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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.
J <<> <-> \
\^t^J
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.
CHRONIC PERICARDITIS
123
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-
HYDROPERICARDIUM
129
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.
H^MOPKRICARDJUM
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
157
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
ACUTE ENDOCARDITIS
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.
ACUTE EXDorAKurns
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
^^^^^^^^^^^^"
ENDOCARDITIS 173 ^^H
^ 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
ACUTE ENDOCARDrns
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
ACUTE ENDOCARDITIS
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
^^^^^^^^B^^^^^^^^^^^^B^^^^^W^^^^^^^^BJI^^^^^^^I
^1
^^H
^^H 250 DISKASES OF THE nEART
^^^1
^^^H to a certaii) aniount of regiirrritatiou. In fact a
pure stenos^i^^^^^l
^^^H very rare* although it Joes occasionally occur.
■
^^^■^ Caniplx'll ingeniously suggests that the shape
of the orifice de- ^^H
^
^ J
^^^^^^1'
^^^H
^^H
^^^^^H
^^^^^^^^B
^1
^H
^^^^^^H
H
^^1
r^^^^^^^^Hj
2 H
^^^^^^^^H
^^H
k ^llb^^l
1 ^^^1
■ ^1
mt j^^P^K^JI
K H
^^^^H W K^^^^ 1 /■'* 1
VilHiHi
^^^^^^^^^^^^^^^V J 1^ ^'^ ' m
V 1 wfl^flT^'
^^Hi ^^1
^^B ^'m -i
N^
r^^iH
^^p ^1
^^v jik^r^j^^^^^l^^^^^^c^