fact that pain is felt in the region of the left nipple or that it radiates from that point into the left shoulder and arm does not warrant the conclusion that it is angina. Indeed, a pain that takes its point of departure at the sternal end of the fourth left interspace or in the fifth left interspace below the breast, whatever
AXUIN'A PKLTOItIS
655
I
tx* its iliroctioB of racliatiim, is iijuri! likely to be au intercostal neuralgia, since the agonizing suffering meriting the name angina |)ectorii^ is most frequently substernal. Moreovery in cases of in- tercostal neuralgia there are usually well-deiineJ tender spots cor- responding to the p^iints of origin of the pain. Another eharacter- istie of these intereostal neuralgias is tlieir coming like a sudden stab or thrust, and then leaving as quickly, the points where they appeared being sore to the touch. When^ as in some instances, the pain is j:iernu.nent or i \ continuous, with exacerbations and remis- sions, the very length of the attack stamps it as intercostal neural- gia and not angina pectoris,
Moreover, these pains are most frequently met with in aim- mic, neurasthenicj or otherwise neurotic individuals, or such as present symptoms of gastric disorder, and although by no means limited to the female sex, they are more frequent in women than in men, and generally in such as have not yet reached the age at which vascular degenerations are to \m expected. In most cases attention to the points just mentioned enables one to readily differ- entiate intercostal neuralgias fruni the true heart-pain of angina. It is far otherwise, however, with those attacks of pra'corjial pain which display the features of true angina pectoris, yet which in reality do not belong to that class.
In other words, is it Heberden's angina with its possibility of judden death i or is the pain a pseudo-angina, and hence not of the ne serious import i The answer to these queries is to be found in the consideration of the following points: (1) the age and aex of the individual, (2) the stale of the arteries and heart, {3} the influence of effort in evoking a paroxysm.
Attacks of pnreordial pain that occur in yonng persons, no matter how closely they resemble coronary angina, are presmnably symptomatic of irritation in some other organ than the heart, and if such attacks are in women the presumption is the stronger that they are false angina. If, on the contrary, they occur at an age when vascular degeneration is conunon, they are much more likdy to be of the grave kind, even though they occur in females.
The detection of stiff arteries or of signs of heart-disease is in favour of true angina, and yet pain of visceral disturbance may occur in women past forty witli hypertrophicd hearts, particularly at the menopause or in such as have suffered all their life from
656 DISEASES OV THE UEART
constipation and defective elimination. The same thing may bo said of young persons of either sex who long before they reach forty are victims of aortic valvular disease.
Consequently in all such cases particular attention is to be paid to the influence of physical exertion over the attacks of pain. If the initial paroxysm took place during exercise, if the pain is aroused by a hurried walk or by walking after a meal or against a cold damp wind, if it compels the patient to stop in his tracks and remain standing until it passes away, it is in all probability a true angina. If, on the other hand, the person is able to con- tinue his walk, if he sits or lies down, instead of standing, during the acme of the pain, and if he is restless, moaning, and throwing himself about, the attack is probably one of pseudo-angina pec- toris.
In cases of a mixed nature described by Huchard, in which cardiac or vascular disease is complicated with attacks of pain of an hysterical nature, there is often great difficulty of diagnosis. Their precise nature can only be determined by noting carefully the influence of effort in provoking the seizures and by the discov- ery of the stigmata of hysteria.
Furthermore, in attempting to distinguish the false from the true angina, one should never forget that the occurrence of pain alone is not sufficient for a trustworthy diagnosis, but that the symptom-complex of pain, constriction of the chest and a sense of impending death, is essential. Pain is the paramount sensation, but in typical coronary angina there is more or less blending of the other two. There are doubtless horder-Une cases, as they may be called, in which it is impossible to assert positively the real nature of the pain, especially in elderly well-to-do males with stiff arteries, yet in whom constriction and the feeling of overhanging death are wanting or not pronounced. If, on the other hand, the patient is young and a female and the two symptoms just men- tioned are absent, the pain may (juite safely l)e set down as a false angina pectoris.
Finally, the pathological condition underlying the angina is to be determined so far as possible. Thickened arteries in a person past forty and signs of sclerosis of the aorta should be carefully sought for. Curschmann has pointed out that the elongation and widening of the arch incident to sclerotic changes may be recog-
ANGINA PECTOHIS
057
nised by careful study of tlie cervical arteries. In the fossa jugti* laris, particularly during the act of swallowing^ may be seen, or, still better, felt the pulsation of the transverse portion of the aorta » while the pulsation of the sulx-l avians is situated abnor- mally biiih and tlie carotids arch unnaturally forward and feel stiff and perhaps slightly irregular. There may be slight dulness at right of the sternum, appreciable only upon deep percussion, and the second aortic tone is sharp and ringing. The detection of such signs %vould strongly snpiH>rt the cuuclusion that the angina was due to coronary degeneration, and was therefore most grave.
Musser has reported a series of cases in which there was typi* eal anginal seizures so long as the left ventricle was hypertrophied, yet in which with snj^ervention of dilatation the attacks of pain , disappeared. These obsen^ations have led JIusser to conclude that in some cases angina pectoris is due to increased intracardiac hlood-pressnre. In all such instances the exact nature of the underlying condition cannot be made with certainty, and one must content himself with the diagnosis of the angina and of the car- diac condition witliout attempting to do more than speculate on the connection between the two.
Prognosis,— As has been repeatedly stated, there is ahvays a possibility, find, according to Iluchard, a strong probability of sudden death in a paroxysm of angina j>ectoris. Even if the patient does not succumb during an attack, the complaint is in- curable, lie should be advised, therefore, concerning the gravity of his affection, and his immediate family should be warned of the likelihood of a fatal termination. How long a patient is likely to live, subject to these attacks, is a matter of too great uncertainty for an expression of opinion by a prudent physician. It is alwavs well to reassure the sufferer, however, hv the state- ment that patients have been known to experience the sjqnptom for a long term of years, and that its severity and the frequency of its occurrence are likely to be modified by appropriate medical treatment and by the care exercised by the patient.
Other things being equal, it may be said that the more severe the attacks the greater the danger of death. Also, the more easily the paroxysms are evoked, the more extensive is the coronary ob- struction, and the graver the complaint. Increasing frequency of 42
05S DISEASES OP THE HEART
rirurreiice is likewise of evil im|)ort. On the contrary, the prog- nosis may be said to improve in proportion as the attacks become less severe and the intervals between them longer.
According to Powell's assiunption, previously mentioned, the prognosis should be better when relief is afforded by slow walking, but the case I have cited of the attorney proves the contrary. Moreover, in the case of my other patient his condition grew stead- ily worse in spite of his ability to endure the exercises to which he resorted in the vain hope of improving his general health, since his attacks of pain became more frequent if not more intense.
Treatment. — This includes, first, measures addressed to the relief of the paroxysms, and second, the management of the pa- tient's daily life during the intervals between the seizures, with a view if possible to lessening their frequency and severity. The treatment of the attacks has already been considered in the chap- ter dealing with myocardial diseases secondary to coronary scle- rosis, but may be again discussed at this time at somewhat greater length.
Very many and divers remedies have been used either solely to relieve the pain, or to strengthen and regulate the heart's action, and are therefore either anodjTies or stimulants. Inhalations of chloroform and ether, Hoffman's anodyne, aromatic spirits of ammonia, opiates, carminative draughts, such were the measures relied upon prior to the discovery and introduction by Richardson and Lauder Brunton of nitrite of arayl. Two medicaments which in the experience of the profession the world over have proved of the highest value in controlling the attacks of angina pectoris, and now imiversally employed, are the nitrites and opium. The action of the nitrite of sodium is too slow, and therefore we have recourse either to the inhalation of a few drops of nitrite of amyl, or to a minim of a 1-per-cent solution of nitroglycerin dropped on the tongue. Tf amyl nitrite is preferred, it should be carried about by the patient in the form of nitrite-of-amyl pearls, containing o to 5 minims each of the remedy. Kept in this way the drug does not lose strength. So soon as the patient perceives his pain a pearl is to be crushed in the handkerchief, or a few drops from a vial may be poured thereon and the fumes inhaled, or the suf- ferer may breathe them directly from the vial. The action of the remedy is usually very prompt, rarely failing to afford relief.
ANGINA PECTORIS
65i)
Tbere is usually no danger attending its use; at the most, only a dull headaclie is produced. If nitroglycerin be preferred, it ia most conveniently and usually administered in the form of a tablet triturate containing 1 minim of a 1-per-cent solution. If tbe tablet is dissolved on the tongue instead of being swallowed, ita effect is more promptly induced. Thh is especially the case if the occasion for its use is soon after the taking of food. The remedy can also be dropped on the tongue or taken in a swallow of water when the solution is preferretl, but this method is not only less convenient, hut it necessitates the loss of valuable time, when seconds of agony seem like hours to the sufferer.
Abatement or cessation of the attack generally takes place in a few seconds; but should this not be tbe case a second or even a third tablet may be employed at intervals of two or three minutes. Special indications for one or another of these remediea are found in pallor of tbe countenance and a small and tense pulse, wbelher slow or acceleratedj regular or irregular, and intermittent or not, and in other signs of arterial spasm. The nitrites are essentially vascKlilatorSj and stimulate the heart only indirectly through their dilating intluence on the arterioles. Through their action, the wiry, and it may be slow, pulse grows softer, fuller, and more rapid, while at the same time there may be felt some constriction nf the throat and tense or throbbing headache, symptoms which to the patient are of small moment in comparison with the relief from his frightful agony.
It has generally been my observation that in elderly individ- uals with sclerosis of tJie temj>oral, and presumably therefore of the cerebral arteries, the heaci symptoms rx'casioned by the nitrites are far less pronounced than in younger persons whose vessels are less stiff, and hence more responsive to the action of the drug. When phenomena of vascular spasm are absent or when relief does not promptly folknv the use of the nitrites, recourse would better be had to opium in some form. A method of administration that yields sf>eedy results is indicated, and therefore it is best to give morijhine hypodermically and in a dose tliat will suffice without rej>etition — e. g,, I or even ^ of a grain.
The lady to whom reference has been repeatedly made was compelled to resort to both nitroglycerin and morphine, and in addition frequently took a teaspoonful of sulphuric ether in sweet-
OGO DISEASES OP THE HEART
died ice-water. Relief was not obtained until under their com- bined effect the pulse became full and bounding, and the skin, pre- viously cold and perspiring, grew flushed and warm. In her case there was extreme aortic stenosis with, it may be, coronary scle- rosis, and a more decided stimulation of the heart was required than was indirectly occasioned by nitroglycerin. Under the influ- ence of the ether, cardiac contractions are both invigorated and quickened, so that the coronaries previously dilated by nitroglyc- erin receive a more adequate supply of blood.
In comparatively mild cases relief may sometimes be obtained by the administration of diffusible stimulants, as aromatic spirits of anmionia, Hoffman's anodyne, camphor, whisky, or brandy, and their effect is hastened by being taken in hot water. Elixir of valerianate of ammonia in teaspoonful doses is a particularly eligible preparation, and admirably meets the indications when rapid stimulation is required. Any one of these remedies may be administered directly following the nitroglycerin and will sometimes obviate the necessity for morphine, a consideration of some importance in elderly individuals who, as well known, are sometimes peculiarly sensitive to this drug.
In nocturnal attacks, which are apt to be severe and prolonged, it is often well to supplement the action of medicinal agents by the api)lication of hot bottles to the extremities or by heat to the pra^conliuin, the ei)igastriuni, or between the shoulders. There is no indication during an attack for the use of digitalis and strych- nine, for not only is their action too slow, but when arterial spasm is responsible for the paroxysm the former will do harm. Aco- nite and veratnim viride should never be employed at such a time.
During the intervals between attacks the daily life of the pa- tient should be so regulated as to minimize if ])ossible both the fre- quency and severity of his seizures. If the complaint has existed for some time the sufferer is likely to have learned by experience that moderation in the matter of exercise is absolutely indispensa- ble to imnninity from his attacks. Nevertheless it may be well to caution him against undue exposure during cold and inclement weather, or going about insufficiently clad, against carrying heavy hand baggage or parcels, against attempting to walk soon after a meal, hurrying to catch a train or street car, etc. He should be explicitly instructed to make use of surface transportation in pref-
ANGINA PECTORTS
^f>i
rcineo to elevatocl mails, wliieli have to Ik:* rcitelied liv tong fiighta of stairs, Biiiee tire incliniitiun to ha^aten iip die last few steps as the train is heard approaching is almost irresistible, and such a 8[)urt may precipitate an attack. Patients should ako be in- structed concerning the hannfiihiess of immoderate coitus, fits of passion, overeating, the Um free indulgence in tobacco and aleo* holic stimnlantSj of ^lecoming exoessivclj fatigued, etc.
The hands and feet should be kept wanidy covered, and it is often well for these patients to wear a chest-protector both front and back. Those who can afford to pass the inclement seasons in a warm, equable climate should be advised to do so, since they can there take outdoor exercise Avithout fear of eijcouuteriug cohi winds and of contracting attacks of bronehitiw.
Sufferers from coronary angina have habitually high and sus- tained arterial tension, and as it is sudden and unexpected aug- mentation of this tension wliieh often precipitates a paroxysm, it is essential that their blood-pressure be lowere<L This can usually be accomplished, in a measure at least, by revision of the dietary — that is, by the restriction, or in some instances by the exclusion, of meats and tlio substitution of a largely vegetable dietary.
Rumpf, of Hamburg, interdicts the use of foods rich in lime- salts, as eggs, milk, cheese, spinach, etc, Tlieoretically, such a restriction is called for when there is arteriosclerosis, but practi- cally, it will be found ditiicult to adequately nourish the patient if all foods rich in phosphates aa well as meats are excluded. Furthermore, a too restricted dietary grows monotonous and leads to anorexia and feeble digestion.
The principles laid down for the dietary of eases of myocar* dial degeneration are equally applicable to these patients, and therefore the reader is referred to that chapter for details. Should arterial tension be not sufficiently reduced by regulation of the diet, then attempts must be made to accomplish this in other ways. To this end appropriate doses of nitroglycerin may l>e given every two or three hours during the day, or moderate doses of an iodide salt, three times daily, may accomplish the result. That such is the effect of iodine internally is generally held, and yet Romlierg asserts that \hA\i clinical observation and experiment show this Dot to be the case. In some cases it may not be necessary to give mtroglycerin daily, but only on those days when the patient finds
662 DISEASES OF THE HEART
walking particularly difficult, or there is a raw easterly wind. I have known striking amelioration of the patient's condition follow regulation of the diet, together with the prolonged use of nitro- glycerin and iodide of soda. Men addicted to the use of tobacco should be informed of its baneful effects and advised to abandon the habit altogether. If this is not acceded to, then the matter may be compromised by the patient's being allowed to smoke only mild domestic cigars. This will sometimes affect a cure of the tobacco habit in those who have been accustomed to choice Jlavanas.
In cases that have begun to manifest cardiac insufficiency or in which abnormally high blood-pressure threatens to soon over- power the heart, attempts must be made to restore cardiac strength or at least to stay its further decline. To this end recourse may be had to the usual heart-tonics. Strophanthus appears to me prefer- able to digitalis by reason of its inferior constricting effect on the arterioles, a virtue of the drug to which Frazer originally directed attention. If digitalis is selected, then its vaso-constrictor effect must be offset by the iodides or nitroglycerin. Strychnine and arsenious acid are also of benefit, and the former may be continued in moderate doses for many months. Strychnine is generally be- lieved to raise pulse-tension, but this action is slight and not to be weighed in the balance as against its value as a heart-tonic.
The one method of treatment that is particularly adapted to this class of patients at this time are the so-called resistance exer- cises, and very favourable results have been reported from their employment in angina pectoris. Theoretical considerations, and indeed actual experience, indicate that benefit is also likely to fol- low the careful use of the saline baths with artificial as well as natural waters. Xcvertheless, the lady whcse case has been so often cited in these pages experienced her first severe paroxysm of angina pectoris shortly after her first bath at Bad Nauheim upon having been wheeled to her hotel, and then . attempting to walk slowly from her wheel-chair to the elevator on her way to her apartments. Subsequent baths, however, were not followed by a similar distressful effect. Details concerning this mode of treat- ment are found elsewhere. (See chapter on Treatment of Valvu- lar Disease in General.)
CHAPTER XXVI
SYPHILIS OF THE MYOCARDIUM — NEW GROWTHS IN THE MYOCARDiUM-ATROPHY OF THE HEART —SEGMENTATION AND FRAGMENTATION OF THE MYOCARDIUM
I. SYPHILIS OF THE MYOCARDIUM
Morbid Anatomy. — The mast common myocardial niani- festiitioii of syphiiitic infection consists in fatty degeneration of the cardiac muscle. This ia not different in any way from fatty degeneration from other causes, and so is not recognisable except in thv jtre.sence of other evidences of the disease. Associated with the arteriosclenK^is of syphilis is a diffuse interstitial myocarditis, which is also usually classed as a luetic lesion. It seems probable, however, that in many eases the induration is due to the presence of the arterial disease, rather than to the direct action of the syphilitic poison,
Gunuua of the heart is very rare, and especially so in the con- genital form of the affection. The part of the heart most com- monly affected is the wall of the left ventricle. The gnmmata appt ar as soft grayish masses surrounded by hyperplastic fibrous tissue, or if older, as dry caseous areas of a yellowish white colour. Very rarely a softening gimima may rupture into one of the cavi- ties of the henrt.
Etiology* — S^T^iliB attacks the myocardiimi only in the ter- tiary i>eriod of the disease, and after a lapse of five or ten years or longer following the initial sore. It is not confined to either sex, but appears to have been rather more frequently discovered in males. As regards age, it may be said to be more frequent at or after middle life, rarely in childhood for the reason that the dis- ease is generally acquired, not congenitaL
664 DISEASES OP THE HEART
SjrniptomB. — Not oiriy is heart-syphiHs a comparatively rare affection, having been for the first time detected by Ricord, but its clinical recognition is still less frequent than is its post-mortem discovery. This is due to the fact of its possessing no pathogno- monic features as yet recognised. Not only have patients, in whom this myocardial disease has been discovered after death, been known to exhibit no clinical evidence of heart-affection during life, but when symptoms were present they were found on analysis to differ in nowise from those displayed by persons suffering from other non-syphilitic forms of myocardial degeneration. Most ob- servers agree in this statement that the cardiac action is likely to be disordered. This is generally though not invariably acceler- ated, and some authors, as Semmola, lay great stress on arrhyth- mia and acceleration of the pulse. Another symptom that has been noted is an indescribable pra*cordial distress which may or may not amount to actual pain. Philips has called attention to angina-like pain as having been present in one or two cases ob- ser^-ed by him. This symptom was remarkably distressing on one occasion in a professional man, who subsequently died suddenly, and in whom Philips found syphilis of the myocardium at the autopsy. Cardiac dyspnoea has also been complained of by some patients, but there was nothing about the difficulty of breathing that was in anywise peculiar.
Upon examination of the patient there may or may not be evidence of specific infection, such as old scars on the skin or mucous membranes, glandular induration, gummata, etc., and the arterial system may or may not furnish evidence of sclerosis. Physical examination of the heart is not infrequently negative, while in some cases there are signs of cardiac disease. When these are ])resent, they are apt to be those of dilatation with feebleness or altered quality of the sounds. Murmurs are not present as a rule unless as an accidental complication or due to the dilatation — i. e., to relative insufficiency of the mitral valves, for example.
Diagnosis. — Unless there is a clear history of previous syphilitic infection the diagnosis of myocardial syphilis is not pos- sible with certainty. On the other hand, even with such a history, one is not always justified in making the diagnosis merely because an individual of middle age displays cardiac symptoms. They may be due to changes in the heart-muscle incident to his age and
SYPHILIS OF THE MYOCARDIUM
6B5
not at all to syphilis. Tf one cannot discover sypLilklos of one sort or another, he .shun hi ^ive the patient tlje henelit of the douht until the futility of iitl other modes of treatment has heen proved. Tho as.soeiation of symptoms and signs of mvfjeardial disease with a history and with clearly demonstrahle lesions of the specific in- feetir>n renders the existence of syphilis of the heart-wall very prohahle. If the cardiac manifestations occnr in an individual not yet fifty years of a<^e ttie supposition is greatly strengthened. Very often the diagnosis will have to Ix* deferred until the results of specific treatment have Ijeen ascertained. Except hy men of wide experience in this particular line of diseases the diagnosis of this cariliac affection must necessarily he a matter of guesswork in most instan(*es. The clinical ohscurity enveloping this affection is shown hy the relative frequency wulh wtiieh it is found at the auto[^sy as coui]>ared with its intra vitam recognition.
Prognosis, — This may Ik* said to be gooil provided the disease is rec^oguised in time to institute proper treatment. Tn undiag- nosed cases the prognosis is bad, since they are likely to terminate fatally. Death is apt to be sudden and unexjtected. I know of no statistics going to show how long may he the duration of the dis- ease, but it is proliahly a very chronic affection, having existed years, it may lx% before the coming on of cardiac symptoms. The rapidity with which death is likely to follow the development of symptoms is likewise a matter of individual difference depending on the extent vi the myocardial cliange, which is itself a matter we cannot obtain definite knowledge of during life. If tlie heart be extensively dilated, its action greatly disturbed, and the pa- tient's symptoms pronounced, the prognosis is grave, and even specific treatment is not likely to do more than effect a partial recovery.
Treatment. — This, it needs hardly be stated, is the employ- ment *if iodides, with or without mercurials, as the physician de- termines. Being a tertiary manifestation, reliance is to be placed chiefly on the iodides. Ordinarily other remedies of the class of cardiac tonics are not necessary. But here again the medical ad- viser must decide. Their eniplo^^nent is symptoraatiCj and digi- talis in conjnncti^m with the specific medication may be of service in cases in which the acrion of the heart is much deranged and the patient's distress from dyspna'a is considerable. What has
666 DISEASES OP TEE HEART
been said in other chapters on the hygienic management of heart patients applies equally to these, so long as cardiac power is de- ficient
II. NEW GROWTHS IN THE MYOCARDIUM
Under this head are included various tumours and parasites. They are rare, some of them as parasites being excessively so, and aside from gummata just considered possess interest for the pathologist rather than the clinician. They will therefore receive only brief mention in this work.
Tubercles of the myocardium may be encountered as miliary nodules scattered through the heart-muscle, or still more rarely as caseous masses. The affection may also be declared as an inter- stitial myocarditis, which, however, possesses no distinctive fea- tures.
Parasites and cysts in this situation are still more infrequent and usually fail to declare their presence by either subjective or objective sj-mptoms. Thus Knaggs, in the Lancet of 1896, vol. i, p. 29, narates the instance of a man who died suddenly, and had not previously manifested evidence of cardiac disease, yet in the wall of whose left ventricle a hydatid cyst was found at the necropsy.
Of other growths in the myocardium cancer is the most fre- quent, and yet this is absolutely very uncommon. Lipoma and fibroma have also been met with, but are still more rare. Ma- lignant tumours occur in either the primary or secondary fonn, but of the two the latter is much the more frequent. The rarity of the primary form may be judged of by Gibson's statement that in 21,954 autopsies mentioned by Koehler, Tanchon, and Willigk there wore only 21 instances of heart-cancer, while Petit found but 7 in the literature.
From Bodenheimer's analysis of 45 cases of secondary can- cer, also cited by Gibson, it appears that the growth occurs most often as multiple nodules scattered throughout the myocardium, since it was limited to the wall of the left ventricle but seven times, to that of the right ventricle three times, and to the right auricle twice. It may occur at any age, even in infancy, but most often after forty-five, and is more frequent in males.
The clinical manifestations of myocardial cancer are too in-
ATROPHY OF THE HEART
667
tlefinite atiJ iineertain to permit an intra-viiam diagnosis. The heart may be irregular and feeble m action, may furnish percus- sion evidence of diktat ion^ but in such findings there is nothing to distinguish these from ordinary cases of uxyocardial degen- eration.
The prognosis is unfavourable^ and yet for the most part life is destroyed in secondary cases by the original disease. In pri- mary heart-eancer the tenure of life will depend largely upon the seat and nature of the tumour.
Treatment is of course purely symptomatic, since if the ac- tion of the heart is disordered and the real cause of the disorder is unsuspected or not, physicians find themselves limited to the administration of heart-tonics,
IIL ATROPnY OF TlIE HEART
By atrophy of the heart is meant a diminution of the organ in weight and size. The condition may be partial or general. The former is exemplified in the smallness of the left ventricle been in extreuie mitral stenosis.
General atrophy may be the result of age, when it is spoken of as physiological, or tbe effect of disease— i. e., pathological. Congenital smaUness of the heart is sometimes designated as atrophy, but, as preferred by \^irehow, should be properly termed hypoplasia of the heart. It is usually associated with con- genital sniallness of the genitalia.
Morbid Anatomy. — The atrophied heart is of a broMmish red or yellHwish tN»lr>m% often firmer than normal, sometimes pre- senting a wrinkled appearance, owing to puckering of the epicar- dium (like a withered pear, Eichhorst), and beneath the micro- scope the individual mu8ele-fihres are seen to l>e diminished in size, their transverse striatron obscured and stained by a deposit of hrowm or yellow pigment near their nuclei. Adipose tissue is everywhere absent.
Etiology, — Various causes of general cardiac atrophy are enumerated, but those most often antl powerfully operative are conditions which induce marasmus — i. e., pulmonary phthisis, cancer, dialietes, and chronic suppuration, as from disease of a bone. Thus W, rhurch is said to have obtained from the body of a woman who died of slow starvation in consequence of pylorus
668 DISEASES OP THE HEART
obstruction by carcinoma a heart that weighed only 3^ ounces. Of 171 cases of phthisis analyzed by Quaiu the heart was atro- phied in 54.4 per cent, while Engel is reported to have found cardiac atrophy in about 25 per cent of males who died of the same wasting disease between the ages of twenty-eight and thirty. It may here be stated that, according to Wunderlich, a heart is to be regarded as atrophied if it weighs less than 200 grammes.
SjrniptomB. — The clinical manifestations of atrophy of the myocardium are obscured by those of the general complaint, but may be said to be such as always characterize cardiac inadequacy — i. e., rapidity and weakness of the pulse, feebleness of cardiac impulse and sounds, without, however, signs of venous stasis other than slight (rdema. As a matter of fact this oedema is due to mal- nutrition rather than to stasis.
DiAg^Osifl. — The diagnosis is likewise obscured by the signs of the primary disease. It rests on the determination by percus- sion, or better by the fluoroscope, of marked decrease in the size of the heart, together wuth evidence of prolonged and extreme emaciation.
Prognosis. — The prognosis is that of the general cachexia, and yet a wasted heart may become so feeble as to cause death.
Treatment. — The treatment is that of the primary disorder, since it can do but little good to administer heart-tonics.
IV. SEGMENTATION AND FRAGMENTATION OF THE MYOCARDIUM
The precise nature of this condition has boon, and still is, a matter of dispute. Opinion is still unsettled as regards its causa- tion, the time of its occurronce, whether prior to or during the death agony, and consequently on the question whether or not it possesses any practical clinical importance. Renaut first de- scribed it as a segmentation of the heart-muscle due to chemical and nutritional changes and assigned to it definite clinical fea- tures. ITis original view was that the muscle-fibres became broken up, segmented, in consequence of softening of the cement sub- stance holding the cells together. Various French and German writers, notably Przewoski and Klein and Browicz, confirmed Renaut's observations and indorsed his views. Others, chiefly von Recklinghausen and Tedeschi, discovered disintegration of
SEGMENTATION AND FRAGMENTATION OF TITK MYDCARDItlM 609
\hv ranlliir inust'Ic-filiri's, 1»iit doelaretl it was ilne h> ruphirc, I. e., fnigiiiOMtarioH of tla* rcll?^, wlii(*li oeriirrtMl during" tlie ileath itgouy in consequence of overstiimilatiuTi ami irregular eiaitrartions.
Ahhoiigli ttiey fuimd fragnientatioti in oflierwise normal hearts of indivulnak who luul died suddenly by viulenee or other- wise, still in the majority uf instances it was in liearts that showed chronic iihrous and fatty ehange, ur the fruginentation was discov- ereil in persons who had suffered from acute infections or lesions of the central nervous system. Indeed, Tedeschi found the condi- tion in 48 per cent of 236 cases of death from all sorts of causes. The statements of von Ivei'kliughausen caused Renaut to modify his views somewhat, and in lst)4, at the first French Congress for Internal iledicine, he described the process as due to swelling, " gigantisui " of tlie muscle-cells and alteration of the intercon- tractile plasma which render the cells brittle and disposed to fracture, while at the same tinje there is softening of the cement that leads to segmentation. Ken a lit still held, therefore, to his assertion that the process constitutes a distinct and recognisable clinical entity.
Since tliut time the subject has Iwen discussed by numerous observerSj chiefly in France and Germany. English and Ameri- can writers have had little or nothing to say on the subject, be- cause, it may be, of its being still sub judiei\ and as yet not be- lieved to possess practical value to the clinician. The only impor- tant contributions that have, so far as I know, appeared in this country at this present writing, are by Ludwig Ilcktotm and John Bruce Mat^Calluin. The former made a careful study of a large number of hearts from lower animals, l)otli .small and large, and from over 100 human beings that had died suddenly as a result of violence, or slowly or suddenly in eonse<pience of a great variety of acute and chronic affections, some of them eases of either in- dependent or secondary heart-disease. llektoen-s observations agreed with those of writers on the Continent aa respects the fre- quency with which dissociation of the heart-muscle occurs in both sexes, at all ages, in all sorts of acute infectious and chronic dis- eases without associated cardiac lesions and in hearts manifest* ing the ordinary myocardial degenerations, hypertrophy and atrophy.
Thus, of 11*0 cases of deaths from a great variety of causes
C70 DISEASES OF THE HEART
and iu both sexes, he found segmentation in 65.78 per cent, while in 10 instances of traumatic and usually instantaneous death the condition was present in all. Hektoen states that whenever s^- mentation was present to any extent there was also more or less fragmentation. It is his opinion that segmentation is due to a disproportion between the violence of fibrillar contractions and the cohesive strength of the cement substance, and thinks that in- travital alteration of the muscle-cells may predispose to cement- softening and consequent segmentation ; it is not impossible, there- fore, for excessive cardiac contractions during excitement, coitus, etc., to lead to sudden death through segmentation of the myocar- dium.
The symptoms attributed by Renaut to disintegration of the muscle-fibres are disordered action and feeble apex-impulse of the heart, some increase in the area of cardiac dulness, an uncertain systolic murmur, and it may be slight oedema. These are, how- ever, not at all peculiar to segmented hearts, but are observed iii hearts that have undergone other forms of degeneration. It is strange, therefore, that Renaut and his pupils should consider the process susceptible of clinical recognition. I shall not devote more space to its consideration, but allow the following sentences, taken from Hektoen's paper, to sum up the whole matter. " All the other authors regard general and focal segmentation as an acci- dental or secondary phenomenon occurring in the course of infections and intoxications in connection with the primary and secondary lesions of asystolic hearts, and with fatal traumatism. It constitutes an episode in the course of the principal affection. While it possesses an anatomical individuality, it is so common that it would be difficult to say in what disease it would surely be absent after, say, the twentieth year, and it would take a very long time to enumerate all the diseases in which it has been found present."
CHAPTER XXVII
PEDUNCULATED AND BALL-THROMBI OF THE
HEART
Among the tiinioiirs of the; hrart iiiav be iiicliiJed those rare fonnations which are found in the cardiac cavities and are in reatity thrombi. They differ from cardiac thrombosis (marantic) in tlie ehrnriieity of tlieir devclyjuneiit, tlie changes they undergo, and in their cHnieal history, since they do not give rise to emboli. Like vascidar thrombi, some of them undergo organization, and when attached to the inner surface of the heart-wall by a pediele are known as peduncitlnird fhrombi or true polypi of the heart.
Others, ealled hftH-fhrotuhi^ ]invp eitliei; become detached from their pedicle, or having l»een formed liy tlie deposition of sue- eessive layers of fibrin npon a primary nnelens, and unattached^ roll about free in the chamber wliere they are formed. Both varieties are exceedingly rarCj but of the two, balbtlirombi have Iteen mnch less frequently encountered.
At tlie Tieunion of Utissiini Physicians at St. Petersburg in 1898, in honour of Pirogoif, Pawh>wski re{)orted a case of true heart polypus that had come under his obser\'ati<)n. In this paper he stated that diligent resc»arch in the literature up to that date had enabled him to collect only 25 eases, including his own. Wil- liam Welch, however, in his admirable article on cardiac throm- bosis in Ailbutt's System of Medicine, states that he has found 8 others in the literature, making *].1 in all. Small as is this num- ber, that of hali'ihromhi is still less. Von Ziemssen, in the report of a case at the Vienna meeting of the German Congress for In- ternal Medicine in 1?^90, stated that he had been able to collect only 4 cases besides his own. His rcsr^arch for publislied cases had been superficiab however, for Welch mentinns 4 cases, with a reference to a fifth, that ha<l been reported in England prior even to von Recklinghausen's, which by German authors was consid-
071
672 DISEASES OF THE HEART
ered the earliest recorded. Since von Zienisson's there have been others reported, so that up to date there have been 20 published instances of ball-thrombi. Some of these I had myself discovered in the literature before I had the good fortune to peruse Welch's article. The others have been taken from Welch's list. The en- tire nimiber will be foimd at the close of this chapter.
Pedunculated thrombi may be found in any of the cardiac cavities excepting the right ventricle, although by far most fre- quently in the left auricle. Twenty-five were in this cavity, 4 in the right auricle, and a like number in the left ventricle. The point of attachment is various, although the interauricular sep- tum seems to be the most frequent seat of the polypi, near the foramen ovale. Of Pawlowski's list of cases, 12 arose from the sseptum, 6 being from the fossa ovalis. Two, including Paw- lowski's, were attached to the posterior wall of the left auricle, 2 within the appendix, and 1 to the mitral valve. In the other cases the precise point of attachment is not stated. In size and form the polypi differ, being likened to a pear, a small heart, a cone, a bullet, a walnut, and a hen's egg, the average comparison being to a walnut.
The pedicle is generally compact and strong, and in most cases the polyp is covered by a thin membrane thought to be an extension of the endocardium (Pawlowski). lie also states that, according to Wilkinson King, some lH)lypi could be injected through the coronary vessels, while in others this did not succeed. In some of the recorded eases the tumours contained calcareous deposits, others were cystic. In all instances of these heart- thrombi there is disease, usually narrowing, at the auriculo-ven- tricular orifice or some other condition, as dilatation, that has led to stagnation of the blood in the cardiac cavity containing the tumour. In Pawlowski's case there was mitral stenosis of an extreme degree.
Von Ziemssen states that hall-ihromhi are for the most part of the size of a walnut, spherical, snuK)th, with no rounded cor- ners, and showing no trace of a pedicle. In his case the mass was beautifully round and smooth, as if turned by machinery, and ex- hibited numerous indentations upon its surface. The thrond)U3 was firm, and upon being sliced into sections showed successive layers of fibrin-fornuition. In the centre was a small nuiss that
PEDLNCULATKD ANI> BALL-THliO^mi OF THP: II HART 6T3
Lad evident] V served as the basis upon which the tibrni hiiJ heen depuiiited. Running up thruugh the thronibus in radiating lines towards the circumference were delicate fibrous bands, which ter- minafed each in a depression on the surfftce, and appeared by their organization and contraction to have occasioned the super- ficial indentations. The mitral orifice was also greativ stt^uosed in von Ziemssen's case. It may be remarked in passing that in his paper von Zienissen alludes to his having had two other cases of jx^dunculated heart-thrombij but Pawlowski does not include them in his list, and I have not discovered where they were pub- lished.
In WfMvd's case the ball measured 1| inch in diameter, was of a dark-red colour, and made up of an outer wall | of an inch thick, composed of a large nnniber of fibrinous lamina and containing a mass of coagulated blood. The feature in this case, considered by Welch as unique, was that ** adherent to the wall ai the auri- cle, near the mitral valve, was a firm, oval thrombus on tlie free surface <>f which was a sujierficial concavity which formed a " kind uf socket for the loose ball to roll in.''
In one of Legg's cases, that of a woman brought into the hos- pital dead, two Icx^se balls were discovered in the left auricle. In Osier's second case Welch states that an ovoid thrombus, resem- bling in siice and shape a thick cliestnut, was fuund with its smaller end sticking in the moderately narrowed funnel-shaped mitral orifice, from which it was readily removed. ** At one pole of the thrombus was an irregular roughened spijt indicating a former attachment, probably to a thrombus in the appendix."
In ArnohTs case the biiU-thrombus was elastic, as if composed of fluid incased by a thin membrane. At one si>ot the surface was roughened and of a speckled apj:»ea ranee, as if at this point it had once been in contact with the wall, while close by w^as a short thread-like prolongation which might have served as its means of attachment. The endocardium of the auricle was smooth and of normal appearance. The appendix was filled by a throm- bus, broken dowTi at its centre, and attached by a ribbon-like ex- tremity to the internal aspect of the tip of the appendix. This mass projected into the cavity of the auricle. It is reasonable to infer, therefore, that these two thrombi were originally one^ a small fragnient having become detached and ultimately converted 4d
G71 DISEASES OF THE HEART
into the ball. The mitral orifice was the seat of obstructive disease.
In Redtenbacher's case there was a funnel-shaped mitral ori- fice and valve that barely admitted the tip of one finger. In the greatly dilated auricle were two thrombi, one a ball 3.6 centi- metres in diameter, round, and even in contour, of a brownish-red colour, and covered with fine fibrous threads, soft and elastic ; the other a long mass, which was attached inside the appendix by a pedicle, extended into the auricle.
From the very meagre description I have been able to find of Stange's case, it appears that a thrombus was found free in the interior of the left auricle, which thrombus was described as flat- tened (abgeplutteten). The mitral valves were slightly insuffi- cient, and there was evidence of old aortic valvular disease. It may be questioned, therefore, if this case can Ixi properly classi- fied with von Ziemssen's and the others, since they all showed more or less stenosis of the auriculo-ventricular ring, and von Ziemssen expressly states that in typical instances mitral narrowing is present.
Ewart and Rolleston have described a cardiac thrombus which was discovered at the necropsy in a forty-three-year-old female. It was hour-glass in form, attached to the lower back part of the foramen ovale, and projected through the mitral orifice into the cavity of the left ventricle, but without disense of the ring or valve. The clot was old at its centre, with fresh fibrin deposits on its surface. The patient had had some chest trouble, probably pleuro-pneumonia, in February, 1S1>G, and afterward a systolic ai)ex-murnuir with a snapping first sound ; subse(iuently a pre- systolic bruit devoloj)ed, and she died with symptoms of failing circulation from mitral disease.
This interesting case aj)pears to be unique, since the orifice was not narrowed.
Pathogenesis and Etiologfy. — Two th(H>ries arc offered to explain the formation of pedunculated hcari-ihromhi. One is that they are due to the coagulation of blood in the dilated cavity in consequence of the retardation of the stream incident to the obstruction at the auriculo-ventricular orifice. To this must also be added, according to von Recklinghausen's view of thrombosis in general, an eddying or whirling motion of the blood. These
PEDrNrULATED AND BALL-TIIROMIU OF THK 11 HART 075
tlirambt beeoiiic HttarLcMl to the wall, iiiid 8ulise<|uently imdorgo orgatiixaliQiL
The other explaiiiition is tlie one advanced by Bostroeiiu and nccepted by both Welch and Romberg as applicable to some of the cardiac polypi at least. This is that true heart-polypi are throm- hosed varices of small veins in the interaiiricular sieptum or result from haemorrhages into the sa-ptum. This view is based on Bos- troein's exaoiination of two snch polypi, one of which he showed to be a thrombosed varix, the other, wliieli tilled the right auricle, to be the result of Itsemorrliage into the wall. *' Therefore/' says Welch, '* it would ap]>ear that the nature of these formations is not always the same.*' It is this difference in the nature of heart* polypi which has led t«» the diversity of opinion concerning their origin.
BaU-thromhi are witliont doubt true heart-clots whieli mav have lieeu fonned l^y the clejiosition of successive layers of fibrin prol> ably upon a central nucleus or matrix. The question that does not appear to have been settled in respect to every reported case is whether they were formed as detache<l masses, or were originally parts of an attached eougulum, from which they had become broken off. Some of the balls have presented roughened s|K>t3 and tiny rudimentary pedicles, which seemed to make it reason- ably certain that they were once attached to thrombi discovered in the appendix. The smooth rounded form appears, as suggested by von Kecklinghausen, to have been caused by their rolling about in the blood-stream.
Neither sex is exempt, yet women are more frequently be- fallen tlian are males, probably for the reason that they furnish a larger contingent of examples of mitral stenosis. Polypi have been found in the young and the old» yet, singularly enough, Paw- lowski's list fails to comjirise any ease between the ages of twenty and thirty, a circumstance which he thinks may l>e utilized in arriving al: a diagnosis. As regards ball-thrombi, however, there are several eases which were observe*! in persons of an age falling in this third decade of life. Finally, there must be a constrictive valvular disease to lead to stasis and coagulation of the blood,
Ssnnptoms. — Whether the tumour is a pedunculated polypus or a ball-tbroiubus, tlie symptoms are such as characterize an ex- treme degree of circulatory embarrassment arising from stenosis
676 DISEASES OP THE HEART
of one or the other auriculo-ventricular orifice, generally the left The patients usually suffer much from dyspnoea, even while at rest, the difficulty often assuming a paroxysmal or asthmatic type. Cough is present in most instances, and cyanosis is a noticeable feature. There is severe congestion of all the viscera, scanty albu- minous urine, and opdema of the lower extremities, it may be of the serous cavities. The pulse may or may not be accelerated, but it is always strikingly small and feeble. Indeed, the scanty filling of the arterial system evinced by the pulse, and the exaggerated congestion in the veins, are features commented on by all observ- ers. The almost total obliteration of the pulse is far in excess of what is obser\'ed even in high grades of mitral stenosis. In rhythm the pulse is not peculiar, since it may be irregular, inter- mittent, or unchanged.
A very striking sjinptom, which von Ziemssen lays stress upon as having been present in all three of his cases, was gangrene of a circumscribed area on the foot, associated with oedema and a truly cadaveric coldness of the extremities: phenomena due, in his opin- ion, not to embolism, but to arterial thrombosis. This results from the very deficient filling of the aortic system and sluggish flow in the arteries of the lower extremities.
In Pawlowski's case the patient, a female aged forty-seven, a school-teacher, the fatal illness lasted five weeks, and was char- acterized by an intermittent pyrexia, which at first gave rise to the diagnosis of tyj)hoid. Great circulatory embarrassment and a mitral nninnur did not at first attract attention, and indeed were variable, particularly the presystolic murmur. At the au- topsy there was found in addition to the polypus and mitral ob- struction a sj)lenic tumour due to infarcts in its centre. These were broken down and purulent, and probably accounted for the septic fever.
One of Hertz's patients, a woman of thirty-nine, was admitted in a state of advanced cardiac feebleness and consequent circula- tory embarrassment, and in spite of treatment died at the end of forty-eight hours. Arnold's patient was a servant-girl of twenty- three who entered the hospital with all appearances of some bron- chial or pneumonic aflFection. A mitral lesion was discovered. Death took place four weeks after admission.
In Proust's case the patient was a man of fifty-eight who was
PEDCNCrLATED AND BALr^TIlUOMBI OF THE HEART »i77
ill fiv'e months with must distressing syiiiptninB of embarrassed circulation, hreathlGssness^ vertigo, tnild sweats, and absence of pulse that were thought to depend upon mitral disease and secon- dary failure of the right ventricle. Death was the resnlt of asphyxia. The necropsy disclose*! a pediuicnbited tlironduis in the right auricle ^3 inches in length and iittaclied to the sH'ptum.
It is thus seen that, however great may he the differences in the duration of the symptoms, these all evince a similarity in the manifestations of valvular obstnietion of an extreme degree.
As regards the physical signs, these nuiy he said to be those of a stenosis of an auricnlo-ventrietdar orifice, usually the left. It must be remarked, however, that the charRcteristic presystolic nmrnuir is not always present. Indeed, von Ziemssen states that after the thrombus has formed and begun to produce symptoms, the diastolic-presystolic murmur which previously existed may disappear. A very suggestive character of the munmir in such a case is its intermitteney, coming and going, audilde ui>on one examination and absent at an ot lien This must depend in some way upon the presence of the mass, at one time the flow heing sufficiently forcible to generate a bruit, at another too languid and small to produce sonorous vibrations.
Diagnosis. — This is obviously a matter of great difficulty if not of aetiuxl impossibility. So far as I can learn, an intra- vitam diagnosis has not been recorded. The existence of the thrombus must always be a matter of conjecture rather than cer- tainty. However, if in a case of apparent mitral disease, or indeed of cardiac feebleness from any other cause, the embar- rassment in the circulation be greater than seems accounted for by the lesion discovered, if localized gangrene of the foot r>ccurs in a case of mitral disease, and evidently not due to arteriosclero- sis or emboli sui, and lastly if a presystolic or other murmur comes and goes in an unaccountable fashion, one may entertain the sus- picion of a heart-thrombus. One cannot from these data diagnose it with certainty.
Von Ziemssen considers three conditions indispensable to an intra-viiam diagnosis of an autochthonous cardiac thrombus: (1) There must be the physical signs of a mitral stenosis, since this lesion was present in all the typical cases on record. The evidence of this valvular defect must have been found at a time prior to
678 DISEASES OF THE HEART
the formation of the thrombus, however, because the murmur characteristic of stenosis disappears after the symptoms of throm- bosis make their appearance. (2) Manifestations of an obstruc- tive lesion of the left heart are not only indispensable, but they must be present to a degree not seen in simple stenosis. These are orthopncra, cyanosis, coldness of the extremities, but, above all, extraordinary smallncss and feebleness of the arterial circulation as evinced by the pulse. (3) The circumscribed gangrene of the foot which was present in all of his and one of Hertz's cases. With regard to this symptom, however, Redtenbacher calls atten- tion to the fact of its absence in his case, although expressly stat- ing that had the patient's life been sufficiently prolonged he be- lieves it would have eventually resulted, such was the feeble- ness of the pulse.
Prognosis. — This is absolutely unfavourable, since the de- gree of obstruction to the circulation is incompatible with recov- ery of the patient or even with a tolerable existence after symp- toms have once declared themselves. The exact mode of death is a matter of discussion. Hertz thought the ball-thrombus acted as a ball-valve and occasioned a total arrest of circulation by being driven into the orifice by the blood-current. Von Recklinghausen showed this to be unlikely, owing to the anatomical character of the stenosed opening. This is apt to present not a fimnel-like cav- ity into which the ball might be pressed, but is a shallow depres- sion of a transversely elliptical form so smooth as to favour the mass being rolled oflF again after once resting against the greatly contracted mitral opening. It is this supposed action present in Osier's case which has led to the api>ellation of ** ball-valve " sometimes given to the condition. Death is likely to supervene, therefore, through strangulation or in consequence of cardiac or general asthenia, or through some of the immediate causes of dissolution, such as occur in severe valvular disease, or by reason of complications on the side of the lungs and general system. The fatal result is usually preceded bv a longer or shorter period of suflFering, and yet in llartell's case the j)atient, a farmer aged fifty-nine, ate breakfast apparently in usual health, went to the field to work, and was found dead three quarters of an hour later.
Treatment. — This is purely syni])tomatic. Xotliing can be done to remove the thrombus, even if its presence can be diagnos-
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680 DISEASES OP THE HEART
ticated. The associated valve-lesion will cause death eventually, and we can do no more than ameliorate the patient's distress. Indeed, we may deem ourselves fortunate if we can accomplish this.
Bibliography of Cases of Ball-Thrombi
Arnold. Beitriige zur pathologischen Anatomie und zur allgemeinen Patho-
logie, Jena, 1890. BosTROEM. Deutsches Archiv f Qr klin. Med., 1895, Iv, p. 219. EwART. Trans. Clin. Soc., London, 1896-'97, xxx, p. 190. IIartill. Brit. Med. Jour., May 22, 1888, p. 973. Hertz. Deutscrhes Archiv fQr klin. Med., Bd. xxxvii, S. 74. OsLER. Johns Ilopkins Hospital Reports, 1890, ii, p. 56. Montreal Med. Jonr.,
1897, XXV, p. 729. Pawlowski. Zcitsehrift fQr klin. Med., 1894, xxvi, p. 482. Proust. Compte rendu d. sc. mdd. ct de biologie, 1864, i, p. 41. Recklinghause.v, vo.v. Handbuch dcr aW^:. Path, des Krcislaufs u. d. Em&h-
rung, 1888, p. 131. Redtenbacher. Wien. klin. Woch., 1892, v, p. 689. RoLLESTOX. Lancet, 1897, vi, p. 1546
Stance. Arb. a. d. path. Inst, in Gottingen, Berlin, 1893, S. 232-234. Welch. Allbutt's System of Medicine. Wood. Edinburgh Med. and Surg. Jour., 1814, x, p. 50. ZiEMssEN, VON. Vortrag gehalten auf dem IX. Congresse fQr inneren Med. in
Wien. 1890. S. 281.
CHAPTER XXVIIT
DEXTROCARDIA
Tills term signifies a transposition of the heart into the right aide of the thorax. This condition may be congenital or acquired. Most congenital displacements of the heart occasionally met with possess interest chiefly for the patliologist. The organ may be situated in the cervical region, within the abdominal cavity or upon the exterior of the chest (ectopia cordis).
COKGENITAL DEXTROCARDIA
This form h the most frequent of all displacements and is of clinical as well as pathological interest, inasmuch as the physi- cian may he called on to determine whether the displacement is patliological or normal to the individxml concerned, and therefore devoid of danger. In most instances this uhnormal situation of the heart is associated with transposition of the other viscera, a condition which has received the name siins tiscerum inversus* That this is not invariahle has been noticed by Breschet.
The displaced heart occupies the same relative position on the right side as it does normally at the left, while the stomach and spleen are in the right and the liver in the left hypocliondrium. The position of the intestines is also reversed, so that the rectum lies in tlie right instead of in the left iliac fossa.
Symptoms, — Congenital di'.rtrocardiu wcasions no symp- toms unless it he associated with other cardiac anomalies, as some- times ia the ease. It is stated, however, that patients with this displacement of the heart are apt to develop pulmonary tubercu- losis. AprojK>s of this possihility I recall >he case of a Miss A., 'who applied to me for an examination because she had had her attention directed to the fact that her heart pulsated upon her right side^ and she desired to learn if it possessed any special im-
681
682 DISEASES OF THE HEART
portance. Examination showed the apex-shoek was in the fifth right interspace, about 1 inch inside the vertical nipple-line. Car- diac dnlness was of normal extent, and beginning a finger's breadth to the left of the sternum, reached nearly to the right mamillary line. The heart-sounds were of normal strength and clearness, and were situated at the right of the sternum. Per- cussion of the abdomen showed gastric tympany beneath the right costal arch and hepatic dulness in the left hypochondriimi. At that time the patient was in perfect health and gave no history of tuberculosis in the family. Yet before two years had elapsed she developed pulmonary tuberculosis, to which she succumbed about a year later.
DiagnosiB. — The detection of the dextrocardia depends upon the recognition of the cardiac impulse, dulness, and soimds to the right of the median line and their absence at the left. Its congeni- tal nature is shown by the transposition of the abdominal viscera, which can scarcely be a matter of difficulty of determination.
ACQUIRED DEXTROCARDIA
Morbid Anatomy. — This form of dextrocardia may be complete, the heart lying entirely within the right half of the thorax, or it may be partial, in which case the organ is situated mainly but not wholly to the right of the median line. As this transposition of the heart is a pathological condition, the other viscera remain in their customary position. The morbid anatom- ical appearances in these cases are found chiefly in the lungs and their investing membranes, since the heart is not necessarily the seat of any other disease than that incident to the torsion of its supports.
The organ is fixed at its base by the ^rroat vessels, and cannot become disj)lace(l in either direction without underiroing more or less rotation upon its long axis. In dextnx'ardia there must be twisting of the arteries and veins at its base, and hence authors have speculated on the direction in which the heart must turn to admit of displacement to the right. Sibson maintained that the heart rotates in such manner as to bring the hit ventricle to the front and the right chambers to the rear, while V(m Schroetter argued that the right ventricle turns towards the left so that the left ventricle recedes still further hito the background.
IlEXTROPARDlA
683
A moniPTit's reflect i cm will convinee one, however, that the direction in whidj the heart rotates is deteriiiined by the displace- ment and twisting of its supports or by the point of attachment of adhesions and the angh' io whirh tbev piilL In a paper on dex- tro<*ai*dia, contributed l>y me in 1S88, this question was fully dis- cussed, and I t lie re reporte<l 2 cases which pruv€*d conclusively that the hetirt nuiy rotate in either direction, so that both Sibson and von Schr(K*tter were right, (For details see Medical News, 1884-1888,)
The twisting and strain to which the aorta and pulmonary artery are snlijeeted may exert a detrimental effect on the heart Thus in the ease of a child which I reported the aorta was found constricted by the superior vena cava, which was stretched tightly across it, and the narrowing of the aorta thus occasioned had led to dilatation of the left ventricle. It is possible, therefore, for this abnormal and constrained position of the heart to lead to its hypertrophy and *lilatation mid to constriction as w^cll as stretch- ing of the large vessels at its base*
Etiology* — This is found in pathological processes that exert either pre ssure or traction ujion the heart. The former is brought about through tlie accirmulation in the left |deural cavity of air (pneumothorax) or of liquids (plcuritis with effusion and empy- ema). With the absorption or artificial removal of the exuda- tion the heart usually returns to its normal situation, but the formation of pleuritic adhesions and obliteration of the left pleural sac may serve to maintain the organ in its acquired loca- tion. The pressure exerted may be sufficient to push the heart entirely beyond tlie me<linn line, so that its apex strikes the cheat- wall outside the right mamilhtry line, and Walshe says this may take place within thirty-six hours. Ordinarily the organ is not greatly displaced, and tlie apex may come to He at any point betwet^n the midsternal line and the right nipple.
W^ien the heart is drawn over into the right side, it is through the traction exerted by pleurf^-perieardinl adhesions acting in con- junction with more or less cirrhosis of the right lung. This was the cause in all three of my cases* The primary cause may be a trauma, or tnberculosis of the lung may he the initial etiological factor. Whatever be the predisposing cause, the pleuritic adhe- sions undergo contraction slowly, and a considerable length of
681 DISEASES OF THE HEART
time must elapse before the dextrocardia is completed. In this class of cases, moreover, are seen the most extreme examples of cardiac transposition, the heart assimiing a nearly horizontal posi- tion in its new situation. It lies, of course, under these condi- tions, immediately beneath the anterior chest-wall and is uncov- ered by lung.
SymptomB. — These may consist of those phenomena ordi- narily associated with venous stasis — i. e., cyanosis, dyspnoea, fee- bleness and rapidity of the pulse, palpitation, and after a time anlema, scantiness of the urine, and other evidences of visceral congestion, or the clinical picture may be rather that of the pul- monary affection with or without symptoms of cardiac insuffi- ciency. The symptoms may be of a severe type throughout, but more frequently the course of the disease is protracted, and the sjTnptoms are mild, depending upon the nature of the associated pulmonary affection. In a word, there is nothing distinctive of the clinical history of these cases unless it be their chronicity.
DiagnosiB. — The detection of the fact of the dextrocardia can hardly be a matter of difficulty, particularly in cases in which it is associated with or dependent upon chronic disease of the right lung. When due to accumulation of air or liquid in the left pleu- ral cavity with compensatory emphysema of the right lung, the condition may escape the detection of the careless observer. It is conceivable also that an aneurysm pulsating low down and to the right of the sterniun, or a pulsating empyema between the ster- num and right nipple, might mislead the inexperienced or super- ficial examiner. The history of the ease and careful exploration of the chest ought, however, to protect against so gross an error.
Inspection and Palpation, — These disclose pulsation in the region of the right nipple and its absence in its usual situation.
Percussion, — This reveals an area of absolute and relative dulness to the right of the sterniun having the characteristic out- line of the heart, while a similar area of dulness is absent on the left. Unlike congenital cases, percussion discloses gastric tym- pany and hepatic dulness in their normal position.
AusciiJtatio7i, — This enables one to perceive that, instead of the heart-sounds being audible in their normal situation, they are heard at the right of the median line.
The physical signs, by which are recognised the pulmonary
DEXTROCARDIA
685
Iiseast»s that lirnig aWut an at*t|iiir€^cl tWxtnwanlia, do not need to be here stated.
If oceasionally eardiac iiiurniiirs are heard in tliia class of cases, it is not always easy to determine whether they are organic from valvnlar disease, or are aeeidental and due in some way to the aherations in the cardiae walls and large vessels ineident to the rotation of the organ. The history of cases of acquired dextro- cardia shows that accidental bruits are not imcummon. For the differentiation of the ninrnuirs one must rely on the rules that have been stated already in the introductory chapter.
Prognosis. — In most instances this may be said to be that of the lung eiaiditioUj and yet in a case of conijilete acquired dex- trocardia with presumably considerable torsion of the vessels, the condition is likely to shorten tlie prospect of the patient's life. Nevertheless, one of my patients %vas alive and in ordinary health fourteen years after my first examination. The prognosis in each case depends upon the evidence or not of cardiac feeble- ness and disordered circulation, all of wdiich signs have been suffi- ciently set forth in previous chapters.
Treatment <— This must be based on the indications of each case and the principles that apply to other forms of cardiac in- adequacy. It is needless to remark tluit nothing can be done for the relief of the dextrocardia in those instances in w^bich it is owing to traction from permanent disease within the right half of the thorax.
CHAPTER XXIX CONGENITAL DISEASES OF THE HEART
Some of these possess a pathological rather than a clinical in- terest, since they render extra-uterine existence impossible. For a detailed description of such the reader is referred to works on pathology. Congenital cardiac affections were the object of much interest and even of superstition in the early days of anatomic investigation. It is to Meckel, Bouillaud, Rokitansky, Dorsch, Peacock, Kussmaul, and Lobert that the profession is chiefly in- debted for a scientific elucidation of their various modes of de- velopment.
Morbid Anatomy. — Of the congenital defects of the heart that are the result of developmental errors, the most frequently found and at the same time the least imj^rtant clinically, is an increase in the number of cusps in the semilunar valves of the aorta or pulmonary artery. This condition is more frequent at the pulmonary than at the aortic o])(Miing. Four and even five segments have been found. The suj)ornumerary cusps are usu- ally smaller than the others, but the ring may be equally divided between the increased number of segments. The presence of a diminished number is of less frequent occurrence. Two cusps have then become united, leaving no trace of the line of union, or at best a very slight one. According to Osier, this condition is more common at the aortic orifice, but two of his twenty-one instances having occurred at the pulmonary. Osier further states that this defect is an important one, as the conjoined cusps are very apt to undergo sclerotic changes.
Stenosis of the pulmonary or aortic orifices may result from the more or less conij)lete fusion of all three cusps (Fig. 78), and this may even proceed to complete atresia. The fusion may be the result of fcetal endocarditis or developmental error. In the former case the valve presents much the same appearance as after 686
CONGENITAL DISEASES OF THE HEART
687
postnatal eiulocnrditis. Vegetations may cover the cusps, project irjto the ventriele, or till tlie sinuses of Valsalva, At other times, however, the iiiiitetl valves may, present no signs of endocarditis, heiijg (HMiihined to form a funnel, which may show signs of very slight sclerosis. 8temksis ur atresia of the auriculo-ventricular orifices is of inneh less frequent occurrence than of the arterial oi)ening8. In eitiier ease The congenital disease is more fre(]nent on the ri^ht side on accunnt of the more frequent location of frrtal endocarditis on that side. Pott says that for one congenital aortic defect ttiero are twenty-five ])ulmonary ami tricuspid.
Fid, 105,— I'BPWfilRATl iNTERrSNTKICITLAm S.«miM.
Pulmonary stenosis, already considered in a special chapter, is a by no means infrequent congenital anomaly. Aortic obstruction is far less frei|uently congenital. In either case if the obstruction
688 DISEASES OP THE HEART
arises earlier than the eighth week of foetal life, it leads to an imperfect formation of the interventricular swptum. This is due to the inequality of blood-pressure in the two ventricles occa- sioned by the stenosis, and the consequent passage of a stream of blood from one to the other through the still imperfect sseptum, with each systole of the ventricles. This stream prevents the union of the two fundaments of the sa»ptum, and in consequence, the imperfection is almost always situated at the pars membrana- ceay or point where the two embryonic fundaments fuse (Fig. 105). This is high up on the sa^ptum in the portion separating the two coni arteriosi.
If the obstruction be established later in embryonic life, the interventricular sa?ptum is usually found entire, but the inter- auricular saeptum is usually imperfect, and the ductus arteriosus open. The stenosis need not necessarily be located at the valve to produce these effects, since narrowing of the conus on either side, the so-called stenosis of the heart, acts in the same way. It is not always possible to say whether the imperfect closure of the sffptum preceded the obstruction of the pulmonary ostium or of the conus, or whether it followed the other lesion. In the light of KiissmauFs conclusions, that defects of development predisposes to endocarditis, the former hypothesis is not unlikely.
Patency of the foramen ovale results from any condition causing a considerable inequality in the blood-j)ressurQ in the two auricles at the time when it is normally closed. This may be due to stenosis of one or the other of the auriculo-ventricular orifices, or obstruction at either of the arterial opening may secondarily influence the blood-pressure in the aurirlos, and so cause persist- ence of the foramen. The condition is often combined with a de- fective interventricular six^ptum, or patent ductus arteriosus, for the reason that all these imperfections are due to the same cause. Patency of the foramen ovale, or rather an incomplete union of the valve with the ring, is by no means always to be considered a pathological condition. According to Romberg, such a condi- tion exists in at least half of all cases. This may not produce symptoms, however, as when the valvular flap is of sufficient size the pressure of the blood in the left auricle keeps it closed and prevents any interchange of blood.
The ductus arteriosus persists as a patulous vessel, when, at
CONGENITAL DISEASES OF THE HEART
689
the time it shmild iioniially be obliterated, the blood- pressure in the aorta and pulMniiiarv artery is so unequal that a curreut riovrs through the duetus from one to the other. Thus in a case of pul- monary stenotiiis develojiing early in fo'tal life, tlie eoutents of the right ventritde, experieneing dirtieiilty in parsing through the pul* monary oritice, enter the left chamber through tiie imperfect in- terventricular sieptuiu, and only ii diminished quantity of blood passes into the [nilnionary artery.
On the otlier handj the aorta re<?eires an increased amount of blfHid on aeoount of the extra supply to the left ventricle from the right ebaniber through the imperfect steptum. Thus the ten- sion in the aorta is rendered higher than that in the pulmo- nary artery, and a portion of blood passes into the latter vessel through the duetus Botalli. The stream in the duetus, it is to be noted, is in this case flowing in a direction opposite to that normal in fu^tal life, which is from the pubnonary artery into the aorta.
Persistence of the ductus may depend on aortic as well as pulmonary defc^ct, and may l>e due to a congenital reduction of the calibre of the vesselj as in Fig, 107, The extreme case of atresia of either artery necessitates the patency of the duetus for the c:i Trying on of the circulation.
Etiology, — There has been nuich s]K*eulation upon the de- termining factors in the development of congenital affections of the heart. Foptal endocarditis is quite generally attributed to the agency of infectious diseases operating through the maternal circu- lation. It has not been at all clear what influences lead to the pro- duction of developmental anomalies. Some have sought to ac- count for these in tendency or inclination to perversion of growth impressed upon the germ by the parent, anfl hence regard such abnormalities as stigmata of degeneracy.* This liyjM>thesia is based largely on the fact that developmental defects of other parts of the body are not infrequently asswij^ted with cnngenital car- diac anomalies. Others, again, hold that these abnormalities, de-
• P, Simpson, in 4.2.12 mitniisios of the insitnt\ found fonest ration of the aortio Talvc^ 75 times; of the right seTuihinHr, 18; of the mitral, 6; fttul of the tricuspii], 2. It wta e«pecially frequeiit in men, Sufwrnumemry imrl nulimontaiy valves were found very often. It would l>e interestinjyr to know how these findings would compare with those from the same numtier of necropgies of the sane.
690 DISEASES OF THE HEART
velopmental as well as endocarditic, are the result of -pathc^nio agencies, the differences in result being determined by the period of fcptal life at which these agencies work. This conclusion ap- pears justified by the results of Fere's experiments.
This investigator found that if eggs in the stage of incubation were inoculated at a sufficiently early period with pathogenic or- ganisms or their toxins errors of development resulted. This is certainly a very satisfactory explanation, and is one that accords with our modern notions of the bacterial origin of most maladies, It is more reasonable also than the assumption that defects in the septa are secondary to an inflammatory process that was limited to the orifice affected, since, as pertinently suggested by Osier, it is difficult to understand how an inflammation could fail to attack the whole heart at a time when the foetus and heart are so diminutive.
The reason for the predominance of endocarditis in the right as compared with the left heart in utero is probably to be found in the greater blood-pressure within the right chambers. After birth has altered the course of the blood-stream by calling into use the vessels of the pulmonic system, blood-pressure becomes higher in the left heart, and this half now becomes relatively more liable to inflammatory processes.
Symptoms. — The disorders now under cousideration do not possess individuality as regards their clinical features. Patency of the foramen ovale even when ot considerable size does not nec- essarily preclude the possibility of lonp: life and may not give rise to symptoms. Duroziez, cited by Gibson, discovered such a condition in a woman who died of erysipelas at the age of sev- enty-six.
When not dependent u]Hm ])uIinonarv stenosis or other valvu- lar defect there may even be an absence of nnirmur or other ob- jective evidence of the ])atencv.
A def(»ct in the interventricular sii^ptum may also fail to manifest itself by subjective symptoms, and there may not be even cyanosis, which, as we shall see later on, is ordinarily one of the commonest and most significant features of congenital heart- disease.
Stenosis or atresia of the pulnumarv orifice or artery, on the other hand, rarely fails to occasion grave circulatory embarrass-
CONGENITAL DISEASES OF THE HEART 891
mentj and 'hence well-inarked subjective and objective symptoms. It is in this tlie most frequently recognised congenital affect ion, thereforCj especially when attended by sa^ptuni imperfections, that
Flo. 106. — ShOITB THB CYANOSift or CONOB?nTAL llSAKT DllXAeX. TIlS DRllf'i^TICK FlNOKV TlP«, THB BrLftFNO Pr^CORDIA, AlfD TH» Dlf«TI3mO!f Of THl AbDOVSN lA IT* Uri'**
ZoxB in 8 T«i Hepatic CoxciisTiojf.
patients complain of symptoms. It is worthy of note in this con- nection^ however, that my patient, whose case was narrated in the
693
DISEASES OF THE HEART
ctuipter on Pnhnfmary Stenosis, tleiiie<l Imving suffered any incon- venience from Im eardiac lesion, although this was pronounced, and indeed was not aware of its existence until infonned of it by niystdf. Even up to the last his symptoms were chiefly attributa- ble to the tuberculosis of the lungs, which was secondary to his valvular disease.
Children who are born with serious disorders of the heart evince notalile backwardness of development, both mental as well as bodily. Their intoUec^tual pnxx^sses are shi|L^gish, and they learn to talk at a later age than do normal childreiL In stature they are usually stunted, even dwarfish, and they are apt to pre- sent certain striking i>ccn]iarities iu ap|K'arance, Tlie nostrils and lips are thick and protruding, and tlie chest is more or less deformed in consequence of bulging of the pnecordia. There is marked clubbing of the fingers and toes with iucurvation of the nails, so that by German authors they are likened to drum-sticks ( Trommelsch laegt* r).
The most characteristic feature, however, in persons with con- genital cardiac affections is cyanosis. This fnorhus caruleus of old authors is a general but not uniform bhieness of the skin and mucous membranes, which is sometimes of so deep a hue as to be actually purple. It is most intense in those parts that are naturally red— the lips, nostrils, ears, cheeks, nails, elbows, and knees. It is always intensified by exertion and during the act of coughing.
The cyanosis and other viniblc circulatory effrvts of congenital cardiac disease is well exhibited in Fig, 106, which is the copy of a photograph taken of a nine-yeafn^ld girl whom, through the courtesy of Drs. Houston and Breid, I had the privilege of seeing at the Maurice Porter ITospital for rhildren. The little patient had been a hlae baby from birth, and was brought to the hnsj>ital on account of attacks of praM!ordial pain during which she moaned continuously and displayed signs of great cardiac feebleness. I saw her in one of these attacks and noted the following: ITniform bluish Inie of the surface, excepting the lips and ends of the lin- gers, whif*h were of a deep purple tint; pronounced emaciation of the extremities, with exquisitely bullnus terminal phalanges; pn> nounced prominence of the cardiac area and distention of the hepatic region as far as the umbilicus ; turgescence of the external
CONGENITAL DISEASES OP THE HEART
G&a
r
jugular?; rapid uml extremely thready pulse; epigastric pulsa- tion, but no uHlema,
Superficial cardiac dulness was greatly increased in all direc- tions, and deep'seated dulness was of a quadrangular outiine, rofiehing from the second Cf»6tal cartilage to the seventh in the median line, and from 2 inches outside of right stermil margin nearly to the left anterior axillary line. Its great breadth at its upper part over the auricles was esijecially noticeable. The heart- sounds^ were very feeble, and over the hodv of the heart was a scarcely audible yet ajiparently systolic murmur. When, however, ft hypodermic injection of f^. of a grain of morphine, given tr* re- lieve the patient's distress, had stimulated the heart and enalded it to partially empty its overdistended chambers* and the littb:* suf- ferer had grown quiet, the bruit came out loud and distinct It was then found to have its maximum intensity in the third left inter- space, close to the sternum, and to possess a very short presystolic portion.
From the great dilatation of the auricles^ the position and character of the nnirmur and evident signs of impeded venous cir- cu I at ion, it was thought likely that this was a case of patent fora- men ovale, or other sa'ptum defect, but whether or not with any other lesion could not be determined. The congenital nature of the defect was attested by tlie phis percentage of ho'inoglohin^ whi(di was 115 per cent, and the nunilier of red ceHs, which were in tlie neighbourhood of 7,000,000,
It is needless to remark that cyanosis is not limited only to congenital heart-lesions, since it is also present at times in ac- quired cardiac disease. In the latter cases, however, it is never so intense.
Many attempts have been made to explain the occurrence of cyanosis, but as yet none is generally accepted as quite satisfac- tory. It has been attributed to venous stasis and to deficient oxygenation of the blood, and apropos of this theory it is stated by Vierordt that JInritz found the COn increase to between 45 and 40 per cent. Komberg thinks the cyanosis may be attributed to the abnormal admixture of arterial and venous blood. The in- tensity of its hue is due to the dilatation of the capillaries (Vie- rordt), which takes place to a far greater extent than can he the case in those diseases in which stasis develops more rapidly.
694 DISEASES OP THE HEART
Striking as is the tint of the integument, there are certain other changes in the blood that are still more remarkable. Toe- niessen first announced that in cyanosis, examination of the blood shows an increase in its specific gravity and its corpuscular in- gredients, llis observations have been abundantly confirmed by numerous investigators. The specific gravity in a boy of ten vears was found bv Banholzer to be 1071.8, while the h»mo- globin was 100, the red cells 9,447,000. The white corpuscles have been rei>oate(lly ascertained to be as high as 16,000. In a case of congenital defect recently observed by me, haemoglobin was 115; total red cells per centimetre 7,120,000; total white cells per centimetre 10,400.
No theory to explain this peculiarity of the blood is gener- ally accepted. Malassez appears to have demonstrated that the bloo<l of the superficial parts contains a greater number of red cells than does that of the deeper parts, and accordingly Penzoldt concludes this cliflFerence is due to an evajwration of fluids at the surface. This theory of a thickening of the blood, which Rom- berg mentions as having been established by Krehl, is objected to by Gibson, and I think justly, on the ground that the volimie of the blood would have to be reduced at least a half in those cases in which the numl)er of red corpuscles is doubled.
It has also been claimed that this augmentation in the mmi- bor of coloured corpuscles is a coTn])ensatorv process on the part of nature in order thorebv to su])])ly more oxygen to the tissues, and also provide a more adequate means of having the COg re- moved. Gibson's hypothesis is so ingenious that it is here quoted at length. ** In venous stasis the corpuscles are insufficiently oxy- genat(Ml, they cannot thoroughly ])erforui their duties as oxygen carriers, and they eannot yield so much oxygen to the tissues. It must further be reinend>ered that in cyanosis tliere is less metabo- lism of the tissues, and theiefore less waste produced. In a word, the functions of the cor])uscles being lessened, the tear and wear which they undergo is reduced, and the duration of their indi- vidual existence increased. The nund)er of the corpuscles must in this way be pro])ortionately augmented, and this must lead to the numerical increase, as well as to the high percentage of Inemo- globin, until a balance is struck between the production and de- struction of the blood-corj)uscles.''
CONGENITAL DISEASES OF THE HEART
695
In contrast to tlie usual results of blood examinations in these cases Alouillt' is cited by Vierordt as Imviog fnuiid a reduciionf the red cells ranging between 3,500,000 and 4,500,000, yet this in no way invalidates the genera] proposition that the corpuscu- lar elements are increased in cyanosis. Finally, it should be stated that a similar though less striking increase is ohservable in cyanosis in acquired heart disorders.
Laennec and Rokifansky attributed to cyanosis a protective influence against the development of pulmonary tuberculosis. Their views are erroneous, however, since it is a well-known fact, as has been stated in the chapter on Pulmonary Stenosis, that ]>atients with this affeetioUj in which cyanosis is particularly apt to oeeur, are esjwcially prone to tuberculous disease of the lungs.
Another symptom in eases of cyanosis is coldness of the skin, particularly of the extremities, and hence these patients are re- nuirkably sensitive to eool atmospheres. They are also very sub- ject to dyspnoea and r*ften manifest pronounced shortness of breath on comparatively trifling exertion, as was present in my case; but this, as we have seen, is a symptom common to all forms of cardiac disease in the stage of defective com|)ensation. In these cases, when dyspnoE'a is a marked feature, there is usually evidence of considerable visceral stasis. In congenital cases, on the contrary, breathlcssness is not infrequently pronounced out of all proportion to the signs of engorgement in the various organs, aside from the capillary dilatation emphasized by Vierordt.
This hick of such venous stasis as would ordinarily I>e ex- pected in cardiac disorders of such evident gravity, is attributed by Romberg to the slow^ness with which the veins have been re- quired to accomnuHiate themselves to their abnormal burden (ueberlastiiHg). Nevertheless, the deficient arterial bkjod-supply and the sluggish return of venoais b1oo<l and the defective met ah* olism lead to disturbances of function on the part of the various viscera more or less severe and commensurate with heart-power. The variations in the pulse will be spoken of in connection with the physical signs now to be considered.
Physical Si^ns. — Inspecfion, — This is of special value only in the cases in which there are cyanosis, a dwarfish appear- ance, clubbing of the fingers, pra^cordial bulging, and other signs
696 DISEASES OP THE HEART
of a long-standing circulatory embarrassment. In such a case, moreover, there is usually the history that the patient " was a blue baby." Scrutiny of the cardiac area may detect displacement of the apex indicative of hypertrophy, but in all this there is noth- ing to attest the exact nature of the lesion. In not severe cases of congenital disease, as persistence of the ductus or patency of the foramen ovale, there may be nothing whatever in the patient^s aspect to suggest the existence of cardiac mischief.
Palpation, — Of the serious congenital defects which come to a clinical recognition stenosis of the pulmonary orifice or conus is by far the most frequent, and it is in this affection that palpation is of special value. This usually detects a systolic thrill in the second and third left intercostal spaces close to the sternum. This may be so soft and weak as to be scarcely perceptible, or so coarse and strong as to tickle the hand. In patency of the foramen, of the duct, or even of the interventricular septum, there may be no thrill unless associated with some obstructive lesion, as just men- tioned.
For the most part authors pay but little attention to the pulse, since it is thought to possess no distinctive characters. It should, however, be given particular study in cases of pulmonary steno- sis, since, according to Starck and Renvers, its volume assists in determining the question whether or not there is closure of the intervciitricMilar sa ptuni. Tf the sa*ptuin is perfect tlie supply of blood to the left heart is diminished, and hence the pulses of the upper extremities are small. When, on the contrary, communica- tion exists between the ventricles, a side channel is provided by which the left ventricle receives a large supply of blood, and hence the pulses are of greater volume. Consecpiently, if in a given case of pulnionarv constriction the pulse shows a degree of strength and volume out of proportion to what would be naturally expected, it suggests the likelihood of incom])lete closure of one or both of the septa.
Kolisko is reported to have stated that when ])ersistence of Botalli's duet (»xists secon<lary to atresia or great narrowing of the isthmus of the aorta or to congenital stenosis of its ostium, the pulses in the lower extremities are larger than those in the upper. This is <lue to the fact that the arteries given off from the aortic arch receive an abnormally small volume of blood, whereas a por-
CONGENITAL DISEASES OF THE HEART
69T
tion of the bkwxl jitmt up in tlie pulmonary artery and intended for tbe oscending aorta through the left ventricle is switched off through the patent duet ant! enters the descending aortii, thus supplying the lower extremities with a disproportionate share of hlood.
Percussion. — As in acquired heart-disease this means of in- vestigation should not he neglected, since it is of extreme impor- tnuee to discover possible mod iticat ions of cardiac dulness. In pnlmnnary ahstructiun the ahsulute and relative dulness are both increased to the right and dowTiward in consequence of tlie right- ventricle hypertrophy. In patent foramen ovale and a defective ventricular Sirptum the cardiac outline may or may not lie in- creased transversely, according to the severity of the lesion* Wlien the ventricular sivjttiim is ineomjdete the greater hkwd- pressure in the left ventricle forces a portion of the contents thrnugh into the cavity of the right ventricle. This ehamher he- comes surcharged, and tends therefore to hypertrophy ant! dilata- tion, which condition i^ shown by increase of cardiac dulness in tliat direction. Nevertheless, in both patency of the sa*ptnm and foramen unassociated with other lesions pnecordial diduess may in some cases remain normal.
Auscultation, — ^This usually furuislies the most valuable in- formation concerning the presence and nature of these congenital affections by the detect icm of a murmur. Yet in cases of sa?ptum defects, including of course tbe furauien, there may be no mur- mur of any kind. ^Vlien such a bruit exists, it is usually a loud systolic mnrmtir heard throughout the cardiac area, particularly over the base. It does not appear to he limited to any area, as are the murmurs of acquired valvular disease; and this fuct, when noted, possesses a certain amount of value.
RoJ^tTt Maguire thinks that the systolic- bruit of a defe^^tivo ventricular sa^ptum is most distinct over the situation of the inter- ventricular gi'oove, and decreases in intensity as the stethoscope recedes from this line in either direction. As, however, the only case he has reported, so far as I have been able to learn, has not yet come to a necropsy, the proof of his contention is wanting, and although the statement may appear plausible, it cannot yet be accepted u n resenT^dly .
Worcester has reported a case of patency of the foramen ovale^
698 DISEASES OP THE HEART
together with a small defect in the interventricular sseptum just below the right semilunar valves, which was discovered post mor- tem in a negro of fifty-seven who died of general paralysis. Sev- eral years before there was detected a long loud systolic murmur audible over the entire chest. The absence of symptoms during life is to be inferred from the fact that he served as a soldier during the civil war. The heart was found only moderately hyi)ertrophied. There is nothing, therefore, distinctive of the mur- mur of foramen or ventricular sa'ptum patency. Cabot speaks of the quality of the bruit as harsh and vibrant; but there is in this statement nothing at all distinctive. In the case of a boy recently seen by me there was a loud systolic murmur not trace- able to any particular ostium.
For a description of the murmur of pulmonary stenosis, as well as the other signs, the reader is referred to the chapter on that subject.
The auscultatory phenomena due to persistence of Botalli^s duct are best described in the narration of a case I had under observation for several years, and which finally came to necropsy. The patient was an undersized woman of twenty-one who suffered from breathlessness upon rapid walking and an uncomfortable pounding of the heart. Iler mother reported her as having been a small delicate babv, but as not having shown cyanosis even dur- ing fits of crying. Her only illness had been scarlatina at the age of nine. The radial ])ulses were small, regular, equal, and in rate between 00 and 100. There was no cyanosis or venous turgoscence. The prsvcordium was prominent, particularly at the left of the sternum, but was not pigeon-breasted. The apex-beat was in tlie sixth left intersj)ace, 2 inclies from the sternum, strong and diffused.
There was a soft, not very distinct thrill in the second and third left interspaces close to the sternum, wliich was not syn- chronous with either systole or diastole, but was most pronounced at the end of expiration and beginning of inspiration. It seemed to follow the a])ex-shock by a very brief instant, and to run into the long pause. Absolute cardiac dulness was but slightly in- cn^ased, whereas the relative appeared rather too broad. The heart-sounds were feeble and obscured by a loud harsh murmur that seemed to be systolic and audible throughout the entire pra>-
CONGENITAL DISEASES OP THE HEART
C99
cordia, but most plainly at the base, and was transmitted to the lower niigle of the left scapula*
Tpon closer observation it was perceived that at the site of the thrill the murmur became a continuous remitting roar, having
I ^^^
Flo, 107.— Hi ART moM CaHI ok r. «»!?, BHOWINO CoJCrKNTKI*- Hvt*XRTIloM(V Of LurT VkXTRlUUE AMI S.tl Nl» VA^tUti TMUolrtH PjlTkXT IlltH-. VRTRIil(J«tJa.
its maxinnim intensity just after the fir4?t sound and its minimum towards the end of the long silence, but never entirely ceasing.
700 DISEASES OP THE HEART
Everywhere the quality of the bruit seemed to be the same. The lungs, abdomen, and urine were negative, but the blood examina- tion showed a pronounced reduction in the percentage of haemo- globin.
The precise nature of this lesion was not clear, but was evi- dently congenital. In time, however, the affection was decided to be either patency of the foramen or of the ductus arteriosus. As conii)onsation appeared threatened, appropriate treatment was in- stituted, and soon a satisfactory degree of hypertrophy became re- established.
To make a long story short, this patient ultimately married and was delivered of a child, passing through both pregnancy and labour without special diflBculty. Unfortunately she became infected through the carelessness of her nurse, and died of seph tica?mia in the second week of her puerperium.
The necropsy was made by Dr. W. A. Evans, who found foci of suppuration in the right kidney and liver, but no evidence of inflammation in the cardiac structures. The specimen is pre- sented in Fig. 107. The left ventricle was concentrically hyper- trophied, its wall measuring 22 millimetres. The wall of the right ventricle measured 11 millimetres, and was therefore also thicker than normal. Both septa were complete and the foramen was not patent. All four sets of valves were healthy, but the aortic orifice was so small as to barely admit the index finger. This was found, however, to correspond in size to the lumen of the artery, which was abnormally narrow throughout. The circumference of the aortic ring was 48 millimetres; of the aorta, just central to branches, 45 millimetres; at opening of ductus, 43 millimetres; and (> centimetres beyond, 40 millimetres. Of ])nlmonary ring, 5.") millimetres; and of pulmonary artery, 55 millimetres.
Tli(^ ductus was patulous, and upon searching for the cause of this persistence it was found that, instead of the isthmus being constrictiMl, or the aortic arch smaller than the portion of the artery below the origin of the duct, it was as a matter of fact half a centimetre wider.
Tn this case the narrowing of the aorta below the origin of the duct, slight as it was, was yet sufficient to cause a portion of the blood-wave to he diverted into the duct and through it into the pidmonary artery, thus giving rise to the murnuir and thrill. The
CONGENITAL DISEASES OF THE HEART
roi
left-ventriole liypertropliy wns see*>iidary to tlie aortic narrowing. This wsm an int^tanee of chlorosis aurtica, and accminteJ for the fact that treatment had never been able to restore the haiuo- globin to its norniol percentage.
I have under observation at the present time two other pa- tients, one a woman, the other a young man, who present almost identical physical signs and who, I believe, are also instances of thi^ i^aine Cdiiirenita! anonialy.
Diagnosis. — As there are several affections embraced by the term Congenital Cardiac Affections, it would be wearisome and unnecessary to recapitulate the physical signs by which each may be diagnosticated, and lience the reader is referred to what 13 stated above under the caption of physieal sujus. It only nec^da to be here stated that the congenital natnre of the affection must be determined by the history and in some eases by a blood exami- nation. If there is a history of the individual having been '* a blue baby" or of his having been feeble from birth with evi- dence of circulatory embarraasment directly after birth, and if the chiM^s appearance corresponds more or less to that described under inspeetton^ there is strong likelihood of the cardiac dis- ease being congenital. In many instances the parents are able to state that the family doctor discovered signs of heart-disease as soon as ihe infant was born or in its earliest weeks of life.
If the person presents well-marked cyanosis, and if exami- nation of the blood discloses the changes previously described — i. e,, an increase of haemoglobin and red corpuscles over the nor- mal—the diagnosis of a congenital defect can Ik? positively made. In some cases, as of pulmonary stenosis, there may be nothing to prove conchisively during life whether the disease is congenital or acquired. In such a case, however, probabilities are always in favour of its prenatal origin, owing to the great rarity of the acquired form.
Finally, in doubtful cases of persistence of BotaUi's duct, it is stated that by means of the tluoroscope a positive diagnosis may be made.
Prognosis. — As stated in the symptomatology of persistence of the foramen, this abnormality may occasion no signs of its pres- ence, and patients may reach an advanced age, and die of some intercurrent affection. Unaasociated with an affection of the pul-
702 DISEASES OP THE HEART
monic or other orifice, a defective sseptum ventriculorura or a patu- lous ductus arteriosus may also in no wise affect the prospect of longevity. It is far otherwise, however, as regards pulmonary stenosis. Even when the patient does not succumb to the heart- lesion directly, he is most likely to develop tuberculosis of the lungs. In comparing the gravity of this with other forms of con- genital cardiac disease, excepting, of course, the uncomplicated sa^ptum anomalies just mentioned, Romberg states that up to the twelfth year of life affections of the pulmonary ostium and conus constitute three-fifths of all cases, whereas after the twelfth year, owing to the mortality of other lesions, these comprise four-fifths of the cases. Taking all forms of congenital cardiac defects to- gether, he cites Stoelker's figures, which, condensed, are as fol- lows: Out of 79 cases of all kinds, 24 died in the first six months of life, 42 had died before the end of the first yeiir, 56 before the tenth year, and 71 had died before the twentieth year of life was reached.
It should be remembered, moreover, that, according to Kuss- maul, congenital disorders of the heart predispose to endocarditis. In other respects the prognosis is influenced favourably or not by all those conditions of environment that have been fully consid- ered in previous chapters. Lastly, when compensation has once begim to fail in these cases there is small prospect of much being accoiiiplislied bv treatment.
Treatment. — As may be inferred from the preceding sen- tonec, this must be largely or wholly symptomatic — that is, in accordance with the indications of each case. The reader is re- ferred, therefore, to the discussion of tlie management of valvular diseases in general for tlie principle's of treatment.
SECTION IV CAEDIAC XEUEOSES
SYN.: FUNCTIONAL DISORDERS OF THE HEART
CHAPTER XXX
PALPITATION, TACHYCARDIA, CARDIAC PAIN, PSEUDO»ANGINA PECTORIS
Pathology. — There is a class of disorders which manifest fheiiiisclves cliiiieally hy a perverted aetitm of the heart, or hy pain and other sensations in the earJiac region, or by a conibina- tion of the two^ yet in which no structural alteration of the organ can be detected. They are < if ten isiioken of, itierefore, as func- tional disorders of the licart. Objection is made to this term on the ground that in organic cardiac diseaf*e there ia a disturbance of function, and, strictly speaking, such affections may also be des- ignated fiint'tional derangements. Furthermore, it cannot be affirmed absohitely that some as yet imdiseoverable alteration of the structure of the heart does not underlie or attend its perver- sion of fonetion. However logical sneh reasoning may be, the term functional has been sanctioned by usage, and is generally understotjd by the profession and the laity to mean an affection which is not associated with demonstrable structural lesion. For this %'ery reason it is often advisnblr in speaking to the patient or his friends to designate the disturbance as functional. A fear or an exaggerated notion of the gravity of the complaint may thus be allayed. Although from force of habit I frequently speak of these affections as funetiona), I yet prefer the designation cardiac neuroses, since one cannot obsen^e these cases without coming to the conclusion that the manifestations on the side of the heart are the expression of a disorder of the nervous system.
708
704 DISEASES OF THE HEART
One may be unable to detect any definite pathological lesion underlying this disturbance of the nervous mechanism, and yet it cannot be doubted that some neurosis is responsible for the cardiac symptoms. In some instances the disorder of the heart's ac- tion points to vagus influence, while in others the accelerator nerves of the heart are responsible for the manifestations. The exciting cause may or may not be discoverable, but an attentive study of the history and close analysis of the symptoms during and between attacks render no other conclusion tenable than that the cardiac and circulatory phenomena are secondary and sub- ordinate to some disturbance of the nervous system, and hence outside the cardio-vascular apparatus.
It would no doubt be more in accord with the pathology of these cases to relegate these so-called cardiac neuroses to the do- main of neurology, where they properly belong ; but the sjTnptoms calling attention to the heart are so often the dominant ones that they mislead the patient into the belief he has heart-disease. In- deed, the correct interpretation of the sensations is often puzzling to the physician, and hence it is customary to consider these cases in works of this kind.
Romberg classifies them as neurasthenic, hysterical, and reflex, in accordance with the nervous disorder underlying them. This would be well if all eases belonged strictly to these categories, or if the pathology of those neuroses was clearly understood. Such is not the case, and therefore I prefer to describe the various manifestations without attempting to divide them according to their apparent etiology into special groups.
Symptoms
Palpitation — This is a transient deran^rement of cardiac ac- tion characterized by an increase in both the frequency and force of its contractions. Witliout warning, the heart suddenly begins to boat in a more or loss disordered manner, and to give to the individual the sensation of a ])ounding or knocking against the ribs. Whatever may be the variations in rate and rhythm in in- dividual cases, it is this sul)joctivo oonsoimisnoss of the heart's action that constitutes the special characteristic of an attack of palpitation, and it appears to bo this feature which alarms the patient. The heart may be rapid, 120, 130, or more, or it may
FUNCTIONAL DISnKDEllS
705
remain below 100, but whatever its rate its action is violent. In the matter of rhvthni also there are differences. Ordinarily the pulse is regular, but it may be irregxilar in frequency and force, and may be even intermittent. When this is the ease the indi- vidual is likelv to be thrown into a 'state of great alarm.
Each time the heart intermits, it is announced by a sensa- tion of the organ suddenly falling or sinking in the chest; it is often described as a ^' sinking feeling," This is succeeded the next instant by a powerful throb, a sensation as if the heart gave a flop or jumped up into the throat, and with this very uncoui- fortahle feeling the patient is apt to make a sudden exclamation or outcrVj and perhaps quickly press the hand against the pnreor- dia, as if trying to grasp the refractory organ. The heart may then quiet down, or it may race off as madly as lK?fore. It appears to nie that in strictly neurotic persons w^ithout any discoverable organic mischief it is more common for the heart*s action at these times to be rapid and regular (tachycardia).
During the attack of palpitation there is often a violent throb- bing or pulsation in the arteries of the neck or in the abdominal aorta, or in both situations. The hand placed against the pne- cordium readily appreciates the energedc beating of the organ, and not infrequently the eye perceives a rapid rising and falling of the cardiac region. As it is bo often expressed by the friends, " you can see the heart beat through tlie clothes/' If the radial pulse is examined during such an attack or ** spell with the heart," to quote the popular phrase, it may be found full an<l quicky or if the rate be extremely rapid, small and feeble, Vaso-motor changes are also very apt to accompany the seizure. The face flushes or pales, as the case may be, and the hands and feet are usually cold.
One of the mo^t typical examples of palpitation was presented in a young nmn who consulted me only a few days ago. lie was twenty-two and an athlete of superb physique, standing 6 feet 2^ inches, weighing 200 pounds, nnd with muscles of steel, lie is an expert boxer, and can endure an arduous sparring-match with- out palpitation or j^hortness of breath. Two years ago he passed through an unusually severe typhoid fever, from which he made a good recovery with the single exception nf sudden attacks of rapid, violent beating of the heart, that almost invariably came on 46
706 DISEASES OF THE HEART
shortly after a meal. They were accompanied and followed by a feeling of exhaustion, and were, naturally enough, very alarming to both the patient and his family. The attacks were of frequent occurrence, sometimes daily. I examined the young man at that time and was unable to discover any indication whatever of car- diac disease.
The history of a recent severe typhoid fever made me con- sider the possibility either of an acute myocarditis during his ill- ness or of the myocardium having been seriously enfeebled in con- sequence of fatty degeneration, such as has been so well described by Quain. But the heart's dulnes3 and the heart-sounds were nor- mal, and inquiry elicited the statement that he was able to exer- cise, indeed had but just returned from a shooting trip in the mountains of Xorth Carolina, without experiencing any shortness of breath, vertigo, or palpitation. The pulse was rapid during mv examination, but its volume and force were excellent. I there- fore assured him that his attacks were of a functional nature and did not indicate heart-disease.
His flesh at that time was rather too flabby, and he said he had been gaining weight rapidly since his recovery from his fever. Minute inquiry into his habits, diet, etc., brought out the fact that he was eating enormously and altogether too much carbohydrates, and was in the habit of drinking a large amount of water with his meals. lie aeknowleilged some feelin*!: <>f l)eing bloated after eating. It was concluded, in the absence of other etiological fac- tors, that gastronomic errors were at the bottom of his complaint, and he was advised to cut out his sweets and starches, to limit his consumption of fluids at meals, to drink lithia water between meals, and to begin his former systematic exercise both in the gynmasium and out of doors.
This regime was faithfully carried out, with the result that his palpitations almost entirely disappeared. During the follow- ing two years he came to see me twice, once a few weeks after his initial visit, merely to report progress, and the second time to re- ceive an examination for life insurance, which on my recommen- dation was granted him.
This i)ast week, however, he came again with his father, who said he wantcnl to know how it conhl he that so robust a young man could still have his attacks of palpitation without there being
FtJXCTlONAL DISORDERS
707
*soiijeHiiii*]^ wron^ with liis lipart. lie tlien explained that the Sun- da j previous liis son was about to start for elmrch with his mother, when all at once he was discovered by his father lying on the floor and his heart beating so fast and hard that it could be seen through the clothes. The attack lasted abint twenty minutes.
The young man ihen spoke up and said lie did not see any use of being concerned about the affair, as he knew perfectly well what had brought the attack <»it. lit* had i^aten too hearty a breakfast, consisting of coflFee and tliree pieces of German coffee cake, besides fried chicken and fruit. An examination was then made, and a more normal heart I have never listened to. The pulse w^as steady, regular, and 80, standing. The apex-beat was in the nor- mal situation, absolute dnlness was not increased, and the rela- tive measured 3 inches to the left and 1 inch to the right of the sternum. The sounds were clear, of normal relative intensity, and entirely free from murmnrs of any kind.
It was without hesitation, therefore, that the opinion expressed two years previously was reiterated. It was not quite clear why the attacks shonld take place in so powerful and an apparently jMi^rfectly well young man, but there was certainly an etiological connection between the attacks and indiscretions in the way of a too liliera! allowance of curlxihyd rates. There was either a teni- porarv alieyance of vagns eontrfd or a stimulation of the acc€*ler- ator nerves of the heart. Whctlupr this was an instance of reflex irritation or of some toxic influence resulting from indigestion, was not at all clear. But it would he ordinarily classified as a reflex cardiac neorosis.
Tn the foregoing case precordial pain or other sensations of an allied uattire were never cotnplaiued of. It is quite common for an attack of palpitation to Im? accoiujianied by a painful sen- sation in the regi*in of the heart or for the exaggerated cardiac action to follow the pain. At other times the patient may com- plain of the heart's pulsations as painful. In still other cases the chief complaint is of an indescribable feeling of distress or dis- couifort *' at tlie heart/' which is usually but not invariably at- tended or succeeded by yvalpitation. Such symptoms are frequent in indiviiluals who are hysterical. This class of cases is well iilustraU'd by the following example:
A physician, aged twenty- four, height G feet 1 inch, weight
708 DISEASES OP THE HEART
156 pounds, gave a history of " heart-weakness " for a year. His parents, brothers, and sisters were all living and in good health and free from neurotic tendency, so far as the patient knew. With exception of measles in childhood he had never been ill, and he denied venereal disease or sexual excess, and did not uso tobacco, alcohol, or narcotics.
During the summer of 1899 he had been particularly hard worked in his profession, and compelled to lose much sleep. In November he suddenly developed attacks of pain in the region of the heart that were speedily followed by accelerated forcible beat- ing of the organ. It seemed to him that every throb of the heart produced pain just below the left nipple. These attacks were pre- cipitated by exertion, such as walking, or even a long drive into the country. After they had endured for about ten days he be- came so bad that he used to faint away during his attacks, and he remained unconscious for an hour or more in spite of efforts to revive him.
This statement made me suspicious that the so-called syncope was not in reality a true fainting fit, and he was asked if he be- came absolutely insensible to his surroundings, or whether or not he knew in a dim way what was being done to him. He then replied that he believed he was vaguely conscious of his surround- ings at those times.
These attacks recurred for about four months, and were finally cured by the taking of | of a grain of codeine 4 times daily dur- ing three weeks. The drug then had to be discontinued because of the obstinate constipation it occasioned. During those four months he was much troubled by insonmia. Since April, 1900, his condition had improved somewhat, but at the date of his ex- amination l)v nie, October, 1900, he was still unable to endure exertion because of the pal])itation it evoked.
The youn^ man was a blond, evidently highly nervous and not stron^r, since he lolled on the lounge in my office, as though too weak to sit up. II is hands were cold and moist, and his arm trem- bled while the pulse was being examined. This was full, tense, regular, and varied from 105 to 110. The apex-beat w^as in the fifth left interspace well inside the nipple, and the strong, rather broad shock was accompanied bv a coarse thrill. Absolute and relative cardiac dulness were normal, the latter measuring 3
FUNCTIONAL DISORDERS
709
inches to the left of the Bternal margin and 1 inch outside the right sternal border.
The first sound at the apex was partially obscured by a rough vibrant murmur of whizzing quality, which was loudest in the erect position, disappeared in the right lateral decubitus, and was scarcely audible when the patient lay on his left side. It was jnereosed in intensity at the end of deep inspiration and grew almost inaudible at the close of expiration- The second pulmonic sound was not accentuated.
The liver was not palpable and its dnlness did not pass below the inferior costal margin^ right nippledine. The abdomen was negative. The patient reported his urine as negative, containing neither allnimin nor sugar. He was not conscious of indigestion, and the bowels were not constipated.
The diagnosis was luado of a enrdiae neurosis with an acci- dental murmur and palpitation.
The patient was advised to spend the w^inter in the Sf>uth, where he could be in the open air, to take moderate, regular exer- cise, and endeavour to build up his nervous system^ and to school himself to regard his malady as not organic. In the way of medication he was advised to take strychnine, give up the use of digitalis and allied heart tonics. Up to the present writing I have had no further report from this case.
This patient illustrated another feature of hysterical patients with disordered heart action. He declared he was always con- scious of its pulsations, and could tell how it was beating without having to feel his pulse. To tost him in this matter I took hold of the wrist and counted the pulse, and then told him to count alotid his heart -heats. In this he iitrerly failed, and I became con- vinced that his sensations were imaginary. This is not always the case, however, for in some instances the cardiac action is suffi- ciently exaggerated to Ix^ perceived by the pa hen t. Sometimes, too, when the pulse-tension is high the individual can perceive pulsations in the extremities.
The powerful influence of the imagination and the readiness with which an attack of palpitation can be elicited by trivial causes are illustrated by the following case:
A law student, aged twT*nty-four, sought advice because of palpitations since the age of fourteen. Family history was nega-
710
BBSASES OF TEE HEART
tire, and the patient had not suffered from any acute disease that might have led to emkic*arditis or pericarditis, lie thought his troiihle with his heart dated from his study of physiology in school, when he obsen^ed tliat his puUe was too rapid.
At all events, from that time on he has lieen subject to fre- quent attacks of virulent, rapid beating of the heart, and has been told rei>eatedly that he had heart-disease. He is greatly fright- ened by his attacks, which often oome on without apparent cause or when fatigued by study, during unworrted exercise and excito- mentj or even too close application to his books. He is greatly troubled with flatulence, and this often sets the heart to palpi- tating. During an attack he is exhausted, alarmed, and notices particularly a violent beating in the stomach. Pollutions occur every two or three weeka^ and are followed next day by extreme weariness, nervousness, and liability to his palpitations.
Examination showed him to be a tall, slender man with thin chest and broad intercostal spaces. The abdomen was thin, rather scaphoid when in the dorsal decubitus^ and the abdominal aorta pulsated visibly. There was gurgling in the course of the trans- verse colon, but no dilatation of the stomach, and no d(*monstrable enteroptosis. The pulse was full, soft, rapid, and regular. The action of the heart was excited and abnormally forcible, and the cervicnl arrerics pulsated strongly.
The ajK'xd>eat was in the nonnal position, cardiac dulness was not increased, and the sounds were clear, hut trni ringing. Xo murmurs could Ix^ <letected. During the examination the patient bec»ame very nervous and exhibited a fine treniorj the hands being warm and moist.
There could be no doubt nf the nature of his fancied heart- disease, and he was emphatically assured that his trouble was a neurosis and that he need apprehend no danger from his attacks. It was concluded also that in this case there was a reflex element, iHid that the cause of his palpitations lay in such an excitability of the cardiac accelerator ner^ es that they were sensitive to con- ditions which would be wholly inadequate to arouse them in a normal individual Tlie chronicity of the affection made prog- nosis rather unfavoura!>le.
So much suffering was caused by the pollutions that the ure- thra was explored, resulting in the detection of nothing more than
FUNCTIONAL DISORDERS
711
hyperu'sthesia of its posterior portion. Lonal treatment, was in- stituted by the specialist to whom tlie patient was referred, but with no apijreeiable effect on his attacks of palpitation.
The following extremely instructive case exemplifies the as- sociation of a veritable phobia with a distinct hysterical element aiid a reflex irritation, or at all events an imaginary reflex irrita- tion :
The patient w^as a German- American, married, aged twenty- six, of medium height ami weight. She sought medical aid be- cause of " weakness, palpitation, and sinking spells/' Her fam- ily history was negative, excepting that her mother and sisters were nervous. The patient was doubtful concerning her having had the ordinary diseases of childhood, but denied rheumatism or other illness of an acute or infectious nature. Said she bad bad stomach trouble and been nervous all her life, and at ten years of age bad heart-trouble that came from ber stonmeh and persisted about a year. From that attack she recovered without treatment, and she remained w*ell with exception of nervousness until two or three years before marriage, at which time she had some nervous trmible that lasted a year and a hall
During her pregnancy she suffered much with her heart and stomach. The confinement was ditfieult, necessitating the admin- istration of chloroform and delivery with forceps. She thougbt the chloroform weakened her heart very much, and she was not strong enough to nurse her baby. That was two and a half years ago, and ever since she has bc*en a nervous wreck.
She has *' heart attacks '' from exercise, excitement » and after eating. These have been much w^orae the last four months in spite of treatment, and last week came as often as twice a day. Excitement, as from anger or domestic wTangles, which nnfortii- nately are too frequent, at once give her a sinking spell, and she lies exhausted for hours, her heart beating very rapidly at such times, occasionally as much as 160 a minute, in this resjx^ct re- sendding paroxysmal tachycardia. At times the taking of some article of food or a remedy which disagrees with her stomach will instantly produce palpitation with extreme exhaustion* At these times she is alarmed, Imt is speedily quieted and her pulse slows dnwn upon the arrival uf a physician. She thinks she has been relieved a little by strophanthus, and has very strong notions re-
712 DISEASES OF THE HEART
garding the effect on her of certain medicaments— €. g., dilute hydrochloric acid, which twice gave her a violent and prolonged attack of palpitation.
Her sjTnptoms are always more likely to occur about ten days before menstruation, but when the menses have become estab- lished, her heart is more quiet and she feels better. Attacks are also very apt to follow looseness of the bowels, and conversely are not so easily called forth when she is constipated. Ever since the birth of her child she has been subject to the appearance on her extremities of " spots that look just like bruises, are dark red, gradually grow yellowish and fade away." Of late she has eaten only beef and wine, because anj'thing else produced gas on the stomach and the attacks of palpitation and sinking spells.
She notices some shortness of breath on fast walking and as- cending stairs; has appetite, and could eat if her stomach would let her, and after eating her stomach feels heavy. The bowel movements arc irregular, but menses are regular, lasting two days. Her sleep is disturbed by palpitation, and she nearly always feels dizzy. During the rapid heart's action she notices pulsation in the carotids and in the stomach, and she has a feeling as if her lungs filled up with blood, her face, feet, and hands are cold, and she feels also as if she could not breathe.
The attacks persist from half an hour to several hours, and are not followed by a flow of copious pale urine. In a word, there is, exeeptin<j: severe pain, scarcely a sensation connected with the heart of which this highly neurotic and imaginative woman does not complain. It is apparent that she is only too glad and ready to talk and dilate upon her symptoms. She is sure she is going to die in one of her attacks.
Physical examination showed pulse 100, small, regular, but not of noticeably low tension, and carotids tlirobl)ed slightly. A|x^x-beat was in fifth left interspace, 3| inches from midstemal line, and accompanied by a slight thrill, which disappeared in the recumbent posture, although the apex-shock became more defined. Relative cardiac dulness reached from 1 inch to right of sternum to 13^ inches to the left of that bone. The first sound was accom- pained by a faint, short, high-pitched systolic whifl^, which was of limited transmission upward and to right and was slightly louder at end of inspiration — and both pulmonic and aortic second
FUNCTIONAL DISORDERS
'V\
sounds seemed aoeentuated. In the standing position the abdomen bulged relatively too ranch below and was too flat above the iiui- bilieus. The right kidney descended to a little below the costal arch, but eould not be grasped. The liver could not be made out ii-s having dropped downward. Gastric tTOipany reached 3 inches below and 1 inch too fur to right of tlie umbilicus, and there was splashing. The abdominal aorta pulsated with abnormal force, but could not be distinctly palpated. The abdominal viscera evidently dragged somewhat upon their supports, and gas- troptosis was undoubtedly present. The pelvic organs were nega- tive. The lungs were negative, and there was no oedema about the ankles.
A week subsequently, after having been limited to two meals a day J and having enjoyed a week of inmiimity from her attacks, her hearths action was found slow but somewhat irregular in fre- quency. The apex-thrill previously noted was discovered to be a sliort but very distinct presystolic one, and the first sound was unmistakably thumping. Tpon the patient assuming the recum- bent posture the second sound, exactly at the seat of apex, was doubled and a low-pitched short murmur acconipanied the first sound. I was therefore forced to concluJe that this patient had mitral stenosis. Nevertheless, her symptoms were those of a car- diac neurosis rather than of an organic lesion.
She was sent to a well-known neurologist, who reported that, although distinct hysterical stigmata were not disco%'erable, he yet be]ie%'ed there was an hysterical element in the case. In addi- tion, T could not rid myself of the belirf that the condition of the stomacli and bowels hud much tu do with the production of her attacks. At one time they would follow an indigestible meal or a relaxation of the bowels sufficient to merit the term of diarrhrra, at another some emotional disturbance, as a quarrel with her hus- band or an ungrafifierl sexual desire — in short, a considerable variety of disturbing causes.
This case gave me endless trouble and perplexity, until at last, acting on a hint furnished by her statements concerning the etiological intluence of diarrh'Ta, I prescribed a combination of astringents which kept her bowel somewhat constipated. She then became more and more free from her fearful attacks, and with in creasing freedom from tliem regained a measure of confidence, so
714 DISEASES OF THE HEART
that at the present writing, 1901, I have not seen her for nearly two months.
August, 1902, hearVB actum being quiet, there was entire dbeenee of eardiae murmur%, and the organ ttas to all appearances free from disease. The presystolic murm'ir and doubling of second sound above noted must therefore hate been ofacd- dental origin and in some way due to the disturbed cardiac rhythm,
A clergyman's widow, German, consulted me because she was sure something was wrong with her heart, and she feared she was suffering from the disease her husband died of. This was Graves's disease, the man having been frequently seen by me during his life and final illness. For two years after his death she remained in her usual health, but about a year ago she began to suffer from " spells with her heart," which were brought on by excitement, and sometimes, she thought, by the taking of food that did not agree with her stomach, for with the eructation of gas the palpi- tation began. At still other times the attacks came on without any apparent cause.
The action of the heart was likened to " rope jumping." She feels a " clutch at the heart," then her heart begins, and the next moment she is " entirely gone," the face being " deathly pale and the hands cold as ice." Nothing relieves her so quickly as a little brandy. Last week she had two attacks. She said she often noticed a gurgling in the loft side of her abdomen, and this gave her nincli uneasiness. Iler appetite was ])<>or, and she was in the habit of drinking eoffee four or five times a day. She was con- stipated, but her menses were regular. Her account of her com- plaint was not that of a neurasthenic, and there was nothing in her symptoms or ap|K'aranee to suggest that she belonged to that class of sufferers. Neither was there any history of neurotic dis- turbances in her family.
She was thirty years ()f age, rather spare, and of medium height. There was no throbbing of the earotids, no tremor, no pers])irations, no enlargement of the thyroid — in short, no indica- tion of Graves's disease. The ])nlse was IM), e(]nal, regular, and of fair tension. The apex-beat was in the normal situation, cardiac dulness was normal, and the heart -sounds were normal excepting, perhaps, that the first was rather too rinii^ing. There were no murmurs. The lungs were negative also. Within the abdomen was the interesting finding that accounted for her gurgling. The
FUX( TION A L DISOKDERS
T15
nlHlntiiinal walls wore relaxed, depemliiig baglike and bulging in tlie hypogastriiim, while the epigastric region was too flat. An indistinct 8phishing was elicited, and gastric tympany extended well down into the pelvis, l>nt not more than an inch to the right of the median line. It began at the level of the ninth instead of tlie .seventh cti.stal cartihage, and was too long vertieally in prfipor- Hon to its hiteral dimensions* The kidneys and other viscera could not l>e nmdc out m pndapsed. She looked anannia
Here, then, was an individual whose organs were apparently normal w'ith exception of the stomacli, which was prolapsed but not dilated. No other condition could he discovered to account for her palpitations, and accordingly she was told that the attacks WTTC probably dne to the gastric disorder, perhaps intensified by the undne use of coffee. She was emphatically assured that her attacks were not dangerous and was ordered to secure an abdom- inal snp[>orter, and fo adjust her cloHiing as to avoid the dragging of her skirts upiin the abdominal parietes and pressure upon her stomach.
Slie was given tincture of mix vomica l>efore and dilute hydro- chloric acid in essence of pepsin after meals. For the attack of palpitation with pallor of face and ctddiiess of the ext remit ies she was given tablets of Tutioglycerin. Coffee was forbidden, and in- structions were given regarding a simple and nourishing diet. At present writing th<^ symptoms still persist, hut are less severe.
Tachycardia. — 'Yhv jdiysician is freqnently called on to treat cases of habitually rapid heart's action^ which are so annoying to the patient by reason f»f his snbfective c«>nscionsness of the same that they may be said to be a jx^rsistcnt [jaljiitation. In many in- stances this is the exaggerated cardiac action of frraves's disease^ yet it is so iirominent a symptom that it brings the patient to the doctor in the belief that the heart is the real seat of the trouble. .\s exojihtbahnic goitre is a disorder of the nervous system instead of the luart, it will nf>t receive special consideration in this work. Tltere is another class of cases, however, wtiieh likewise present taebyeardia and attacks of palpitation as their main symptoms, and which because semietiines associated with thyroid enlargement wonld seem to be incomplete forms of Graves's disease. The indi- viduals arc highly nervous, easily agitated^ manifest more or lesa tremor, and in some instances have a warm unduly perspiring
716 DISEASES OP THE HEART
skin. They do not show exophthalmos, and if goitre is not pres- ent, it is often exceedingly difficult to say whether they belong to the category of exophthalmic goitre or not. Most, if not all, the cases I have seen have been in women, who, as a rule, are below the age of forty.
T have frequently discovered enteroptosis in these persons, and I am not able to escape the conviction that there is some intimate etiological connection between this condition and that of the nerv- ous svstem. In some there has been evidence of moderate cardiac hypertrophy and in others, not.
This form of cardiac neurosis, as it may not inaptly be termed, was well illustrated by the case of a married woman of twenty- seven who came for treatment on account of symptoms that made her fear heart-disease. One sister had died of pulmonary tuber- culosis at the age of twenty-four, and I may say, in passing, that in my cases I have been struck by the frequency with which a history of consumption in some near relative has been obtained. The patient had not been in her previously good health since her last confinement, two and a half years before. Her home was in a remote suburb in a lonely situation, and as night approached and her husband did not return she regularly grew nervous and appre- hensive. She had lost weight, and for a considerable time had noticed that her heart beat too fast. Recently it had taken to giving a " flop," and everv time this occurred it threw her into a state of alarm and agitation. Her neck had grown full, but she had given this no attention in comparison with the action of her heart. She was a hearty feeder, and all her functions appeared to l)e normal. Physical examination showed pronounced enlarge- ment of the thyroid, which was firm and without thrill. There was no prominence of the eyeballs, but there was a fine tremor and the pulse was so rapid, in consequence of extreme nervous agi- tation, that no attempt was made to count it. Cardiac impulse Avas exaggerated, but the area of dnlness was not demonstrably increased, and the sounds were clear, ringing, and free from mur- murs. The lungs were negative and there was no enteroptosis. The case was regarded as one of incomplete exophthalmic goitre, and a guarded prognosis was expressed. The patient was assured that she had no heart-disease, and T observed that this assurance at once favourablv influenced the heart's action and nervousness.
FUNCTIONAL DiSQKDKRS
717
Tn conclusion^ it may be stated that iiiuler the prolonged use of iodine to the neck and intereal medication addressed to relief of symptoms and improvement of digestion and general health, this patient ultimately made a complete recovery, the thyroid becoming of normal size and the tachycardia disappearing en- tirely. There was evidently a neurosis in this case, as shown by the powerful domination of her emotions over the action of her heart. Wliether there was any direct connection lx*tween the thy- roid enlargement and the tachycardia and paljjjtations I am not able to say, but her nervousness certainly disappeared pari passu with the decrease in the size of the gland. Nevertheless, her pulse- rate was invariably influenced by the state of her digestion and elimination.
I recall another case of rapid and pounding cardiac action in a female who presented fine tremor of the extremities, but no other sig^ns of Graves's disease^ and who was ultimately found to be pregnant at the time. As she was positive that her symptoms had first attracted her notice after the cessation of her menses, and the heart's action quieted dowii somewhat as the pregnancy advanced, I have not been able to determine what the connec- tioUj if any, was between the two conditions. This patient was unmistakably neurotic, as shown by both her family and personal history. Whether such cases are instances of inei]nent or incom- plete Graves's ilisease or not, they are instances of cardiac neuro- sis so far as the action of the heart is concerned.
The foregoing cases present some of the symptomatology of heart-neuroses so graphically that it was thought Ijest to intro- duce them before considering the etiologyj although in so doing the general plan of this work is departed from. It is believed they will throw some light on the causation of some of tlie most common manifestatinns of functional cardiac disorders. As there is no demonstralde alteration in the structure of the refractory organ in typical cases, there is no morbid anatomy to be described. If a valvular lesion or dilatation of the heart is found in a person displaying the s\iuptoms of neurotic disturbance of cardiac ac- tion, a combination which is not at all infrequent, the anatomico- pathological changes on the part of the heart are not to be re- garded as dependent upon the neurosis. There may be an etiologi- cal connection in so far as the organic heart-lesion may, through
718 DISEASES OP THE HEART
its influence over nietabolism, aid in the development or the main- tenance of the neurosis and may help to explain the ease with which the heart's action is perturbed. It may also be claimed that the palpitation and tachycardia induce the dilatation; but in my experience these cases do not display permanent cardiac enlarge- ment to an extent that calls for treatment.
As previously stated, the pathology of palpitation is obscure. It is argued that it may be due to loss of vagus control, which allows the accelerator to gain the ascendency, or that there may be stimu- lation of this latter independent of an abeyance of the inhibitory apparatus. Again, it is not at all certain that there may not exist some histological change in the heart structures or nerve-centres which may account for the readiness with which the action of the heart becomes disturbed under conditions that are inoperable in the healthy individual. As Romberg says, arteriosclerosis some- times develops in neurasthenics at an unusually early period of life ; and who can say that there may not be some connection be- tween this fact and the cardiac manifestations ? These are mat- ters of speculation purely, and in the present state of our knowl- edge we must content ourselves with speculation and theory.
Cardiac Pain. — This is another exceedingly frequent symptom in neurotic patients who suflFer from fancied disease of the heart. It possesses no imiformity in intensity or diaracter, being in one case sharp and darting, in another dull and continuous. Its one feature, coninion to all, is its location in the heart-region, usually in close proximity to the left nipple. It is sometimes intensified or even evoked by exercise — e. g., sweei)ing, which calls into use the muscles of that portion of the chest. In some instances it seems to l>e influenced, in i)art at least, bv atniosi)lieric conditions. Very frequently this pain is associated with a feeling of anxiety or oppression in the prarordia, which, hocanso it occasions a vague feeling of ajiprehension, is by the (iennans called herz angst, or anxiety of the heart.
This sensation may be wholly independent of any demon- strable change in the heart action, hut is apt to be attended by palpitation, coldness of the hands and feet, and other indications of vaso-motor disturbance. As stated, it may accompany, but as a rule it seems to re])lace, actual ])ain. Whatever the exact char- acters of this pra'cordial feeling, it is very unlike, and is not to
FUNCTIONAL PtSOUDKHS
710
confounded with the [nunfvil seizures which are dosigimted iiiigiiia pectoris^ whetlier true or iahv. The differences are so iriiirked that no mistake ought to be nuide^ and yet it is possible f«o' the feeling ni eardiae anxiety to be mistaken for the constric* tion of the ehest j>res?eiit in grave angina and tlie feeling of appre- hension for the sense of iiiqx^nding death.
Fseudo-an^ina Pectoris*^ — ^From the standpoint of scientific ac- curacy this term may be and doubtless is objectionable, since there can be no sneh thing as a false chest jjain. Nevertheless, this term is sanctioned by the usage of the best writers in this country and Europe. It includes those prteeordial pains which closely re- semble attacks of coronary angina^ and are therefore spoken of by Osier as ** allied states/* The essential difference between them lies in the fact that psendoangina is independetit of structural disease of tlie heart or its nutrient vessels, and that it is not likely to cause sudden death.
In true angina there is some condition within the heart which initiates the stimulus sent to the nerve-centres. In the pseudo form the starting-point uf tlie jiainful attack is, aeeording to Hucliard, not the heart, but some jKn'ipheral (*r visceral nerve, most commouly one of the intereostals. The impulse thence passes to the medulla, and there, reaching the sensory centres, evokes a sensation of pain ihat radiates into the chest or down the arm with phenrjiiu»na that point to a coincident stimulatirm of the vaso- nit*ti»r antl vagus centres. Often it is some painful point on the chest, generally one in the region of the left nipple, which acts as the starting-place for an attack, Wliether such is the pathology of these cases or not, it certainly seems to me to afford a fairly satis- factory explanation of the essential difTerenee between the^e two forms of angina.
Writers recognise three great varieties of this neurotic form; the rellex, the vaso-motor, and the toxic. Of these, angina re- flectoria is the most common, although no one can observe these eases without coming to the conclusion that they an? all very apt to blend indistinguisliably with each other. Irritation w^ithin the abdoDiinal organs is thought to be the most common start ing-jx^int oi an attack of the reflex variety, and yet the vaso-motor form may Hkewii^e find its origin in some disturbance within the abdo men as well as in any ]>art of I he body, Ilucliard dwells much on
720 DISEASES OF THE IIBAKT
the toxic angina and finds its causation in toxic agencies intro- duced into the system from without, such as tobacco.
An attack of pseudo-angina pectoris is agonizing, and because it usually begins in the cardiac area it excites a feeling of fear or apprehension that is closely allied to a sense of imi)ending death. Ordinarily, however, the patient admits that this feeling is subor- dinate to that of pain. This latter radiates throughout the chest and into the left arm, which is apt to feel numb and cold. There is often a " clutching feeling at the heart," and the patient is apt to have a sensation as if she were " sinking away." At such times the pulse is said to become " very low," by which seems to be meant slow and weak. In cases of the vaso-motor type the face is pale and anxious, the extremities cold and clammy, and the pulse is small, usually slow, and often irregular or intermittent.
The sufferer from pseudo-angina is not compelled to assume an erect, motionless attitude, as in true angina, but lying on the bed or couch moves about restlessly and moans or cries aloud with pain. It is this feature of the attack on wliich reliance is chiefly placed in the determination of its real nature. Exceptionally, patients pass into a cataleptic state, apparently though not actu- ally unconscious, rigid, and it may be cold, presenting in this state an appearance which is very alarming to the friends, who think it presages speedy death. The attacks usually come on sud- denly and without warning, frequently at night, but in some in- stances there are prodromata, such as chilliness, restlessness, or vague nervous sensations. Some authors state that this neurotic form of angina displays a tendency to periodicity by recurring at the same hour on successive days.
The duration of the seizures is longer than that of true angina, lasting for one or more hours; their departure is apt to leave the patient weak and exhausted. They may abate gradually or suddenly or they may terminate in an attack of violent palpita- tion. Xunibness and helplessness of the arm into which the pain radiates are not infrequent sequels of a paroxysm. Patients are naturally terrified, not only by the seizure, but also by the pros- pect of its return. Its frequency of (>ccurrence is variable, but usually the intervals of freedom from ]>ain are not long. IIu- chard observed cases in which as many as 200 or 300 attacks were experienced in the course of a single year.
FUNCTIONAL DISORDERS
721
In pure angtJta reflecioria without vaso-motor phenomena irritation originutes in some distant part and the pain radiates thence into the cardiac area^ from which it spreads along the in- tercostal nerves and even into the left arm. There is nsnally an associated feeling of anxietj and constriction^ Init the neuralgic element is the more pronounced, lluehard cites a case^ not ob- served by himself, however, in which the paroxysms of pain origi- nated in the cicatrix of a woimd received many years before. This was situated at the hend of the elbow, and the attack of pain was precipitated by movements of the joint, by friction of the clothing, and even by gentle stroking of the scar. Squeezing of the middle finger was also capable of arousing a paroxysuiy and this fact together with their cure by acupuncture led him to con- chide there nmst have been an hysterical element in the case, lie also qnotes the instance of an officer who experienced an attack of pseudo-angina in conserjuence of painful irritation of his foot by one of his decorations, which had fallen into his Ixiot, and there remained during tlie day. In such an individual there must be a highly neurotic tendency. Osier narrates a single ease in which this form of angina followed attacks of vomiting, and there- fore appeared due to gastro-intestinal irritation. Such attacks have also been known to result from exposure to cold.
In the vaso-molor form the exciting cause may likewise be exposure to cold or even the washing of the hands in very cold water. In this gronp there are phenomena of widespread vaso- motor spasm as well as pain, as might be expected.
The strictly toxic form is exceedingly uncommon and presents considerable diversity as regards the severity of the attacks and the prominence of certain features. Pain is often suliordinate to a feeling of anxiety or priecordial oppressiun and there is dis- turlK'd cardiac rhythm in the way of retardation or acceleration, irregularity, and interrnittence of the pulse. In tobacco angina there may be vertigo, pallor, a contracted pulse, tendency to syn- cope, pra»cordial anxiety, coldness of the hands and feet, and cold perspirations. According to Iluchnrd, there may be other asso- ciated symptoms which are referable to nicotine intoxication, as dizziness, tinnitus anriiim, dysphagia, and cephalalgia, a sense of suffocation or dyspnma, general weakness, cerebral confusion, spinal tenderness, and disorders of vision. Although anginal
T9S
DISEASES OF THE HEART
attacks from tobacco may be iiicoiaplete in all their manifesta- tions, thoy are none the less severe, and may be of great intensity.
Utiologry* — Although the automatic action of the heart prob- ably depends ui>on some quality inherent in the cardiac musele- cells, and not upon the nerve tihiments or ganglia situated in the heart-walls, still there can be no doubt of the powerful influence of mental and nervous states upon cardiac action. The class of disorders now considered is generally thoug^ht independent of structural diseai^e of the hearty although pers^iUK with organic car- diac lesions may undoubtedly present some sjinptoms closely akin to those of the so-called cardiac neuroses.
The predisposing causes of the so-called functional or neurotic disturbances of cardiac action and of the various sensations refer- able to the heart are those disorders, neurasthenia, hysteria, etc., which for want of definite knowledge of their pathology are called neuroses. Psychoses, such as hypochondria, may also be attended by disturbance of cardiac action and other symptoms referable to the heart. Consequently in every case of cardiac neurosis the physician should endeavour to ascertain and expect to deal with some such underlying neurotic or psychical eleiiient.
Heredity, age, and sex have an undoubted etiologie influence over functional disorders now considered. Most of these patients present a clear family history of neurones, and some of them have manifested unstable cardiac action from childlux>d, Tt is particn- larly in the female sex that the s^Tnptoms which have been de- scribed are encountered, and yet some of the most pronounced cases are seen in young men. Women appea especially prone to these symptoms during the child-bearing period and at the meno- pause. Their attacks of palpitation, heart-pain, or what not, are very apt to be evoked during the days immediately preceding menstruation. This is not because of any direct etiologie connec- tion between the two, but simply because at this time, as at the climacteric, the nervous system is more than usually unstable. Whatever serves to lower nerve tone, or otherwise deteriorate the general health, predisposes to cardiac neuroses, and therefore mas- turbation, excessive venery, loss of sleep, sorrow, worry, too close confinement to mental pursuits, are all predisposing factors.
The influences which act as exciting causes are too numerous and various and often too obscure to warrant the attempt to enu-
I
FUNCTIONAL DISORDERS
W8
merate them in detail. Patients are very apt to speak of having a " nervous shock," by which may be meant some sudden start or fright, an unexpected piece of bad news, and the like. In many instances the mere suggestion, whether subjective or made by an- other, that thoy have heart-diHease suffices to excite an attack of palpitation. This is particularly the ease with hysterical sub- jects, and I have known a word casually dropped, by being wrong- ly understood to apply to lumself, to throw- such a person into a violent rit of palpitation with coldness of the hands and a feeling of intense anxiety. On the other hand, a reassuring word w^ill iometimes as promptly quiet the action of the heart.
There is often a close connection between the laking of food or a remedy and the onset of symptoms. This is sometimes doubtless the result of suggestion, at others of the formation of products of indigestion^ and when this latter is the case it is dif- ficult to say whether it is through a reflex or mechanical action or is the effect of the absorption of toxins. The symptoms not infrequently conje on so quickly tiafc there would hardly seem to be time for the formation and action of toxins. In neurasthenic individuals fatigue is undoubtedly an exciting factor. I have known a woman to take a short walk and immediately upon her return to be seized by a sinking spell w^ith either rapid or slow and feeble pulse and coldness of the extremities, symptoms easily thouglit to indicate hcnirt-failure, yet in reality due not at all to cardiac weakness. Ordinarily in cardiac neuroses an attack of palpitation is not produced by a reasonable amount of exercise. In fact, moderate exercise, as w^alking, is more likely to quiet dow^n the heart. Xevertheless exceptions may occur, as was the case with one of my patients, a highly neurotic young man with- out demonstrable signs of organic disease.
Cases of psendo-angina reflector ia have been shown in the de- scription of symptoms to result from irritation of the abdominal viscera, from irritation of a peripheral nerve, and undoubtedly also from disturbances within the pelvic organs. It is my opinion that the same sort of influences may excite an attack of palpita- tion instead of pain. The same thing is true, I believe, as regards the impressions %vhich are said to arouse an attack of pseudo angina through the vaso-motor centres. Palpitation of this origin is not common, how^ever, any more than is pure vaso-motor pseudo-
724 DISEASES OF THE HEART
angina. Instances in which an attack of pain is called forth by washing the hands in too cold water or by the impression made by a cold wind upon the intercostal nerves are certainly excep- tional. Of the toxic agencies accredited with the production of pseudo-angina pectoris, disordered action of the heart, precordial anxiety, oppression, etc., tobacco is by far the most frequent This influence of the weed is not very common, and yet I have under observation at the present time a gentleman who assures me that he cannot smoke a single pipeful of mild tobacco without feeling h\» heart beat more rapidly and strongly than ordinary.
DiagnosiB. — In deciding the question whether or not a pa- tient's symptoms warrant their being classified as a cardiac neu- rosis, one should bear in mind that they are independent of struc- tural alteration of the heart, and are in reality one of the mani- festations of a disordered nervous system. Consequently one must first seek in the personal and family history and by a care- ful analysis of the symptoms for evidence of hysteria, neuras- thenia, or of a highly neurotic temperament, conditions which have been shown to possess an etiologic influence over the phenom- ena that form a clinical picture of cardiac neurosis.
This being so far as possible settled, it is next necessary to determine the presence or absence of organic heart-disease. If such can be excluded, and the patient belongs to the age and sex in which neuroses are most prevalent, a correct diagnosis cannot for the most part be difficult. If, on the contrary, structural altera- tion of the heart is dotoeted, or if the patient has arrived at the time of life when myocardial degeneration is likely, then one should be most cautious about expressing a positive opinion. It is very possible that he has to do with a case in which there is a blending of neurosis with structural cardiac disease. In all in- stances, even in the young, one must carefully study the nature of the symptoms, carofully discriminating those pointing to insta- bility of the nervous system from such as indicate cardiac as- thenia. One should therefore inquire minutely concerning the effect of exercise, for although one cannot assert positively that physical effort is without influence upon symptoms in cardiac neuroses, still such is ordinarily the case. This applies as well to anomalies of cardiac action as to the differential diagnosis of pseudo-angina.
FUNCTIONAL DISORDERS
n&
Furthermore, without wishiDg to set it down as an infallible
guidcy I desire to give it as the result of years of observation that, if the patient is not subjectively aware of disorders of his cardiac rhythjii, there is probably myocardial disease even if objective proof of the same cannot be had. The reverse does not obtain, llie matter of dyspTura requires close study. Patients with car- diac inadequacy from whatever cause experience shortness of breath upon exertion and not during repose except in an advanced stage. Neurotic individuals, on the contrary, unless markedly neurasthenicj are able to walk without breathlessness, whereas they are very apt to complain that they are unable to draw a long breath, or that they feel a '^ catch in their breath." They breathe superficially, and cwerv now and then take an unusually deep in- spiration, which is followed by a feeling of great relief.
If one is summoned hastily to administer relief to a patient in an attack of |)alpitation, a sinking spell, etc., a correct diagnosis is not always easy at first. Valuable infnnnation may be ohtainedj however, from impiijw into tlic history as regards previous at- tacks, mode of onset, etc.» and from attention to the absence of signs of organic lieart-disease and of secondary stasis. Fnrther- niore^ the patient generally tlisplays nervous agitation, fright, etc.
Tn those cases of palpitation whirh manifest throbbing of the aorta either in the episternal notch or in the epigastrium, the dif- ferentia! diagnosis from aneurvsni may be made by attention to tbe following points: (1) The history of attacks of palpitation and their association with sjmptoms of neurasthenia «»r hysteria; (2) the r.ge and sex of the patient, who is generally young and more often a female: (3) the absence of pain, of signs and symp- toms of prcssnre, of a l*K*nlixed tiimonr having an expansile pulsa- tion and thrill; (4) the absence of an area of dulness upon the manubrium stern i or at cither snlc, or at some point along the course of the abdominal aorta; (5) the failure to detect the aua- cultatory plicnomena, of bruit and accentuation of the vascular smmds usually present in aneurysm; (6) the evidence derived from the ^phygnmgraph and the X-ray.
In determining the significance and nature of pain in the car- diac region one should meet %vith but little difficulty if he remem- bers the frdlowing points: fl) The absence in neurotic cases of signs of structural cardiac disease; (2) the spontaneous origin of
726 DISEASES OF THE HEART
the pain, independent of exercise or of any other evidently excit- ing cause; (3) the presence of painful areas in the course of the fourth and fifth intercostal nerves, shown by Head to be symp- tomatic of both functional and organic disorders of the stomach. These hypera?sthetic zones are generally found on the left side as follows: (A) near the left nipple, upon the fifth rib, or in the in- terspace immediately above or below; (B) another upon the fourth costal cartilage or in the fourth interspace near the ster- num; (C) at the lower end of the sternum or upon its appendix. There are frequently other painful points upon the back near the inferior angle of the scapula. The tender areas symptomatic of disorders of the thoracic organs are, according to the same author, located higher up, being in front on the sternum near the level of the third costal cartilage, and on the third rib, or near by, just within the vertical mamillary line. When the tender points first mentioned are discovered close inquiry will usually elicit symp- toms of indigestion or the so-called auto-infection.
For the most part the correct diagnosis of the pseudo-anginas is difficult only in patients at or after middle age, and in them the question is likely to be rendered still more difficult by the dis- covery of cardiac hypertrophy or arterial thickening. In such an event a positive diagnosis must often be deferred until time throws further light on the case. In most cases, however, a cor- rect diagnosis is possible by the discovery: (1) That the attacks, as previously mentioned, arise independent of, and are as a rule uninfluenced by, physical eflFort ; (2) the sufferer is not compelled to seek the erect posture, but frequently prefers to lie down; (3) he does not present a picture of silent motionless agony, but moans or cries aloud and moves about restlessly; (4) the attack is of much longer duration, often lasting several hours; (5) it is often possible to discover signs of peripheral disease that may exert a reflex influence or to get a history of influences that are operable through the vaso-motor system or act as a toxin. As regards tobac- co, however, it should be needless to suggest that in middle-aged men who are smokers coronary sclerosis is much more likely to be the cause than is their tobacco.
Prognosis. — This is practically that of the underlying neu- rosis. These cases are often of very long standing, and therefore present a correspondingly unfavourable prospect of cure. In the
FUNCTIONAL DISORDERS
Tsr
'^oiing, when the case is unmistakably one of neurosis, the assur- ance can iinliesitatiiigly be gi\'en that death will not result from the attack of palpitation or pseudo-angina. When the diagnosis is doubtful, the patient may, for the moral effect, be told that his oardiac i^yniptoms are functional, yet the friends should be warned of the possibly grave nature of the case. In strictly neu- rotic subjects the prognosis depends, moreover, upon the possi- bility of the removal of all tho§e influences of environment which unfavourably affect the patient. In Graves's disease, or those allied states ass^^ciated with enteroptosis, the prosj^ect of obtaining immunity from their tachycardia and palpitations is very un- promising.
Treatment. — This must be directed not alone to the relief of the paroxysms of palpitation or pain, hut also to the removal if possible of the underlying neurosis. It is not the province of this work to disenss the numagement of neurasthenia and hysteria, and therefore the reader is referred to works dealing with the sub- ject. It need only be remarked here that the physician who would successfully treat cardiac neuroses must command the entire con- fidence and respect of his patient, and he must use the influence thus gained for their proper moral management. He must dis- play no hesitation or vacillation in his suggestions and no irreso- lution in their enforcement.
Treatment of the Attack.— In most instances the medical at- tendant first sees the patient in one of his seizures, and is there- fore called on to act energetically and promptly. Yet he should never be in such haste that he cannot first gain a tolerably correct notion of tlie nature of the disorder. lie should never display alarm, and even if he thinks so, he should never tell the patient he is in danger of dying. On the contrary, he should endeavour to reassure the patient both by word and the calmness of his manner. Whether the attack is one of pal imitation merely, or one of intense pain, the treatment is essentially the same, for there are usually associated s\Tnptoms of vaso-mofor disturbance.
Palpitation. — I have never be<^n able to see the wisdom of re- sorting to digitalis or remedies of similar action for the arrest of an attack of palpitation. These remedies are slow of action, the attack is in most instances short-lived, and before the digitalis takes effect the tumultuous heart-action subsides spontaneously, or
728 DISEASES OF THE HEART
because some other measure has met the indication. If there are pallor of the countenance, coldness of the extremities, and a small contracted pulse, a rapidly diffusible stimulant- is indicated. The arterioles should be dilated so as to cause warmth and flush- ing of the surface, even though the pulse be rapid as well as small. To this end nitroglycerin is eflScient and usually affords prompt relief. It is better to dissolve a tablet or to drop a minim of a 1-per-cent solution on the tongue, for its action is more prompt than when swallowed. Whisky, ammonia, camphor, or even hot ginger tea or hot peppermint water may be given, while heat should also be applied to the extremities and prspcordium. If in- stead of being cold the surface of the body is warm and the face flushed, pulse full and bounding, then diffusible stimulants are contra-indicated. It is now better to apply ice to the prsecordium and to give a full dose of one of the bromides, with possibly 2 or 3 drops of tincture of aconite root. This may be followed by a dose of digitalis or strophanthus. In most cases fear plays an impor- tant part in maintaining the attack, and consequently the very presence of the doctor, provided his manner is calm and reassur- ing, will do much to aid the action of remedies. If the seizure is unusually refractory and the patient's agitation does not subside after a sufficiently long trial of the line of treatment indicated above, then it may bo well to inject | of a grain of morphine for its calmative effect.
The Attack of Pain, — If the pnvcordial distress is not suflS- cient to merit the term of pseudo-angina, being plainly a pleuro- dynia with cardiac anxiety, it may yield to the application of a sinapism or of simple heat to the chest. If there are signs of vaso-niotor spasm, or if the pulse is weak and perhaps slow and irregular or interniittont, a rapidly acting stimulant of the kind mentioned above should be given.
If the paroxysm is a psendo-angina either one of two remedies is indicated: nitroglycerin where there is arterial spasm, and morphine subcutaneously whore there is or is not such spasm. This latter not only allays pain and acts as an efficient cardiac stimulant, but it calms the patient and promotes subsequent sleep. Nevertheless it is wtII to bear in mind that there is always danger of these neurotic patients, who suffer from frequent attacks of pain, learning to depend upon the drug, and thus in time becom-
FUNCTIONAL IHSOKDERS
729
iBg victims of the morphine habit. The same ohjet'Hnn applies to the use of alcoholic sliiriulantsi for the treatment of an attack of palpitation, eiuking spells, etc., and therefore it is better to rely on other harmless but equally effective stinmlants.
In coneliit^ion, the physician should search for and endeavour to remove all those sources of visceral or peripheral irritation which serve to disturb the nervous system between attacks or may seem to act as exciting causes.
Enteroptosis, dilatation of the stomach, digestive indiscre- tions, or any other comlition that may account for the cardiac symptoms are to be treated in accordance with the principles ap- plicalile to such cases and the special intHcations of each case. Great amelioration and sometimes entire relief of the distressing Ettacks of palpitation follow so simple a measure as the wearing of a properly fitted abdominal supporter in cases of ptosis of the stomach or other viscera. In addition, attention must be paid to the clothing, that too tight skirt-bands or corsets may not in- crease the dragging of the abdominal contents upon their sup- ports. Properly given, massage is often of much benefit in these cases.
Finally, in all cases the exciting causes should be carefully sought out antl fht^ patient impressed with the necessity of avoid- ing all those influences which may precipitate an attack. He should he told that if he is to get better he is to aid in his cure by obeying instructions to the letter, since medicines alone are in- capable of eradicating his disorder.
CHAPTER XXXI ESSENTIAL PAROXYSMAL TACHYCARDIA
Tuis is a highly interesting and very puzzling derangement of the heart's action which has received much attention from the medical profession since 1867, the date, according to Herringham, of the publication by Payne Cotton of the first i^ecorded case. This disorder of cardiac rhythm consists in exceeding rapidity of action, and occurs in attacks of variable duration and frequency, during which the heart-beats number 160 or more to the minute. Medical men in the British Isles have always been keen observers, and here again, as in angina pectoris and bradycardia, have sig- nalized their powers of observation. Cotton, Edmunds, Watson, and Bowles led the way, and in the next few years other observa- tions were recorded by Nunnely, Cavafy, and Farquharson. On the Continent we find the names of Tuchzek, Gerhardt, Bouveret, Oettingcr, Probsting, and many others. Gerhardt suggested the term Tachycardia in the year 1881, and in 1888 Bouveret sug- gested the appellation Essential Paroxysmal Tachycardia, to dis- tinguish cases in which the paroxysms of excessively rapid action furnished the only clinical evidence of cardiac disease.
Acceleration of the heart's action to 140, 150, and even to 170 in the minute is sometimes observed in cases of valvular lesion, and may be assumed to depend in some way upon structural alter- ation of the walls due to the valve defect. But in those cases which Bouveret characterizes as essential tachycardia there is no clinical evidence of cardiac disease, and therefore the paroxysms cannot be considered symptomatic. This distinction is objected to, however, by Herringham, Gibson, and others, who prefer to call the condition simply paroxysmal tachycardia, since this ap- plies broadly to all cases in which typical attacks of excessively rapid action occur. 730
ESSENTIAL PAROXYSMAL TACHYCARDIA
731
Clifford Allbiitt objects to the term paroxysmal, sayings " The interpretation is that tachycardia ib a fairly uniform symptom group; and, as one of its eminent characters is its paroxysmal occurrence, the addition of this qualification to the name is super- fluous."
Pathology, — There are no anatomical changes that can be definitely associated with essential paroxysmal tachycardia, and likewise there is no established pathological basis upon which an explanation of the phenomenon may rest* Prior to 1897 six post- mortem observations had been made in this class of cases, but they failed to disclose any constant or uniform lesion. In one, the wall of the left ventricle was in a state of pronounced fil>rou3 degeneration, and in two the hearts were extensively fatty, while in three others no special changes were noted aside from dilata- tion. As these alterations have been found over and over again, indeed, are very common in hearts that have never manifested this peculiar disorder of action, it is plain that there is nothing in these post-mortem findings to explain the occurrence of parox- ysmal tacliyeardia. Consequently various theories have been offered to account for the attacks.
Tuchzek suggested paralysis of the vagus, and Xothnagel, irri- tation of the sympathetic, sutficient to overcome the controlling influence of the pneumogastric. It has also been suggested that there may be a combined action of the two, vagus paresis and ac- celerator stimulation. Objections are urged against all of these theories* Tuehzek's theory has l>een widely accepted, and yet ex- periments on animals have failed to produce so extreme a rapidity of heart-action as is seen in these attacks, and Allbutt believes that in man abeyance of the inhibitory control of the vagus would not send the pulse up beyond 120. Likewise, stimulation of the cardiac accelerator nerve is said not to increase the pulse-rate beyond 150. Ascribing the rapid action to a combination of both neeessitates the assumption of some cause which acts simultane- ously on both nerves, and this, in Allbutt's emphatic w*ords, *' sins against the economy of causes."
Bouveret's suggestion that it is a bulbo*spinal neurosis, and Talamon's that it is of an epilpetie nature, are both not aceeptable. Samuel West has urged that the attacks are due to alterations in the myocardium, to which Herringham woidJ add changes in the
732 DISEASES OP THE HEART
nerve endings situated in the heart, a view that seems to appeal strongly to Gibson. Other suggestions, as a neuritis, are of still less importance. They are all mere surmises ; and in the present state of our knowledge, without numerous and careful necropsies to throw light on the anatomical changes underlying this interest- ing symptom or disease, whichever it may be, we can only say with positiveness that we know nothing concerning its true nature.
Etiology. — This is likewise obscure. Most of the recorded cases have been in adults. Of the 53 cases collected by Herring- ham, the age was stated in 40, and of these there were 7 instances in children, 12 between the ages of twenty and thirty, and 13 in the following decade of life, the remainder being in persons past forty. Age, therefore, cannot be said to exert special predispos- ing influence. Both sexes are subject to attacks, and although 30 of Herringham's collected instances were in males, the prepon- derance of this sex is so slight that it scarcely warrants the con- clusion that in sex alone resides any predisposing influence.
That in some cases there may be an hereditary element ap- pears to be established by Oettinger's case, since there was history of the same sort of attacks in three preceding generations. In some of the reported cases there has been a history of previous disease — rheumatism, influenza, diphtheria, malaria, aniemia — that may possibly have boon a predisposing factor, but a definite relationship of this kind has not boon ostablishod.
In the way of possible cxcHiiKj causes have been a blow on the chest, fright or other strong emotion, and a sudden physi- cal effort. Attacks have also followed disturbances in the digest- ive tract.
Romberg states that paroxysmal tachycardia rests on a nerv- ous basis, and may arise rofloxly from disordor in any of the vis- cera or may result from some cause acting directly through the central nervous system, and is independent of any demonstrable cardiac disease. Thus it is plain that after all has been written on the subject of its pathogenesis we are no wiser than we were before.
Features of the Paroxysm — Two conditions are essential if rapid action of the heart is to be considered an instance of essen- tial paroxysmal tachycardia: (1) The apparently healthy heart must beat at least 160 times a minute. (2) The onset and ter-
ESSENTIAL PAROXYSMAL TACHYCARDIA
733
minatioii of the attack rnii8t Ik? so sudden and abrupt as to give it the character of a paroxysm. Although a pidse-rate of less than 160 is frequently observed in persons with some structural disease of the heart, still in essential tachycardia the number of cardiac contractions is often vastly in excess of this number, running as high as 200, and in a few instances even to ^^00 a minute. The pulse is small, thready, and often imeountable, because the ex- treme frequency of the waves and the emptiness of the vessel cause the pulse-waves to run together in an indistinguishable manner. To determine the heart-rate, therefore, one must count the heart beats by auscultation instead of by palpating a periph- eral artery.
The rhythm of the contractions is usually regular, but irregu* larity and inequality in their force are sometimes observed. The extreme rapidity of the cardiac systoles is at the expense of their
Fio. 108. — SpHioiiOiiK .
. <A»lt Oir rAKOXV«SJAL TArHyOARDIA.
strength and efhciency, blood-waves of normal volume are not dis- charged into the aorta » the arterial system becomes relatively empty, and the pulse is one of strikingly low pressure. This is illustrated by the appended tracing (Fig. 108) kindly furnished me by Dr. E. F. Wells from one of his cases.
The paroxysms begin abruptly and generally without premoni- tion. Indeed, upon the (X'currenee of the first attack the patient does Hot always know what is the matter with him, and is only able to say he feels bad. If the tachycardia is short lived, the patient may experience nothing more than a vague feeling of dis- comfort and his outward appearance may not disclose anything unusual to the ordinary observer. There may be, however, pallor or ilushing of the countenance. In some instances there are pne- cordial oppression and even pain, numbness or tingling of the arm (Gibson ). Palpitation or fluttering of the heart may be com- plained of, and vertigo is sometimes experienced. Most suflFerers from this complaint, notwithstanding repeated attacks and the
734 DISEASES OP THE HEART
fact that experience has shown the termination to be in sudden recovery, become greatly alarmed, and if the attack is prolonged to several days fall into a state of great mental and physical dis- tress.
If the case is seen early there is usually so little evidence of the actual state of things in the patient^s outward appearance that the medical attendant on feeling the radial pulse is usually struck with astonishment and even dismay at its rapidity.
If the attack lasts long enough it leads to cardiac inadequacy and the blood tends to accumulate in the heart-cavities. The heart becomes overdistended and the venous side of the circulation en- gorged, as shown by increased cardiac dulness, cyanosis, and it may be by pulsation of the jugulars (Gibson). There is pulmo- nary congestion, possibly also a small amount of oedema, and even albuminuria. The heart-sounds are feeble and the first at the apex may become almost inaudible.
In most cases the duration of the paroxysm is not sufficient to lead to such marked signs of stasis. The attack subsides sud- denly after a few hours and the patient is left very much as he was before, feeling perhaps tired and dreading a recurrence, but able to return to his ordinary duties.
A striking peculiarity of such a paroxysm, whether long or short, is the persistence of the tachycardia even during sleep. Such attacks are usually repeated through a series of years, and yet cases have been observed in which but a single paroxysm was noted. Although recurrences are the rule, there is no regularity in their repetition.
Their duration is likewise variable, since the paroxysms may last from a few minutes to one or more days. In one or two in- stances the tachycardia persisted for two or even three weeks.
If the tachycardia is a sjnnptom of some visceral disturbance, or, in other words, is a functional derangement of reflex origin, then it is easy to conceive of but a single attack and to understand how this may be of short duration. But, if it is due to some deli- cate and as yet unrecognisable alteration in the myocardium or bulb, then recurrences should be the rule, as indeed they are, and the attacks should be of considerable duration.
Diagnosis. — The determination of the fact of tachycardia is not difficult. The point to be decided is whether the rapid ac-
ESSENTIAL PAROXYSMAL TACHYCARDIA
r35
tion is an instance of essential paroxysmal tachycardia or is of the kind called riyinptomatic. If it belongs to the former class, it should fnliil the following requirements: (1) A heart-rate for the time being of at least IGO a minutej (2) abruptness of onset and equal suddennesi» of termination^ (3) failure to detect evidence of heart-disease either during or between attacks.
If J on the other hand, there is evidence of myocardial or endo- cardial disease, the taebyeardia is symptomatic and not essential, no matter how rapid may be the pulse. In this class, however, it is not usual for the heart's action to exceed 150 a minute. Most instances of ** heart hurry " belong to this class, and yet it is prob- able that the essential form occurs more often than is reported, either because the attacks come to the notice of the family doctor rather than of the consultant, or because the attacks are so tran- sient that no physician is called in. Although I have repeatedly observed symptomatic tachycardia and have known several indi- viduals who gave a history of the essential form, among them a medical man, I have not actually witnessed a paroxysm.
Prognosis,— In the essential form the prognosis may be said to be favourable so far as life is concerned. There is always an element of uncertainty in any case of extreme and protracted ** heart Imrry," but if a paroxysm terminates speedily no damage to the heart may be sustained. The real difficulty lies in the uncertainty of the length of time during which an attack may endure. In the aged, the feeble, and persons having a definite cardiac lesion such paroxysms are not devoid of danger. In most cases of paroxysmal tachycardia the seizure may be expected to ternnnate abruptly and sjMntaneously, but how long the patient 18 to remain immune from a repetition is a matter of too nmch uncertainty for the prudent physician to express an opinion. The history of cases shows that in most instances other attacks are to be expected.
Treatment. — The plain indication is if possible to arrest the paroxysm. This is called for, notwithstanding the fact that in the majority of cases the tachycardia has not caused death. Al- though a patient may have had repeated attacks that have ceased spontaneously, yet tachycardia is such an uncertain quantity that one can never be quite sure how another paroxysm may affect the Iieart Unfortunatelv it is the same with this as with other mala-
736 DISEASES OF THE HEART
dies; our therapeutic resources do not always enable us to meet indications satisfactorily.
Theoretically, digitalis ought to enable us to slow down a run- away heart, but experience has shown its inefficiency in most cases; This remedy should not be administered recklessly in paroxysmal tachycardia, for if the attacks were to terminate spontaneously soon after the administration of a single very large dose or of several massive ones in quick succession, there might be positive danger of poisonous effects. If, as stated by Allbutt, digitalis produces diuresis even when it does not control the heart's action, it is likely to be eliminated and evil consequences will not result. Nevertheless, it is well not to administer more than 10 minims of the tincture hourly for six hours, and if at the end of this time no appreciable slowing of the pulse is produced, to have recourse to other means.
Ice may be applied to the pra?cordia, or one may try the effect of prolonged but not too vigorous friction of the skin over the upper portion of the spinal column, which has been said to slow the heart. The vagus may be compressed in the neck, or it may be stimulated by an electric current.
It has also been recommended that the patient take a deep inspiration, and then with his arms folded across the front of the chest and his feet pressed firmly against the foot-board of the bed to make a powerful expiratory effort while the glottis is kept closed. One of my patients who is a sufferer from essential paroxysmal tachycardia assures me that she has sometimes been able to chock her heart by drawing a full breath, then while her body is flexed so as to compress her abdomen, making a powerful expiratory pressure. In her case also a paroxysm has been knowTi to be arrested by the pouring of cold water over her wrists.
Whatever remedy is administered or whatever method of im- pressing the nervous system is tried, it is often found useless. It then becomes the physician's duty to support the heart until the tachycardia subsides spontaneously, and when cardiac dilatation sets in, this is imperative. To this end reliance must be placed on strychnine, caffeine, digitalis, etc., while the patient is kept at rest. The diet is to be simple and nourishing, and tea, coffee, or other stimulants are to be forbidden. In prolonged attacks it may be well also to administer a gentle cathartic.
ESSENTIAL PAROXYSMAL TACHYCARDIA 737
It may not be possible to prevent recurrences, and attempts in that direction may seem to be something like firing in the dark, yet the patient should receive medical attention between attacks. In cases exhibiting subsequent signs of cardiac strain or in which there is an unstable nervous system, such regular treatment is spe- cially advisable. Gibson recommends tonics, a course of the Nau- heim baths with resistance gymnastics and such other measures as the experience of the medical attendant and the exigencies of each case suggests. In some instances it may be well to give digitalis or other heart-tonics for a long time. Every effort should be made to discover and remove any source of reflex irritation, and the daily life should be as healthful and free from excitement as possible.
47
SECTION V DISEASES OF THE AETERIAL SYSTEM
CHAPTER XXXII ARTERIOSCLEROSIS
Degenerative changes in the coats of the blood-vessels were observed as long ago as the days of Senac and Morgagni, and by these investigators were described as an inflammatory process. It is to Rokitansky and Virchow, however, that we are indebted for thorough and systematic investigations concerning the origin and nature of the process to which Lobstein had previously given the name of arteriosclerosis. Virchow regarded it as a chronic arteritis and pointed out its siitiilarity to the slow inflammatory process so often seen in the viscera, which is attended by the devel- opment of fibrous tissue. The inflammatory nature of arterio- sclerosis was accepted bv other pathologists also, but by certain of them was regarded as an evidence of some infectious process.
On the other hand, the cause of the sclerotic change was by Traube and others found in mechanical factors — i. e., in an in- crease of the arterial blood-pressure following persistent contrac- tion of the arterioles. Indeed, some went so far as to attribute to high blood-pressure every case in which they recognised sclero- sis and secondary cardiac hypertrophy.
The latest view of the pathology of this vascular change and the one that is coming into general acceptance is that of Thoma. Concisely stated, his conception of the process is that in conse- quence of lessened resistance of the media the vessel becomes widened with resulting slowing of the blood-stream. Connective tissue then develops in the subendothelial layers of the intima as a compensatory process by which to restore the normal relation be- 738
ARTERIOSCLEROSIS
739
tween tlie artery and its contents. Although in most instances the vasenlar change is an attempt to make good a loss of elasticity and widening of the artery, still it may develop when the normal relation between the vessel and its contents is lost by reason of decrease in the volume of the blood. Romberg, to whom I am in- debted for the historical data just given, finds Thoma's view highly satisfactory, since it seems to explain the development of arteriosclerosis in cases which were jirevionsly nnaccountable by Tranbe's theory. Moreover, it has been founded on an immense amount of carefully studied material
Morbid Anatomy. — Arteriosclerosis consists essentially in a degcHcratiou of the media with secondary compensatory thicken- ing of the intima. It may be localized, constituting the nodular form of Councilman, or it may be diffuse. In the nodular or cir* cuuiscribed form whitish or yellow- ish patches are scattered along the inner surface of the vessel^ wdiich stand up from the surround- ing level and are of a rounded contour. In the diffuse variety the arterial wall is stiiF, and more or less dibited, while on the surface of the intima nuiy be zones of nodular thickening and calcareous or atheromatous patches. In ohl pers^jns tlie arteries are stiff, more or less tortuous and dilated. The inner surface presents numerous calcareous plates and atheromatous ulcers.
Examined microscopically, the thickening of the intima is found due to development of connective tissue between the endo thelium and underlying elastic tissue. After a time, degenerative changes take place in this newly formed connective tissue w^hich consist in hyaline transformation of the outer portion with areas nearer the endotheliuni of fine detritus in which fat droplets are seen. These areas of necrosis constitute the so-called atheroma- tous abscess. When these areas break into the lumen of the vessel depressions are left, known as atheromatous ulcers. The borders and bottoms of such ulcers are rough, and hence may become the Beat of white thrombi. By the deposit of lime salts in these ath- eromatous patches calcareous plaques are formed which project above the surface of the intima, while b}* formation of chalky particles in the wall the artery may become transformed into a tube of almost bony hardness.
In the middle coat changes of a degenerative nature take place which lead to weakening and dilatation of the artery and conse-
740 DISEASES OP THE HEART
quent thickening of the intima. The middle tunic becomes thinned in consequence of atrophy and degeneration of its muscle- fibres and of more or less extensive destruction of its elastic ele- ments. In some cases these elements disappear entirely and are replaced by connective tissue. The adventitia in its turn does not escape, but becomes infiltrated with round cells, especially in the neighbourhood of the vasa vasorum. The investing membrane be- comes tough and fibrous and may also be of increased thickness.
The changes of arteriosclerosis which have been thus briefly described are not distributed uniformly in the aflFected vessel or in all parts of the arterial system. The lumen of small arteries is apt to be greatly narrowed and even obliterated by the hyper- plasia of their coats, or it is blocked by thrombosis. The aorta and large arteries, on the contrary, are apt to become more or less dilated while their walls are rigid and the intima rough from the presence of calcareous plates and atheromatous patches, as pre- viously described.
As already stated, the various parts of the arterial system are not equally involved in the sclerotic process. Thus Bregmann found as a result of analysis of the cases investigated under Thoma's direction, that the ulnar was involved in 94 per cent, anterior tibial in 93, subclavian in 88, cerebral arteries in 87, in- ternal carotid in 87, radial in 86, splenic in 82, popliteal in 79, external carotid in 78, axillary in 71, femoral in 60, common ca- rotid in 68, ascending aorta in 67, abdominal aorta in 64, external iliac in 58, and brachial in 55 per cent. This list shows some very remarkable differences which it is difficult to explain, and so far as I know have not been satisfactorily explained. Why, for instance, should there be so marked a discrepancy in the fre- quency with which the ulnar and radial are affected ?
This matter will again be referred to in considering the eti- ology.
It should also be mentioned that arteriosclerosis of the nodular variety is encoimtered in some arteries with greater frequency than in others. These are such as do not run in straight or nearly straight directions, but make numerous turns in their course or give off branches at a sharp angle. The sclerotic process is here found at the points whence the branches depart or where the vessel undergoes a bend or curve. A glance at Bregmann's
ARTERIOSCLEROSIS
741
tables, quoted bv Romberg, ami eoiiipiled with special reference to tlie nodular form, shows that the abdotuinal aorta heads the list, while the coiiinion carotid, internal earotidj ascending aorta^ and cerebral arteries follow close after in this order.
On the other hand, the radial is generally aflFected %vith the diffuse form, owing probably to its nearly direcl course and the arrangement of its not numerous branches, conditions which per- mit uniformly high blcKid-pressure, and hence development of sclerosis thronghout its length.
Associated with siderotic changes in the vascular system are alterations of a similar nature in the various organs, particularly heart, kidnevs, and liver. In the senile form the Iieart mav he decreased in size, whereas in the diffuse variety, that encountered in comparatively young and robust men, the heart sometimes reaches enormous dimensions. Councihnan found instances in which the heart weighed two and nearly three times the normal. The myocardium is apt to show tibrous degeneration, the eoro- naries to be ^'clerotic, and the aortic valve to he opaque, sclerotic, and in some cases incomjietent.
The kidneys are especially likely to show the sclerotic change on microscopic examination, although to the naked eye the changes may be so slight as to be easily overhx»ked. The capsule is adher- ent and somewhat ronghened on its surface, which may present dark red depressed areas due to atrophy. The capillaries of the glomeruli are thickent^d and may be obliterated and exhibit ex- tensive hyaline degeneration. Atrophic changes may be present in the liver, particularly in connection with snnile arteriosclerosis.
Etiology. — The great frequency of sclerotic changes in the arteries of old people very naturally attracted attention and sug- gested a close etiological connection Itetween age and this disease. It has been thonghf directly due to senility, and hence a necessary part of advanced years. That arterifisclerosis is not an invariable accompaniment of age, however, is well knoivn, and Gibson states that when Thomas Parr died at the age of one hundred and fifty* two his arteries were found bv ITarvev to be free from any evi- dence of degeneration. Such facts indicate that to the mere influ- ence of age per se cannot be attributed the development of arterial dej^encrafion. The explanation given by Komlierg of the connec- tion between the two conditions seems to me to be the best I have
743 DISEASES OF THE HEART
yet seen, and is, that when arteriosclerosis is found in an old man, it is because the conditions of blood-pressure which lead to the change have been operative during his many years, and therefore have come to manifest themselves more extensively than in a younger individual.
Males are without doubt more often and extensively affected with this change than are females. This is owing not to any special influence inherent in sex, but to the greater exposure of men to occupations, habits, and conditions of life in general which affect blood-pressure injuriously. The influence of occupations which necessitate arduous physical exertion, and thereby subject the arterial system to strain, has long been recognised and empha- sized, particularly by the English. Thus day labourers, smiths, miners, etc., are very apt to develop arteriosclerosis, sometimes at a comparatively early age, and Romberg points out that in them it is the vessels of the extremities that are specially prone to dis- ease. It is probable, also, that among the labouring classes other factors are at work beside physical toil, such as abuse of alcohol and syphilis. Nevertheless, strain of the vascular coats by severe and oft-repeated muscular effort cannot be ignored in the produc- tion of sclerosis.
Of diseases which lead to this degenerative process syphilis is perhaps the most important. Its relation to the form of endar- teritis known as obliterans was deseril)od bv Ileubner, and is quite generally recognised. Chronic lead poisoning and chronic alco- holism are also recognised etiological factors, as is likewise gout. I low those act is not quite clear, whether as suggested by Traube by causing persistent augmentation of blood-pressure or through the action of their poisons directly on the vascular coats. The excessive use of tobacco is also l)elieved bv some writers (Iluchard, Romberg) to cause arteriosclerosis, particularly of the coronary arteries. Romberg likewise states that neurasthenic subjects are prone to arterial degeneration, as he believes, in consequence of the frequent alternations in blood-pressure occasioned by their unstable and excitable nervous state.
The manner in which these, and other predisposing conditions to be mentioned presently, act in the production of arterial degen- erations has long been thought to be through the persistent in- crease of blood-pressure occasioned by them. Nevertheless expla-
ARTERIOSCLEROSIS
743
nation bas^d on siieh hypothesis was not altogether satisfactory and did not clear! v account for the pathology or etiolog^^ of the changes observed. In the light of Thoma"s investigations and views, howeverj we are now able to understand much in the etiol- ogy^ whicli was before obscure.
It will be remembered that, according to his view, the thicken- ing of the intima is an attempt at the preservation of the normal relation existing between the calibre of the vessel and the pressure of its contained bltx>d. The loss of siu*h proper relation or equi- librium, as it may be termed, is brought about either by dilata- tion of the artery in consequence of lessened elasticity or by dimi- nution in the volume of the contents. Loss of elastic resistance on the part of the vessel is due to degeneration and atrophy of the elastic fibres of the media, and this destructive change in the mid- dle coat may be due to the long continuance of excessive blood- pressure or to sudden, frequent alternations of blood-pressure.
Diminution of the volume of blood is seen very much less fre- quently, but is met with in the arteries of amputated extremities (Romberg), and, according to the same author, in tlie renal artery in interstitial nephritis. Of course tlie former requirement- — i. e., increased pressure — is far more often and widely operative than is lessened blood-pressure. Accordinglv, when we have to do clinically with arteriosclerosis we have to seek out some under- lying condition, disease, oeeupatinii, or habit, that has caused long'Continued and greater internal or endarterial strain than the vessel was able to bear. Slowly the miildle coat has been forced to give way before the intravascular bliXMl-j>rcssurc, pari passu the intima has taken on compensatory thickening and by degrees the sclerotic process has declared itself,
Tn some individuals blfM-Kl- pressure has been abnormally high quite uniformly throughout the Ix^dy and arteriosclerosis is gen- eral. More commonly, perhaps, the conditions influencing the change are local and the degeneration is confined to or at least far more pronounced in certain parts, as extremities, brain, coro- naries, etc. Tor example, the frequency with which the anterior tibial is involved is explained by the fact that this artery is com- pelled to hear the distending weight of a column of blood which U heavy by reason of hydrostatic pressure (Romberg).
It has been frequently and forcibly pointed out (Fraenkel,
744 DISEASES OP THE HEART
Hasenfeld) that corpulent persons of a sedentary mode of life are especially prone to the development of sclerosis in the splenic, hepatic, and superior mesenteric arteries, and, according to Hasen- feld, earlier in these than elsewhere.
The explanation is, that owing to their sedentary pursuits and their habitual consumption of more food than the requirements of their inactive lives demand (luxus consumption) the vessels of. their digestive organs are persistently overtaxed. In other words, blood-pressure within them is habitually too high. In time abnor- mally high and sustained pulse-tension is everywhere established, more or less wide-spread arteriosclerosis develops, and in conse- quence secondary cardiac hypertrophy (Fraentzel's idiopathic en- largement of the heart) results.
Another interesting phase of this question of blood-pressure relates to the development of sclerosis in vessels which are ex- posed to varying degrees of pressure, oscillations from low to high pressure, " schwankungen " (Romberg). Such alternations subject the artery to undue strain and probably account for the sclerotic change so frequently present in the arteries of the arms of workingmen. According to Romberg, they also explain the fact that sufferers from migraine sometimes manifest sclerosis of the arteries of the side of the head affected by the pain.
It is on this hypothesis likewise that we may explain the pre- ponderance of arteriosclerosis in the cerebral vessels of persons who are engaged in literary pursuits or whose occupations call for spe- cial activity on the part of the brain during a certain number of hours each day. ^lay it not be for this reason that many an ambitious business man succumbs to the stress of modern com- mercial life ( Itoniberg ex])lains the greater frequency of coro- nary sclerosis in hypertropliiod hearts as compared with those that are not hypertropliiod, on the ground that coronary blood-pres- sure is higher in the former on account of their more forcible contractions.
If his view is correct, then one is tempted to query if the car- diac excitoniont ex])erienood by stook-l)roker8 and men of affairs under the influence of rapid fluctuations of the stock or grain market may not liave much to do with the relatively great fre- quency of coronary angina in modern business men. In illustra- tion of the important etiological influence exerted by variations
ARTERIOSCLEROSIS
745
ot blood- pressure in circuniseribed a reus , Romberg eites the re- markable case reported by Erb of an ardent angler who developed a liigh degree of arteriosclerosis in the lower extremities, in con- sequencCj it is thought, of liis standing and walking for hours together in the cold water of the streain^^ wliere be fished.
Additional instances of the injurious effect of long-continued high blood-pressure are seen in the degenerative changes found in the pulmonary artery of mitral patients and in chronic phthisis as well as the general arterioselerosis of ditdietie patients (Rom- berg). In short, upon the basis of Tbouni's conclusions we are now able to understand many a ea^e of arteriosclerosis the de\'elopment of wb it'll was jTreviously almost nn intelligible.
Symptoms.-^ A rterioselerosis is latent so htng as it is of minor degree and nt^t very wide-spread. When at length symptoms are produced, they dejx*nd u|X)n the degree and distribution of the proce*ss and the organs affected. In some cases the clinical ])icture 13 that of i*eual inadequaeyy in others of cardio-vascular disorder, in others again of disturbed cerebral circulation^ and in still others of interference with the bloofl-supply to the extremities, digestive organs, or heart-musele, as the ease nniy be.
Sclerosis of the renal arteries may be secondary to already ex- isting interstitial nephritis in consequence of diminished supply of blood to the renal capillaries, but in most cases it precedes or accompanies the development of the nephritis. The augmented htood'pressure occasioned, first declares itself clinically by in- creased secretion of urine, particularly at night. Examination of the urine in this early stage generally shows nothing more than a lowered specific gravity. When at length the sclerosis has be- come so extreme as to materially interfere with flow of blood in the renal capillar! es^ the urine grows scanty, and is apt to present characters like those of genuine contracting kidney.
In these cases there is apt to Ik* more or less sclerosis of the arteries of other parts, particularly the heart, or general pulse ten- sion becomes too high to be snccessfully combated by the hyper- trophied left ventricle, and STOiptoms of cardiac incompetence are added to those of renal disease. Thus I recall the case of a middle- aged physician who, aside from cardiac breathlessness, developed symptoms of serious renal inadequacy. Urine grew jx^rsistently scanty, contained an occasional trace of albumin, but rarely casts.
746 DISEASES OF THE HEART
He ultimately died with symptoms that were ursemic rather than cardiac^ and the autopsy disclosed almost complete obliteration of the renal arteries.
In other cases the picture is that of slowly increasing, or per- haps suddenly induced, failure of heart-power, with renal symp- toms of very inferior importance. Only to-day I examined a man of seventy-one who for two years past has noticed breathlessness, which of late has become serious cardiac dyspnoea. For more than twenty years he has had increased nocturnal micturition, but no other evidence of renal disease. He has been closely confined to his desk daily, and has been " a pretty heavy eater, particularly at breakfast." His chest is capacious and abdominal corpulence is quite marked. The radials, temporals, and carotids are stiff, and the heart is enormously enlarged, its impulse feeble, and its sounds distant and muffled. This case is a fair illustration of the etiology and symptomatology of the cases in which the clinical pic- ture is what may be termed cardio-vascular, the chief, it may be the only, complaint being dyspnrra of effort.
Many such cases, like the foregoing, very well represent the clinical picture of chronic myocarditis. In others, symptoms of failing heart-power and of chronic interstitial nephritis are so in- timately blended as to make it difficult to determine definitely which organ is the more seriously involved. In others again, gly- cosuria and renal cirrhosis precede the symptoms of vascular and cardiac disease, yet when the latter become marked they may domi- nate the scene. In all these cases, when cardiac incompetence su- pervenes, it is apt to prove most serious and to progress under the every-day appearance of increasing and unconquerable stasis, since the extreme degree of peripheral resistance incident to arte- rial rigidity renders restoration of heart-power impossible. They have been sufficiently portrayed in preceding pages and do not re- quire repetition.
In comparatively few cases the symptoms are mainly, almost exclusively, referable to the arteriosclerosis as such. The arteries everywhere feel wiry and nodular, like a string of beads, or thick- ened and tortuous, and the pulse is small and weak. The super- ficial veins stand out prominently; the heart manifests slight if any change, being in some moderately and in others not at all enlarged ; the urine is scanty and of poor quality, and if any albu-
ARTERIOSCLEROSIS
747
min is present, it is a mere trace, while casts are scanty, being hya- line or granular; the patient complains of increasing inability to work or exercise; appetite and digestion fail; slight oi'dema appears at the ankles; the individual emaciates, grows sallow, pale, steadily more feeble, and at length takes to bed and dies from what appears to be general asthenia.
I have notes of such a typical case in an Englishman who was a farmer of about sixty-eight years of age. Up to a year or so prior to my seeing him he was hale and hearty, and able to perform active work of a not too severe kind.
Examination disclosed no distinct evidence of heart or renal disease, but the radials, ulnars, tomporala, femorals, and tibial? all felt hard and empty and most of them contained deposits of lime that gave them a pronounced beady character. Venous stasis was evident in the turgescent veins, palpable liver, and slight pit- ting of the ankles and shins. He did not complain especially of dyspn(.ea, but was much concerned over his growing weakness and loss of weight
Treatment benefited him for a time, but he ultimately grew too feeble to report at my office, and as he resided in the country was lost sight of. It was ultimately learned, however, that he died after a few months of what appeared to be general feebleness with failing circulation. In his case, as in many, the heart seemed to he comparatively unaffected and the difficulty of circulation to be due to the impermeability, so to speak, of the arteries.
The rigidity of the arterial system interferes with proper dis- charge into the capillaries^neither are the arteries able to receive the full supply of bkxid sent from the veins, and stasis occurs.
In a considerable proportion of cases the clinical manifesta- tions are not those of disturbed circulation in general, but of dimin- ished or abolished bloixl-supply to a part, as the brain, extremities, heart, etc. The result is perverted function and structural altera- tion of a more or less serious kind. In some instances such disturb- ances are plainly apparent, while in others the manifestations of arterial degeneration are obscure and often misinterpreted or over- looked altogether.
Thus sclerosis of the cerebral arteries may be shown by impair- ment of memory and intellection, headache, transient vertigo, espe- cially upon quickly assuming the erect position, change in disposi-
748 DISEASES OF THE HEART
tion, increasing weakness, in a word, by the manifold symptoms due to cerebral aniemia or areas of softening (encephalomalacia) which result from the shutting off of blood-supply to definite areas. One should not forget also that when epilepsy develops at or after middle age, it may be due to arteriosclerosis within the brain (Ilochhaus). Disease of these vessels is also a very frequent, ac- cording to Romberg the most frequent, cause of apoplexy. There may be either haemorrhage into the brain from rupture of a miliary aneurysm, a condition of the arteries shown by (Charcot to be very common, or the apoplectic seizure may result from thrombosis of a narrowed cerebral artery.
Sclerosis of the arteries in the medulla is a recognised cause of slowness of the pulse and of recurrent bradycardia known as Stokes- Adams disease, and which has been previously considered. (See page 627.)
Sclerosis of the arteries of the feet and legs is not uncommon, but apart from the change it creates in the elasticity of the vessel — i. e., stiffness and tortuosity, as perceived by the palpating finger — it docs not often lead to serious disturbance of circulation in the region supplied by the sclerotic artery. The sclerosis may, how- ever, according to Erb, be responsible for disorders of sensation and motion, vaso-motor and even trophic disorders. The first may be shown by panesthesia, formication, pain, and a feeling of heat or coldness; disorders of motility, by intermittent lameness and extreme degrees of arterial narrowing by cramps, rigidity, etc. ; vaso-motor disturbances, by coldness, pallor, cyanosis ; and nutri- tional disorders, by circumscribed slouching of the skin. In cases of obliteration from sclerosis, as is well known, there may be local- ized gangrene (senile gangrene).
According to Romberg, sensory and motor disturbances make their appearance at first only when the muscles are put in use — i.e., when there is a call for more blood to the part than can be fur- nished by the thickened arteries. In more advanced degenerations these disturbances are produced by insignificant movements, and at length the limb becomes stiff and useless.
Xot only are vaso-motor neuroses, such as pain, redness, swell- ing, stiffness, etc., phenomena of arteriosclerosis, but, according to Romberg, there may appear symptoms of Reynaud's disease, cyano- sis, pallor, and even gangrene of portions of the skin, such phenom-
AHTERIOSCriEROSlS
749
ena heing particularly liable to affeet the fingers. Fortunately, however, such serious disturhaneos are rarcj aud for the raost part only minor degrees of sensory and vaao-motor perversions are present.
The heart may be affected by arteriosclerosis in either or both of two ways; It may be degenerated and feeble in consequence of thickening, narrowing or thrombosis of the coronaries, with angina pectoris and the symptoni-i'<unplex of myocardial incompetence, or the heart may be secondarily hypertrophied in eonsei|iience of diffuse sclerosis of the arteries supplying the abdominal viscera, Ilasenfeld has dwelt on the intimate connection between sclerosis of the mesenteric vessels and general cardiac hy]jertropliy, and Romberg also states that it is degeneration of these arteries which calls forth secondary hypertrophy of the left ventricle. Extensive vascular change uf the brain and extremities may exist, he states, without appreciable enlargement of the heart. This coincides with my clinical exi)erience, for the largest and most inadequate hearts I have ever seen have been in men whose abdominal cor- ]iulcnce and sedentary lives have furnished the conditions neces- sary for the development of vascular disease in tlie splanctmic area* Moreover, their stiffened radials and high-tension pulse have borne out the correctness of that assumption. On the other hand, I have seen old men with emaciate<l ahdomcns, peripheral arteries that were like wires strung with tiny beads, and feeble, even flickering pulses, and yet whose hearts could not be made out as hyper- trophied* In some of these cases, to be sure, pulmonary emphy- sema renders the results of percussion uncertain^ but the clinical picture is that of ad\mamia or of a cachexia, hut not of myocardial failure, as in men of the other type.
Lastly, there is still another group of cases which present them- selves in guise of chronic bronchitis and emphysema. They are usually at or past middle age, not confined to either sex, yet in my experience more often males of the labouring class. The vascular system is everywhere stiff, urine is of poor quality or may contain a small amount of albumin, and there is manifest hy[Dertrophy of the right ventricle. This may be due in part to the emphysema, but a contributing factor of importance is the sclerosis of the pul- monary arteries. It is not always easy to determine whether this disease of the pulmonary vessels is primary or secondary^ but as it
750 DISEASES OF THE HEART
is associated with retrograde change of the aortic system it is fair to assume that it plays a role in the causation of the emphysema and bronchial catarrh.
For the most part the course of this vascular disease is slow and indefinite. Years are usually consumed in its development, and even after symptoms appear the course is protracted or more or less rapid, according to the portion of the arterial system chiefly affected and to the degree of the sclerotic change.
Fhjrsical Signs. — Inspection. — There are two main types of individuals with arteriosclerosis. In one class they are large and imposing, more or less corpulent and with rather too flabby abdom- inal walls. In such, there may or may not be evidence of vascular disease in the peripheral arteries. The other type is quite the re- verse. The individual is thin, looks ill-nourished, and the tem- poral, perhaps also the carotid, arteries are seen distinctly, the former looking like stiff tortuous cords and pulsating visibly. Superficial veins are also prominent, but cyanosis is not present. The only other information obtained by inspection relates to changes in the strength and location of the apex-beat, and to epi- gastric pulsation, signs which may be directly connected with arteriosclerosis, yet may be independent of the same.
Palpation. — This is the best and usually most reliable means of detecting arterial degeneration. If an artery which rests on a firm foundation, as the radial or tibial, is carefully palpated, it is perceived to be thicker and stiffer than normal. It can be rolled beneath the finger like a cord, and the vessel is difficult to compress. In many cases this is all, but in others the vessel is tortuous, and when the finger is passed along its course, presents small elevations that feel hard like beads, and hence lead us to speak of the vessel as beady. In some instances the artery shows minute elevations, which when carefully studied are found to be dilatations of the vascular wall — in other words, miliary aneurysms.
Particular attention should be paid to the cervical arteries, noting their position, size, reguliarity or smoothness, rigidity, etc., since changes in them may furnish valuable hints concerning the state of the aorta and infercntially of the coronaries. When the arch of the aorta is thin-walled and dilated it may sometimes be felt pulsating abnormally high up in the suprasternal fossa. Litten is authority for the statement that when the abdominal aorta is sole-
ARTERIOSCLEROSIS
751
rotic and acceasiWe to palpation, thrill is elicited by very much less pressure than m required if the vessel is healthy.
Percussion is of value only in the detection of changes in the si^e of the heart secondary to vascular disease. It may, therefore, by demonstrating hypf*rtrophy of the left ventricle, afford a certain amount of corroborative informatioD. Careful and deep percus- sion of the areas overlying the ascending portion of the aortic arch may detect a slight degree of duliiess due to dilatation of the vessel. In such a case rescjnance is apt to be impaired in the first and sec- ond right interspaces close to the sternum. Dilatation and elonga- tion of the arch may displace the heart downward, the same as does true aneurymn ; and hence in eases in which the aorta is suspected of being sclerotic, it is well to percuss the heart carefully, with view, if possible, to ascertaining its exact location*
Aiiscultatlon. — Almost the only value of this means of investi- gation lies in the study of the second sound in the aortic area. This tone is nonnally more intense than is the pulmonic second in per- sons after thirty years of age, and hence it is the quality of this sound more than its mere intensification that is significant. Gen- eral arteriosclerosis catises accenhiation of the aortic second tone, but so also do other conditions, eispeeially chronic interstitial neph- ritis. Taken in connection with left-ventricle hypertrophy, un* due intensification of this sound is significant of arterial or renal disease or both. If the sound is not only intensified but is also sharply ringing, even of a metallic quality and is associated with stiff arteries in persons of middle age, it is generally consid- ered to indicate sclerosis of the aorta. Should the sound be not quite pure^ as well as accented, it is likely that the valve is also involved in the degenerative process* Not infrequently in persons whose vessels are resisting, there is a systolic murmur heard along the course of the ascending arch, and when present is, in the absence of signs and symptoms of aneurysm, to be regarded as due to roughening or dilatation or both of the aorta, not of steno- sis of the ostium. Any other modifications of the cardiac sounds are indicative of secondary or associated changes in the heart- muscle and valves.
Diagnoflifi,— ^The recognition of sclerotic changes in periph- eral vessels that can be reached by the palpating finger, as radial, uLnar^ tibial^ etc., is a very simple matter, and has been sufficiently
752 DISEASES OF THE HEART
described under palpation. It is far othen^'ise, however, with the diagnosis of sclerosis of the arteries within the cranial and other cavities. In such, diagnosis is usually a matter of inference in- stead of absolute demonstration, and must be arrived at by study of the patient's history, age, sjTnptoms, etc. It is manifestly beyond the scope of this work to discuss the diagnosis of disease of the cerebral vessels. It may be stated, however, that tortuosity and rigidity of the temporals may, in connection with the head symptoms previously noted, be taken to point strongly to sclerosis of the cerebral arteries. If doubt still remains, or the external vessels are negative, the ophthalmoscope may be appealed to and is said to furnish early and reliable information concerning the state of the cerebral arteries (Thoma, Rehlmann, Koenig). The changes said to indicate sclerosis are pulsation and tortuosity of the retinal artery (when not due to chlorosis or amemia), opacity of its coats, narrowing, and it may be thrombosis of the artery of the papilla, and miliary aneurysms and punctate haemorrhages into the retina, the choroid, and the enveloping capsule of the optic nerve (Koenig).
The diagnosis of sclerosis of the aorta cannot always be defi- nitely made. Romberg states that the condition of peripheral vessels, as radials, affords no criterion of that of the aorta, and hence stiffness of the arm or leg arteries does not warrant a con- clusion that the aorta is also sclerotic. The state of the latter must be inferred, therefore, from careful study of the cervical ves- sels and of changes in the size of the heart or of its sounds. If the carotids appear healthy, if the heart is not appreciably en- larged nor displaced, and the aortic second tone is not unduly ac- centuated, then the aorta is probably healtliy. If, on the contrary, the carotids are unyielding, the subclavians are situated abnor- mally high and feel stiff, if the left ventricle is hypertrophied, and lastly, but not least, if the aortic second sound is ringing and metal- lic, there is probably sclerosis of the ascending portion of the arch.
The question of the existence or not of arteriosclerosis within the domain of the splanchnic nerves may present great difficulties. The recognition of stiffened radials in a corpulent individual who complains of dyspna^a of effort out of proportion to recognisable changes in the heart, renders extremely probable a similar state of the vessels deeply situated in the abdominal cavity. If, on the con-
ARTERIOSCLEROSIS
758
trary, accessible arteries are not stiff » one must depend for diagno- sis on the history, symptoms^ degree of blood-pressure, and adequaey as well as size of the heart A history of sedentary pursuits and of luxus consiiiiiption ; gradiudly developed and increasing shortness of breath ; abdominal corpulence ; high tension but slow pulse; cardiac Iiypertrophy without dilatation; these point strongly to arteriosclerosis as the cause of the symptoms.
In suspected cases one should test the efficiency of the heart- nuiscle as well as search carefully for indications of overstrain of the right ventricle. If the pulse is unduly rapid and feeble during repose, if cardiac dulness is increased transversely and downward with pulsation in the epigastrium, if superficial veins are engorged, there is reason to conclude that the heart is no longer quite ade- quate and that the dyspnrra is cardiac. Then if on the patient's making extra exertion^ as by hojjping alnrnt the room, the action of the heart grows unduly accelerated, perhaps irregidar or inter- mittent, and the sounds become feeble, perhaps accompanied by an apex-murmur, but little doubt is to be entertained of myocardial instifficiency*
Even then the state of the internal vascular system may be a matter of doubt. Prolonged higli tension of the pulse, as shown by Gaertner's tonometer, and a ringing metallic quality of the aortic second sound strengthen the assumption that the heart weakness is secondary to arteriosclerosis. It is, of course, presupposed that all other etiological data are wanting.
The differential diagnosis of such cases from the cardiac insuf- ficiency of the obese (the so-called fatty heart), is often iuipossible^ and, as a matter of fact, the two conditions are not infrequently combined. In the obese, how^ever, there is a general distribution of adipose tissue far in excess of what exists where there is only excessive abdominal corpulence with arteriosclerosis.
Quite recently T examined a gentleman of fifty-three com- plaining of breathlessness on more than moderate exerti^^n, Uis abdomen was very bulging and flabby, while bis extremities and chest were rather thin, h!a radials were distinctly stiff, but the heart was not appreciably enlarged except on the left, and did not grow too rapid or irregular from the effort of hopping up and down my office. In this case I felt no hesitation in attributing bis symptoms to arteriosclerosis, and not to myocardial inadequacy, 48
754 DISEASES OP THE HEART
particularly as his habits were such as tended inevitably to its de- velopment. Unfortunately all cases are not so clear, and hence necessitate great reser\'e.
With regard to the diagnosis of vascular disease in other inac- cessible regions, it may be stated that coronary sclerosis is not often possible of positive recognition. It may be assumed when angina pectoris develops in a man past middle age, when there is reason- able evidence of sclerosis of the aorta and its great branches with subjective and objective symptoms of myocardial incompetence.
Sclerosis of the pulmonary artery cannot be diagnosed with any degree of certainty, but may be assumed if a patient with stiff arteries is a sufferer from chronic bronchitis and emphysema, and in addition there is unusual hypertrophy of the right ventricle.
Renal arteriosclerosis may be inferred if in conjunction with ' stiffened peripheral vessels there is nocturnal micturition, the urine being of poor quality. When in an advanced stage there is evidence of positive renal change, as shown by albumin and casts, it is practically impossible to say definitely how much is due to nephritis and how much to arteriosclerosis.
PrognosiB. — This depends upon the degree of the vascular change discovered and upon the extent and nature of the visceral disturbance resulting therefrom. The process is inherently pro- gressive, and I believe incurable. Symptoms may, however, some- times be held in check by proper treatment.
Cardio-vaseular symptoms are for the most part subject to the conditions which influence prognosis in cases of myocarditis, and need not here be dwelt upon. For the prognosis of cerebral and renal arteriosclerosis readers are referred to works devoted to dis- eases of the respective organs. The ])rognosis of sclerosis of the pulmonary vessels is essentially that of the cardiac or pulmonary affections to which it is secondary, while when vascular decay of the arteries of the extremities has once led to definite disturbance of circulation the prognosis is highly unfavourable. Progressive emaciation and loss of strength in general arteriosclerosis indicate so serious an interference with nutrition that it may be regarded as the commencement of the end.
Treatment. — This is to be divided into (1) prophylactic, (2) curative, and (3) symptomatic. The institution ot preventive measures necessitate (A) the earliest possible recognition of vas-
ARTERIOSCLKHOSIS
T65
eular change and (B) the proper regulation of habits, diet, exercise, and excretion with a view to lessening undue vascular strain and correcting injurious fluctuations of blood-pressure. The disas- trous eflFect of sedentary pursuits must be counteracted hy appro- priate gymnastic and abdominal exercises, ineludling massage in cases of excessive abdominal corpulence. Heavy feeding must be restricted and its effects offset by outdoor exercise and sports, as golf, hunting, and fishing. Furthermore, the character of the dietary should be revised so as to exclude or reduce the eating of meats which are tissue- forming foods and are also harmful on account of the extractives they contain.
Theoretically, also, the diet should not consist of foods rich in lime-salts, and as a matter of fact Runipf, of Hamburgj cuts out such articles from the dietary of his patients. He includes among such forbidden articles milk, eggs, cheese, rice, and spinach. For my part, I aiu of the opinion that quantity cuts a far greater figure than does quality, since it is a matter of every -day (observa- tion that the individuals who live the longest and are the most active with advancing years are those who eat sparingly and of a dietary relatively rich in vegetahlea, cereals, milk, and fruits. I regard it as a good iudieatitm when a person past middle age tends to lose weight gradually rather than to gain. Best of all, he should strive to hold his weight about at a standstill until well on in years.
Exercise in the open is a very important matter, especially for tlie man who having been accustomed to plenty of exercise in col- lege sudtlenly finds himself tied down to his office desk many hours each day. He should endeavour in every way possible to get out for some sort of active physical exertion. If his profession or busi- ness duties tax his mental powers severely and keep him keyed up to the highest pitch day after day and month after month, then he should make whatever sacrifice is necessary to secure a yearly vacation, during which he can obtain perfect relaxation and recrea- tion. Otherwise sclerosis of cerebral or other arteries will be his fate after middle age.
If, as is l>elieved, the splanchnic nerves regulate blood-pressure and irritation of these nerves increases blood-pressure, particularly within the abdominal cavity, then, from a prophylactic standpoint, digestive derangements, including of course chronic constipation,
756 DISEASES OF THE HEART
should be corrected. This is desirable from another point of view — ^namely, that by improving excretion the system may be rid of toxines which may be of influence in augmenting arterial tension, and eventually leading to arteriosclerosis.
In a word, the prevention of degenerative changes in the blood- vessels calls for the removal, or at least the minimizing, of all in- jurious influences which are believed to derange blood-pressure, and thereby subject the vascular system locally and generally to strain.
The curative treatment of arteriosclerosis is, I believe, unprom- ising. The French, and of late some German clinicians, as Vie- rordt, express faith in the ability of iodine to arrest and even cure vascular degeneration. The remedy is administered in the form of iodide of sodium rather than of potassium because of its being better tolerated. It is begun in small doses, 2 or 3 grains twice or thrice a day at first, and as the system learns to tolerate the remedy it is gradually increased until 15 grains three times a day are reached. In this dose the iodide is continued over a long time — i.e., from eighteen months to three years — ^but with occasional intervals during which the drug is not taken. Vierordt is said to omit the remedy one week out of five and one month out of every five months. Given in this manner, and from the start increased so cautiously as not to cause imdue irritation, he has seen very gratifying results. I have made repeated attempts to get my private patients to perse- vere in the use of iodide of sodium after the manner recommended by Vierordt, but always without success. It lias invariably disor- dered appetite and digestion, and at length has had to be discon- tinued.
This therapeutic agent may favourably affect the patient's gen- eral condition, and even the vascular disease in cases of syphi- litic origin (although I believe the claim is made that favourable results are obtained even when there is no specific taint), but it is very difficult to see how any drug can promote resolution of the sclerotic process, or why it should be well to do so. If the develop- ment of connective tissue in the intima is, as Tlioma believes, a compensatory process by which is attempted to make good atrophic changes in the media, then how can any line of therapy be bene- ficial that does not restore the media to its former normal state? The iodide may in some way prevent or remove deposits of lime
ARTERIOSCLEROSIS
167
and the hyaline degeoeration that ultimately occur in the newly formed connective tissue^ but can it do naore or would it be well to have it do more ?
It seems to me, therefore, that when arteriosclerosis has once become pronounced, our efforts must be limited to the prevention or lessening of symptoms — in short, must he symplomaiic* To do this we must endeavour to pramote better circulation in the arterial system, since it is in this respect that evils' arise.
Cardio-vascular derangements are to be combated in the same manner as disorders due primarily to cardiac insufficiency, and these do not need to be repeated. I should like to urge the neees- siry, however, of freely using vaso-dilators, as the nitrites, that if possible the arterial paths may be somewhat opened up and the labour of the left ventricle thereby lessened. In this class of cases nitroglycerin, etc., should always be given whenever it is necessary to resort to digitalis. It is because of the constricting action of digitalis on the arterioles that strophanthus ought to be tried instead, and only replaced by digitalis when it has proved in- efficient.
Nothing is of greater sennce in cases of diffuse arteriosclerosis with secondary venous engorgement timn a periodic purge by means of calomel. The catharsis should be brisk to be of benefit, for relief does not follow until several waterv stools have been secured. I have seen truly surprising results from such simple treatment. One instance in particular comes to mind as I write, that of an old German with verv stiff vessels who exhausted both my patience and my resources in a vain endeavour to procure relief from formication nnd coldness of the thighs. At last, in despair, I prescribed 5 grains each of calomel and jalap for the purpose of preventing his return to my clinic. He did not reappear for two or three months, when one day he returned, and on entering the clinic room cxchiimed that he bad come back for another powder, as he bad never hod anything do him so much good.
I recall also an Irishman with stiff arteries and an obstinate chronic bronchitis that had defied the efforts of several well-known practitioners, and who obtained greater relief from his dyspna^a and cough by a single dose of 5 grains of calomel than from all the cough mixtures he had previously taken.
Fraenkel reports the highly interesting and instructive case
758 DISEASES OP THE HEART
of a man with general arteriosclerosis who was relieved of his nocturnal asthma for a period of three months by a single sharp attack of epistaxis. This suggests that in cases of cardiac asthma, which so often form a distressing feature in the clinical history of arteriosclerosis of the cardio-vascular type, it might be well to resort to venesection when catharsis has failed of ameliorating the symptom.
In cerebral arteriosclerosis I am of the opinion that stimulants and vaso-dilators are indicated. Judgment and caution should be exercised in their administration, however, lest the heart be too vigorously stimulated and rupture of a miliary aneurysm result The safety of such medication may be estimated by the state of the cardiac muscle. They are certainly indicated when the systoles are feeble and the brain is not suflBciently flushed.
The treatment of coronary sclerosis and its resulting angina pectoris has already been considered in the chapters on Chronic Myocarditis and Angina Pectoris.
The management of renal sclerosis is essentially that of chronic nephritis, since the two conditions are so frequently com- bined. When vascular disease in the extremities has led to gan- grene, the treatment is of necessity surgical. Sclerosis of the pul- monary artery is practically that of arteriosclerosis in general plus that of bronchitis and emphysema.
Only general principles can here be laid down. In every case special symptoms must be left to the judgment of the practitioner.
L
CHAPTER XXXIII
ACUTE AORTITJS - ACUTE ARTERITIS - SYPHILITIC ARTERITiS-ENDARTERlTJS OBLITERANS-PERIAR- TERITIS NODOSA-STENOSIS OF THE AORTA AND PULMONARY ARTERY-CONGENITAL StVIALLNESS OF THE ARTERIES
L ACUTE AORTITIS
When acute inflammation of the aorta is discovered it is in moat cases associated with the changes of sclerosis in the same situ- tion or with an acute endocarditis* French authors, however, have described a form of acute aortitis which they chiim is independent of antecedent sclerotic change and occurs in the course of acute infectioua diseases. Such statements are received with consider- able reserve by the Germans, and von Schroetter in NothnageFs System seems qnitc sceptical on the subject, particularly as regards its clinical reco^ition.
Morbid Anatomy*— The aorta is found more or less dilated, and tiie surface of the intima looks rough from the presence of reddish or grayish translucent more or less thickly scattered patches of a gelatinous consistency. These are minute thrombi, and it is through the detachment of these that cutaneous and other infarcts occur, the same as in acute valvulitis. Indeed, acute aor- titis is so similar to acute endocarditis that the description of the latter may answer for the former.
The process may he of a benign type and proceed to the forma- tion of so-called vegetations, or it may b€?ha\*e like ulcerative endo- carditis and lead to serious destrnetion of the vessel and rupture. In this manner communication may be established between the aorta and one of the auricles, a contiguous vessel or the pericar- dium with fatal ha?ujorrhage (Romberg). The media and even the adventitia becomes infiltrated with round cells, and if the pro-
759
760 DISEASES OF THE HEART
cess is sufficiently prolonged newly formed vessels may penetrate into the intima.
As already stated, degenerative changes are usually found as- sociated with the evidences of acute inflammation. There may also be an associated valvulitis affecting previously healthy valves or more often as an acute process ingrafted on an old-standing aortic-valve lesion. In other distant parts of the body there may be discovered local changes due to benign or septic emboli cast off from the aortic intima.
Etiology. — The aorta may become acutely inflamed in conse- quence of direct extension of an identical process of the endocar- dium. French clinicians (Huchard, T-.eger, Siredi, etc.) maintain that acute aortitis may arise in the course of scarlatina, measles, variola, independently of involvement of the endocardium, and Fiessinger is said to have seen it in a case of influenza (Gibson). The latter says also that acute aortitis may be associated with acute pneumonia, pleurisy, and pericarditis. The disease has also been attributed to trauma, and has been observed in the course of chronic nephritis.
Symptoms. — Acute aortitis in most instances is latent or is overlooked by reason of its occurrence in the course of some other distinctive affection. The case discovered by Thoma, and which occurred during measles, had produced no symptoms whatever. Von Schroetter appears to think that the clinical features de- scribed by Huchard in such a brilliant and interesting fashion are not to be attributed to acute aortitis per se, but are such as are so often observed in cases of arteriosclerosis affecting the aortic arch. In Chapter IV, page 158, I have depicted a case which I took to be acute endocarditis because of the subjective symptoms and clinical findings, and in which post-mortem examination dis- closed an aortitis together with endocarditis, the acute process hav- ing developed on top of old sclerotic changes that had masqueraded under the guise of aortic insufficiency.
I will briefly portray the features that are claimed by the French to have been observed in acute aortitis unconnected with other aortic or endocardial lesions. Fever is usually absent, but if present it is due to the primary infection, not to the aortitis as such. The countenance is apt to be pale and anxious. The pulse is small and weak, regular or not, as circumstances in each case may die-
ACUTE AORTITIS
7fil
tate. The patient is likely to complain of pain in tlie upper ster- nal region, and sometimes extending through tlie iiiediaatinnni and clown the back along the spinal column. The pain is described as burning^ sticking, smarting, etc., and in some instances is said to radiate into the left shoulder and down the arm, very like that of angina pectoris. The resemblance to this latter is enhanced by a feeling of oppression and anxiety in some cases,
Peter has observed tenderness on pressure in the intercostal spaces to the left of the manubrium, and undue throbbing of ihe right subclavian ban been noted by French writers (Laboulbeue, Faure)j and by them is attributed to the greater liability to in- flammation of the left suh^lavian than of the innmninate artery. Von Sehroetter, however, believes that if such difFerenee in the pulsation of the two subclavia exists, it is due to sclerotic changes, an opinion in which Gibson concurs.
Dysphagia, cough with expectoration, and disturbance of the digesti%x* tract shown by vomiting and flatulent distention of the bowels, have been observed in some cases.
In short, the symptoms of this affection are often wholly want- ing, and w^hen present are not at all distinctive. There is noth- ing in them which may not be observed in other affections involv- ing the heart, and hence Romberg states that even when the malig- nant form of acute aortitis occurs, there is nothing in its clinical picture to distinguish it from ulcerative endocarditis.
The course of acute aortitis is often protracted and the termi- nation is usually in death.
Physical Signs are usually indefinite, or are such as are found in other acute inflammations in%*olving the cardiac stnie- tures, or are those of the infection in the course of which acute aortitis occxirs.
Inspecfwn, — The countenance may be pallid and anxious, the carotids throb strongly, and the right subclavian may pulsate more powerfully than does the left.
Pal pat ion is negative unless pressure elicits sensitiveness in the intercostal spaces to left of the sternum and along the course of the aorta,
Percussion is likely to be negative unless dulness be revealed at right of the manubrium in cases in which the inflammation leads to dilatation of the aortic arch.
762 DISEASES OP THE HEART
AtLSCultation. — This is not likely to furnish information of a positive kind. A systolic murmur over the situation of the ascend- ing arch may be evoked by dilatation of the vessel, and in cases in which the valve is also affected there may be impurity of the aortic second tone.
Diagnosifl. — This can rarely if ever be more than conjectural. If the character of the pain and oppression simulate that of angina pectoris, it may possibly be differentiated from it by the fact that in acute aortitis this symptom is likely to persist, or at the most show only remissions, not intermissions.
The differentiation from acute endocarditis is not possible in all, perhaps not in most cases. Aid may be obtained, however, if one notes that in the course of a disease resembling endocarditis no changes in the area of cardiac dulness or in the heart-sounds are developed, or if on repeated examinations one should be able to detect increasing dulness over the ascending aorta indicative of dilatation. In my case this was noticed, but was not correctly in- terpreted, owing perhaps to the coincident dilatation of the right auricle.
Prognosis. — This may be said to be very unfavourable. The occurrence of embolic phenomena renders the outlook most un- promising. Rupture of the aorta is a possibility that should always be borne in mind in suspected cases of the disease.
Treatment cannot be expected to do more than relieve symp- toms. Rest in bed is imperatively indicated, and the strength of the patient must be sustained by highly nourishing, easily digested food. Pain, when severe, should be allayed by morphine, counter- irritation, hot applications, etc. Nitroglycerin may be of service by diminishing intra-aortic blood-pressure, and strychnine is a val- uable general and cardiac tonic. Digitalis is only useful in case of threatening cardiac inadequacy.
II. ACUTE ARTERITIS
Morbid Anatomy. — (.Circumscribed inflammation of the larger arteries is t»onietimes observed in connection with an in- flammatory process of surrounding tissues or in consequence of embolic plugging. Infiltration with small round cells takes place in the outer and middle coats, later on also in the intima. The endothelial lining becomes swollen and of increased thickness.
ACUTE ARTERITIS
7fi3
while the imderljing layers of the intmia show the development of newly formed eonnectix'e tissue.
In cases in which the inflammation is the result of plugging, thromhoais also occurs, and in time the throniLiis undergoes organ- iziihon* If the embolus is infective, the inflammation may spread to the parts outside of the vessel and set up abscess. When the arteritis results from surrounding inflammation, thrombosis and subsequent or^^anization may likewise take place.
The etiology has already been stated in the opening sen- tence. Acute arteritis results either from adjacent inflammation or from embolic occlusion.
Symptoms are likely to be recognised only when the arteritis is situated in an extremity or a part accessible to palpation, and when thereby one can detect either embolism or tlirombosis, or when there is phlegmonous inflannnation <>f the tissues surround- ing an artery of considerable size.
When local intlanmiation invades the artery, involvement of the latter is likely to be masked by the symptoms of associated phlebitis. In the latter event there are circulatory disturbances due to interference with return flow, swelling, and more or less cedema, together with pain and great tenderness»
In the case of embolism there are pain and phenomena of obstructed circulation, coldness (local syncope), cyanosis, and numbness.
Physical Signs consist of such phenomena of local inflam- mation or of the accompanying phlebitis.
Inspection perceives swelling and redness of the affected ex- tremity.
Palpaiion is of greater service. The limb is hot, painful to touchy usually pits on pressure, and at some point careful palpa* tion is generally able to detect resistance due to the embolus or to thrombosis extending for a variable distance above the seat of the plug.
Diagnosis. — This is to be made by the history, local symp- toms, and the result of palpation. The differentiation of acute arteritis from phlebitis is not always easy or possible.
Prognosis depends upon the nature of the cause and the completeness of collateral circulation. Acute meningitis is a pos- sibility in certain cases, and of course affords a very grave outlook.
764 DISEASES OF THE HEART
The prognosis is always unfavourable in cases in which the arte- ritis is secondary to acute malignant endocarditis.
The treatment of acute arteritis is partly medical and partly surgical. The affected limb should be elevated, kept at absolute rest, and enveloped in moist heat, as poultices to which anodyne remedies may have been added. Pain is to be allayed by local sedatives or by the use of opium in some form. Should an abscess occur, it is to receive appropriate surgical management
III. SYPHIUTIC ARTERITIS
Vascular changes observed in syphilitic subjects have been the object of careful study by numerous investigators, among whom should be mentioned Lancereaux, Heubner, Weigert, Doehle, Baumgarten, Vendeler. Some of the changes are unquestionably of luetic origin, while others are by some authors, as von Schroet- ter, accepted with considerable doubt.
Morbid Anatomy. — The inflammatory changes in the arter- ies are of a chronic nature and invade circumscribed portions of a vessel or are limited to the arteries of certain regions, as of the brain. The process may show itself as circumscribed patches of a grayish white translucent appearance, or the entire vessel may be changed into a whitish or grayish cord in consequence of the trans- formation of its coats into fibrous tissue. In this form the adven- titia, and ultimately the media and intima, become infiltrated with round or fusiform cells. The process may remain in this stage of inflammatory infiltration (von Sohroetter), but as a rule it goes on to formation of fibrous tissue in the several coats.
This hyperplasia of the walls is often extreme and leads to very considerable narrowing and even occlusion of the lumen of the artery.
In this respect syphilitic arteritis differs from arteriosclerosis, which is more apt to lead to dilatation than to obliteration of a ves- sel, although it may do this latter in the smallest arteries.
It has been shown, furthermore, particularly by Baumgarten, that minute gummata are scattered in the middle coat in imme- diate proximity to the vasa vasorum. Atrophy and rupture of the media result, and in time the rents are repaired by the formation of cicatricial tissue. The subsequent contraction of these areas leads to pouchings of the intima, which, when they are found in
SYPHILITIC ARTERITIS
T65
the ascending aorta^ are almost pathognostic of syphilis (Rom- berg), These ponchings of the aortic intima may prove the start- ing-place of future aneurysms*
In another form of arterial disease due to syphilis the vessel becomes invaded by a syphilitic process in its neigh bt>urhood. The vessel is surrounded by a gummatous mass or by dense cicatricial tissuCj and the coats of the artery are more or leas thickened and altered (Zicgler). In the early or inflammatory stage th*^ outer and inner coats are rich in cells, but as the process advimccs fibrous tissue replaces the cells wholly or in part The media is not so much invaded by fibrous tissue as are the adventitia and intima.
The cerebral arteries appear to be the ones most frequently affected. The aorta and coronary arteries may, however, be the seat of syphilitic disease, and in a few cases the vessels of the extremities have been affected. C 0. Weber is said by von Schroet- ter to have found the right branch of the pulmonary artery in a syphilitic girl greatly narrowed by reason of a gumma in its walL Zeissl is also stated by the same author to have found the left brachial artery invaded by a gummatous iu filtration, while Lang- enbeck saw the same sort of process in the right brachial of another case.
Utiology, — Syphilitic arteritis is a late manifestation of lues.
Tiie symptoms are determined by the seat of the arteritis. In the case of the brain they are those of disturbed or obstructed circulation^ loss of memory, dizziness, headache, mental confu- sion^ epilepsy, etc. — in short, such as arise from areas of acute softening,
"ft'hen the disease affects the aorta it may lead to aneurysm or to the symptom-complex of sclerosis of the arch.
Arteritis of this origin may be a cause of angina pectoris by leading to sclerosis and occlusion of the corouaries, particularly the left anterior descending branch. In very rare instances a coronary artery has been said to be invaded and obliterated by a gumma of the myocardium.
In the extremities s3T)hiHtic arteritis occasions clinical mani- festations of obstructed circulation the same as may other forms of arterial disease, pallor or cyanosis, coldness, and eventually gangrene.
706 DISEASES OP THE HEART
The diagnosis must depend upon the history of luetic infec- tion and on the discovery of unmistakable lesions indicating a late stage of the disease. Even in such a case one cannot always say positively that the vascular changes observed are of specific origin. They may be due to arteriosclerosis and be independent of syphilis per 86. In some cases one may be obliged to await the result of treatment before being able to arrive at a definite diagnosis.
The prognosis is not always favourable as regards recovery, although appropriate therapy may in some cases affect a restora- tion of health. If the arteritis has led to pronounced fibrous thick- ening and considerable obstruction, to pouching, or even to aneu- rysm, there is small prospect of favourably influencing the process by antisyphilitic medication no matter how vigorous.
The treatment should consist of the administration of ap- proved specific remedies — i. e., mercury and iodides. In addition, one may have to treat certain sjTiiptoms, as angina pectoris, cardiac inadequacy, gangrene, cerebral disorders, etc. The management of aortic aneurysm will be found in a succeeding chapter.
IV. ENDARTERITIS OBLITERANS The following account is a condensed statement taken from von Schroetter's excellent description of the disease in Noth- nagel's Spocielle Pathologic und Therapie. No apology for such a transcript is necessary, since the disease in question is rare, and comparatively few contributions to the subject have been made. The designation obliterans was suggested by Winiwarter, whose case is considered so typical bv von Schroetter that he makes use of Winiwarter's description, l^illroth gave it the name Hyper- plastica, while Orth called it Productiva. Other observers to whose views or eases von Schroetter refers are Weiss, Brochard, Schlesinger, Sternberg, Wiedermann, Ortmann, lladden, Gold- flam, Wel)er, Collet, Cliatin, Kocine, Brann.
Morbid Anatomy. — The disease occurs most often in the smaller arteries of the foot or leg, occasionally also in the upper extremity, and excej)tionally in other parts. Upon macroscopic inspection the vessels are seen to be enveloped by a tough fibrous sheath which binds them firmly together. The individual artery — e. g., posterior tibial — is converted into a firm whitish cord, and on section is seen to be filled with a whitish gray or grayish brown
ENnARTERITlS OBLITP-JRANS
707
maaS| so that a probe can l>e passed into the %'essel only with diffi- culty or not at all.
The artery is nevertheless not uniformly so filled, yet on the whole is transformed into a rigid cord in consequence of its inte- rior being filled with a somewhat yielding wide-uieslied tissue. The process hegius at the periphery and extends upward, reaching from the plantar peroneal and posterior tibial arteries, even in some instances to the femora!, or in the case of the arnij to the brachial.
Histological examination reveals in different places a somewhat variable condition, yet which is in reality a hyperplasia of the intima which may augi:nient its thickness to even eight times the normal. In the larger vessels the newly fiKrmed connective tissue is composed of ronndj spindle-shaped, or stellate cells, between which can he recognised an intercelluhir substance made up of delicate threads. According to Winiwarter and others, several strata of elastic fibres may be seen in the outer portion of the in- tima next to the media. Finally, minute blood-vessels are seen to exist within tlie connective tissue of the interior, which Winiwarter regartla as an extension or formation of new channels by which an attempt is made to provide a collateral circulation, and not as an organization of a thrombus. The capillaries thus formed permit a partial injection of the mass filling up the lumen of the artery. In spite of this attempt at a collateral circulation the slump after an amputation does not bleed freely when the Esmarch bandage is removed.
Etdolagy.^ — This is practically unknown. It has been ob- served in men far more frecpiently than in %vomen, and what is especially strange about it is that it attacks comparatively young and previously healthy individuals. The process drx^s not neces- sarily invade all the arteries of a limb, for it has been found in the posterior tibial, Avhile the anterior tibial was free. It has been attributed to occupation, but in von Schroetter's opinion without sufficient warrant. The only theory that seems to appeal to von Schroetter is that the tiflTpetion is, in some manner as yet unknowTi, dependent on some ner%^ous influence.
Symptoms are made up of prodromata extending through a period of years, as many as twelve, and of such phenomena as depend upon interference with local circulation. Individuals thus
768 DISEASES OF THE HBABT
afflicted complain for years of pains in the leg or arm which are generally thought to be either rheumatoid or neuralgic, and are likely to be treated as such, yet without benefit.
After a time perversions of sensation occur (parsesthesise), as formication, numbness, etc. At first the pains are lessened or disappear when the extremity is at rest, but at length grow extreme, and on use of the affected member become intoler- able. As the obstruction to circulation increases movement be- comes difficult and the extremity feels heavy, so that the patient favours the limb so far as possible and may actually walk lame.
When at last the artery is wholly occluded areas of gangrene make their appearance. These may be superficial or may invade a toe or the whole foot, and show a tendency to spread rapidly upward. The extremity now looks either pale or livid and feels cold and lifeless. Unless the gangrenous area is removed by the surgeon septic phenomena may develop and lead to a fatal termi- nation of the case. The course of the disease is progressive, and the termination is usually or invariably fatal in the course of years.
The diagnosis is surrounded by considerable difficulty, par- ticularly in the prodromal stage. The pains are likely to be con- sidered rheumatic or simply neuralgic, and cannot very well be correctly interpreted before there is evidence of rigidity of and want of pulsation in the arteries.
Obliterating endarteritis is to be distinguished from arterio- sclerosis mainly by the age of the patient, since it has been observed most frequently between twenty and thirty, next between forty and fifty, and arteriosclerosis occurs most often past fifty. The disease is likely to be localized, while evidence of vascular degen- eration is usually more wide-spread. Moreover, arteriosclerosis, although it may cause gangrene, does so far less constantly than does the endarteritis, and then usually in persons who present well-marked evidence of the arterial change in both legs.
Reynaud's disease, for wliich the endarteritis may be mistaken, occurs most frequently in children and young adults, especially in females, sets in abruptly, and the dead feeling of the fingers of both hands is attended with slight anaesthesia. Moreover, the condition is due to a cramplike constriction of the vessels, and is not attended with rigidity and pulselessness of the vessels.
PERIARTERITIS NODOSA
769
le prognosii i.s unfavourable, since the affection is pro- gressive,
Treatnient ig of a necessity symptomatic and restricted to Bitch measures as may alleviate suffering. The occurrence of gan- grene calls for surgical interference.
V. PERIARTERITIS NODOSA. SYN,: CONGENITAL ANEURYSM
The very remarkable and rare affection which hears the above titles was first adequately dcscribc^d by Knssmaiil and Jlaier in IStif], although it appears that Rokitansky in 1852^ and possibly Pelletan in 1810, observed each a single case (von Schroetter). The designation Periarteritis Nodosa was bestowed upon it by Kussmaul because of his conception of the process as an inflam- mation originating in the adventitia. The term Congenital Aneu- rysm is applied to it because it has been thought to be due to con- genital weakness of the arterial coats (Eppinger), leading event- ually to the development of multiple aneurysnis. According to von Schroetter, only thirteen authentic eases liave been reported.
Morbid Ajiatomy.— The afTectcd artery is studded with nodular thickenings of a whitish colour and of variable size» from that of a pin's head to a pea, which are due to circumscribed fibrous thickening of the intima with cellular infiltration of the adven- titia and media. The lumen of the vessel may be narrowed or the weakening of its coats may lead to circumscribed dilatations — i. e,, multiple aneurysms. These may reach such numbers as to be uncountable. The disease affects arteries of medium calibre, and is found with special frequency in the arteries of the muscles and viscera, as the heart, intestines, spleen, liver, and kidneys, and also of the ^kin.
Its etiology is entirely unknown, but inasmuch as the clin- ical picture is very like that of sepsis or an infection it may have some such origin (Romlx^rg). Tlie disease appears to attack both Bexes about equally and to occur between the ages of twenty and fifty-two (Osier).
SymptomB. — The most striking featnres of the affection are
weakness, rapidly progressing anaemia, and rapidity of the pulse
out of all proportion to the temperature. Fever may be present in
the beginning, but is of moderate height, and tends to ultimately
disappear. There is pain in the muscles which may eventually 48
770 DISEASES OP THE HEART
show atrophic changes and paralysis. Digestive disturbances are present, as anorexia, thirst, and vomiting, and there may be con- stipation or diarrhoea. There may be albuminuria and casts, and when the arteries of the abdominal organs are aflFected there is severe epigastric distress. Hemorrhages from the bowel may also be observed (Romberg) in cases in which the arteries of the intes- tines are the seat of the disease.
The course of the malady is progressive as a rule, and a fatal termination occurs in from six weeks to three months. Very ex- ceptionally, however, recovery may ensue.
Diagnosis is impossible unless the nodular thickenings can be felt along the course of peripheral arteries or such as situated within the abdomen are yet accessible to palpation. In suspected cases a nodule may be excised and subjected to microscopic exami- nation.
Prognosis is unfavourable, although recovery does not appear to be imjx>ssible.
Treatment is purely symptomatic and is limited to attempts to alleviate suffering, build up strength, and check or overcome the destruction of the blood.
VI. STENOSIS OF THE AORTA AND PULMONARY ARTERY Stenosis of the Aorta may be Congenital or Acqnired. — In the
foriiKT variety the narrowing is situated at the isthmus and may 1h» caused by a toi> early closure of Botalli's duct and conse- quent failure of the descending aorta to receive the amount of blood nei'essarv for its proper development or expansion, or a membrane may ho stretcheil across the vessel at the isthmus, having at its centre an oixMiing through which the stream of blood must j>a<s.
Acqnired stenosis may Ix* caused by a fibrous band that con- stricts the aorta at some point within the mediastinum, or it may l>e compressed by a tumour. Such con<litions are, however, rare as regards the arch, since this jx^rtion of the aorta is capable of suecessfnlly withstanding encroachment u]K">n it by new growths iHomhcTf:).
In the chapter on Dextrocardia is mentioned the case of a child in whom the rotation and dis]>lacement of the heart had caused the suj>erior vena cava to be stretched tightly across the aorta and
STENOSIS OP THE AORTA AND PULMONARY ARTERY 771
constrict its lumen. I have also in tht* chapter on Aortie Ke^irgi- tation mentiuued the? case of a man whose ascending aorta was greatly narrowed by a ring of fibrous tissue that completely encircled the vessel and had induced relative insulKciency of the valve.
Symptoms depend upon the degree and seat of the stenosis. In the congenital form collateral circulation may become estab- lished through the intercostal arteries, the internal mamniary, or arteries in the integument and muscles of the back. If such side channels are sufficient there may be no obvious hindrance to the blood-supply of the lower parts of the body^ and no untoward effects are experiencetL
Romberg mentions a case observed by bini in which the arter- ies of the back provided a means of maintaining the circulation below the point of stenosis, and in which he detected a loud vascu* lar bruit on the posterior aspect of the trunk between the vertebral column and right ifcapula. The niurniur was attributed by him to dilatation of the arteries at that point.
In the acquired form narrowing of the aorta is likely to occa- Bion compensatory hypertrophy of the left ventricle and possibly also incompetence of the aortic valve, as in my case. The ulti- mate effects are those of cardiac inadequacy. In cases in w*hich relative insuffieieney does not occur, but the stenosis leads to left- ventricle hypertrophy, the clinical history is likely to be that of narrowing of the ostium or of the disease which causes the con- striction of the aorta*
The dla^OSis is very difficult as a rule, and may be impos- sible. One may recognise the signs of obstruction to outflow from the ventricle, but may not be able to determine its real nature. The detection of a mediastinal tumour or of chronic fibrous medi- astinitis, together with the signs of obstruction — ^i. e., a systolic hruit over the course of the aortic arch with accent itation of the aortic second tone and left-ventricle hypertrophy — might lead to a correct diagnosis. This would be strengthened if as time went on evidence of regurgitation should appear.
Congenital narrowing of the isthmus might be diagnosed if one were to discover compensatory dilatation of the arteries by which collateral flow is established together with hypertrophy of the left ventricle.
772 DISEASES OP THE HEART
Prognosis depends upon the cause and decree of the stenosis, the effects on the heart, and in congenital cases the completeness of collateral circulation. The general health may not be seriously influenced, or the heart may suffer in its integrity, and death be ultimately brought about through cardiac inadequacy. In a few cases the prognosis may be that of the etiological condition.
Treatment is to be addressed to obviating so far as possible the injurious consequences of the acquired stenosis. We can do nothing towards removing the cause.
Stenosis of the Pulmonary Artery is acquired, and is a relatively infrequent condition. It may be due to constriction by a fibrous band, to compression by an aortic aneurysm and a few other con- ditions, of which isolated examples have been reported. Thus Romberg states that Litten found stenosis of the pulmonary artery from an " echinococcus embolus," while Gerhardt discovered a case of slight compression of the vessel by the left auricle in conse- quence of this having become distended by a clot. C. O. Weber, cited by von Schroetter, obsen^ed pronounced narrowing of this artery by a bean-shaped gumma in its wall. One of the branches of the artery may be constricted through retraction of the lung in interstitial pneumonia.
Symptoms are confined in the main to the secondary effects on the right ventricle or to congestion of the lung back of the seat of stenosis when this is situated within the lung at a distance from the bifurcation.
If the obstruction is in the main trunk or in a branch suffi- ciently close to the main stem, the right ventricle imdergoes hyper- troi)hy and perhaps dilatation with consequent turgcsconce of the veins of the aortic system and corresi>onding feebleness of the pulse. It may even lead to relative incompetence of the pulmonary valve with its evil consequences.
Diagnosis is attended with great difficulty, and is likely to be impossible. It must depend upon the recognition of right-ventri- cle hyj)ertrophy for which no other cause can be determined, or on this with a systolic murmur in the pulmonic area together with intensification^ instead of diminution of the second tone, as is the case in stenosis of the pulmonic ostiimi. Systolic pulsa- tion in the situation of the trunk of the artery — i. e., in the second left intercostal space close to the sternum — together with
CONGENITA!. SMALLNESS OF THE ARTERIES 778
d Illness in this area, would greatly strengthen the other signs just men t i oned ( Koinberg) .
The prognosis is determined by the nature and degree of secondary disturbance. It is of necessity more or less unfavour- able.
Treatmant is entirely symptmnatic, and, as in stenosis of the aorta, must aim at maintaining cardiac adequacy, since the cause cannot be removed.
VII, CONGENITAL SMALLNESS OF THE ARTERIES
This state of the aorta an*! arterial system was studied by Virc'how, who pointe<l out its association with chlorosis. Not only are the vessels uf small calibre, hut their coats are thin and deli- catCj rendering them particularly liable to rupture, and they are abnormally elastic. In extreme cases the lumen of the arteries may he reduced to a third of the nornuil (Romberg),
The heart is also abnormally !?mall, the genitalia are likely to remain undeveloped, and the individuals are small and delicate in appearance* This is especially true of those who present the chlo- rosis spoken of. In other not (jmnounced cases of arterial hypo- plasia there may be nothing in the appearance and no lack of body development to suggest its existence.
Symptoms of this condition as such cannot be said to exist. The heart, by reason of its snialhiess, is weakened in its re- sistanee, and is more than usually liable to infection (Romberg), and indeed general vigour and resistance may be said to be below par. This is readily compreheu?^ible in cases character- ized by chlorosis. The bypiplasia is found more often among feuuiles than males.
Fraentzel was of the opinion that congenital narrowness of the arteries predisposed to hypertrophy and dilatation of the left ven- tricle, and in support of his view cited instances of the kind in young recruits, Romln^rg, however, thinks the clinical picture draw^n by Fraentzel is to be interpreted as the result of prema- turely developed arteriosclerosis. This is favoured possibly by the sniallness of the arterial system ; and yet, as a matter of fact, such arterial degeneration does not occur with special frequency in the subjects of arterial hypoplasia.
It is worthy of note that rupture of the aorta and dissecting
774 DISEASES OF THE HEART
aneurysm are said to occur with relatively greater frequency when it is congenitally narrow. The patients are also said to bleed more easily than normal persons owing to the thinness of the vascular coats.
BiagnosiB of arterial hypoplasia is difficult to make with cer- tainty. It may be considered as possibly present when palpation of the large cervical arteries and percussion of the heart show what seems to be abnormal smallness of the same, and when, in addition, the individual is poorly developed, chlorotic, and possesses deform- ity or an infantile state of the genital oi^ns. It is possible that an expert in the use of the fluoroscope might be able to recognise that in a given case the heart and large vessels were abnormally undersized.
Fngnosis. — Congenital narrowness of the arteries affects life prospect only when the hypoplasia is considerable and is at- tended with chlorosis. In such cases there is danger of some of the consequences that have already been considered.
Treatment cannot affect the underlying condition, and is therefore limited to attempts at relieving or modifying such effects as may result
rTTArTEK XXXIV ANEURYSM OF THE THORACIC AORTA
AxEi uvsMs liave been tlie objrct of interested study for several centuries both to anatomists and clinicians. The names of many celehruted men are connected with the history of this arterial dis- ease, and, as might be expected, they were at first tlie name^^ of anatomists who stndied the subject mainly on the deud body. Methods of diagnosis were crude and, very naturally, not equal to the (Hst^overy of such obBCtire affection!^ as intrathoracic aneurysm. Xevertheless it is worthy of record that Vesaliua made a diagjnosis of aortic aneurysm in 1507, JIalpighi and !Mor^agni wrote on the subject and added to tlie facts euneerning it. There has been scarcely an author of note since wlio has not attempted to add to our knowledge rm the subject, and to some of tlieoi the profession is greatly indebted, Lancisi, Scarpa, Corvisart, Hodgson, Stokes, and in our own tinje Eppinger and Thoniaj are names that are inti- mately linked with tlie history of anenrysni.
In this cbajiter it is propr>sed to deal exclusively with the dis- ease as it affects the aorta within the thorax, a cnnditinn tbut pos- sesses peculiar interest for the physician. Aneurysms of periph- eral arteries belong to the prnvinee of the surgeon and hence are left to surgieal works for consideration.
Morbid Anatomy, — An aneurysm is a circnmseribed dilata- tion of an artery; and as siieh must be distinguished from the uni- form widening of an artery, wliieh results from sclerosis. The three main divisions that are made of aneurj^sms are, (A) true, (B) dissecting, (C) false. By false aneurysm is meant a circum- scribed collection of blood that has escaped from an artery into the surrounding tissues, hence a ha^raatoma. The walls of the tumour are not composed of the arterial coats, and therefore, ac- cording to von Scbroetter, it should not have the term aneurysni
775
776 DISEASES OP THE HEART
applied to it at all. A dissecting aneurysm is one in which the stream of blood penetrates through a rent in the intima into the parts beneath, and burrowing its way either between the inner and middle coats or in the layers of the media, thus dissects up the intima for a variable distance. In some instances the blood-current again breaks through the intima and becomes reunited with the main stream. This condition may be of long standing and is scarcely open to recognition.
True aneurysm is therefore the condition in which are ful- filled the requirements stated in the definition. The two sub- divisions of this form of tumour which best meet the facts as observed by the clinician are (1) fusiform and (2) sacculated aneurysm. By the former is meant a localized dilatation of an artery involving its entire circumference; while by sacculated is meant a dilatation limited to one side, and hence involving but a portion of its circumference.
Aneurysm of the aorta may be either fusiform or saccular, but the latter is the more common. All three coats are involved in the bulging but are not all retained in the wall of the aneurysm. The intima extends into the sac to a greater or less distance, but is then lost. The portion that persists usually presents the changes of arteriosclerosis, as does also the inner coat of the aorta, in the neighbourhood of the tumour.
The media is also involved in the destructive process which has favoured the fonnation of the aneurysm. Its muscular fibres are degenerated or wholly lost and its elastic elements show signs of granular change. In places, the middle coat may be entirely destroyed; and when such is the case, together with loss of the intiina, the wall of the sac is composed solely of the adventitia. This latter is also thickened and infiltrated with inflammatory products.
The j)ouch which has thus been formed communicates with the lumen of the aorta by an opening of variable size, but almost al- ways smaller than is the calibre of the sac. The interior of the aneurysm is apt to be lined by coagula in the form of layers of a whitish colour. The most internal of these lamina is likely to be reddish and soft, while the more deeply situated layers are firm as well as white. The degree of thrombus formation within the aneurysm is variable, but does not usually fill up its lumen.
ANEURYSM OF THE THORACIC AORTA 777
Except ioB a II J, however, Avlien the sac is not very large and its opening into the channel of the aorta is small, its cavity may be entirely tilled with eoagula so as to obliterate the sac. The inner- most layer of fibrine then forms a firm wall nearly on a level with the intinia. Its surface is apt to be rongh and calcified. Altliongli an aneurysm may in this manner undergo spontaneous arrest, still the degeneration of the arterial coats which led originally to the formation of tliat aneurysm h likely to favour the development of others^ so that multiple aneurysms are not at all uncumuion.
Aortic aneurysms differ much in shape and size. Thus a sac- culated aneurysm may have other sacs springing from its walla so that the tumour presents an irregiilar outline. In size the sac may vary from that of a small nut all the way to that of a man's head. Aneurysms may he situated at any point along the course of the aorta from just above the ring to the termination of the abdominal portion,
The disastrous effects of aortic aneurysm are not confined to the vessel, but consist of all the changes in structure and position of neighbouring organs produced by presstire of the sac. The na- ture and extent of these secondary pressure effects arc determined by the situation as well as the size of the aneurysm. Aneurysms involving the sinuses of Valsalva are not apt to attain much size, yet their influence on the lienrt is very disastrous and they are especially liable to rupture into the perieardimn, causing sudden death.
Aneurysms of the arch displace the heart dowTiward (Fig- 109) and it may be forward or to the left, l»ut they rarely occasion hypertrophy of the left ventricle unless the aortic valves have been rendered incompetent. The latter condition is likely to result when the sac springs from the ascending or transverse arch and has attained great size, I recall a man whom I treated for months for aortic regurgitation without suspc^cting the existence of an aneurysm until quite suddenly signs of pressure on the left lung arose. Even then other sii^ns of the aneurysm were not at all dis- tinct, yet were of such a kind as to render its presence certain*
Other effects of aortic aneurysm than those already mentioned will be left for consideration under Symptoms.
etiology. — Arteriosclerosis has long been recognised as pre- disposing to the development of aneurysm. It is objected by Ep-
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77S DISEASES OF THE HEART ^^^^H pin^r that the changes of sclerosis tend to render the vessel more rather than less resisting, an objection that is also recognised by Thonia. Consequently the latter points out thftt aneurysm is likely to develop dnring the time of primary degeneration and weakness of the media* before compensatory thickening of the inner coat has taken place. This will be referred to again. Fio. 10».— Seiaoraph iHowtwo Axiuiiybm o? Aoiita wrrti Dfii^LACxmesfT of tus ffKAin' DoWNVTARI* ANl» TO TUlt LeFT, Syphilis is an nndonbted factor in the eansation of aortic aneurysm, and yet wide differences exist in the opinions of writers concerning the frequency of its relation to this form of vascular disease. The extremes are represented by iL Schmidt, who finds syphilis present in 29 per cent of cases, and Dmmmond, who be- lieves that hies is responsible for aortic aneurysm in every in- stance— i, e., 100 per cent, ily experience leads me to look upon |
ANEURYSM OF THE THORACIC AORTA
we
Dninimand^s opinion as too extreme, and to accept Gerhard t's 53 per cent aa much nearer the truth.
Age IB a predisposing factor of great importance, since aneu- rysm of the thoracic aorta is undoubtedly more frequent after than before the fortieth year, Tbe decade of life in which it is most common is still unsettled, and figures differ all the way from the fourth decade (Crisp) to the seventh (Juda^ Barsdorff). Thoma's notion is that persona are especially lialde to the development of aortic aneurysm at or about the ai^e of forty, in consequence of diminislied resistance of the vascular coats at this time. There is, he thinks, a period of about a year at this age when the weakness of the media has not yet become offset by growth of connective tissue in the intirna, and during which time the coats of the vessel are therefore liable to yield to excessive blood-pressure at one or more points resulting in future aneurysm.
I bave under observation at the present writing a muscular man of furty-four who gives no history or signs of previous syphilis, but who has been a more than usually active, energetic business manager in a line of %vork that necessitated much physical exer- tion. This patient suffers from symptoms which, together with stiff arteries and suggestive but not conclusive physical signs, are yet auspicious of fusiform aneurysm of the arch- The age of this person, his occupation, and the state of his arteries, are all, from an etiological standpoint, highly suggestive and strengthen the conclusion to be drawm from the clinical findings.
Sex 19 likewise a predisposing element in the class of cases now under consideration. Men are without doubt far more liable to aneurysm than are mendjcrs of the gentler sex. Thus of a total of 425 cases of aortic aneurysm analyzed by Hodgson, Bizot, and Brow^ne, and cited by Gibson, 3R0 occurred in males and only 45 in females. This striking preponderance of men is not to be at- tributed to any quality inherent in sex per se as inferior vascular resistance on the part of men, but to the greater liability of males to all those factors which favour the development of arteriosclero- sis as well as their greater exposure to syphilis and conditions of vasciilar strain which, acting in conjunction wn'th vascular degeneration, are known to predispose to the occurrence of aneurysm. Sex is therefore only incidentally of etiological in- fluence.
780 DISEASES OF THE HEART
Two other factors that are mentioned as predisposing to aortic aneurysm are the abuse of alcohol and occupations which necessi- tate vascular overstrain. Both are recognised causes of arterio- sclerosisy and as such operate in the production of aneurysm ; but, in addition, overwork subjects the aorta to strain at a period of life when, according to Thoma's view, the vessel-wall is least able to endure high intravascular pressure. Such influences are inde- pendent of sex, and yet are some of the things which render men more liable to aneurysm than are women.
Kace, which is said to exert a certain degree of influence, can scarcely be separated from conditions of work, habits, etc, to which peoples of some countries are especially subjected. Thus aortic aneurysm is particularly frequent in England. The English appear to be more than commonly subject to arterial degeneration, and this fact, acting in conjunction with heavy toil in the manifold workshops of their country, probably accounts for the relatively great frequency of thoracic aneurysm among them. Traumatism cannot be ignored in the production of aneurysm of peripheral arteries, and probably also of the abdominal aorta, but it is difSr cult to see how injury can have direct etiological relation to aneu- rysm of that portion of the vessel which is situated deeply within the thorax and is protected by its bony walls. It certainly could only act in connection with already existing degeneration of the media. If under such conditions trauma — e. g., a fall from a heiglit — were to suddenly raise blood-pressure, it might possibly induce laceration of the middle coat and thus be an indirect cause of aneurysm.
The influence of malignant endocarditis in the causation of so-called mycotic aneurysms has been emphasized by Eppinger and is generally recognised. Aneurysms of this origin are usually lo- cated in peripheral vessels, and yet it is possible for such aneu- rysm to be aortic, as showTi by the case mentioned by Osier as hav- ing occurred in the Montreal General Hospital. In this case there were, in addition to ulcerative endocarditis, four saccular dilata- tions of the aorta, one large and three sinall ones. Embolism may also be a cause of aneurysm of the arch as well as of other arteries, as shown by reported instances in which the lodgment of an em- bolus on the intima of the ascending aorta has been discovered and was associated with circumscribed inflammatory change. Osier
ANEURYSM UK THE THORACIC AORTA
781
iinks it possible for such aii embolus, if consist ing of a calcareous plate, to lacerate the intima and thus initiate aneurysm.
Lastly, Osier believes there may be an inherent weakness of the vascular coats which predisposes individuals to aneurysm, and cites the instance of Dn Thomas King Cliambers, who^ after hav- ing had one of the left popliteal artery, and eleven years after- ward another in the right leg, finally developed ** aneurysms of the carotid arteries."
Symptoiris. — Cases of aortic aneurysm may be divided into three groups :
( 1 ) Those in which the timiour fails to declare its presence by either .subjective or objective symptoms. Such aneurysms are usu- ally small aud are only discovered at the necropsy, when they may be found associated with some other clinically recognisable disease or as the cause of unexpected death through rupture. When the sac is situated jtist above the aortic ring, it is very apt to rupture into the pericardium. This was found to be the case in 75 out of 289 cases of rupture from a total of 953 instances of aortic aneurysm analyzed by Hare and Holder.
(3) Aneurysms which occasion subjective symptoms as the leading feature of the case. In the majority of cases objective signs are also present, but often of so indefinite a character as to furnish no clear information concerning the nature of the tumour ocx^asion- ing pressure. Such cases belong to Bram well's second category. They may be said to correspond also to Broadbent's subdivision of cases which occasion symptoms but not signs of aneurysm.
(3) Aneurysms which produce distinctive physical signs. These are generally united with symptoms of greater or less severity, but the objective manifestations of the disease are sufficiently pro- nounced to warrant their classification in a separate group.
Aortic aneurysms may also be classified according to their situation — e. g., of the ascending, of the transverse, and of the descending portion of the arch, etc. Indeed, one cannot deal with this subject adequately and clearly without describing the features distinctive of aneurysm in the several locations. There are, however, certain general features shared to a greater or less extent by all aneurysms, whatever their position along the course of the thoracic aorta, and hence these will be considered first
Such symptoms are the result of pressure, and hence it is plain
782 DISEASES OP THE HEART
that variations in pressure phenomena are determined by several factors, as the size of the sac and the direction in which it grows^ as well as the portion of the aorta from which it springs. More- over, aneurysms are liable to change their direction of growth, so that symptoms sometimes differ in character and intensity from time to time. Indeed it may be said that such lack of constancy is generally regarded as one of the points of distinction in favour of vascular as against solid tumours.
Pain is one of the earliest and most constant symptoms of tho- racic aneurysm. Its nature and severity depend upon the direction in which the sac develops. If this is towards the surface of the chest, or, as Walshe termed it, " centrifugal," pain appears earlier, is more constant, and more like what is called neuralgic, is sharp and lancinating or dull and aching, and is not infrequently described as boring, grinding, cutting, burning, etc. As it is due to pressure upon the intercostal nen^es or branches of the brachial plexus, it is apt to radiate along the lines of these nerves, hence around the chest, up into the side of the neck, down the arm, etc.
As a rule, the pain is confined to nerves connected with the first, second, third, and fourth spinal segments (Head), and is associated with tender areas in the upper part of the thorax at either side, but especially at left of the sternum. Such areas of tenderness are not characteristic of aortic aneurysm, however, for they may be symptomatic of various diseases of the intrathoracic viscera. The pain of aneurysm is apt to be very constant, and in this regard indicative or suggestive of tumour rather than of any other disease not occasioning pressure.
If the sac grows inward towards the more yielding and less sensitive structures, it is not so apt to give rise to such severe pain, and hence this symptom is likely to be oversliadowed by some other more distressing symptom, as dyspna^a or cough. The character of the pain, too, when this is experienced, is apt to be more dull and oj)pressiye, and does not radiate so widely in the wall of the chest or the uj)per extremity. Although the pain of aneurysm is apt to be constant, it is liable to paroxysmal exacerbations which greatly increase the suffering. Pain is also apt to be influenced somewhat by the position of the patient's body. For example, it is apt to be intensified when the patient lies in such a manner as to permit the sac to gravitate or press more strongly upon the irritated and
ANEURYSM OF THE THORACIC 2VORTA
783
painful nerve* Per contnij suffering is lessened by attitndes which allow the sac to fall away from the part previotislj pressed upon. Such postural variations in the pain are not often marked, but are seen sufficiently often to merit attention.
It is stated also that in some cases the pain is what is known as intrinsic, by which is meant pain experienced in the sac itself or in the aorta either from acute aortitis or from internal pressure. Pain of this origin is evoked or aggravated by increase of blood- pressure, and is dull or aching in character and substernal in loca- tion. It is likely to be lessened whenever vascular tension is low- ered. Extrinsic pain or that due to pressure may disappear after the structure subjected to pressure has been destroy ed- — e. g., after the bony wall has been eroded and the tumour is permitted to grow without the restraint of rigid structures. I recall the instance of an enormous aneurysm which had thus penetrated the chest-wall and was covered only Ifv a thin layer of skin, and in which eas6 the man made no complaint of pain whatever.
Dyspntm is another very common sjTnptom of aortic aneurysm, but varies much in severity. It is of course most pronounced when the growth of the tumour is inward and pressure is exerted on the trachea, large bronchi, or lungs. Very distressing paroxysms of dyspnoea are occasioned by irritation, not paralysis, of one of the recurrent laryngeal nerves, more often the left, and are due to laryngeal spasm. There is apt to be an associated feeling of con- striction and jK^rliaps pain in the side of tlie throat. In a case of the kind coming under my observation, the man felt the painful sense of constriction in the side of the neck corresponding with the recurrent nerve affected, and described the sensation as beginning in the left side of the larynx and running thence along the side to the back of the neck.
I have quite recently seen, in consultation with Dr. Gorgas, a man i>f fifty with aneurysm of the ascending and transverse arch whose dyspnoE'a was extreme, and compelled him to maintain the right lateral tlecnbitus. Change of position induced a paroxysm of air-hunger accompanied hy uncontrollable coughing. It was impossible for him to rest on the left side, or indeed to lie back against the pillows. In this respect his dyspncea corresponded with what appears to be a cpTite common ex|)erience — i. e., the influence of posture over the intensity of the dyspncea and of
784 DISEASES OF THE HEART
change of position in evoking a paroxysm of respiratory di£Sculty that is very like an asthmatic attack. The subsequent history of this case is interesting and instructive. Having received a hope- less prognosis from his medical advisers, he resorted to a Christian Science healer. Owing to a coincident change in direction of pressure, his sufferings abated and he again got about, the im^ provement being attributed by himself and family to this treat- ment. After a respite from suffering of several weeks, his former symptoms recurred with aggravated intensity and shortly there- after the man died.
Dr. Gorgas made an autopsy and discovered an enormous sac that had not only produced pressure on the right lung and sur- rounding structures, but had caused the erosion of several dorsal vertebra.
Difficulty of breathing is very apt to be accompanied by stridor, which may be so intense as to be audible at a distance and occasion pronounced fremitus. This stridulous respiration is due to con- striction of the trachea or of a bronchus and consequent interference with the expulsion of mucus accumulated behind the point of com- pression.
Cough is a very common symptom in cases of thoracic aneu- rysm, but is variable in both frequency and severity. In some cases it is 80 distressing as to rob the patient of needful rest, and when once excited is so prolonged and intractable as to necessitate abso- lute repose in a given position and even require the free use of morphine. When due to pressure upon tlie trachea, as occurs most fre(|uently in cases of aneurysm of the transverse arch, the cough is ai)t to possess a harsh strident character; that by Wyllie was likened to the note of a gander, and bonce is known as the " goose cough." In some instances it may be of a toneless, muffled charac- ter, probably in consequence of paralysis of a vocal chord. The causes of cough are various, as (A) reflex irritation from pressure on the vagus or recurrent laryngeal nerve, (B) compression of trachea or bronchus, (C) direct impingement on the lung with re- sulting retention of secretions or with an actively destructive process.
Expectoration is apt to be associated with cough, and may con- sist of mucus and serum, muco-pus, and in cases of pulmonary gan- grene, of offensive material characteristic of this affection.
AI^EURYSM OF THE TnOEACIC AORTA
785
Ilmmopiysis is by no means nnconinion in cases of aortic ancu* rysm, in which event the blooJ may come from granulations situ- ated on the tracheal mucosa ( Osier ), from bronchial congestion, or from destruction of a lung, or from the sac itself, what is then known as weeping of the aneurysm. Sueh liannoptyses may occur from time to time over a protracted period, even for months*
I vividly recall the instance of a man with unmistakable aneu- rysm of the upper portion of the descending aorta, whose clinical picture was that of phthisis. The tumour occasioned destructive pressure on the left lung, with pronounced dulness, bronchial res- piration, and a multitude of coarse and fine bubbling rales, fre- quent harassing cough, and copious purulent sputum which was occasionally streaked with blood. In another case of aneurysm Bimilarly situated » pressure was chiefly exerted upon the left bron- chus with consequent dyq^noea, cough, and copious riles due to retention, since there was very little expectoration.
Dysphagia is another very frequent subjective symptom, which is occasioned by aneurysms of the transverse and descending por- tions of the arch, or when a sac situated on the descending aorta exerts pressure uix>n the a?sophagiis. The patient not infrequently speaks of the ingesta seeming to stick at a certain point in their passage do^Tiward. If the aneurysm is situated low down near the diaphragm it may cause regurgitation of the food. Digestive disorders, properly speaking, do not form a part of the clinical history of thoracic aneurysms. They may be present nevertheless, and are then the result, in part at least, of the stasis within the portal system and its tributaries oeeasioned by pressure on the great veins in the thorax.
All aneurysms of the arch do not occasion appreciable inter- ference with the flow of blood out of the venous system. When, however, an aneurysm attains considerable size it can scarcely fail to afl'eet circulation by mechanical pressure. One or both of the venae cavfe may be compressed, and to such a degree that the circulation can only be carried on 1>y means of collateral vessels.
Sueh a condition is admirably showTi in Fig, 110, which is taken from a photograph kindly furnished me by Dr. Emil Beck. This man, aged thirty-seven, was first se^n by Dr. Beck in October of 1901, at wdiich time his complaint was of cough, dyspnoea and in- ability to lie down. He gave a history of syphilis sixteen years 50
786
DISEASES OF THE HEAltT
t.
Fio. 110— Dn.Ar.ui N
I'LitruiAL Veins .Sicr<>NtiARV to Pressure by Avnvntffn ow
Venjj CAV-lt.
before, for which he received very inadequate treatment. His occu- pation was that of a metal-polisher, which necessitates the putting forth of considerable strength in pressing the metal against a
1
ANEURYSM OF TUE THORACIC AORTA
m
two factors both operative iu
polishing wheel, lloroj then, were the etiology of aneurysm.
His one initial symptom of hreathlessness on exertion devel- oped slowly, and did not necessitate abandonment of work and the sport of playing baseball until nearly a year after it was first noticed. Wlien Dr. Beek exaiiiineil the patient there was a pcr- eeptible fulness of the neck and bulging in the aortic area. This tinnonr pnkared and gave a systolie bruit. The pulses of the right half of the neck and of the eorre8pt*uding arm were distinctly smaller than their fellows on the left side. The diagnosis was accordingly made of aneurysm of the ascending and transverse aorta.
Cyanosis and turgescent veins were marked, lie was then ad- vised to enter St. Joseph's Hospital, in the service of Dr. Carl Beek, for the purpose of treatment. Rest and iodide of jwtash did not seem to ameliorate his condition, and he left the hospital.
An aggravation of syrtiptoms and evident increase in the size of the sac led the patient tt! re-enter, in January, \UU2, when ho was given hypodermic injections of gelatin (2 per cent iu 30 cubic centimetres nf normal salt solution) which were administered once a w^eek, snbscipiently increased to 45 cubic centimetres^ until he had received ten such injections iu ail.
Un<ler this treatment pressure symptoms nearly disapjieared^ and the patient felt so well that he again left the hospital. Through the courtesy of Dr. E. Beck, I had the opportunity of exanu'ning him a number of weeks later. The distention of Uie superficial veins was then as shown in Fig. 110, while, viewed from the side, there was the evident bulging of the chest shown in Fig. Ill* The arteries of the right arm ami corresponding half of the neck were manifestly less filled than those on the opposite side. There was a feeble pulsation in the prominent area^ and tracheal tugging could be plainly felt.
Percussion elicited an area of flatness having a semicircular outline below and extending from beneath the middle of one clavi- cle across the upper sternal region to about the same distance on the other side. This area is shown by a shaded area in Fig. 112. Over this area could be heard a dull first tone accompanied by a systolic bruit and succeeded by a loud, ringing second sound.
The area of relative cardie dulness is also shown in Fig, 112,
DISEASES OF TEE HEART
Fiu* U L— pHOTooiiAni or Cahz ow AoRTio AmEtniTsif, anownco Slight Biloino of
AimiuoB Chut Wall.
and from its position indicates displacement of the heart doira- ward and to the left. Its sounds were clear, but the aortic second waa very loud and metallic
ANEURYSM OP THE TnORAClC AORTA
789
The liver, as indieated by the outline at the bottom of the figure, was evidently eiigorgeLl as well as probably somewhat de- pressed, being palpable and having an area of greatly increased flatness.
The man admitted having previnnsly noticed some diffietilty in swallowing. He had not experienced pain to any extent, but in the last two weeks had begun to notice some dull pain in the front of the chest at right of the sternum. This, it seemed to me, indi- cated an increase of pressure upon the parictes, the sac hav- ing changed its direction of growth, and hence its pressure, in the weeks following his abandonment of the gelatin injections. It may be stated in addition that the nature of this case was contirmed by an X-ray examination.
The interference with ve- nous circulation in these cases may not only be declared by turgescence of sui>erficial ves- selsj but by general or h^-al- ized iTdema. Thus the neck and upper extremities may be- come dropsical, or the cedema may be limited to one arm and a portion of the thoracic wall. Inequality of the pulses on the two sides is very connnon, owing to partial obliteration, dis- placement, or twisting of the great branches given off from the arch. Displacements of the heart occur and the function of the valves, espe^'ially ihe aortic, is quite likely to be seriously inter- fered with. Pressure effects in detail will be considered in con- nection with the description of aneurysms in the various situations.
(1) Aneurysms of the ascend ituj portion of the arch. — These may be situated close to the aortic ring and involve the sinuses of Valsalva, or they may spring from the convex or concave surface. In the first situation they are apt to be small and to escape detec- tion, first declaring their presence by rupture into the pericardium and death.
Fio. 112.— Shows Dclkem aku Liveh Ot:T-
rt*u
DISEASES OF THE HEART
t
If the sac arises from tbe cguvcx aspwt, it is likely to attain great size and exert very obvious pressure effects. If its direction of growth is forward as well as lateral, it produces a pulsating tumour in the second and third interspaces at the right of the sternum, and not infrequently leads to erosion of the bony cover* ing, Aneurysiim in this situation may attain truly enormous di- menslonf^, and projecting with only the integument for a coverings
■^
♦v
<n«j Fig. 115),
necessitiitt' the wearing of a metal shield, lest the tumour be acei- dentfllly struck and caused to hurst. Figs. 113-115 show an aneurysm in this location whi<'h had an external diameter of several incites. I vivifUy recall another man sent to me by Dr* G* Frank Lyilstmi, who |>re!^ented a pulsating prominence which oc- cupied tlie entire pmcnrflin, extendi n^r from one nipple to the other, and from the nj>per border of the second rib to the inferior
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792 DISEASES OP THE HEART
extremity of the sternum. As nearly as could be determined by measurement with calipers, the tumour projected 4 inches at its highest point above the level of the surrounding chest, and its diameter was 7X8 inches. In places the enveloping skin was so thin and blue that it seemed on the verge of rupture, and made me actually shudder to touch it. I dared not place a stethoscope upon it firmly enough to auscultate with accuracy, but so far as could be ascertained the dull, distant sounds were not accompanied by murmurs. WTiere the heart was I could not determine. How this man had been able to thread his way through our crowded streets without receiving a fatal blow on this thin-walled sac I do not know. He was advised to protect it by wearing strapped to his chest a framework or cage of woven wire. He was seen by me but twice, and it is probable that death from external rupture took place not long thereafter.
Aneurysms in this situation may encroach upon the pleural cavity and hmg, as witness an instance seen in the Cook County Poor-House in which the necropsy revealed a sac of enormous size that nearly filled the entire right half of the thorax and had caused collapse of the lung, the same as would a massive pleuritic exudate. The side was motionless and moderately enlarged during life, flat and intensely resisting on percussion, with complete absence of cardiac tones and murmurs. Breath-sounds were heard feebly at the suniinit of the chest behind, close to the spinal column, all of which findings, together with distention of the superficial veins, were held to indicate pressure by a solid tumour rather than aneu- rysm.
Aneurysms of the convex portion of the ascending aorta are likely to impinge upon the sujierior vena cava and have been known to rupture into this vessel. They may press also upon the right subclavian vein and occasion passive congestion of the arm and other parts drained by this vein. In some instances the right recurrent laryngeal nerve is subjected to pressure, with consequent paresis of the right vocal cord. The heart is also likely to be crowded downward and to the left, while the aortic valve is apt to be rendered relatively incompetent. The hypertrophy of the left ventricle in such cases is the result of the regurgitation rather than of the aneurysm per $e.
Aneurysms springing from the concave portion of the ascend-
ANEURYSM OF THE THORACIC AORTA
793
ing aorta may, aeeonling to Osier, oecasiuimlly give rise to a tumour at the left of the &torniim iukJ then oeetision great dispkce- ment of the heart. There is at the present time in Ward 10 of Cook County Hospital a man who presents sneh a tumour. It lies in the situation normally occupied by the Iwdy of the heart — i, e., between the second and sixth costal eartilages, the left border of the sternum, mid 1 ineh outside of mamillary line — has a slowly heaving expansile pulsation and gives forth a distinct, harsh double bruit that has replaced the normal cardiac sounds. The heart, as shown by percussion aud the location of what appears to be the apex-beat in the seventh interspace midaxillary line, is greatly displaced downward and to the left* Its tones are rather feebly audible in this situation and are accompanied by the same to-aud- fro murmur, though less distinctly than on the body of the tumour. Vascular signs of aortic regurgitation are presentj and there is an indefinite tracheal tug. There are no signs of pressure on the left recurrent laryngeal nerve, antl pressure etfeets on veins are not present. Without wishing to affirm that this sac arises from the concave aspect of the ascending aorta, I yet incline to the opinion that such is the location, since the incompetence of the aortic valve is not so likely in cases of aneurysm developed from the descending portion of the areh^ and were the transverse arch the portion aifected, the tumour wouhl be likely to have a different location. This patient has been an inmate of the hospdtal at various times for the past four years. Occasional dull pain over tlie seat of the growth and dyspna^a of effort are the only symptoms of wdiich he complains,
(2) Aneurysms of the transverse arch^ in the eame manner as those just considered, produce a variety of effects according to their size and direction of growth. They most frequently develop in a backw^ard direction, and then, when even of small size» occasion pronounced symptoms in consec|uence of pressure on the trachea and oesophagus, interfering with respiration and deglutition. Paroxysmal cough is a very common symptom and inspiration ia attended with stridor.
Growth of the sac forward produces a tumour at the upper part of the sternum and to the right, with absorption of the bony struc- tures. The tumour may occasionally present at the left of the breastbone, but does so so much less commonly than at the right of
794 DISEASES OF THE HEART
the median line that, according to Osier, O. A. Browne found it but 4 times out of 35 cases of aneurysm of the transverse arch. These tumours sometimes reach enormous size and fill up the superior mediastinum so that they spread out into both pleural cavities.
Pressure of these aneurysms is exerted on the left recurrent laryngeal nerve and left bronchus, producing such characteristie phenomena that these cases have been described by Dieulafoy as Aneurysms of the Recurrent Type. In this class of cases symp- toms vary according to whether the nerve is paralyzed or merely irritated by pressure of the growth. Paralysis of the recurrent nerve is shown by paralysis of the corresponding vocal cord, which, examined laryngoecopically, is seen in a state of cadaveric rigidity.
Wlien the nerve is merely irritated laryngeal spasm is evoked, shown by paroxysmal dyspnoea, lasting from a few minutes to sev- eral hours, and causing very great distress. There is also apt to be painful deglutition, and there may be attacks of angina pectoris from pressure on the cardiac branches of the recurrent (Preble).* Pain in swallowing is due to spasm of the muscles of deglutition in the pharynx and gullet Variations in the quality and power of the voice are observed in these cases, and the left vocal cord may be paralyzed for a transient period.
Mr. M., a school-teacher, aged thirty-two, was referred to me by Dr. Bayard Holmes because of paroxysms of dyspncra that were thought by the patient to be attacks of asthma. The history was, that a year earlier he had, one evening, without previous warning, been seized with a fit of coughing that was immediately succeeded by difficulty of breathing lasting the greater part of an hour. As he had become chilled the night before on the deck of a steamboat, he had attributed his attack to having taken cold and thought no more about it.
That was not his last attack, however, but during the next few months he experienced several recurrences. During the six months last past his attacks had increased in frequency and intensity. They came on at any time, hnt more often in the early morning, waking him out of sleep, and lasting: from twenty minutes to half an hour. They were accompanied by loud wheezing in the throat or upper part of the chest and gave him the sensation of being strangled. When the attacks subsided he felt as well as ever. In other respects he felt in good health.
ANEURYSM OF THE THORACIC AORTA
795
It was apjiuroiit that this was not the dinical history of hroii- chial asthma, hut was highly suggestive of some organic disease, especially of intermittent pressure. I therefore inquired concern- ing syphilitic infection and learned that he had had a chancre twelve years lief ore. This fact in connection with his symptoms suggested thoracic aneurysm as the possible cause of pressure on the recurrent laryngeal, and led to minute inquiry regarding pain and cough. With exception of a trifling dry cough to which he paid no attention, he declared he was free from all symptoms ex- cept the spasnifxlic dyspntra already described.
The results of examination may he l)riefly stated as follows: Tlie left radial and carotid pulses seemed not quite so full and strong as the right, hut the differ€?uce was so trifling that I hesi- tated to accredit my senses lest I might he deceived hy my sus- picion of aneurysm into recognising an asymmetry that did not actually exist. Likewise I was not ahle to positively identify any abnormal finding in the invest igiit inn of the heart and cervical vessels, hut I thought T recognised a slight difference in the in- tensity of the second tone on the two sides of the neck» tluit above the left clavicle l>etng somewhat louder and more ringing tlian at the right. There was certainly no abnormal pulsation or inequal- ity in the vessels to the palpating finger. The heart appeared in its normal position.
Upon examination of the lungs, however^ certain abnormalities were at once detected. Over the upper portion of the chest there was a single inspiratory sibilus with each act, the rale seeming to he more pronounced on the left. But the change that was most notewortliv was dulness of the left apex above the clavicle and in the first interspace close to the left edge of the sternum. This impairment of resonance was not intense and yet was distinct. Over this area the breath-sounds were obscured by suhcrepitant rSles, After several forced inspirations the dulness became less pronounced and the rales partially disappeared.
These findings convinced me that the loss of resonance was due to atelectasis, anrl that from the history of spasmodic dyspnoea the collapse of this portion of the left upper lobe was probably caused by pressure. From the history of syphilis twelve years before and from the absence of positive signs on the part of the circulatory apparatus, I was led to make an inferential diagnosis of aneurysm
796 DISEASES OF THE HEART
of the transverse portion of the arch and consequent irritation of the left recurrent laryngeal nerve.
Laryngoscopic examination was next made, and aside from slight congestion of the left arytenoid cartilage was negative. The patient was then submitted to an X-ray examination with the re- sult that the fluoroscopic screen revealed a pulsating tumour be- hind the left edge of the sternum, while a skiagraph showed a distinct though small shadow in the same situation.
The diagnosis was thus confirmed and the case was shown to be one of the type just described. It is interesting, furthermore, in two respects : first, on account of the early age (thirty-two years) at which thoracic aneurysm has developed, and second, because it was the peculiar character of the dyspnoeic attacks which sug- gested the possibility of the disease.
The attacks, which in this case were considered asthmatic by the patient, were in reality due to laryngeal spasm ; and could the lamyx have been inspected during an attack, the arytenoid carti- lages would probably have been foimd approximated and the left vocal cord occupying the median line. As a matter of fact, an at- tempt to inspect the larynx during a spasm was made, but the attack was passing off and the laryngoscopic examination was negative.
It is further worthy of note, that paroxysmal dysphagia was not experienced and that pain was never complained of by this man. This accords with the fact that dyspntra and dysphagia are not necessarily associated in all cases.
Pressure on the left bronchus is another effect of aneurysms of the transverse arch of the type now considered. If the tube is but slightly constricted, the lung becomes retracted only suflBciently to occasion immobility of the side, tympanitic resonance and di- minished respiratory sounds. When the bronchus is greatly nar- rowed the side becomes perceptibly smaller than its fellow, the percussion note is dull, and respiratory sounds are abolished. There may be retention of tlie secretions with rales, bronchorrhoea, and bronchiectasis — symptoms which, in the iLontreal General Hospital, are characterized as *^ aneurysmal phthisis" (Osier).
Aneurysms of this portion of the arch sometimes occasion pres- sure on the thoracic duct. If they develop in such a direction as to involve the innominate or carotid artery, the condition is apt
ANEURYSM OF THE THORACIC AORTA 797
to be shown by a symmetry or delay of the pulses on that side. Pressure on the sympathetic is another manifestation of tumours in this situation, and is shown by dilatation and immobility of the
pupil when the nerv^e is irritated, and by contraction when the sympathetic is paralyzed. Tracheal tugging is another result of aneurysm of the transverse arch, as was first shown by Oliver, It
798
DISEASES OP THE HEART
is due to the dowiiward traction of the sac on the trachea at its bifureatiLHi. This i?ign will he spoken of again at greater length under Palpation. AneurysmB in this situation may rupture into the trachea (Figs. 11*1, 117).
(3) Aneurifsms of the descending portion of the arch grow laterally and posteriorly in the majority of instances, and yet it is
Fifj. 117.— i)rr
ir^Roni ly UFEiriJffo ittto Traoiiia.
M I - W >- i M
stated that a tumour of this portion of the vessel may present at the left of the sternum (Sansom^ Walshe). Phthisical symptoms are the result of jiressnre on the left lung or bronchus, dysphagia of compression of the gullet, pain from erosion of the dorsal vertebrsB
ANEURYSM OF THE THORACIC AORTA
Y99
(third to sixth), and a tiimoiir in this situatioD may be the result of backward pressure^ CompressioB of the spinal cord may oc- casion characteristic effects-^e. g,, paraplegia.
(4) Aneurysms of the descendijig thoracic aorta are usually located low down near the diaphragm and produce oftentimeB very obscure syniptoms. In an instance of the kind which I saw with Dn Bayard Ilulnies, and which was not recognised as aneuryani, the only coniplaint was dull pain vaguely felt in the lower zone of the thorax and upper abdominal region. The only thing that could be disctjvered on examination was an area of iinpairL*d resonance and feeble broncho-vesicular breath-sounds in the left infrascapn- lar region, close to the spinal column. From the history of previous illness, that seemed to have been pleuritic, and from the physieid findings, this area was erroneously thought to indicate old adhe- sions. The autopsy, months subsequently, revealed a sac filled with dense coagula pressing on the base of the left lung just above the dia]>hragm.
Anetirysms in this situation may, as previously stated^ cause dysphagia and regurgitation of solid ingesta, but they rarely occa- sion respiratory embarrassment. Aside from deejvseated pain they are not likely tc produce subjective symptoms, and unless, by reason of tlieir size, they give rise to lateral dulness and other signs of pressure on the hmg, they are likely to escape recognition.
It should l>e Ivorne in mind that an aneurysm which in the beginning is confined to one jwrtion of the arch may as time pro- gresses so increase in dimensions as to eventually invade other divisions of the vessel. Thus, a sac at first limited to the transverse arch may in time spread to the ascending portion, or one in this latter situation may at length involve the entire arch ; so that both subjective and objective symptoms are very liable to exhibit changes correspoTuling to the extension of the anenrysm,
I recall the case of a locomotive engineer who was for many months an inmate of the Cook County Hospital in wdiom such a change took place. His aneurysm at first presented in such a situ- ation that it was believed to implicate the descending portion of the arch. As months went on^ however, the tumour grew enormously towards the front, and at the necropsy was found to have involved the entire arch, which had consequently lost all semblance to an arch, being, in fact, but a huge sac from heart to descending aorta.
800 DISEASES OF THE HEART
Physical Signs. — Inspection. — In some cases this is wholly negative, minute scrutiny failing to detect signs of pressure, and the general appearance being that of robust health. In other in- stances, on the contrary, patients look cachectic, and their chests being uncovered present unmistakable evidence of aneurysm. It is not to be supposed that all the signs are present in any one case. Consequently the following are the points to be carefully looked for :
(1) Circumscribed bulging of the chest-wall in the following areas : (A) At the right of the sternum, especially in the second and third intercostal spaces, but also the first, and including the sterno-clavicular articulation ; (B) at the upper end of the sternum, including the regions at either side and the fossa jugularis; (C) in the intercostal spaces at left of the breastbone, from clavicle to fourth rib ; (D) in the left interscapular region below the level of the fourth dorsal vertebra. These are the areas in which tho- racic aneurysm most commonly makes its appearance.
The integument at these points may appear smooth and shin- ing, the prominence being slight, or a tumour of such size may pro- ject and have so eroded the overlying structures that the skin is of a dark red or bluish hue, or may have disappeared in spots, leaving the wall of the aneurysm visible.
(2) Signs of interference with the circulation: (A) visible cutaneous capillaries on some portion of the chest, as over the area of bulging; (B) distended, tortuous veins denoting the establish- ment of collateral circulation in consequence of pressure on some of the great internal veins, as superior vena cava, one of the in- nominates or subclavians; (C) localized cpdema, as of one arm and corresponding half of the neck, or when bilateral, of the upper part of the body, but not of the lower extremities. Walshe speaks of the neck being in some instances so distended and spongy from capillary turgescence as to look " like a collar of flesh."
(3) Pulsation in some abnormal situation — e. g., one of the areas in which bulging may appear; or an exaggeration of a pulsa- tion in a normal situation — e. g., of the cervical arteries, particu- larly on one and not the other side or in the episternal notch.
(4) Dislocation of the cardiac impulse, in most instances downward and to the left. The organ may, however, be pushed strongly forward against the anterior chest-walL
ANEURYSM UF THE TflOHAClU AORTA
801
(5) Diminution or absence of respiratory movement of one half of the tliurax, more often the left, with, in some cases of marked bronchial compression, also retraction of the side. This sign in conjunction with pressure-symptoms is highly suggestive.
(6) Immobility of one pupil, which may be larger than its fellow, but is more often contracted,
(7) Sweating of the head, sometimes unilateral, and by Walshe said to be very profuse in sonie instances. This is another sign of pressure on the sympathetic^ and taken in conjunction with other pressure-symptoms may be of value, but found alone pos- sesses no significance as respects aortic aneurysm,
Pafpaiio7i is of value ehiefiy as a means of detecting abnormal pidsatron, its extent and character. It is especially likely to give information when employed as bimanual palpation, one hand being pressed firmly against the chest in front and the other behind. In this way, deeply situated pulsation may sometimes be appre- ciated that otherwise would escape recognition. If a bulging area is perceived to pulsate, one should endeavour to feel the extent, force, and direction of the pulsation. If the tumour is due to aneurysm, it is likely that the pidsation includes the whole area. If this is forcible, so forcible in fact as to equal in this regard the beat of the heart, it is highly suggestive of aneurysm (Balfour). Finally, the pulsation of aneurysm may be slowdy heaving and is expansile, and when by palpation this character can be determined^ there is no doubt of the nature of the tumour* Pulsation imparted to a solid tumour by a vessel beneath is a simple forward thrust or shock.
In some cases the hand laid upon a tumour due to aneurysm perceives a distinct diastolic shock which succeeds the systolic im- pulse. This is very characteristic, being due to elastic recoil in the wall of the sac. In some instances a thrill is detected in the bulg- ing area, but in my experience is not at all common, and is of diag- nostic aid only in connection with other signs.
Palpation is of value also in the study of the pulse wnth a view to ascertaining whether or not it is equal and synchronous in cor- responding arteries, since when the innfmiinate or the left common carotid and subclavian arteries are implicated, smallness and per- haps retardation or obliteration of the pulse in the arteries of the
corresponding half of the neck or arm are likely to be occasioned. 51
802 DISEASES OF THE HEART
Palpation is of value also in ascertaining displacement of the heart, as well as hepatic congestion due to pressure.
The finger pressed gently into the epistemal notch may sometimes detect pulsation of the transverse arch of an abnor- mal character, or a thrill, as well as the jogging impulse of aneurysm.
The tracheal tug is another phenomenon sometimes elicited by palpation. It is a distinct downward pull of the trachea caused by the impact of the sac against the windpipe at its bifurcation or against a main bronchus, and although feebly present in some other conditions — e. g., free aortic regurgitation — is never so marked as in aneurysm of the transverse arch. To elicit tracheal tugging the examiner instructs the patient to raise his chin so as to strongly extend the neck, whereupon he inserts the tips of his forefingers into the notch between the thyroid and cricoid cartilages and pulls gently upward. If the sign sought for is present, the trachea is felt to be jerked distinctly downward with each cardiac systole. When well marked, this tug cannot be mistaken, but when not pro- nounced considerable care is required for its detection.
Percussion is a valuable means of diagnosis in cases of aneu- rysm, especially when there is no visible tumour. Before the sac leads to protrusion of the chest-wall it may occasion retraction of a lung-border or more or less collapse of a lobe, so that dulness in one of the areas in which aneurysm is usually situated may be de- tected by firm percussion and form an early sign of such tumour. It is especially important to percuss carefully in the right infracla- vicular region close to the sternum, since loss of resonance in this location is, together with s\Tnptoms and signs of pressure, strongly suggestive of aneurysm. Dulness over the manubrium is not so suggestive as at either side. Percussion is necessary also for the recognition of pressure effects on the lungs and of displacement of the heart.
Auscultation, — Aneurysms do not always produce acoustic phe- nomena, a statement which applies to some large as well as small ones that are deeply situated. A sac may be filled with coagula, and be thus to all intents and purposes the same as a solid growth, in which event no adventitious sounds are generated and the aneu- rysm remains silent.
In most instances, however, aneurysms occasion abnormal
ANEURYSM OF THE THORACIC AORTA
803
sounds or bruits which are audible over the sac or in some neigh- bouring vessel or part to which they are propagated*
There is no auscultatory phenomenon pathognomonic o£ aneu- rysm, but certain sounds are more suggestive than are others. The two tone* normally heard over one of the great vessels at the base of the neck and in the aortic area are usually altered by the devel- opment of aneurysuL Either the systalie or the iliastolic may bo modified — i. e*, intensifiedj diminished, or impure.
Perhaps the most frequent and striking change is a loud pecul- iarly ringing quality of the second tone heard over the growth or in one of the cervical arteries but not the others. In some instances such a sound is impure or split, in others it is clear and clanging, while the first is not pure or has been replaced by a murmur of harsh quality. In other cases again the systolic tone is pure and accentuated and the diastolic is accompanied or obscured by a dis- tinct bruitj while in still others there is a double to-and-f ro murmur of wide propagation.
Intensification or modification of the normal vascular soimda occurring in immediate proximity to the heart — e. g*, in the aortic areaj are not so suggestive as are such changes in regions in which they do not normally exist — e. g., the left interscapular region or one side of the neck. Another very valuable auscultatory sign is the propagation of the heart-tones to a much greater distance than normal^ — e. g., to the outer limit of an infraclavicular region or into an axilla, the lung tissue not being indurated. This condition is essential, for solidification of lung from tuberculosis may lead to wide transmission of the cardiac soands without aneurysm.
We do not yet understand the conditions which determine changes of one kind and another in the tones heard over an aneu- rysm. These sounds are probably not generated de novo in the wall of the sac, but are mc^roly eonducte*l tbitlier from the heart and are tliere intensified, reduplicated, or otherwise modified by vibra- tions set up in the sac-wall or by some other condition that escapes our ken. It may well be that bruits are generated in some cases in the sue itself in consequence of the blood-stream swirling into or out of the sac, hut probably the mnrmur is due in other instances to atheromatous roughening of the aorta between the heart and sac or to insufficiency of the aortic leaflets. This is believed to be the explanation of the double aortic brnit not infrequently heard in
804 DISEASES OF THE HEART
aneurysm of the ascending portion of the arch. Indeed, Gibeon states that he can recall only three cases in the literature in which such a double bruit was found without associated incompetence of the semilunar valves. It is not strange, therefore, that all possible combinations of tones and murmurs may be heard in cases of intra- thoracic aortic aneurysm.
Drummond has called attention to the fact that the pulsation of an aneurysm may be communicated to the trachea and manifested by rhythmical interruption of the expiratory murmur. This is perceived by placing the stethoscope upon the manubrium and aus- cultating while the patient expires slowly through only one nos- tril, the other being closed by his finger. This phenomenon is not peculiar to aneurysm, being perceived in health, but is more pro- nounced.
In some cases an aneurysmal bruit may be plainly heard when the bell of the stethoscope is placed between the patient's teeth, his lips being closed about the instrument. Sansom speaks of having thus been able to detect a systolic murmur, and Dr. E. J. Abbott, of St. Paul, has narrated to me an instance in which the detection of such a tracheal bruit was the only evidence of aneurysm he could discover. In Cook County Hospital at present writing is a man with aneurysm in whom both a systolic and diastolic bruit can thus be loudly heard. The phenomenon is due to the conduction of the munnur to the column of air within the trachea. This sign may be of diagnostic value in cases of small sacs of the transverse arch which are too deeply situated to declare their presence by outward pressure-eflFects.
Diagnosis. — Under some circumstances the diagnosis of aneu- rysm of the thoracic aorta may be made almost at a glance, by the discovery of an external tumour displaying the expansile pulsa- tion and other characters of an aneurysm. There are other cases, on the contrary, in which the most painstaking examination fails to positively establish the nature of the malady. Between these two extremes are to be found cases which, although obscure, are yet susceptible of elucidation by minute investigation- and by ex- clusion.
In a suspected case the following points may be considered of diagnostic importance: (1) A history of syphilis years before or of strain, as by occupation, to which some would add chronic alco-
ANEURYSM OF THE TIIORACR? AORTA
806
holic excess. (2) Age, the patient being at or after the middle period of life. (3) The male sex, since men are vastly more liable to aneurysm. (4) Symptoms indicative of intrathoracic pressure; as, (A) intractable pain of the characters previously de&eribed ; (B) djspncea, especially if influenced by posture; (C) cough of a brazen clang, also evoked or intensified by posture; (D) dys- phagia or regurgitation of food. These four symptoms, if all pres- ent, form a very strong chain of evidence in favour of an existing aneurysm.
If to the foregoing history and symptoms the following physi- cal signs are added, reasonable doubt can scarcely be entertained: (fj) Bulging, even if slight, in some one of the areas in which aneurysm is likely to be present, (6) Dulness in one of these areas even without perceptible bulging. (7) Displacement of the heart, most often downward and to the left. (8) Some of the auscultatory phenomena already described, especially a harsh, aortic systolic bruit with a clanging seeoml sound. If such second tone is split or doubled and is heard most plainly or solely over a dull area or in the cervical arteries, especially if on one side and not on the other, and is accompanied hy a diastolic shock, the evidence, taken in connection with pressure-symptoms, may be considered almost conclusive.
Aside from an external tumour having a distinctly expansile pulsation or a diastolic shock, there may be said to l>e no signs so distinctive as to be pathognomonic. Diagnosis is to be found in the association of several important signs rather than in any one alone. Nevertheless attention nuiy be especially directed to w*hat Balfour considers very trustworthy evidence^ — -namely, a pulsation in an aneurysmal area et|ual in intensity to the apex-beat, so that there may be said to be two areas of maximum impulse. Even this is not absolute, liowever; for a kyphoscoliosis has been known to push the convex portion of the aortic arch so strongly against the anterior chest-wall at right of the sternum as to simulate, with respect to the force of its pulsation, a thoracic aneurysm.
Tracheal tugging is a very strong sign of aneurysm of the trans- verse arch, esy>ecially in conjunction w^ith other signs; but as it may l>e produced by other conditions, it is not infallible.
Differential Diafpto.^is.^ — This concerns especially the three fol- lowing diseases, which taken in order of frequency and importance
806 DISEASES OF THE HEART
are: (1) A solid intrathoracic growth — e.g., carcinoma and the varieties of sarcoma; (2) mediastinal abscess; (3) pulsating em- pyema in close contiguity to the base of the heart.
(1) Malignant Tumour. — This disease when situated within the thorax occasions symptoms of pressure so identical in some re- spects with those of aneurysm that they cannot be distinguished. The chief differential points are to be found, therefore, in the his- tory and physical signs. As a rule, the history is of more rapid growth than in aneurysm, accompanied by more pronounced ema- ciation and loss of strength. In the physical signs the main dif- ferences are found in the character of pulsation, when such exists, and in the auscultatory phenomena.
A solid tumour occasions pulsation which is not expansile, but is a fon\'ard impulse, owing to the circumstance that the growth itself does not pulsate, but receives an impulse imparted to it by the aorta or some other artery or by the heart against which the tumour lies. More commonly, however, such a mass possesses no impulse. It must not be forgotten, on the other hand, that when a sac is filled with dense coagula, it is practically also a solid tumour, and hence under such conditions may be also incapable of producing any perceptible pulsation. I recall such an instance in Cook County Hospital. A large, dense, intensely resisting, non- pulsating tumour protruded close to the sternum in the right infra- clavicular region. It was, moreover, perfectly silent, and very naturally was for a long time mistaken for a malignant growth. Only after the lapse of time had somewhat altered the size of the sac and permitted vascular sounds to be generated was a correct diagnosis possible.
As regards the sounds audible over a solid tumour, it may be stated that when such are present they are usually clear and im- changed. It is possible, however, for the cardiac or vascular sounds to be modified in eonsetjuence of pressure by the growth. Under such circumstances bruits may be generated or the second sound may take on a ringing intensification. It is not likely to be so clanging as is sometimes the case in aneurysm. Moreover, a tu- mour of the mediastinum which, from its situation and resulting area of dulness, simulates aneurysm of the transverse arch, does not occasion a tracheal tug. Neither is such a solid growth when situated in the area at right of sternum, and hence simulating
ANEURYSM OF THE THORACIC AORTA
807
aneurysm of the ascending aorta, likely to lead to signs of insuf- fieiency of the semilunar valves. It does not change its direction of growth and cause sudden modifications of symptoms, nor is it apt to create as^jTiimetry of the pulses. Finalh% in cases of malig- nant growths there may Ije history or s^Tnptoms of an ante- cedent tumour elsewhere, or there may be induration of some of the lymph-nodea in axilla or neck which may aid in the correct inter- pretatiou of the case.
(2) Mediastinal Abscess, — In this infrequent affection there is history of more sudden invasion, and pain is an early symptom, even before pressure has become sufficient to occasion dyspnfea. Fever is likely to be present, and is an early sjinptom, whereas when it exists in aneurysm it is apt to he late, after the sac has begun to exert pressure on the bronchus or lung with phthisical symptoms. In abscess^ moreover, there is not likely to be the change in the vascular sounds or the production of new ones as occurs in aneurysm. The disease may arise at any age and in either sex, showing no predilection for the male sex*
(B) Puhaiing empyema may simulate an aneurysm %vhen an empyema necessitatis forms in close proximity to the base of the heart. It is, however, exceedingly rare, and may occur in children as well as in adults. The history and examination of the lungs ought to clear up the natm^e of the ease. Should a circumscribed empyema in immediate contiguity to the heart display bulging and pulsation as well as dulness, it may occasion considerable difficulty of correct diagnosis, but ought at length to be diagnosed by exclusion, if not by history and physical signs indicative of its real nature.
Other diseases producing signs in the aortic area — i. e.^ dila- tation of the ascending arch associated with aortic regurgitation, stenosis of the aortic ostium, and sclerosis of the ascending arch — may and have been mistaken for aneurysm. In the case of the first mentioned a positive differential diagnosis is sometimes ex- tremely difficult, when the regurgitation occurs in the male past middle age, but as a rule pressures-effects are absent. Thrill and systolic murmur mmy in cases of stenosis give rise to suspicion of aneurysm, but error may ordinarily be avoided by study of the liistory, agCj the second sound, the position and size of the heart, and the characters of the pulse. Sclerosis of the aorta may occa-
808 DISEASES OP THE HEART
sion a systolic bruit and ringing second sound very suggestive of aneurysm, but does not occasion pressure-effects noted in aneurysm. In all these three affections the subsequent progress will probably clear up the case.
Pulmonary tuberculosis, fibrosis and retraction of the lung and throbbing of the aorta sometimes obsen-ed in neurotic subjects ought not to occasion material difficulty if due attention is paid to the history, symptoms, and clinical findings.
Formerly the sphygmograph used to be depended on to aid in the detection of thoracic aneurysm, and may in favourable cases afford reliable information, by furnishing a tracing of one or both radials in which the usual characters are wholly wanting, but in many instances it fails to record positive evidence.
Nowadays we are accustomed to resort to the X-ray in all doubtful or suspected cases. The reader is referred for details to the appropriate article in the Appendix.
Prognosis may be said to be extremely unfavourable, for although spontaneous cure through obliteration of a small sac or one with a narrow pedicle sometimes takes place, it is unlikely for such to happen. Furthermore, the results of medical or surgical treatment are not encouraging. The progress of the disease is not of a necessity steadily downward, although such is apt to be the rule. Remissions may occur both in the gravity of subjective symptoms and growth of the sac.
Thoracic aneurysm may run a comparatively rapid course, par- ticularly if the sac develops externally and ruptures, but the dis- ease may persist for years, depending of course upon the size, direc- tion of growth, and physical conditions of the sac. Ten years may be said to be a long period of time for the continuance of thoracic aneurysm, and yet this limit has been reached and even surpassed. Finally, the outlook is influenced largely by the habits, general status, and environment of the individual, the same as in any other form of cardiac or vascular disease.
Modes and Causes of Death. — The fatal termination may be said to occur either from rupture or the direct or indirect effects of pressure. Death from rupture is not the most frequent mode of termination, as shown by Hare's and Holder's figures, previously quoted, according to which it was the cause of death in 289 out of 953 cases. Rupture may take place externally or into any one of
ANEL'RYSJl OF THE THORACIC AORTA
809
the coDtiguoiis structures, pericardium, heart, pleural cavity, bronchus, trachea^ a^sophagiis, vena cava, puhiKmary artery. In such an event death may be immediate or protracted over a period of hours.
More conmionlvj life is terminated in consequence of mechani- cal interference with respiration or circulation and cardiac inade- quacy, or the patient succumbs to " aneurysmal phthisis '* or gen* eral exhaustion and cachexia. Under such circumstances the end may come slowly or suddenly after weeks of slowly progressing loss of strength. The last hours are in many cases fraught with ex- treme sutTering and death is hailed as a blessed deliverer.
Treatmeiit.^ — The not infrequent post-mortem discovery of the si>oiitiHjeous cure of thoracic aneurysm by coagulation of the blood within the sac has furnished the hint upon which all thera- peutic measures are based that airn at anything more than pallia- tion of symptoms. The aecomplishment of this object presupjioses certain favouring conditions in the sac itself. In the first place the aneurysm must be of the saccular variety, and in the second it must communicate with the aorta by a narrow opening. Given tliese essentials, it is jmssible for clotting within the sac to take place.
If these conditions are not present, there is little or no prospect of cure, and medical skill is powerless to do more than mitigate suffering or furnish advice, which if carried out may retard prog- ress. In the majority of cases, unfortunately, we are compelled to content ourselves with palliative measures and watching the course of the disease.
Our aim should be, however, to effect a cure in every case in which there seems to be such a possibility. Consequently, the first measure to be advised is rest in the rentvibent posiiion. The object of this plan of management is the reduction in the number and force of cardiac contractions that thereby the flow of blood within the aneurysm may be less sw^ift. Ever since its introduction by Val- salva the value and importance of this measure has been recognised. To be effective the rest must be absolute and must include rest of mind as well as of body. WHiatever excites the heart to more rapid and powerful systoles iruist l>e avoided, and to attain as complete rest as is necessary, the patient should be clearly instructed con- cerning its advantages and neceBsity.
810 DISEASES OP THE HEART
It is also advisable that arterial tension be reduced and the vol- ume of the blood diminished. To this end the diet must be re- stricted, as was recommended by Tufnell^ of Dublin. His dietary was extremely rigid, consisting as it did of 2 ounces of bread and butter with 2 ounces of milk for breakfast and supper alike, while for the midday meal 2 to 3 ounces of meat and 3 to 4 oimces of milk were allowed.
Such a rigid restriction in the amount of food requires for its successful carrying out courage and determination on the part of the patient, and few persons will submit to such an almost starva- tion diet. It is probable that the daily allowance may be somewhat greater than Tufnell's dietary permitted without destroying the aim of treatment, provided one remembers that if blood-pressure is to be lowered the quantity of fluid allowed must be small. Fur- thermore, if such management is to accomplish results it must be persevered in for several months or until the aneurysm gives evidence of having diminished in size. While carrying out this or any other mode of treatment the bowels are to be kept freely open that there may be no straining at stool or increase of blood-pressure incident to constipation.
The next plan of management that promises beneficial results is the administration of iodide of potassium. This mode of treatment was at very nearly the same time recommended by Bouillaud and Chuckerbutty, but has been especially advocated by Balfour. It is not advised because of the syphilitic history obtained in most cases of thoracic aneurysm, but for the purpose of influencing the sac in some as yet unknown manner. Balfour is of the opinion that this salt leads to thickening and contraction of the aneurysmal wall, while others believe its beneficial action lies in decrease of blood-pressure and slowing of the heart's action.
Whatever be its modus operandi, it is not necessary and it is not advised to prescribe enormous doses, as used to be done, but to administer it in doses of 5, 10, or 15 grains thrice daily, since these moderate doses accomplish exactly as much as do larger ones. The dose of the salt must not be large enough to produce acceleration of the pulse, the rate of which during repose should have been pre- viously determined. The remedy should be continued for many months, and is advantageously combined with rest and a restricted diet.
ANEURYSM OP THE THORACIC AORTA
811
Testimony is universal that the first and pronounced effect is relief or very considerable amelioration of pain due to the aneu- rysm. Why this is cannot be said, but there can be no doubt of the empirical fact. This plan of management should be instituted in all eases, yet to promote a cure of the disease favourable condi- tions of the sort explained above must be present in the tumour.
The foregoing are the simplest measures, and in most instances are likely to aeeompHsh as much as any other of the various plans of management that have been recommended and will now be mentioned.
The siirgkal procedures sometimes employed in the treatment of this formidable complaint are five in number, as follows;
(1) The introduction into the interior of the sac of many feet of fine iron or steel wire, horsehair, catgut^ or silk thread* The object of such treatment is the coagulation of the blood in the meshes of this foreign material, wire being prc^ferable to the others. This operation, known as the Moore or Loreta method, has been done a number of times, but not with sufficiently brilliant results to make it a jjopnhir mode of treatment. Of the 16 eases collected by White and Gould (Gibson) ^ only 2 were successful, while of the 8 cases of thoracic aneurysm so treated and collected by Hunner prior to 1900 (Osier), all died. The great objection to this method of management is the resulting inflammation and aggravation of the condition.
(2) Electrolysis, which consists in passing a galvanic current through the contents of the aneurysm by means of two insulated needles introduced through the wall of the sac. The points of the needles are to be left uncovered by the insulating material. They must not be in contact when inside the tumour. The electrical current thus applied cau^^^s coagulation of the sac contents, and in Gibson^s opinion promises well, although the results as yet have not been very satisfactory. It is worthy of trial in suitable instances.
(3) The Moore-Corradi method, which consists in the combi- nation of the two procedures just mentioned. A fine gold, silver, or steel wire is passed into the sac, and then a galvanic current is »ent through the wire. This method is said to have yielded sat- isfactory results in a few instances. It has been performed by Burresi and Hershey. Of 17 cases of thoracic aneurysm thus treated prior to 1900 only 3 were successful According to ilun-
812 DISEASES OP THE HEART
ner, this method is not devoid of the following dangers: (1) embolism; (2) the formation of a secondary bulging of the wall of the sac; and (3) obliteration of an artery springing from the wall of the aneurysm.
(4) The scratching of the inner surface of the sac-wall with the point of a thoroughly sterilized needle, a method said to have been introduced by Macewen (Gibson). After the integument has been carefully sterilized an aseptic needle is passed through into the aneurysm until its point comes in contact with the internal surface at the opposite side. The needle may then be left in situ to be moved about and made to scratch the lining of the sac by the pulsations of the aneurysm, or the surgeon may irritate the wall by moving the point of the needle about first in one place and then in another, but without removing the instrument. If the needle is left in situy it should not be allowed to remain for longer than twenty-four to thirty-six hours. This method is simple, said to be safe, and to promise well.
(6) The subcutaneous injection of a 1-per-cent solution of pure white gelatin in normal salt solution. This method was introduced by Lancereaux in 1896, and by him was highly praised. At first a 2-per-cent solution was employed, but at Mic suggestion of Hu- chard was reduced to half this strength as being safer.
The gelatin solution should be carefully filtered and sterilized under pressure at the temperature of 120° C. Two hundred or 250 cubic centimetres of this 1-per-cent solution at a temperature of about 100° F. are to be very slowly injected into the loose subcutaneous tissue of the thigh or abdomen, after which the patient is to be kept perfectly quiet.
Injections should be repeated every six to eight days until 20 in all have been given. The objections to this plan of treatment are the intense pain and sometime.^ local and general reaction that follow. In the case of the patient treated in this manner by Dr. Carl Beck, and previously mentioned in these pages, the tempera- ture rose to 101° F. or thereabouts after the injections.
Cures have been reported in France, but in this country, so far as I know, the results have been unsatisfactory. It may be tried in desperate cases; but so many difficulties and dangers attend its use, that it is not likely to become widely employed. Among the dangers is the risk of sepsis or tetanus, since 10 per cent of
ANEURYSM OF THE THORACIC AORTA
813
commercial gelatin is said to contain germs, especially the tetanus bacillus. Moreover, iiot many ])atients will Ite found willing to bear the pain from the injections and the subsequent febrile re- action. Finally, of the cases in which this treatment has been tried, but a small percentage has shown really eucouraging results. The use of gelatin in this manner does not appeiir to increase the coagulability of the bloody and since the action is a8 yet not under- stood, it has been suggested that the remedy be given by the mouth as food, 15 graunues being consumed daily*
When one considers the pathology of thoracic aneurysm, the great internal pressure to which the \vall of the sac may be sub- jected in cases in which the mouth of the aneurysm is a wide one, and usually the advanced stage of the pirocess when the individual applies to the surgeon for relief, it is not strange that failure, or at best only amelioration^ of symptoms follows any attempt at a cure.
The most that can be done in the great majority of cases is to mitigate the patient's distress. If the iodide of potash does not relieve the pain, recourse must be had to opium in some form. Subcutaneous injections of moridiine are the best» since they not only rid the sufferer of his pain for a time, but they also lessen his sense of dyspnoea and promote sleep. I have not yet prescribed heroin in a case of aneurysm^ but think it ought in the dose of one-twelfth grain not only to prove efficient against the cough, but should diminish the sense of dyspna^a.
Venesection is highly recommended for relief of venous con- gestion and to decrease blood -pressure for a time, and thereby the dull pain arising from pressure within the sac. Only a few ounces, 3 to 5, should be taken at a time, since it may have to be frequently repeated, and the abstraction of too much would only serve to weaken the patient without doing more good than do the few recommended.
When the sac is external and large, it is said to minister to the patient's comfort to have him wear an elastic bandage over the tumour (Oeler). It certainly ought to lessen the tension to which the integument and thoracic parietes may be subjected, and thereby mitigate pain. In some cases it may be necessary to protect the tumour against violence from external blows by having the patient wear a shield of thin metal or woven wire strapped to his cheat.
814 .DISEASES OP THE HEART
The diet of these sufferers should be light, even though they are not placed at complete rest, and they should never be allowed to become constipated, since straining at stool is sure to prove harm- ful. They should take a daily laxative, and now and then, when blood-pressure becomes too high, they should receive a sharp purge from calomel.
They should be informed of the dangerous nature of their malady and be warned of the risk attending severe physical efforts, excitement, excesses, etc.
There are times when from cardiac inadequacy digitalis or one of its congeners may appear indicated, but one should remem- ber that such agents are likely to injure rather than benefit the aneurysm. Consequently if such a remedy is called for, it should be administered with caution and its effects should be carefully watched.
When at length it is plain that the end is near, and, as it approaches, suffering is intense, I am of the opinion that the phy- sician is warranted in the free administration of morphine injec- tions to promote euthanasia. I certainly should not hesitate under such circumstances to inject a dose that would hasten the patient's death. I know of an instance in which this was done to prevent the terrible shock to the friends that was sure to follow the impend- ing rupture of a large external sac.
APPENDIX
MECHANICAL DEVICES AS AIDS TO DETERMINING CARDIAC DISEASE
THE X-RAY
Percursion^ and auscultation are not entirely satisfactory methods of examining the heart, for the reason that thick, rigid parietes, pulmonary emphysema, or other conditions may prove sources of error. Much depends also on the skill of the examiner or on his delicacy of hearing, so that if is quite common for two or more examiners tn ohtaiu results that do not wholly agree* When, therefore, the Roentgen-ray came into use it was quite naturally hoped it would furnish a reliahle means of detecting diseased con- ditions in the heart.
Accordingly, considerable work along this line has been done both in Europe and this country. As a result of such investiga- tions we now know that the X-ray is in many cases a valijahle aid to the diagnosis of internal diseases, but cannot altogether replace other and older means of investigation. This is pre-eminently true of cardiac disease.
Francis P. Williams, of Boston, is a particularly diligent in- vestigator with the X-ray, and it ia to his elabcirate paper in the Philadelphia Medical Journal of January 6, 1900, that I am in- debted for much of what is here stated. Percussion of the cardiac area was made by Williams and his friends in a large series of cases both healthy and diseased, and after the limits of deep-seated dul- ness had been carefully marked out on the bare skin the results thus obtained were compared with those of the X-ray by means of the fluorescent screen* The conclusion Williams arrived at was that the fluoresce pe is a much more trustworthy means of judging of the size of the heart. He found that in normal hearts the dis-
li-
816 DISEASES OP THE HEART
crepancies between percussion and the fluoroscope were not so marked as when the heart was either undersized or oversized, and that the greater the enlargement of the organ over the normal, the less frequent is the error by percussion, although the more pro- nounced is such error when made.
He furthermore discovered the X-ray to be a more precise method of determining the shape and position of the heart. Thus Williams found that in one case, in which the situation of the apex-beat and the results of percussion led him to conclude that the heart was hypertrophied, the X-ray showed the organ to be merely displaced downward so as to lie transversely. Trans- positions are also discovered by means of the fluorescent screen more certainly than by percussion. This was brought out very clearly in cases of left-side pleuritic effusions.
Congenital malformations are stated to be capable of diagnosis by the X-ray, and by this means patency of the ductus arteriosus has been determined. It also enables one to diagnosticate a peri- cardial effusion, as is well illustrated by the figure opposite kindly furnished me by \V. C. Fuchs, who took the skiagraph from which the cut has been made (Fig. 118). Cardiac contractions can be observed and differences in size between systole and diastole noted, particularly in cases of valvular incompetence.
The value of the X-ray in the diagnosis of aortic aneurysms has been repeatedly proved. Williams finds that certain aneurysms can be more surely detected by this means than by any other mode of examination. It enables one to determine their location and extent and whether or not the tumour is increasing in size. Final- ly, if the aneurysm is situated at the left, it is best seen from behind, while those at the right of the heart show best from the front. Although it is possible for even skilled observers to commit error by incorrectly interpreting normal pulsations seen by aid of the fluoroscope, still there can be no doubt of the positive value of the X-ray in this class of cases.
To sum up, it may be stated that aside from the detection and study of aneurysms the real practical value of the X-ray in cardiac disease lies in its greater accuracy in detorniining the size of the heart in general, enlargement of any of the chambers, displace- ments and transpositions and certain obscure congenital malforma- tions. Even if it could replace percussion and auscultation, which
818 DISEASES OF THE HEART
it cannot, its lack of portability would preclude the possibility of its supplanting older methods.
THE SPHYGMOGRAPH
The sphygmograph is at the same time one of the most useful and most useless of the instruments used in clinical medicine. If used as a routine in his practice by the observing physician it will exceed in value the feeling of the pulse by the fingers, which it should supplement and not supplant. The educated tactile sense, which is always quickly and easily available, can appreciate nearly everything which the sphygmograph can show, and some features which this instrument is unable to delineate, but the impressions cannot be intelligently described and are evanescent On the con- trary, the sphygmograph, which is not always at hand nor readily applicable, can graphically show nearly everythijig that the finger can detect and some characteristics which this member cannot appreciate, and the results may be preserved for deliberate study, comparison, future reference, and exhibition to others.
The clinician will be able to do good work with any one of the standard sphygmographs, but he can use with the greatest facility, and can interpret most readily and accurately the tracings made by the instrument with which he is most familiar. My own pref- erence is for Dudgeon's sphygmograph, which, because of its por- tability and adaptability, readily lends itself to the exigencies of all kinds of practice.
In the practical application of the sphygmograph certain ele- mentary rules must be followed, but the whole secret of success in manipulating the instrument lies in placing and maintaining the metal pad upon the artery in such manner as to give the greatest possible amplitude to the excursions of the lever. The wrist band should be clastic ; the pad properly placed ; the tension correctly adjusted ; the pressure gauged to give the greatest amplitude to the writing lever. In adjusting and maintaining the instniment in proper position it is essential that the operator should rely, mainly, upon his fingers and not upon mechanical appliances. Facility in the use of the sphygmograph can only be attained by practice.
It may be noted that the most convenient strips of paper which can be used are made from ordinary heavy writing paper, cut thirty-one thirty -seconds
THE SPHYGMOGRAPfl
819
of an Inch wide^ and blackened with smoke from burning camphor. The beet varnish for preserving the tracings is the ordinary sandarac vjirnish used by dentists, suitably thinned by the addition of absolute alcohol.
Flo* 119. — Fkom a IIealtmt 3iA?r, Furttfive Yeah» or Age,
Tracings of the norraal pulse in health vary infinitely in their charac teristici?, and no two are ever exactly alike. The above sphygraogram (Fig. 119) may be considered fairly typical of the pulae in the healthy middle-aged adult.
ho. 120.^Frum a WctM^N, AoKD FyRTv-mrH, Di ring an Attack or Paboztsiiai* Taokycaruia- PrL»E, 196 per Miji'lte.
Between tlie extreme frequency of the pul&e in paroxysmal tachycardia and the remarkable slowness of bradycardia lies a wide gap which is filled by the rapid pulses of infectious fevers, the varying pulses of health and the slow pulses of age, some of the intoxications, c*tc. (Figs. 120 and 121).
Flo. 12L— Fkom
Man, Aok& Twekty-ei<*^iit. wttij RBcrRiutST Bradycardia.
iJ5 PER MlNlTE,
PtTLAE,
The sustained arterial tension as shown in the pulse varies within wide limits. The lowest tension is found in some of the acute infections — e, g., general gonorrhoea! or pneumococcal, in which there occurs, very early, profound capillary paresis. In many of these cases the powerful left ventricle throws the blood
830 DISEASES OF TOE HEART
forcibly into the arteries and tliron^h tlie riipillari(\s with prac- tically no resistance, as i^hown in the following tracing (Fig. 122).
iNritCTlO&l.
In some of these easeis the capillary and arteriole vaso-motor reflexes resixmd energetically to an unnatural stimulus, and the dicrotic pulse of every prade is the result, an example of which is
Tin, 123-— FhoM a MaA, All£ll FoBT¥, WITH DkCLLMSU TVPIIOlO FXV'EJI.
given in Fig, 123. The hyperdicrotic \mhiu as shown in Fig. 124, is so often seen in lurnHirrhages acc<jnipanied hy nervous excite- ment— e, g., in liienioptysis — tliat it may be considered somewhat distinctive*
In aortic regurgitati(»n the powerful left ventricle vigorously propels a large voluine of blood into nearly collapsed arteries,
Fm. ISS4.— Hrf»»t)ioROTio PruMii from a Womax, Aged TwiitTT-ftvit, awtmu Twitvi
quickly and widely distending theni, but the flow of blood through the capillaries, during and iuiiaediately fallowing the systole, and the reflux of blood through the open valve, the instant ventricu-
|
^^^^ lar aetioi H typical p Fio. ia5,-Fi In thij equrtl, the or more fr according 1 the seoondi At th liigh-teDs H Fio. 12tJ.— b K arteriosc] ^m nephritis, ■ 127). H Fio. 127,— S ^H f V fairly rej V and IB tv] H Id thi^ H FifihygMio^^r ^1 have iH'tn ^m their merits |
^^^^ THE SPHYG.MOGKAril 1 ceases, as qtiirkly reduce the arterial tension ilse of this eondition is the result, as shown in *OM A WuMAN, AOKD IVeNTV-FIVE, WITH Mi'DEBATE AoJtTtC 1> Well Coiri"ii:Ni*ATED- } connection it should be remembered that, other condi mbe will be less frequent and approximate the normal ii equent and with exaggeration of the distinctive chi* 0 the de^^'^ree of valvular incompetency. With failing coi iry curves in the line of desct^nt may disappettr. e other end of tlie scale we Itave the initial and ion piilseSj wdiieh are so often tlie aceoinpaninien fTTlAL HioH-TeXSIOM PcLfiE, FROM A MaX, AoED FoRTY-ElOir lUiKlLEBOCli A>U A SmaLL AxfitHYSM Of THE ArcH OF THE Ao] erosis, aneurysms of the aorta, and chronic ir typical tracings of which are given (Figs. rBTAiNKO HiohTenmow PtxaB Fiiosi a Womajt, Aoed Sixty Chronic Inteiiktitial Niu'hriti«. ollowing sphyn:mogram (Fig. 128) may be cons ^resenting the average in chronic interstitial i [deal of tho^:e oftenest encountered in this affect » connection it is fair fr>r me to state that» highly as iph, it U my ojiinion that it?? tracings in chronir jnlerstiti accorded, in wme <pi trrers, n diagnostic value altoget *, This is not to the discredit of the instniment, for it |
821 ^U and the ^^M Fig. 125. ^H a pr iciiif or, ^^^H tions being ^^^H 1 character, ^^^^| mcteri«itic^f ^^^H npeusutiou^ ^^^H sustained ^^H t of early ^^H wrm Ar^ ^^^H iterstitial ^^H and ^H TEffRZB, WITS ^^H ^idered aa ^^| aepbritisi ^^| al nephritis ^^^| Ker beyond ^^^H affords the ^^H |
8S3 DISEASES OF THK HEART
best practicable means for quickly and rfinvcnientlj estimating and permanently recording the state of the circulation^ cardiac energy, peripheral resistance, arterial resilience, and arterial tension. On the cootrary, this fictttiou» value usually de]>endii upon a faulty appreciation of the inl3nite variationa of the pulse in health and disease^ and io the same person at different times.
Flo. 1S8. — Faoii 4 Mak, Aomo FosTY-riTx, with Cmbokio Ixtsbatitijll Nspuaini^
The rhnliin of the pulse is very clearly and only satisfactorily shown by the sphygmograph. In health, the rhythm, in every par- ticular, U fairly but not absolutely regular. A nioinent's reflec- tion uix»n the physiology of the cardiac cycle and the vaso-motor mechanism should lead iis to expect this, and an inspection of any
Ftu. IW. — Fbum X WuitAX, .\ucD F»j|iTV-roLB» WITH Mild MYx«CDEitA.
large collection of sphygmograms will confirm the inference. Xevertheless, in ordinary health, the points of difference between the individual pulsations are minute and well within the limits of physiological identity, Ilowever, in certain conditions, some of which are understood while others are not, the pulse becomes
Fio. ISO.— Fjium a ilAJT, Aged TwijcrrrorR, with W«LL-CoMF*Jf bated Mitbal In^
eumcttifcT.
decidedly and morbidly irregular^arrhythmie. These irregu- larities may be of almost every conceivable degree and character, some of which are strikingly peculiar.
Thus there may be a marked inequality in the interval be- tween some of the pulsations, as shown in Fig. 129, or beats may
THE SPHYGMOGRAPH
bo entirely lost, as seen in Fig. 130. It will be found that under these eireimistant'es ilie line of descent reaches a lower level than it doea in the regular pulsations, because the artery has had a longer time in which to empty itself througli its distributing chan- nels. In some cases the pulsation is not entirely lost, one or more aboriive beats showing in the line of descent, as illustrated in Figs. 131 and 132, Such pulses are denominated bigeminal, trigemi- nal, etc. It is to be noted that the elevation that marks the abor-
Fjo. i3L— From a Woma»» Aoitti SiJtTT^itviN, with Abteiiio.- Well-Co MPKNAATED Mitieal iNcoaiPtTExrx.
WD FAIBLT
tive pulsation in the bigeminal pulse is located nearer the pre* ceding than the following full beat, and that the second abortive pulsation in the trigeminal pulse lies nearer the first alx>rtive beat than docs the latter to the jirecc^ling full stroke.
The arrliythniias thus far mentioned may l>e irregular in their occurrence, or the prolonged j missed, or abortive pulsations may be repeated at regular intervals. The irregularities of this group may be found rarely in apparent health, and frequently in patients
Fig. 1^^,— From a Woman, Aokd Seventv-threi, with Ahtkiuo?- i.rjc<*^is, autd MitbaL
iNaurriClENCV, FaILIJ^O CoHPEKeATl'X.
suffering from digesti%'e disturbances, various intoxications — aSy e. g., tobacco, renal insufficiency, organic disease of the central nervous system, the vagus and the cardiac ganglia, arteriosclerosis of the coronary arteries, myocardial changes, etc. They occur, therefore, in conditions of no, or varying degrees of danger. They often lead to tlie discovery of conditions which without such warn- ing might be overlooked. They may, by the strain thrown upon the ventricular walls, lead to dilatation, and relative valvular in-
824
DISEASES OF THE HEART
competence and thus become an element of danger. As a matter of fact, however, many persons pass through the greater portion
Fi©^ i i i^ \i A Mas, Auto SKvi^KTv-TiniKt, with AKttHKJ^t i^euohiis Chro»:ic Iw-
Tm#TITlAL NltPimfTlH, AKU MtTRAL InbCI HCIE3ICY, WITH FAJLUf^ OoMrJCK&ATIOlV.
Cheyne-Stori^ Keshkation.
of u Umg life with sjiu-h irre^ilarities an J without any iTn^onvr^nU enct.* whatever.
In HtMition to the above arrhythmias we have another group
Flo. 134 — Fkom a Womax, Agcu Sixty tth'O^ wim MttiiAt < ►usTutcTiax anh Rxomat- TATioir, wrrii FAtLixa CoKrxxaATioif. Irrxoularly K&ccrjujcu Dxlikjcv Coiuijs.
in which the irregiihirities of the pulse, as shown by tracings, abso- lutely defy either analvi^is or de^^cription. Such pulses are simply
Flo. 1^5. — From a Maic, Aosd Fifty, wirit Mitral Regurgitation, Lost CoifPKNtA* Tiow, RgLATivi TRictariD I^scrrrciRKizv, Aj*crrKH, and (Edema of Legs- Later
CoMFARATITtt RecOVSRY WITH QctOU CoMPElfftATIftN,
irregularly arrhythmic, mid are eiidlejis in their variety, as may be seen in the few examples shown (Figs. 133, 134, 135, and 136).
Flo, 136. — From a Woman, Ar*Er» TiimTv-EiaiiT, v^w-. i i , , i ,|, xsu I»-
AtTFtCISTVCY, L«>eT CuMFEXBATtON, ANl> Ul^LATIVR LltiHJMP&T&hclb <iM 1 M£ TrICUSFID. DkURIUM CoRlilt.
THE SPHYGMOGRAPe
825
This form of arrhythiiiia is met with, particularly, in mitral gtenosi^ aiul innjinpeteBcej and in iiiyoeanlial insufficiencv. It is often a late j>henomenon in mitral disease. It is of grave, but not necessarily of fatal iiiiport, os the lost compensation may be restoredj or the weakened mym:ardimn may reii;ain its tone.
Fig. IBT.—Fkom a Roy, Ameu Twelve, with a PisKviuriaLv Normal Pi l*k. Tex Dati III TviTJ! Acute KiiKiMATisii^ and un thk Sto^Nn Day of Enrocahui-xis, No
In endocarditis the t^phygmognipli usually furnishes ns with diagnostic evidence of valvuhir involvement several hours or days before murmnrs can be heard with the stethoscope. This evidence
Fio. 188.— FyioM Tiii: !^A 1
STtNOf*lJJ.
NT, Two VtARH Later, with Developed Aoimo
<CoNVAJ.£8CKNT FROM MtMrs,)
13 shown in a more or less radical change in the character of the pulse, as shown in the above sphygnifigrams (Figs, 137 and 138),
In ifilnKliicifig the above tracings it is proper for tne to aay that, during the past Qve yeara, I have hud under ohBcrvaHnn for one, three, and five years Tespcctively, three cases of aortic :*teno»is in yonn^ persfms, from eacli of whom tracings of a Mmiiar chameter were ohtained. In ttie slighter ctises of aortic stenosis the character of the pulse approximates the normul. In this connection a word of caution is due. In nsin^ the sphyjy^mograph in cases of considerable or great aortic oljstruction the most del irate adjustment of the instrutneot is required to ohtain satis;fortnry resultSv It may l>e sai<l, however, that the greater the care bestowed uywn this p<Hnt the more diffieidt it will he to pro- duce tracings corresponding to some which have been ninde classic by moTQ than a generation's text-book currency.
In early jnilmonary tuberculosis the pulse is often of a pecul- iar character, approfiehin^, more or less closely, the infantile type, and the tracings, at this lime, possess a distinct diagnostic value-
826
DISEASES OP THE HEART
One of the curiosities of clinical Bphjgmography is the mani- fest family resemblance, inherited from the father or mother bj their ehildreBj often shown in the pulse tracings.
Fio. IS^.-^Cahdiooraji moM a iiiKLu, Ao£o Nine, with Mitral iNdurncixiroT,
The sphyg^ograph may be used to obtain tracings from the heart (an example of which is given in Fig, 139), aneurysms, pul- sating veins, pulsating tumours, etc, but the information to be derived from such tracings is not very great.
OAERTNER'S TONOMETER
The examination of the circulation includes the observation of
the pulse for what is termed the arterial or blood pressure. This is determined by heart contraction, the peripheral resistance in the arteries and tissues, and the quantity of blood contained in the vessels. Among skilled physicians there is often a difference of opinion in regard to the degree of the arterial pressure, even in general terms, such as hard and soft, while subtile differences are entirely beyond registration, and, to most jjhysicians, beyond perception. Numerous attempts have been made to overcome this difficulty in pulse examinations by means of instruments; if suc- cessful, we would then have a more accurate method of comparison of the blood-pressure of individuals, and also of the blood -pressure of the same individual under different conditions. The invention of the sphygmograph was expected to bring accuracy into the subject, but this hope was not realized. Mosso, von Basch, ITuer- thle, Frey, Oliver, Riva-Rocei, and Hill and Barnard may be mentionc^d as inventors of such instruments. Of these, the von Baseh instrument was the most used up to 180D, since when the Oaertner instrument, on account of greater simplicity of its mech- anism, has supplanted it in the hands of many, and has also intro- duced the practice of taking the arterial pressure to a greater extent than had heretofore been customary. Opinions still vary as to the preferable instrument. James MacKenzie (1902) com-
GAKRTNERVS TONOMETER
82T
pares the action of the Tlill and BarniirJ inatniment to that of the sphygmograph and regards it unreliable for blood-presaure registration. So also with the Oliver instrument. Jarotxiij be- lievefi the Hill and Barnard device superior to those of von Basch^ Gaertner, etc. Hirsch considers the Gaertner less reliable than the von Basch instrument.
As the latter is at present the chief rival of the Gaertner in* stnunent it may be well to state the principle on which it works. There is a small compressible rnbber pelote connected by a rubber tube to a metallic manometer. By pressure with the rubber cyl- inder (pelote) a suitable artery may be compressed and the amount of necessary pressure at the point of disappearance or reappearance of the pulse on the peripheral side of the instrument is registered on the manometer. The radial artery may be used, but the temporals are usually selected. The sense of touch is re- quired for this instrument, while in the Gaertner method, soon to be described, sight is em]>loycd for observing the re-establish- ment of the circulation; and because in most people the sense of sight is more acute than the sense of touch, the Gaertner instru- ment requires less practice for its use, and also is believed by many to be more accurate.
Von Basch calls his instrument a sphyginomanoraeter. Gaert- ner's tonometer consists of a mercury manometer, a rubl:>er bidb, a ** Y '* rubber tubing, and a small ring consisting of a metal frame- work and encased in a rubber envelope^ which on inflation stretches inwardly only, ami thus compresses the finger that is introduced into the ring. These rings are of different sizes to fit large and email fingers snugly. One end of the *" Y '' tube is attached to the manometer, another end to the rubber bulb, and the third end to the riibl>er finger ring; thus pjressiire made on the bulb transfers itself to the manometer and the rubber ring, and the elastic rubber on the inside of the ring unfolds itself and makes inward pressure in proi>ortion to the pressure put on the bulK The manometer, being f>n the same closed tubing, regit^ters the increase or decrease of the pressure. A small clamp is serviceable for compressing the bulb firmly and steadily. The. rubber ring is pressed over the first or second phalanx of any finger or the thumb. It is to fit loosely, and is not to rest on a joint. An ordinary small rubber elastic is now rolled from the tip of finger to the rubber ring. This produces
828 DISEASES OP THE HEART
an anaemia of the finger. Pressure is now put on the rubber bulb to a degree that is regarded sufficient to maintain the anaemia. This is usually 180 to 200 millimetres of the mercury manometer. The rubber elastic is now pulled off the finger, after which the antwnic appearance continues on account of the constriction of the ring. The pressure on the rubber bulb is now gradually lessened, 5 millimetres at a time. After each diminution, the finger is ob- served for a few seconds. When the pressure is sufficiently lowered for the arterial pressure to force the blood through the arterioles compressed by the rubber ring, the ana?mic finger first shows a few spots of purple congestion, and after a little more reduction of the pressure on the bulb, the finger becomes entirely suffused with the purple colour of congestion, showing that the circulation is re- established. At this point the height of the mercury column is observed on the scale of the manometer. This is the arterial pres- sure expressed in millimetres of mercury.
One of the principal objections is the small size of the arteries utilized, but Gaertner and others state that the pressure in the digital arteries is the lateral pressure in the volar arch, and that this is probably only 8 or 10 millimetres lower than the pressure in the radial arteries. Another objection is that such small peripheral arteries are more under the influence of the vaso-motor variations than large vessels, and especially subject to local influences. Cold anii'inic tinkers soinetiinos must be imniorscMl in warm water before tlie t(»st can bo made.
It is well to follow his instructions for the use of the instrument vcrv closely. The individual may be in the horizontal or upright posture. In the former the pressure is a few millimetres lower than when the person is erect. The nianoni(»ter must be on a level with the heart. A difference of 10 centimetres in the levels of the heart and manometer produces a clianij:e of 7 millimetres in the mercurv acconlingly. The individual is to breathe regularly. A cough renders the result unreliable on account of the sudden in- crease of the blood-pressure. The test is not to be repeated on the same fin<rer immtMliately on account of a possible persistence of an arterial spasm. Thirty seconds will suffice for a test. There is no j)ain, but at the time of the re-establishment of the circulation the })erson feels a throbbing and tingling in the finger.
For portability a metallic manometer may be used, but it is not
GAERTXER'S TONOMETER
829
as reliaWe; it should be fre<]iient]y compared with the mercury manumeter. Tiie advocates of the vuii Basch method admit the requirement of much more experience and careful mauipuhuion in its use than in that of the Gaertner, The values obtained by both instruments agree fairly, those of the von Basch instniment are prohalily H to 10 millimetres higlier; tlie range of normal blood-pressure under ordinary conditions is from 100 to IGO milli- metres of merenry. These limits may be narrowed down to 110 to 135 for the greater nundjer of persons. Constant pressure of 150 to 160 should be regarded suspiciously high. li is probable timl each organisni has a mettn arleritd pressure towards whose ififiinfefiftnre the refjutalory mvrhfttiism feitacionsJif strives as soon as a disitirbance occurs. Active intluences are nuoierous. For instance; Posture, food, sleep, physical and mental work, psychical conditions. Several readings should be obtained and the average taken; according to some authorities the lowest reading is the correct IdiKjd-jjressure, as more causes are active in increasing than low^ering the blood-pressure. According to Jellinek the ar- terial pressure in the fingers of the right side is usually slightly higher than on the left, but Eckart and Hirscli, using von Basch's spliygmonuiuomcter, fiumd the pressure usually higher in the left temporal arteries, and ascribed this to the direct origin of the left carotid artery frum tlie aorta. Ilirscli, who ])refers von Basch's sphygmomanometer, maintains that the Oaertner instrument reg- isters the blood-pressure 10 to 20 niillinietres higher than the von Basch instrument, but admits that in general the values obtained by both instruments agree as to being high, medium, or low.
The high pressures are of special irjterest on account of bein^ associated with diseases in which many of the threatening symp- toms are thought to be due to the high pressure; thus in uricmia and arteriosclerosis pressures of 170 to 240 or more niillinietres are the rule, AH observers state thai hifjh pressures are frequently found in spite of an apparently soft pulse by palpation; here, then, as the general accuracy of these instruments camiot be doubted, their value is undeniable. In many illy defined conditions of mid- dle age an unusually high pressure is found, which returns within the normal limits in the course of treatment. Such cases are often described as due to arteriosclerosis or to some intoxication produc- ing increased arterial pressure. In the treatment of nephritis a
830 DISEASES OP THE HEART
lowering of the arterial pressure is associated with improvement of the subjective symptoms. In advanced cases of nephritis a sink- ing of the blood-pressure is considered to presage fatal termination. The influence of muscular efforts on arterial pressure has always been a mooted point. Both moderate increase and decrease have been claimed. This is possibly explained best according to Schott, who finds in such muscular exertions, as wrestling, at first a slight increase of 10 millimetres, but after prolonged dyspnoea a lowering of the pressure from 10 to 25 millimetres. There is certainly not an increase in the pressure directly relative to the amount of muscular exertion (Kornfeld). A cold bath in health as well as in fever increases the blood-pressure from 10 to 15 millimetres. A bath at 104° reduces the pressure slightly; so also do hot air and electric light sweat baths. Exceptions are occasionally found. There is an increase with digitalis, ether, and camphor, but this is less marked, and very frequently absent in fever. In fever the cold bath alone may be relied upon to increase the pressure (Mer- candino with the Kiva-Rocci instrument) ; psychic excitement regularly increases the blood-pressure from 10 to 20 millimetres, hence first examinations often are too high. In neurasthenia an increase of 10 to 20 millimetres is so common that Fedem, Kraus, and Ileim regard it a sign of diagnostic value, especially in chil- dren. In hflpmatemesis and haemoptysis there occurs a slight in- crease of arterial pressure on the second and third days; in acute fevers there is sometimes a slight rise, sometimes a slight sinking of the blood-pressure. The fever does not seem to have a constant influoneo, but, rather, the blood-pressure varies on account of other factors occurring in the course of the fever. For phthisis a constant low pressure indicates progression, but in the early stages there is usually little change ; as the disease progresses the pressure sinks on account of the diminution in the peripheral resistance (Burck- hardt-IIensen). There is a diminution in anaemia, cachexia, sleep, and acute cardiac weakness. A pressure of 60 millimetres is con- sidered very grave.
Gaertner states that his instrument registers mean and not maximal pressure. This is not accepted by all. However this may be, we must remember that the actual blood-pressure can be obtained only by the introduction of a cannula into an artery, as has been done in the course of operations by Albert, who found the
GAERTNEB'S TONOMETER 831
pressure to be in the anterior tibial artery between 100 and 160 millimetres of mercury; Knhe-Wiegand during ursemia^ 155 mil- limetres in a radial artery; Faiore in the femoral and brachial arteries, 120 and 110 millimetres; but such direct methods are out of the question for ordinary clinical purposes. The Gaertner in- strument, as well as all the other instruments, are influenced by the resistance of the tissue of the artery and the surrounding struc- tures. Von Basch estimates that the resistance of an empty tem- poral artery to compression is 1 millimetre and that of an ather- omatous artery 5 millimetres. The resistance of the soft tissues over the temporal artery is about 6 to 8 millimetres. So after all we are not dealing with figures of the actual pressure within the artery, but with relative figures. If all precautions are observed, these figures may surely be used for comparisons of blood-pressure changes in the same individual with a great degree of reliability ; while in comparisons among different individuals much more cau- tion must be observed. Although no defined clinical value can as yet be claimed for these researches except in diseases of high arte- rial pressure, the necessity for more attention to arterial pressure has become very apparent within the last ten years, as shown by numerous articles appearing on this subject, especially in Ger- many; and since there are now several instruments giving practical results, we may hope that soon a clearer understanding of the blood- pressure problems will be forthcoming, especially in cardiac dis- eases and acute fevers, so that both diagnosis and therapeutic in- dications will become more accurate than has thus far been possi- ble, even with the acumen of the most experienced.
INDEX OF NAMES
Abbott, 804.
Adams, 324, 328, 344, 376, 528, 627,
638, 748. Albert, 830. Allbutt, 139, 300, 580, 625, 671, 731,
736. Andrae, 505. A parti, 76. Apenta, 612.
Arnold, 646, 673, 676, 680. Arnozan, 376.
Babes, 150.
Bacelli, 397.
Balfour, 27, 263, 353, 496, 501, 541,
640, 801, 810. Bamberger, 43, 153, 638. Banholzer, 694. Banting, 608. Barie, 19, 366, 368, 374. Barnard, 826. Barsdorff, 779. Basch, 826.
Bauer, 43, 46, 57, 73, 206. Baumea, 638, 651. Baumgarten, 764. Baumler, 49. Bax, 629, 636. Beck, 785, 787, 812. Beniveni, 505. Billroth, 766. Biroh-Hirschfeld, 150. Bizot, 568, 779. Bodenheimer, 666. Botalli, 568. Bouilland, 19, 153, 366, 505, 638, 686,
810. Bouveret, 730. Boviard, 376. Bowles, 730. Boyer, 627.
Bramwell, 28, 353, 619. Braun, 766. Bregmann, 740. 53
Breid, 692.
Breitung, 81, 85.
Breschet, 681.
Broadbent, 9, 62, 99, 119, 142, 265, 269,
308, 361, 368, 486, 494. Brochard, 766. Brotroem, 680. Browiez, 668. Browne, 779, 794. Brunton, 445, 658. Budd, 153.
Burckhardt-Hensen, 830. Burresi. 811. Busse, 6.
Cabot, 698.
Campbell, 250.
Calon, 87.
Cavafy, 730.
Cay ley, 150.
Cejka* 79.
Chalmers, 653.
Chambers, 43, 781.
Charcot, 628, 748.
Chatin, 45, 766.
Chauveau, 22.
Cheyne, 237, 531, 537, 539, 550, 616,
632. Christophe, 108. Chuckerbutty, 810. Church, 666. aark, 197. Collet, 766. Collin, 57. Comil, 150. Corradi, 811. Corrigan, 298. Corvisart, 505, 575. Colton, 730. Councilman, 741. Cred^, 171. Crisp, 779. Cruveilhier, 376. Culture, 195.
834
DISEASES OF THE HEABT
Cuitsclimann, 656. Curtin, 445.
Davidson, 22.
Davis, 424.
Dessy, 150.
Dieulafoy, 794.
Doehle, 704.
Dorsch, 080.
Dreschfeld, 150, 150, 192.
Drummond. 35, 30, 778.
Duchex, 70.
Duckwoith, 137.
Dudgeon, 810.
Duroziez, 280, 305, 311, 399, 498, 690.
Kberth, 182.
Ebstein, 6, 11, 47, 73, 78, 506, 608, 625.
Eckart, 829.
Edes, 627.
Edmunds, 730.
Edwards, 171.
Eichhoret, 81, 139, 567.
Einhorn, 470.
England, 444.
Eppinger, 709, 775, 780.
Erb, 748.
Esmarch, 707.
Eulenberg, 038.
Evans, 112, 101, 359, 642, 700.
Ewart, 72, 75, 77, 81, 674.
Fagg. 153.
Faiore, 831.
Farquharson, 730.
FcMiern, 730.
Fenger, 293, 370. 379.
Fenwick, 133.
Fer(^, 090.
Fiessinger, 700.
Figaroli, 70.
FlexncT, 42, 45, 150.
Flint, 300.
Forlniiini. 370.
Fothergill, 422.
Foxwell, 28, 353.
Fraenkol. 150. 743, 757.
Frapntzcl, 19, 321, 520, 534, 544, 558,
ntis, 7.H. 773. Fran(;ois-Franck, 19. Franz-Josef. 612. Frazer, 002. Freund, 512. Froy, 820.
Friedreioha, 120, 038. Fuchs, 810.
Fuller, 153. Ftttterer, 460.
Gaertner, 571, 615, 629, 753, 826.
Gairdner, 262, 557, 639, 653.
Galen, 505.
Geigel, 22.
Gerhardt, 254, 730, 772, 779.
Gibson, 2K, WjI 139, 195, 343, 403, 640,
648, 666, 090, 694, 730, 760, 779,
804, 811. Gilbert, 150. Gintrac, 038. Uivadiiiovjtc*h» 45. Goldflam, 706. Goodhart, 254. Gorges, 783. Grave, 714, 727. Grob, 625. Gutch, 565. Guttman, 638. Guy, 251, 255, 269.
Hadden, 766.
Halberton, 628.
Hale, 482.
Hall, 498.
Hampeln, 534.
Handford, 353.
Hanford, 27.
Hanot, 209.
Hare, 130, 781, 808.
Harris, 99, 104.
Harrison, 590.
Hartell, 078.
Harvey, 741.
Hasonfpld, 150, 744.
Haskin, 170.
Ilayden, 139, 153, 209.
Hayem, 500.
Hcborden, 637, 054, 055.
Heidman, 110.
Hrim, 830.
Hektoen, 116, 009.
Horriok, 350, 301, 304.
Herringham, 730.
llcrshey, 811.
Hertz, 076. 078, 080.
Ileubncr, 742, 704.
Hill, 820.
Hirsoh, 829.
Hirschfeld, 500.
His, 027.
Hoohhaus, 748.
Hodgson, 775, 779.
Hoffman, 027, 035, 658, 660.
IND£X OF NAMES
885
Holder, 130, 781, 808.
Holmes, 168, 794, 799.
Holt, 376.
Hope, 505.
Homkohl, 6, 8.
Houston, 289, 481, 489, 692.
Howard, 156.
Huchard, 505, 555, 628, 632, 638, 644,
056, 742, 760, 8131 Huerthle, 826. Hllfler 470. Hunner, 811. Hunter, 637, 647. Hustedt, 248, 270, 308, 341, 354. Hutterbrenner, 617.
Janeway 327 Jaquet, 627 Jarotzny 827. Jellinek, 829. Jenner, 637. Johnson, 68, 294. Jom, 470. Josephson, 70. Josseraut, 150. Juda, 779.
Kaczorowski, 358. King, 344, 672. Klebs, 150, 157. Klein, 668. Klemperer, 195. Knaggs, 666. Koehler, 376, 378, 666. Koenig, 752. Kolisko, 696. Komfeld, 830. Krannhals, 377. Kraus, 830. Krehl, 555, 570, 694. Krester, 150. Kreysig, 638. Kuhe-Wiegand, 831. Kussmaul, 99, 102, 117, 120. 686, 688, 702, 769.
Laennec, 123, 505, 638, 695.
Lajard, 137.
Lancereaux. 139, 638, 764, 812.
Laneisi, 775.
I^andois, 638.
Latham. 639.
Lebert, 153.
1.^8, 87.
Loger, 760.
Legg, 673.
Leube, 35, 78, 83, 260.
Leudet, 356, 364.
Lewis, 34.
Leyden, 407, 411, 506, 636, 600, 638.
Lion, 150.
Lobstein, 738.
Loeffler, 157.
Lowrence, 288.
Loreta, 811.
Lorry, 637.
Lovewell, 196.
MacCallum, 669. Macewen, 812. Mackenzie, 421, 826. Maguire, 12, 697. Maier, 769. Malassez, 694. Malpighl, 775. Massa, 505. Massip, 82. Mayer, 377. Meckel, 686. Mercandino, 830. Merck, 481. Miller, 141. Minor, 436. Mitchell, 482. Mollet, 509. Moore, 811.
Morgagni, 637, 738, 776. Moritz, 692. Moaqiiera, 191. Mfisso, 826. Mouill^, 695. Mracek, 139. Munnely, 730. Murchison, 169. Murri, 623. Musser, 657.
Naunyn, 27. Netter, 150. Neusser, 181. Nothnagle, 638, 731, 769.
0*Byme, 279.
Oertel, 454. 608, 611.
Oliver, 797, 826, 827.
OrmcTod 43.
Orth, 139. 766.
Ortmann, 766.
Osier, 38, 137, 151, 166, 606, 626, 667, 625, 639. 646, 673, 678, 686. 690, 719, 721. 769, 780, 786, 793, 796, 811.
Otis, 331, 333.
836
DISEASES OF THE HEART
Parr, 741.
Parry, 637.
Pftssler, 512.
Paul, 376.
Pawlowski, 671, 676, 679.
Peacock, 153, 686.
Pellatau, 769.
Pembrie, 623.
Perez, 121.
Peter, 638.
Petit, 666.
Philips, 664.
Pick, 100, 123.
Pins, 80.
Pirogoff, 671.
Pi teal rn, 42.
Pleischl, 57.
Popoff, 260.
Potain, 19.
Powell, 191, 197, 643, 653, 658.
Poynton, 43, 49, 62, 184, 609.
Prei>lt% 4(), titiO, 794.
Pr^ntis, 6^7
ProlMtinp, 730,
PnouBt. G7n. cm
Pnidden, 144, 150.
Przewoski, 668.
Purser, 150.
Quain, 706.
Quincke, 28, 298, 301.
Radizewsky, 260, 534, 589.
Rwkl njLihauH4»n, (UiH, 674, 678.
RedtenWchtT 674, 678, 680.
Reeder, 638.
Regnard, 433, 509, 625, 630.
Rehlniann, 752.
Renaut, 668.
Rendu, 377.
Renvera, 696.
Richardson, 658.
Ricord, 664.
Riegel, 349. 625.
Rinsenna. 377.
Riva-Rooro. 826, 830.
Roberts. 42. 44, 49, 60, 72, 87, 99, 102, 121, 593.
Hokitiinskv 254, 276, 506, 686, 695, 738. 769.
Rolleston, 674, 680.
Romberg, 169, 171, 506, ,508, 511, 516, 558, 577, 599, 600, 609, 625, 638, 675, 688, 692, 694, 702, 718, 741, 748, 752, 759, 765, 769, 770.
Roque, 766.
Roeenbauch, 77, 150, 164, 328, 506, 618,
;i.:t;, (i-ii). 638. Ronensteiii, 1 RoU'h, Tu, Td, 78, 96. RougnoiJ, 633, 637. Roux, 150. Rumpf, 661, 766. Russell, 27, 353.
Sam ways, 251, 269.
Sansom, 7, 17, 28, 78, 192, 252, 267,
277, 445, 618, 625, 798. Savart, 22. Scarpa, 775. Schlesinger, 766. Schmaltz, 510. Schmidt, 778. Schott, 328, 331, 693. Schroetter, 683, 759, 772, 775. S#e, 638. Semmola, 664. Seneca, 637, 738. Sewall, 17, 19, 433. Shattuck, 77, 96. Sibson, 43, 49, 66, 76, 683. Simpson, 689. Siredi, 376, 760. Smith, 361. Sommerbrodt, 569. Southey, 492. Stadelmann, 623. Stangp, 674, 680. Starck, 696. Starr, 440. Steele, 300. Stein, 506. Sternherp, 766. Sloelker 702. Stokes, 237. 324, 328, 417. 505, 528,
532, 536, 537, 550, 567, 602, 616,
627, 632, 748, 775. Streeter, 440. Sturpea, 44, 184. Stybr, 377, 378. Sweninger, 608.
Talamon, 731.
Tanchon, 606.
Tedesohi, 668.
Teissier. 253.
Thonia, 567, 743, 752, 756, 760, 775,
778. Thome, 9. Tice, 382. Tiedemann, 638.
INDEX OF NAMBS
837
Traubc, 264, 618, 638. Tripier, 628. True, 32. Tuchzek, 730.
Unverricht, 623.
Vaughn, 197.
Vendeler, 764.
Veronese, 512.
Vesalius, 775.
Vierordt, 5, 11, 693, 756.
Villy, 511.
Virehow, 143, 150, 738, 773.
Walker, 178. Walsh, 57, 139. Walshe, 602, 640, 683, 798. Watson, 730. Weber, 765, 766, 772. Webster, 284. 292. Weichselbaum, 150. Weigert, 764. Weirdermann, 766. Weiss, 766.
Welch, 209, 671, 680.
Welles, 329, 631.
Wells, 136, 733.
Wessner, 471.
West, 731.
Wharry, 617.
White, 811.
Wilks. 99.
Willigk, 666.
Williams, 141, 579, 584, 595, 816.
Wing, 55.
Winge, 143.
Winiwarter, 766.
Wood, 680.
Worcester, 697.
Wunderlich, 153, 668.
Wyssokowitch, 144.
Yung, 273.
Zeissl, 765.
Zenker, 506.
Ziegler, 101, 765.
Ziemssen, 83, 279, 417, 639, 671.
|
^^^^^^^^^^^^^ i:n^dex ^^^^^H |
1 |
|
|
Aberrant cords, 30, |
Angina pectoris, 637; f |
^^M |
|
Abortion, oauiing acute endocarditiBf |
aconite, not itaed in, 660; |
^^^^^^^H |
|
180. |
amyl nitrite in, 058; |
^^^1 |
|
Adherent poncArdium* 99; |
a noil y lies in, 060; |
^^^1 |
|
BroadlM?nf8 siffn hi, 119; |
brandy in, 060; |
^^H |
|
Frieilreiclm' h\gn in, 120; |
cases of, 045, 652, 653 ; |
^^^1 |
|
Kussraaurs si^ii in, 120. |
chloroform and ether in, 668; |
^^H |
|
Adhesions, clironic mediasUnoperi- |
diagnosis of, 654; |
^^^1 |
|
eardial, 102; |
digitalis in, 062; |
^^^H |
|
formation of, in chronic perii-arditia, |
etiolcTgy of, 040; |
^^^1 |
|
103. |
nitroglycerin in, 658; |
^^^1 |
|
Age, influence of, in mitral stenosiB, |
opium in, 658, 059; |
^^^1 |
|
254; |
pathology of, 640; |
^^^1 |
|
in valvular lesions, 407. |
prognosis in, 057; |
^^^1 |
|
Air luingf^r, 1:>7, |
etropliantlius in. 062; |
^^^1 |
|
Alcolioli^m, in acute endoeardittSr 47; |
syphilis in, 640; |
^^^1 |
|
in aortic reg^urgitation, 2S0. |
treatment of, 658. |
^^^1 |
|
Aniyl, nitrite of, in angina pectoris, |
Angina pseu do pectoris, 719. |
^^H |
|
'65a |
** Angina-sclcro-tabagi^ne," 648, |
^^H |
|
Aneurysm^ congenital, 709; |
Anodynes, 88. |
^^H |
|
caHo's of, 01, 746. |
Antistreptococcns serum. (See |
■ |
|
Aneuryjtm. of thoracic aorta, 775; |
mm.) |
H |
|
asMK'iiittHl with expectoration and |
Antitoxin, in amte endocarditis, |
193; ^M |
|
congh, 784; |
in arufc myocarditis, 516. |
^^H |
|
auscultation in, 802; |
Aorta, stenosis of (!*ee Stenosis) ; |
^^H |
|
cases of, 779, 794, 799, dD4; |
thoracic, aneurysm of. 775, |
^^H |
|
diagnosis of, 804; |
Aortic regurgitation {see Regurgita- __^^ |
|
|
dyspmta in, 783; |
tinn) ; |
^^^1 |
|
electrohsis in, 811 ; |
stenosis (see Stenosis) » |
^^^H |
|
etiology of, 7*7; |
Aortitis, acute, 759; |
^^^^ |
|
injection of gelatin in» 787; |
etiology of, 760; |
^^^1 |
|
of gelatin and salt solution, 812; |
inspection in, 761; |
^^^1 |
|
inapeition in, 8O0; |
in mcanles, 760; |
^^^M |
|
morbid anatomy of, 775; |
morKid anatomy of, 159; |
^^^M |
|
morphine in, 813; |
nitroglycerin in. 762; |
^^^M |
|
pain in, 782; |
palpation in, 761 ; |
^M |
|
palpation in, 801; |
percussion in, 701 ; |
^^^B |
|
percnssion in, 802; |
physical signs in, 762; |
^^^H |
|
physical signs in, 800; |
in pneumonia, 760; |
^^^1 |
|
prognosis in, 8flfi ; |
progno?«is in, 762; |
^^^1 |
|
«ymf>toms of, 781; |
in warlnlina, 760; |
^^^^M |
|
syphilis in, 778; |
^tnchnine in, 762; |
^^^M |
|
treatment of, 809; |
gj'mptoms of, 700; |
^^^M |
|
luhereuTosis in, 808. |
treatment of, 762. |
^^^H |
|
N |
m 1 |
1 |
840
DISEASES OF THE HEART
Apnoea, in Cheyne-Stokes respiration,
615. Applications, cold (see Ice-Bag ) ;
hot, in acute endocarditis, 190. Area, aortic, 25;
cardiac, 25;
mitral, 26;
pulmonary, 25;
tricuspid, 26. Arrhythmia, in chronic endocarditis,
214. Arterial syntem, diseases of, 738. Arteries, con^^enital smallness of, 773;
diagnosis of, 774;
prognosis in, 774;
symptoms of, 773;
treatment of, 774. Arteriosclerosis, 738;
bronchitis, chronic, resulting from, 749;
calomel in. 757;
cases of, 746, 753;
diagnosis of, 751;
digitalis in, 757;
etiology of, 741;
jalap in, 757;
morbid anatomy of, 739;
nitroglycerin in, 757;
physical signs in, 750;
prognosis in, 754;
strophanthus in, 757;
symptoms of, 745;
syphilis in, 742. Arteritis, arnto, 762;
diapriK)>is of, 763;
digitalis in, 762;
ins|)oction in, 763:
morbid anatomy of, 762;
palpation in, 763;
physical sijjns in, 763;
prognosis in, 763;
sympt4>nis of. 762:
treatment of. 763. Arteritis, syphilitic. 764;
diagnosis of, 766:
etiology of. 765;
morbid anatomy of, 764;
prognosis in, 766;
symptoms of. 765;
treatment of, 766. Artery, cerebral, rupture of, in hyper- trophy of left ventricle, 574;
pulmonary, stenosis of (see Steno- sis). A8cit(»s, in adherent pericardium. 117. Asthma, cardiac, 237. 613.
Asthma, bromides in, 563;
in mitral stenosis, 270. Atheroma. (See Arteriosclerosis.) Atrophy of the heart, 667;
diagnosis of, 668;
etiology of, 667;
morbid anatomy of, 667;
prognosis in, 668;
symptoms of, 668;
treatment of, 668. Atropine, in Cheyne-Stokes respira- tion, 623;
in valvular lesions, 500. Attack, neuroses, treatment of, 727.
Bacilli. (See Micro-organisms.) Bacteria. (See Micro-oi^nisms.) Baths, hot, evil effect of, in valvular lesions, 427. in valvular lesions, 427, 466, 503; Nauheim, 110, 115, 464, 503, 592; saline, in valvular lesions 466; Turkish, 552. Belladonna, in pericarditis, 88. Benign endocarditis. (See Endocardi- tis.) Bloodletting, in dilatation of heart,
591. Blue baby, of congenital heart disease,
692, 701. Bradycardia, 624;
diseases associated with, 625; Breathing, Clieyne-Stokes, diseases in
which, observed, 617. Bright 's disease, in pericarditis, acute, 45; chronic, in Cheyne-Stokes respira- tion, 617; in myocarditis, chronic, 539; in regurgitation, mitral, 237. Broad bent's sign in adherent pericar- dium, 119. Bronchial disr)rderfl, in valvular le- sions, 407. Bronchitis, in pericarditis, acute, 47; in pericarditis, chronic. 102.
CaflTeine. in tachycardia, 736;
in valvular lesions, 4.32. Calcification in pericarditis, chronic,
101. Calomel, in arteriosclerosis. 757;
in pericarditis, chronic. 125;
with effusion, 89:
in valvular lesions. 432. 448, 491, 493. Cancer, of the myocardium, 666.
INDEX
841
Cardiac asthma (see Asthma) ; neurosis, 703; pain, 718. Catarrh, bronchial, in mitral lesions,
407. Cathartics, in dilatation, 592; in endocarditis, chronic, 202; in valvular lesions, 492. Cheyne-Stokes respiration, 617; case of, 622 ; in diphtheria, 617; morphine in, 623; in pneumonia, 617; prognosis in, 622; treatment of, 623. Chilis and fever, in suppui*ative peri- carditis, 72. Chloralamide, in chronic myocarditis,
563. Chloral hydrate, in valvular lesions,
501. Chloral osc, in valvular lesions, 501. Chlorosis, in mitral insufficiency, 597. Chorea, in acute endocarditis, 153, 154,
155. Cirrhosis, atrophic hepatic, differen- tiated from adherent pericardium, 122; renal, leading to tricuspid regurgi- tation, 345. Climate, cliange of, in valvular lesions,
432. Clothing, in valvular lesions. 425, 476. Codeine, in pericarditis, 88, 91. Compensation, imperfect, in valvular lesions, 435. lost, 478; perfect, 413, 414;
prevented, in chronic pericarditis, 105. Congenital aneurysm. (See Aneu- rysm.) Congenital diseases of the heart, 686; case of, 698; diagnosis of, 701 ; etiology of, 689; inspection in, 695; morbid anatomy of, 686; morphine in, 693; palpation in, 696. Congenital smallness of arteries. (See
Arteries.) Congestion, ab<lominal viscera, in aor- tic and mitral regurgitation, 397; cerebral, in mitral regurgitation, 237.
54
Congestion, chronic pulmonary, 231;
venous, 397. Cords, aberrant, 30. Corpulent, cardiac inadequacy of the,
599. Cough, in aneurysm of thoracic aorta,
784. Cusp, rupture of, in aortic regurgita- tion, 278. Cyanosis, in acute endocarditis, 171; in aortic stenosis, 335; in dilatation, 585; in tricuspid regurgitation, 347.
Death, mode and causes of, in aneu- rysm of thoracic aorta, 808;
in regurgitation, aortic, 307;
mitral, 247 ;
pulmonary, 374;
tricuspid, 354;
in stenosis, aortic, 340;
mitral, 270;
pulmonary. 388;
tricuspid, 364;
sudden, in syphilis of the myocar- dium, 665.* Deglutition, painful, in dry pericar- ditis, 49. Delirium, in mitral stenosis, 270. Devices, mechanical, as aids to deter- mining diseases, 815. Dextrocardia, acquired, 682;
diagnosis of, 684;
etiology of, 683;
inspection in, 685;
morbid anatomy of, 682;
palpation in, 684;
percussion in, 684;
prognosis in, 685;
symptoms of, 684;
treatment of, 685;
tuberculosis in, 681. Dextrocardia, congenital, 681;
case of, 681 :
symptoms of, 681. Diathesis, rheumatic, in valvular le- sions, 406. Digitalis in arteriosclerosis, 757;
in arteritis, 762:
in angina pectoris, 662;
in dilatation, 591;
in endocarditis, acute, 189;
in endocarditis, chroni'. 202;
in fatty heart, 611;
in functional disorders, 709;
in hypertrophy, 575.
842
DISEASES OF THE HEART
Digitalis in mitral insufficiency, 598;
in myocarditis, acute, 516;
in myocarditis, chronic, 552, 564;
in pericarditis, chronic, 126;
in pericarditis, dry, 54;
in pericarditis, with effusion, 83;
routine administration, objection- able, 89;
in pneumopericardium, 136;
in regurgitation, aortic, 288, 290;
in regurgitation, mitral, 225;
in stenosis, aortic, 326;
in stenosis, mitral, 272;
in stenosis, tricuspid, 359;
in Stokes- Adams disease, 636;
in syphilis, of myocardium, 665;
in tachycardia, 736;
in valvular lesions, 394, 430, 480;
wai-ning in regard to use of, 497. Dilatation, 576;
baths in, 592;
bloodletting in, 591;
blue mass in, 591;
cases of, 582, 584, 593;
cathartics in, 592;
cyanosis in, 584;
diagnosis of, 586;
digitalis in, 591;
etiology of, 577;
influenza in, 577;
inspection in, 585;
morbid anatomy of, 576;
morphine in, 593;
nitrof»lycorin in, 591, 593;
palpation in, 585;
percussion in, 585;
physical signs in, 585;
prognosis in, 587;
resistance exercises in, 592;
rheumatism in, 401, 429;
secondary to pericarditis, 101 ;
strychnine in, 591 ;
symptoms of, 580;
treatment of, 590. Diphtheria, in bradycardia, 625;
in Cheyne-Stokes respiration, 617;
in endocarditis, acute, 150;
in myocarditis, acute, 508, 511;
in pericarditis, acute, 46;
in tachycardia, 732. Diphtheritic endocarditis. (See Endo- carditis.) Disorders, functional. (See Function- al Disorders.) Dropsy, in hydropericardium, 130;
in myocarditis, chronic, 530, 563.
Dropsy, in r^pugitation, mitral, 210, 236, 245; cause of, in tricuspid regurgitation,
348; in regurgitation, tricuspid, 351; in valvular lesions, 470. Drugs, use of, in valvular lesions, 430. Duroziec's sign, in aortic regurgita- tion, 305. Dyspepsia, chronic, in bradycardia, 625. Dyspnoea, in aneurysm, aortic, 783; in endocarditis, acute, 171; in regurgitation, mitral, 238; in stenosis, mitral, 257.
Electrolysis, in aneurysm of thoracic
aorta, 811. Embolism, septic, in acute endocar- ditis, 158, 172, 184. Emphysema, in hypertrophy, 570. Endarteritis obliterans, 766;
diagnosis of, 768;
etiology of, 767;
morbid anatomy of, 766;
prognosis in, 768;
symptoms of, 767;
treatment of, 769. Endocarditis, acute, 143;
abscess in, 156, 181;
aconite, not used in, 189;
alcohol in, 192;
alkalies in, 187;
applications in, hot. 190;
associated with myocarditis, 157;
associated with pericarditis, 101,157 ;
bacillus of diphtheria in, 151, 156;
of influenza in, 151, 156:
of typhoid fever in, 151;
bacteria, pyogenic, in, 149, 156;
blister in, 188;
brandy in, 191 ;
bromides in, 189;
camphor in, 191;
in cancer, 156;
cases of, 158, 164, 170;
chorea in, 153, 154, 155;
course of, 163:
cyanosis in, 171 ;
diagnosis of, 163:
diagnosis, differential, from typhoid fever, 182:
digitalis in, 189;
dyspnoea in, 171;
emboli in, 172;
ether in, 191 :
etiology of, 143.
|
^^V ^^^^^F INBEX ^^^r 843 ^^| |
|
|
^B Endocarditis, acute, hemiplegia in, |
Endocarditis, yegetative, 143. ^^^H |
|
^M 15B, 184; |
Endocarditis, verrucoset 143. ^^^^H |
|
^H iic-ltag ID, m9; |
Endocardium^ diseases of, 143. ^^^H |
|
^H iiulieiiied by rheumatic feveri 157; |
Knteric fever. (See Fever.) ^^^H |
|
^H infarction in, 158; |
Epilepsy, in mitral stenosis, 212. ^^^H |
|
^m in k^lat life, U3; |
Ewart's sign, in pericarditis with effu- ^^^H |
|
^H inspection in, 176; |
^^^H |
|
^H lencoeytoaiH in, 181; |
Exercii^e, in dilatation, 592; ^^^H |
|
^H in niea$le», 154; |
resist a Ui'^\ 455, 592; ^^^H |
|
^H morbid anatomy of^ 143; |
in valvular lesions, 414, 454, 502. ^^^H |
|
^H morphine in, 175; |
Expectoration, in aneurysm of tbo* ^^^^H |
|
^H opium tit, 190; |
racic aorta, 784, ^^^^H |
|
^H oxy^'en in, 101 ; |
^^^^^ |
|
^H palpation in, 170; |
Fatty heart, 599; ^^H |
|
^H in pi vie disease, 155; |
af>ertenis in^ 612; ^^^^| |
|
^H percii^iHiou in, 177; |
camphor in, Oil; ^^^^H |
|
^H phyfiieal si^ns in, 176; |
of, 007 ^^^^H |
|
^H in pnc^nnionia, 186; |
diagnosis of, 605; ^^^^H |
|
^H in p3'a^niia, 156; |
608; ^^^H |
|
^H pyrt'xia in, 171 ; |
digitalis in, 611; ^^^^^| |
|
^H resulting from pnterie fever, 154; |
etiology of, 6O0; ^^^H |
|
^H resulling from gallstones, 156; |
gentian in, 610; ^^^^^ |
|
^H resulting from seark't fever, 154; |
gluttony, predisposing to, 601; ^^^^| |
|
^M rheumatiftm in, 140, 152, 153, 157, |
hypo phosphites in, 610; ^^^^| |
|
^m 181, 186, IH7; |
insfM^^tion in, 004; ^^^^| |
|
^m m'pHis in, 170, 103; |
in, 610; ^^^^| |
|
^H serum, antialreptoeoccus ID^ 103; |
morbid anatomy of, 599; ^^^^^| |
|
^H in small- pox, 154; |
nitroglycerin in. Oil; ^^^^^| |
|
^H atrophanthus tn, 169; |
nux vomica in, 010; ^J^^^^l |
|
^P strychnine in, 100, 101; |
orthopntra in, 603; ^^^^^1 |
|
symptoms of, 157; |
palpation in, 604; ^^^^H |
|
in ton?^tllitis, 150; |
pathology of, 599; ^^^| |
|
treatment of. 187. |
fx^rcttSMion in, 604; ^^^^| |
|
Endoi-arditi^, benign, 143. |
physical signs in, 604; ^^^^| |
|
Endocarditis, ebronic, 190; |
prognosis in, 000; ^^^^| |
|
arrhji;hmta in, 214; |
strophanthus in. Oil; ^^^^| |
|
1 eases of, 201, 206, 210; |
strychnine in. Oil; ^^^^| |
|
cathartics in, 202; |
symptoms of, 602 ; ^^^H |
|
digitalis in, 202; |
treatment of, 606. ^^^H |
|
etiolofjy of. 201 ; |
Fever, in pericarditis, dry, 51; ^^^^H |
|
morbid anatomy of, 199; |
in pericarditis, with effusion. S9; ^^^H |
|
nitroglycerin in, 202; |
enteric, in endocarditis, 154; ^^^H |
|
rheumatism in, 204; |
rheumatic, indicating acute eiido- ^^^H |
|
strychnine in, 202; |
carditis, ^^^H |
|
symptoms of, 205; |
ecarlet, Cheyne-Siokea respiration ^^^H |
|
1 siypbilis in. 204; |
^^H |
|
treatment of, 202. |
in myocarditis, ,'i22: ^^^H |
|
Endoearditis, diphtheritic, 143. |
leading to acute endocarditis, 154; ^^^H |
|
Endoearditi**, malignnnt, 143. |
leading to pericarditis with eflTu- ^^^H |
|
Endocarditis, mycotic, 143. |
^^^1 |
|
Endocarditis, simple, 143, 150, 157. |
Fever, typhoid, Cheyne-Stokes respi- ^^^H |
|
Endocarditis ulcerative, 143, 154, 163; |
in, 017; ^^^H |
|
course of, 172; |
diagnosis of, differential, from aciit€ ^^^H |
|
diagnofiia of, 179; |
enducardttis, 1R2; ^^^H |
|
morphine in. 106; |
in bradycardia, 625; ^^^^| |
|
. trtatment of, 191. |
in endocarditis, acute, 151, ^^^^| |
844
DISEASES OP THE HEART
Fever, in myocarditis, acute, 508;
in myocarditis, chronic, 522;
typhoid, in pericarditis, acute, 46;
treatment of, in acute myocarditis, 516. Fibroma, of myocardium, 666. Fii-st rib sign, in pericarditis with ef- fusion, 75. Foetal life, acute endocarditis in, 143;
developmental anomalies in, 690;
perforate interventricular saeptum in, 688. Fomentations, in pericarditis, 88. Food, in valvular lesions, 428. Fragmentation of myocardium, 688. ** Fremissement eataire," in mitral ste- nosis, 259. Friedreich's sign in adherent pericar- dium, 120. Friction-sounds. (See Sounds.) Functional disorders, 703;
cases of, 705, 714;
digitalis in, 709;
neuroses in, 703;
strophanthus in, 711;
strychnine in, 709;
tuberculosis in, 716.
Gangiene of foot, in arterial throm- bosis, 676; of leg. in mitral regui^tation, 238. Gastritis, chronic, in chronic myocar- ditis. 5.')!. (U'latin, injection of, in aneurysm,
787. (iorins. (See Micro-orpanisnis.) Olonoin. in valvular disease, 432, 446. (Hut tony, inducing fatty heart, 601. (ioitrc, exophthalmic, hypertrophy in, 570; taeliyeardia in, 715. Gonorrhd'a, in acute endocarditis, 154, 181: in acute myocarditis, .')08. Gout, in mitral stenosis, 254; in regurgitation, aortic. 280, 206.
Habits, in valvular lesions, 410, 420,
476. HaMnopericardium, 130. Ila^mopliilin, in acute pericarditis, 47. Heart, area, aortic. 3;
mitral, 4:
pulmonic. :? :
tricuspid, 3. Heart, atrophy of. (See Atrophy.)
Heart, auscultation of, 12;
deep boundaries of, 6;
dilatation of (see Dilatation);
diseases of, congenital, 686;
disorders of, functional, 703;
enlargement of, 5;
fatty (see Fatty Heart) ;
hypertrophy of (see Hypertrophy) ;
location of, 1 ;
musical, notable example of, 30;
position of, attempt to fix, 2;
relation of, to anterior thoracic wall, 1;
size of, how ascertained, 5;
valve lesions of the right, summary of physical signs of, 389;
vessels and valves, position of, 3. Heart sounds. (See Sounds.) Hemiplegia, embolic, in acute endocar- ditis, 158, 184. Heroin, in pericarditis with effusion,
88. Home surroundings, in valvular le- sions, 410. Hydropericardium, 103, 127, 131;
diagnosis of, 129;
dropsy in, 130;
etiology of, 128;
ina|)ecti(m in, 128;
morbid anatomy of, 127;
palpation in, 128;
percussion in. 129;
physical signs in, 128;
prof-nosis in, 129;
pyrexia in, 129;
rheuntatism in, 129;
symptoms of, 128;
treatment of, 129. Hypera»inia, chronic, 116. Hypnotics, in valvular disease, .'>00. Hypophosphitea. in fatty heart. 610;
in valvular lesions, 448. Hypertrophy of the heart, 565;
aconite, not used in, 575;
diagnosis of, 572;
digitalis in. 575;
etiology of. 568;
following emphysema, 570;
inspection in, 571 ;
morbid anatximy of, 565;
palpation in, 571 ;
percussion in, 571 ;
pliysical signs in. 571;
prognosis in, 574;
symptoms of, 570;
treatment of, 575.
|
^^^^^^9^^^^^^^ ^^^r ^^M |
|
|
^^^^^ Ice. in paroxysmal tachycardia, 736* |
Liver, in pericarditis, chronic, 100, ^^^H |
|
^H lee ba^^ in ni'Ute eiKkx'aiditis, 18S): |
lO-l, 1U5. UMK 117, 122; ^^^^| |
|
^H in p^^iii'tirditis, 87 , 8U> |
in {K'ricarditis, dry. 63; ^^^^^ |
|
^H lllneBsei^ in viilvular le^^lon4t 421). |
in ptricardiliH. with cfTusion, high ^^^^^ |
|
^H Inadw[Liat'y, cardiac, of the cnrjmlpnt» |
pi>i^ition of, 70; ^^^^H |
|
^B |
in regurgitation, aortic, 28H; ^^^H |
|
^H Int'oinpetency, cariliae, 5S5. |
in regurgitation, mitral, 2 19, 233. 23S; ^^^H |
|
^H Individual tendeneiein, in rhmnic endo- |
in regurgitation, tricuspid, 347. 3.50; ^^^H |
|
^M curdiliH, 200. |
in stcnoHiH, mi) ml, 257, 268; ^^^^| |
|
^H Infarction, in acute endocarditis, 158; |
in valvular dii^as(>, 405, 464; ^^^H |
|
^H in rtcute niyrH-drditia. 514. |
p^cmlo-, I*ick's {>encarditie, 123. ^^^H |
|
^m . Infection. jifTcctin|r valves. 185. |
^^^M |
|
^H Influenza, in dihitattiin. 577: |
Macula^ tendinis*, 101. ^^^^M |
|
^^1 in acute en<loi-uidili8, 151, 156; |
Magnem, flulpUate of, in valvular ^^^H |
|
^m in Tatty heart, 6(K); |
disease, 447, 4S)2. ^^^f |
|
^H in myocarditis, chronic, §22, 561; |
Maliguaut endocarditis. (See Kndo- ^^^H |
|
^H in paroxyHnml tacliycardia, 732. |
^^^^^ |
|
^H Injection of <?cldtin in ;inciiry»ni. 787; |
Marriage, in valvular dinease, 422. ^^^H |
|
^V of j^elatin and ^^alt Siilulidn, 812. |
Massage, in chronie myocnrclitis, 559. ^^^H |
|
^H Insonmia, in mitral regnrrritatioti, |
Meastea, ref^ulttug in acute aortitis, ^^^H |
|
^m 237; |
^^H |
|
^H in mitral stenosis, 2.56. |
resulting in acute endocarditis, 154; ^^^H |
|
^H In«ufTicicncy, milra!. (See Mitral In- |
resulting in acute pericarditis, 46. ^^^^| |
|
^H c^ulHcicncy.) |
^Icchanii-til devices as aids to deter- ^^^^| |
|
^H Insurance, life. (See TJfe Insurance.) |
mining disease, 815, ^^^^| |
|
^H Iron, in fatly heart, 610; |
^Icdiastinitis, associated with pert- ^^^^| |
|
^H in in^ulticiency, mitral, 507; |
101, ^^^^1 |
|
^H in myocarditis^, acute, 517; |
Mediustinopcricnrditis, 103. 104. 105; ^^^| |
|
^H in valvular lesions, 448. |
Pcick's sign in, t2L ^^^^^| |
|
Medicinal agents, in valvular disease, ^^^H |
|
|
^H Kidneys, in artcrinwderosis, 741 ; |
^^H |
|
^g in cmlocarditi-s acute. 1 mi }m, 1S5 ; |
Miero-organif^ms, in Abseen^ 508; ^^^H |
|
' in endrK'arditis, chronic, 203; |
^^^1 |
|
in myocarditis, acute, 514; |
in (liliUatiou, 577; ^^^H |
|
iu pf^ricarditis. atute, 45; |
of diphtheria. 151. 1,50: ^^^| |
|
in peri<'arditis, chronic, 112; |
in eiidociirditis, acute, 144, 149, 150; ^^^| |
|
in KHTU I "citation, mitral, 238; |
gas forming, 133; ^^^H |
|
in valvular disease, 4W. |
of intlucnzji, 151; ^^^H |
|
Knowledge of lesion, effect on patient, |
in myocarditis, acute, 508; ^^^H |
|
411. |
in [K'Hcarditis, acute. 40, 42; ^^^^^ |
|
KuHsnuiur^ s[|m, in adherent pericar- |
in pen umopericard turn, 133; ^^^H |
|
dium, 120. |
pyogenic, 140; ^^^H |
|
Kyplioscoliosis, resulting in hypertro* |
of tuhcrculoais, 42. 332; ^^^H |
|
^^^^ phy of right ventricle, 570. |
of typhoid fever, 151. ^^^H |
|
^^^B |
Mitral insu6^cieney, relative, 504; ^^^H |
|
^^^i Lesions, valvular, (See Valvular Le* |
chlorosis in. 507; ^^^H |
|
^m^ siauH.l |
diagnopiis of, 500; ^^^^^H |
|
^B I^uoocvtosis, in acute endocarditis, |
digitalis in, 508; ^^^H |
|
■ |
etiology of, HM; ^^^H |
|
^H Life i nan ranee, relation to, of prog- |
in, 507; ^^^H |
|
^H misis in valvular disease, 412. |
nitroglycerin in, 504; ^^^H |
|
^B Lipoma, of luyoeardium, 560. |
patholngy of, 504; ^^^H |
|
^H Liver, cirrhoais of, 102, 156; |
physii-al signs in, 500; ^^^^H |
|
^H in dilatation, 584; |
prngnnsis in. 597: ^^^^H |
|
^H in endocarditis, acute, 156, 171, |
in rheumatism, 505; ^^^^H |
|
^^^ 185. |
symptoms of, 506. ^^^H |
846
DISEASES OF THE HEART
Mitral insufficiency, treatment of, 597. Mitral regurgitation (see Regurgita- tion) ;
stenosis (see Stenosis). Mode and causes of death. (See
Death.) Moderator bands, 30. Morbus eeruleus, in pulmonary steno- sis, 385 Morphine, in aneurysm of thoracic aorta, 813;
in Cheyne-Stokes respiration, 623;
in congenital diseases, 693;
in dilatation, 593;
in endocarditis, acute, simple, 175;
in endocarditis, ulcerative, 196;
injection of, in aneurysm, 814;
in myocarditis, chronic, 533, 561;
in pericarditis, dry, 69, 88, 91;
in pneumopericardium, 135;
in regurgitation, aortic, 288, 290, 316;
in stenosis, aortic, 333;
in stenosis, mitral, 272;
in Stokes- Adams disease, 635;
in valvular disease, 446, 481, 499. Murmurs, accidental, 26, 32;
differential diagnosis of, 34;
not accompanied by secondary changes, 35;
detection of, 13;
endocardial, 21;
exocardial, 36;
muRical, 29;
pericardial, effect of pressure on, 59;
transmission of, 25. (See also Sounds.) Muscle, papillary, degeneration of, a cause of mitral insufficiency, 696. Mycotic endocarditis. (See Endocar- ditis.) Myocarditis, acute, 505;
antitoxin in, 515;
associated with endocarditis, 157;
diagnosis of, 514;
digitalis in, 516;
diphtheria in, 508, 511;
etiolofjy of, 508;
infarction in, 158;
iron in, 517;
micro-organisms in, 508;
morbid anatomy of, 506;
palpation in, 514;
percussion in, 514;
in physical signs in, 514.
Myocarditis, prognosis in, 515;
pulse in, 511, 513;
rheumatism in, 508, 513, 515;
scarlatina in, 508, 516;
small-pox in, 508;
strophanthus in, 516;
symptoms of, 510;
treatment of, 515;
in typhoid fever, 508, 516. Myocarditis, chronic, 518;
atropine in, 562;
baths in, Turkish, 552;
brandy in, 561;
Bright's disease, associated with, 539;
bromides in, 563;
bronchitis, acute, in, 551;
camphor in, 561;
cases of, 526, 531, 540, 541;
chloralamide in, 563;
diagnosis in, 122, 547;
digitalis in, 522, 564;
dropsy in, 530, 563;
etiology of, 522;
gastritis, chronic, in, 551;
influenza in, 522, 551;
inspection in, 543;
massage in, 559;
morbid anatomy of, 519;
morphine in, 533, 561 ;
nitroglycerin in, 553, 560;
palpation in, 543;
percussion in, 544;
physical signs in, 543;
pneumonia in, 551;
prognosis in, 549;
pulse in, 529;
rheumatism in, 522, 541;
strophanthus in, 553, 561;
strychnine in, 553;
symptoms of, 526;
treatment of, 551;
typhoid fever in, 522. Myocardium, cancer of, 666;
degeneration of, in chronic pericar- ditis, 101;
diseases of, 505;
fibroma of, 666;
fragmentation of, 668;
lipoma of, 666;
segmentation of, 068. Myocardium, syphilis of, 663;
diagnosis of, 664;
digitalis in, 665;
etiology of, 663;
iodides in, 665.
|
^^^^^ ^H^ ^7 ^^1 |
|
|
^m Myocardium, ayphUis of, merciiry in, |
Pathology of Stokea-Adamfl disease, ^^^| |
|
■ 665; |
^^H |
|
^H morbid anatoDij of, 663; |
of tachycardia, 731. ^^^M |
|
^H prognosis in^ 665; |
Pectoris, angina (see Angina Pec- ^^^| |
|
^H syaiptoms of, 664; |
^^^1 |
|
^B tre&tmeDt of, 665. |
pf^udo angina, 710. ^^^B |
|
Percussion, "abgediLmpfte" method, 7; ^^^| |
|
|
^B Nephritic, in iicute }K^ricarditiB, 44, |
auscultatory, or stethoscopic, 8; ^^^H |
|
■ Neuroses, 703, 717» 731; |
palpatory- J 10. ^^^H |
|
^m iliiigtioiiia of, 724; |
Perez's sign in chronic mediastino^ ^^^| |
|
^1 etiology of, 722; |
pericarditis, 121. ^^^H |
|
^M pain in, 728; |
Pericarditis, acute, 37; ^^^H |
|
^B pathology of, 703; |
ab^ci^ in, 47; ^^^H |
|
^B prognoi^is in, 726; |
atcoholigm iu, 47; ^^^H |
|
^H symptoms of, 704; |
Brtght's disease in* 45; ^^^^B |
|
^H treatment of, 727. |
bronchitis^ in, 47; ^^^| |
|
^H Nitroglyeerin, in anpna peetons, 658; |
cancer in, 47; ^^^| |
|
^H in aortitis, acute, 762; |
earieH of rib in, 47; ^^^| |
|
^^^^. in arterio^lerosis, 757 ; |
cholera in, 46; ^^^^B |
|
^^^H in dilatation, 591, 593; |
dipbtheria in, 46; ^^^B |
|
^^^^B in endocarditis, chronie, 202; |
eryKipelu!^ in, 46; ^^^H |
|
^^H in fatty heart, 611; |
etiology of, 41; ^^^| |
|
^^^^H in mitral inBiillicicncy, 594; |
measles in, 46; ^^^B |
|
^^^^1 in niyoearditis, olironte, 553, 560; |
micro orgartismK in, 40, 42; ^^^B |
|
^^^^" In pseudo-anijina peetoris, 728; |
morbid analomy of, 37; ^^^^| |
|
^m in regurgitation, aortic, 288, 314,316; |
nephritiK in, 44; ^^^B |
|
^" in stenosis, aortic, 332, 333; |
pritonit'uni, dimmses of, in, 47; ^^^| |
|
in ftlenosifl, mitral, 272; |
pleuritic in, 47 ; ^^^B |
|
in StokcS' Adams disease, 635; |
pneumonia in. 46; ^^^B |
|
in tachycardia, 715; |
[111 ni lent fonn, 40; ^^^B |
|
in valvular diseases, 442, 444, 446, |
purpura bumiorrhagiea in, 47; ^^^B |
|
488, 408. |
rheuinatii^m in, 42, 46; ^^^B |
|
scarlatina in, 46; ^^^B |
|
|
Occupation, effect of, in valvular dis- |
in, 47; ^^^^| |
|
eases, mh 410, 476. |
seroiibrinaua form, 40, 42; ^^^| |
|
CEdema, in mitral stenosis, 256; |
simplest forui, 37; ^^^| |
|
in valvular diseases, 405; |
small-pox in, 46; ^^^^B |
|
digitalis in, 405. |
BtQX'hntne in, 5)6; ^^^B |
|
Orthopnea, in fatty heart, 603; |
suppurative form, 42; ^^^B |
|
in pcriearditis with effusion, 67, |
tonsillitis in, 44, 47; ^^^B |
|
Oxygen, in acute endocarditis, 191; |
typhoid fever in, 46; ^^^B |
|
in Stokes- Ailams disease, 635. |
^^^B |
|
valvular defects resulting from, 49* ^^^B |
|
|
Pain, in aneurysm of thoracic aorta. |
Pericardili.'i* chronic, 09; ^^^B |
|
782; |
huthii HO, 115; ^^H |
|
attack of, in neuroses, 728; |
calomel in, 125; ^^^B |
|
cardiae, 718; |
caseti of. lai, 114, 123; ^^H |
|
in pt^ricarditis, drj, 40. |
c4>mpeni^atlon prevented in, 105; ^^^B |
|
Palpitation, in cardiae neuTo«eB, 727* |
couri<e and termination of, 117; ^^^| |
|
Paroxysmal tat-hycardia, 73U; |
diagnosis of, 122; ^^^^| |
|
features of, 732, |
diagnosis, drfTerential, from cirrho- ^^^B |
|
l*athogencsi9, of thmmbi, 674. |
sis of liver, 122; ^^B |
|
Pathology of angina pe^-toris, 640; |
digitalis in, 126; ^^^B |
|
of fatty heart, 590; |
diuretin In, 126; ^^^B |
|
of mitral instilliciency, 504; |
etiology of* 103; ^^H |
|
of neuroses, 703. |
morbid anatomy of, 10C» ^^^B |
848
DISEASES OF THE HEART
Pericarditis, chronic, palpation 120;
percussion in, 121;
physical signs in, 118;
prognosis in, 123;
rheumatism in, 117;
stasis in, 117;
strophanthus in, 114;
strychnine in, 114, 125;
symptoms of, 104;
treatment of, 124. Pericarditis, dry, 48;
cases of, 50, 52, 61;
course and termination of, 56;
deglutition in, painful, 49;
diagnosis of, 60;
differential, 60;
digitalis in, 54;
inspection in, 56;
morphine in, 69, 88, 91;
pain in, 49;
palpation in, 57;
percussion in, 57;
physical signs in, 56;
pneumonia in, 60;
prognosis in, 61;
pyrexia in, 51;
rheumatism in, 50, 54, 61;
strychnine in, 53;
symptoms of, 48;
hsemorrhagic. 40, 47. Pericarditis, with effusion, 64;
anmlyncs in. 88;
atropine in. 92;
bolladoniui in. 88;
blister in, 80. 87;
calomol in, 80;
cases of, 08, 70, 92;
chloroform in. 8S;
codeine in, 88, 91;
course and termination of, 73;
diagnosis of. 81 ;
dilTerential, 82;
digitalis in, 83;
fever in, 89;
"first rib" sign in. 75;
fomentations in, 88;
heroin in, 88;
ice-bag in. 87, 89;
inspection in, 75;
opium in. 88. 91 ;
orthopnu'a in, 07;
percussion in, 70;
physical signs in, 74;
prognosis in, 84;
puncture in, site of, 94, 96.
in, I Pericarditis, resulting from pneumo- nia, 73;
with effusion, resulting from scar- let fever, 72;
rheumatism in, 68, 70, 73, 84;
sepsis in, 72;
signs in, " first rib," 76;
Ewart's. 80, 81 ;
Pins*, 80;
Rotch's, 78;
strychnine in, 91;
symptoms of, 64;
treatment of, 86. 90;
tuberculosis in, 84. Periarteritis nodosa, 769;
etiology' of, 769;
morbid anatomy of, 769;
prognosis in, 770;
sepsis in, 769;
symptoms of, 769;
treatment of, 770. Pericardium, adherent, 99;
bacteria in, 45;
signs in, Hroadbent*s, 119;
Friedreich's, 120;
KussmauKs, 120. Pericardium, carcinoma of, 141;
diseases of, 37;
perforated by gastric ulcer, 133;
sarcoma of, 141;
syphilis of. 139;
tuberculosis of, 136. Pick's pericarditic pseudo-cirrhosis of
the liver. 123. Pins' sign, in pericarditis with effu- sion, 80. Pleurisy, mistaken for pericarditis, 83. Pneumonia, in aortitis, acute, 760;
in bradycardia, 02.^;
in Cheyne-Stokos respiration, 617;
in endocarditis, acute, 185;
croui)ous, lo4, 150, 181;
recovery from, 155;
in niycx-arditis, chronic, 551 ;
in pericarditis, acute, 40;
in pericarditis, chronic. 103;
in pericarditis, dry. 00;
in pericarditis, with effusion. 73, 97;
in regurgitation, mitral, 224;
in stenosis, aortic, 341;
in valvular disease. 440. Pneumopericardium, 132;
bacilli in, gas forming, 133;
brandy in, 1.35;
cases of. 133;
diagnosis of, 135.
|
^l^r ■ |
||
|
^^^ Piieumopericardium» digitidis in, 1^6 ^ |
Regurgitation, aortic, Ditroglycerin in, ^^H |
|
|
^^H etioJogy of, VS2; |
2b8, 314. 3iti; ^^M |
|
|
^^^K jtisp^ctmi] in, 134; |
palpation in, 2U8; ^^^H |
|
|
^^^H morbid anatomj of, 132; |
percussion in, 301; ^^^H |
|
|
^^^H morphine in, 135; |
physical signs in, 207; ^^^H |
|
|
^^^H progBOsifi in, 135; |
prognosis in, 300; ^^^^| |
|
|
^^^K re^sulting from trauma^ 133; |
pulse in, 208, 301; ^^H |
|
|
^^^H resulting from ulcer, 133; |
Quincke's sign in, 298; ^^^H |
|
|
^^^H atrychnim^ in, 130; |
rheumatism in, 280; ^^^H |
|
|
^^^H syriiptoma of, 133; |
scarlatina in, 30O; ^^^| |
|
|
^^^" treatment of, 135, |
atrophanthus in, 288, 201 ; ^^^| |
|
|
^T Pregnancy, in valvular defects, 400, |
strychnine in, 2fKV, 3IG; ^^^| |
|
|
■ 422. |
symptoms of, 282; ^^^H |
|
|
^m Pressure, efTect of^ on pericardial mur- |
syphilis in, 284. ^M |
|
|
H mur, 51^. |
Regurgitation, aortic and mitral, com- ^M |
|
|
^M P^'udo' angina peetoris, 710; |
bined, 397; _^H |
|
|
*^ -cirrhosis of liver, Pick's pericar- |
diag^nosis of, 391, 397; ^^^M |
|
|
ditis, 123. |
pmgnoflis in, 308; ^^^H |
|
|
Pnlinonary artery, stenosis of (>see |
symptoms of, 397. ^^^H |
|
|
\ |
Stenosis). |
Regurgitation, uortiu, and aortic ate- ^H |
|
I |
Pulmonary regurgitation |»ce Re- |
no<<is combined, 300. ^H |
|
' |
gurgitation ) ; |
Regurgitation, aortic, and mitral ste- ^M |
|
Btenoeis {see Stenosis ). |
no&is combined, 393; ^^^H |
|
|
Pulse, capillary, in aortic regurgita- |
inspection in, 395; ^^^H |
|
|
tion, 301 ; |
palpation in, 395; ^^^H |
|
|
inequality of, in aortic aneurvsm, |
percussion in, 395; ^^^^H |
|
|
SOI; |
prognosis in, 394, 396; ^^^1 |
|
|
inequality of, in mitral stenosis, |
symptoms of, 393. ^^^H |
|
|
257, 25SJ, 260; |
Regurgitation, mitral, 216; ^^^H |
|
|
instability of, in aeute myocarditis, |
Bright'^ diseane in. 237; ^^^| |
|
|
611,513; |
cases of. 224, 229, 232^ 247; ^^H |
|
|
tension of, in chronic myocarditis, |
congestion in, 237; ^^^H |
|
|
529; |
diagnosi^^ of, 245; ^^^H |
|
|
venous, in aortic regurgitation. 301 ; |
digitalis in, 225; ^^^| |
|
|
"waier liammi^r," in aortic reguii^i- |
dropsy in, 219, 236, 245; ^^^| |
|
|
tation, 298. |
dyspnoea in, 238, 257; ^^^H |
|
|
Puncture, site of, in pericarditis with |
etiology of, 252; ^^^| |
|
|
off 11 si on, iJ4, 00. |
inspection in, 239; ^^^H |
|
|
Pyrexia, in endocarditis, acute, 171; |
in^^omnia in. 237; ^^^H |
|
|
in hydropcritardium, 120; |
morliid anatomy of, 216; ^^^H |
|
|
in pericarditis, dry, 51; |
palpation in, 239; ^^^^H |
|
|
in regurgitation, tricuspid, 346* |
percussion in, 240; ^^^^^ physical signs in, 239; ^^^| |
|
|
Quincke's sign, in a.ortic regurgita- |
pneumonia in, 224; ^^^^| |
|
|
tion, 208. |
prognosis in, 246; ^^^H resulting in gangrene, 238; ^^^H |
|
|
Regurgitation, aortic, 278; |
rheumatism in, 222, 247; ^^^H |
|
|
alcoholism in, 280; |
ficariatina in. 222, 224, 229; ^^H |
|
|
oa!«os of. 2S2. 2H«, 293, 308, 313; |
in, 230; ^^^1 |
|
|
cusp, nrpturetl in, 278; |
strychnine in. 225; ^^^H |
|
|
dia^osis of, 305; |
symptoms of, 223; ^^^H |
|
|
digitalis in, 288, 290; |
tuberculosis in. 232. ^^^H |
|
|
Duroziez's mgn in, 305; |
Regurgitation, mitral, and aortic tte- ^^H |
|
|
etiology of, 280; |
nosis combined. 396. ^M |
|
|
gout in, 280, 296; |
Regurgitation, mitral, nnd mitral 9t«- ^M |
|
|
1 |
inspection in, 288, 2W, 316. |
nosis combined, 392. ^^^B |
850
.DISEASES OF THE HEART
Regurgitation, symptoms of, 391. Regurgitation, of pulmonary artery, 772;
diagnosis of, 772. Regurgitation, pulmonary, 3tt5;
case of, 368;
diagnosis of, 387;
etiology of, 380.
morbid anatomy of, 365;
palpation in, 371;
percussion in, 371;
physical signs in, 370;
prognosis in, 374;
stasis in, 367;
symptoms of, 367. Regurgitation, tricuspid, 343;
case of, 354;
cyanosis in, 347;
diagnosis of, 363;
dropsy in, 351;
etiology of, 356;
inspection in, 349;
morbid anatomy of, 344;
palpation in, 350;
percussion in, 350;
physical signs in, 349;
prognosis in, 354;
pyrexia in, 340;
resulting from cirrhosis of lung, 340;
from fibroid phthisis, 346;
from renal cirrhosis, 345;
secondary to chronic bronchitis, 346;
stasis in, 347;
syniptoiiis of, 347. Rhcnmatisiii, acute, in bradycardia, 625;
in endocarditis, acute, 146, 181, 186;
in endocarditis, chronic, 022;
in myocarditis, acute, 51,'^, 515;
in pericarditis, acute, 42;
in pericarditiH, chronic, 117;
in pericarditis, dry. 50, 54;
in rcgurjfitation, aortic, 289;
in regurgitation, mitral, 222;
in stenosis, pulmonary, 377;
in tachycardia, 732;
in valvular disease, 401, 429. Rhcuinatisiii, articular, 32, 34;
in dilatation, 583;
in endocarditis, acute, 152, 157, 187;
in hydropericardium, 129;
in mitral insunicicney. 595;
in myocarditis, acute, 508.
Rheumatism, articular, in pericarditis, acute, 42; in pericarditis, dry, 61; in pericarditis, with effusion, 70; 'in regurgitation, mitral, 247; in stenosis, pulmonary, 376; in stenosis, tricuspid, 356; in valvular disease, 441, 479, 485. Rheumatism, inflammatory, in endo- carditis, acute, 153; in myocarditis, chronic, 541 ; in pericarditis, with effusion, 68, 73,
84; in stenosis, mitral, 274; in valvular disease, 436. 441. Rhythm, gallop or canter, 18;
a sign of the end, 20. Rotch*8 sign, in pericarditis with effu- sion, 78.
Scarlatina, in aortitis, acute, 760; in congenital disease, 698; in endocarditis, acute, 154; in myocarditis, acute, 508, 516; in pericarditis, acute, 46; in regurgitation, aortic, 309; in regurgitation, mitral, 222, 224,
229; in stenosis, mitral, 274; in stenosis, tricuspid, 358. Scarlet fever. (See Fever.) Sclerosis, 246, 286, 573. Scurvy, in pericarditis, acute. 47. Second sound, simulated doubling of,
17. Segmentation of the myocardium,
668. Sepsis, in acute endocarditis. 170, 193 in |>criarteritis nodosa, 769: in pericarditis with effusion, 72. Septicaemia, in acute endocarditis,
155, 156. Scrum, anti-streptococcus, in acute en
docarditis, 19.3. Signs, Broadbent's. in adherent peri cardium, 119; Durozier/s, in aortic regurgitation,
305; Ewart's. in pericarditis with effu
sion, 80, 81; " first rib," in pericarditis with effu
sion, 75;
Friedreich's, in adherent pericar- dium, 120: Ku^ismaul's. in adherent pericar- dium, 120.
INDEX.
851
Signs, Perez's, in chronic mediastino- pericarditis, 121;
Pins', in pericarditis with effusion, 80;
Quincke's, in aortic regurgitation, 298;
Rotch's, in pericarditis with effu- sion, 78. Simple endocarditis. (See Endocardi- tis.) Smallness of arteries, congenital, 773. Small-pox, in acute endocarditis, 154;
in acute myocarditis, 508;
in acute pericarditis, 46. Sound- friction, intensity of, 59;
location of the pericardial, 58;
quality of, 50;
rhythm of, 58. Sounds, heart, normal, 13;
reduplication of, 16, 18;
second, simulated doubling of, 17. Spleen, abscess of, in acute endocardi- tis, 150, 185. Stasis in pericarditis, chronic, 117;
in regurgitation, aortic, 207;
in regurgitation, mitral, 236;
in regurgitation, pulmonary, 367;
in regurgitation, tricuspid, 347;
in stenosis, mitral, 257;
in stenosis, tricuspid, 358. Stenosis, of aorta, 770;
symptoms of, 771;
treatment of, 772. Stenosis, aortic, 310;
cases of, 323, 330, 339;
cyanosis in, 335;
diagnosis of, 338;
digitalis in, 326;
inspection in, 335;
morbid anatomy of, 319;
nitroglycerin in, 332, 333;
palpation in, 335;
percussion in, 336;
physical signs in, 335;
pneumonia in, 338;
prognosis in, 339;
strychnine in, 332;
symptoms of, 323. Stenosis, aortic and mitral combined, 392;
diagnosis of, 392;
prognosis in, 393;
symptoms of, 392. Stenosis, mitral, 249;
bronchitis in, 256;
cases of, 253, 263, 270, 273.
Stenosis, mitral, deliiium in, 270;
diagnosis of, 268;
digitalis in, 272;
epilepsy in, 212;
" fremissement cataire" in, 259;
gout in, 254;
insomnia in, 256;
inspection in, 258;
morbid anatomy of, 249;
morphine in, 272;
nitroglycerin in, 272;
oedema in, 256;
palpation in, 259;
percussion in, 260;
physical signs in, 258;
prognosis in, 269;
pulse in, 257, 259, 260;
rheumatism in, 264;
scarlatina in, 274;
stasis in, 257;
strophanthus in, 272;
strychnine in, 272;
symptoms of, 255;
syphilis in, 254. Stenosis, mitral, and pulmonary ste- nosis combined, 387. Stenosis, pulmonary, 376;
cases of, 377, 380;
diagnosis of, 373;
inspection in, 385;
morbid anatomy of, 376;
percussion in, 386;
physical signs in, 385;
prognosis in, 374;
rheumatism in, 376, 377;
symptoms of, 380:
tuberculosis in, 380. Stenosis, of pulmonary artery, 772. Stenosis, tricuspid, 355;
cases of, 379, 380;
diagnosis of, 353;
digitalis in, 359;
inspection in, 361 ;
morbid anatomy of, 355;
percussion in, 362;
physical signs in, 361;
prognosis in. 364;
rheumatism in, 356;
scarlatina in. 358;
stasis in, 358;
symptoms of, 357. Stokes- Adams disease. 627;
cases of, 628, 630, 632;
digitalis in, 636:
etiolopy of. 627;
morphine in, 635.
|
^^1 852 DISEASES OF |
THE HEART ^^^| |
|
^^^H gtokes-Adams disease, mtrogl^rcerin |
Tachycardia, etiology of, 732; ^^H |
|
^^H |
^^^1 |
|
^^^H oxygen in^ 1^; |
influenza in. 732; ^^^^ |
|
^^^H pathology of, 627; |
malnria in, 732; ^^^| |
|
^^^H prognosiB io, 635; |
nitroglycerin in, 715; ^^^^ |
|
^^^B syniptoms of, 62Q ; |
pathology of. 731; ^^H |
|
^^^H Bjphilis in. tj2S; |
prognosis in, 735; ^^^^ |
|
^^^^1 treatment of, 635. |
rheumatism in, 732; ^^^| |
|
^^^H Stroplianthu». m angina pectoris, 662; |
strychnine in, 736; ^^^| |
|
^^^H in arteraoscIeroBis, 757 ; |
treatmetii of, 735. ^^H |
|
^^^H in ondocarditi*^, acutCj 169 j |
Tettjpeniments, of cardiopathi, 408. ^^H |
|
^^H in fatty heart, 611; |
Tendencies, iudividwal, 206, ■ |
|
^^^H in fynt-tional disorders, 711; |
Terrain cure, in valvular diseose, 454. ■ |
|
^^^H in iiivocarditis, acute» 510; |
Thoracic aorta, aneurysm of, 775. H |
|
^^^H in myocarditis, ehronie, 553, 561; |
Thoracic cavity, L ^^^^ |
|
^^^^B in pprii^arditiH, I'limnic, 114; |
Thrombi, ball, 674; ^^1 |
|
^^^H in regurgitation, aortic, 288, 291 ; |
bibliography of, 680; ^^^| |
|
^^^H in Btenosift, mitral, 272; |
cim-s <»f, 676, 680; ^^H |
|
^^^H in valvular diBea«<.c. 432. |
dia^TiOi^is in, 677; ^^^f |
|
^^^H Strychnine, in aortitis, acute, 762; |
etiology of, 674; ^^^^ |
|
^^^H in dilutution, 591 ; |
pathogenefiis of, 674. ^^^| |
|
^^^H in endocArditii^, acute, 169, 191: |
Thrombi, pedunculated, 074; ^^^| |
|
^^^H in endocarditis, chronic, 202; |
prognosis in, 678; ^^^| |
|
^^H in fatly hciirt. (Ill; |
symptoms of. 675; ^^^| |
|
^^^H in func'liunal dlMiniers, 709; |
treatment of, 678. ^^B |
|
^^^H in niywardittB, chronic, 553; |
Thrombosis, arterial, causing gan- ■ |
|
^^^^H in pericarditis, acute, 516; |
grene, 676; ^^H |
|
^^^H in pericarditis, chronic, 114, 125; |
venous, in valvular disease, 209. ^^H |
|
^^^H in pericarditis, dry, 53; |
Tissue, adipose, in syphilia of pericAr- ^^H |
|
^^^H in pericarditis, with effusion, 01; |
dium, 139. ■ |
|
^^^H in pneunioperieardium, 136; |
Tonics, accessory, 499; ^^^^ |
|
^^^H in regurgitation, aortic, 290, 316; |
cardiac, 44 1 ; ^^^| |
|
^^^H in regurgitation, mitral, 225; |
nerve. 517. ^^B |
|
^^^H in stenosis, aortic, 332; |
Tonsillitis, in endocarditis, acute» 1^; ■ |
|
^^^1 in stenosis, mitral, 272; |
in periLiirditis, acute, 44. 47. ^^H |
|
^^^H in taehyeardia, 736; |
Totio meter, (laertner'a, 826. ^^^| |
|
^^^B in valvular disease, 430, 443, 445. |
Tricuspid regurgitation <«« R«gUlgi* ^^B |
|
^^^H Syncope, in aortic regurgitation^ 287* |
tation); H |
|
^^^H Syphilis, in aneurysm, 778, 795; |
stenosis (see Stenosis). ^^^| |
|
^^^H in arteriosclerosis, 742; |
Tiiherculoftif*, of p*»ricjinlium, 136j ^^^| |
|
^^^H in angina pectoris, 646; |
of lungs, 103. ^^B |
|
^^^H in endocarditis, chronic. 204^ |
Tuberculosis, pulmonary^ in aneu* fl |
|
^^^H in regurgitation, aortic, 284; |
rysm, 808; ^^M |
|
^^^H in stenosis, mitral, 254; |
in dextrocardia, 661; ^^^^ |
|
^^^B in stenosis, tricue^pid, 356; |
in functional disorders, 710; ^^^| |
|
^^^H in Stokes Adams distafle, 629; |
in pericarditis, with cfTuaion, 84; ^^^| |
|
^^^H Syphilis of the myocardium, 663; |
in regurgitation, mitral, 232 ^^H |
|
^^^H of the |>ericardium, 139. |
in stenosis, pulmonary, lim); ^^H |
|
^^H By^pbilis vs. rheumatism, in aortic ste- |
In valvular diseaae, 406. ^^H |
|
^^m nosis, 3Sg. |
Typhoid fever, in pericartlitis, 40. ^^H |
|
^^M Byphllitie artentiA, 704. |
TyphuSf in acuta myocarditis, 509, ^^H |
|
^^H Tachyeaniia. 730; |
Ulrerative endocarditis, (8«a £iido> ^V |
|
^^^1 cftflTeine in, 730; |
carditis.) J |
|
^^m diagnosis of, 734; |
^^H |
|
^^H digitalis in. 736; |
Valvular lesions comMocdt tMi ^^H |
|
^^m diphthena in, 732, |
atropine in, 500. ^^H |
INDEX
853
Valvular lesions, baths in, Nauheim,
427, 464, 503; baths in, saline, 466; caffeine in, 432; calomel in, 432, 448, 491, 493; cases of, 393, 436, 440, 469, 479, 482,
485; cathartics in, 492; chloral hydrate in, 501; chloralose in, 501 ; change of climate in, 432; clothing in, 425, 476; compensation imperfect in, 435; compensation lost in, 478; compensation perfect in, 413; complicated with catarrh, bronchial,
407; with dropsy, 470; with pneumonia, 440; with rheumatism, 406; convallaria in, 432, 497; diet in, 428, 470; digitalis in, 394, 430, 480; drugs in, 430; exercise in, 414, 454, 502; exercise, resistance, in, 455; glonoin in, 432, 446; habits in, 410, 420, 476; haematics in, 448; home surroundings in, 410; hypnotics in, 500; illnesses in, 429.
Valvular lesions, jalap in, 493;
marriage in, 422;
medicinal agents in, 444;
mercury in, 432;
morphine in, 446, 481, 499;
nitroglycerin in, 442, 444, 446, 488, 498;
occupation in, 409, 419, 476;
cedema in, 495;
pregnancy in, 409;
prognosis in, 401;
rest in, 448, 502;
rheumatism in, 401, 429, 436, 441, 479, 485;
strophanthus in, 432;
strychnine in, 439, 443, 445;
Terrain cure in, 454;
treatment of, 413, 435, 478;
tuberculosis in, 406. Vegetative endocarditis. (See Endo- carditis.) Vemicose endocarditis. (See Endo- carditis.) Vessels and valves of heart, position of, 3.
Whisky, in acute endocarditis^ 192; in angina pectoris, 660; in pseudo-angina, 728; in myocarditis, chronic, 561; in valvular disease, 493.
(«)
THE EKD
NORMAL HISTOLOGY
BY
JEREMIAH S. FERGUSON, M.Sc, M.D.
Instructor in Histology, Cornell University Medical College, New York City
With 462 Illustrations, many in colors Cloth, $4.00 Half Leather, $4.50
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— A'ew York Medical Record.
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APPLET ON AND COMPANY, Publishers 436 Fifth Avenue, New York.
DISEASES OF THE ANUS, RECTUM, AND PELVIC COLON.
SECOND REVISED AND ENLARGED EDITION. By JAMES P. TUTTLE, A.M., M.D.
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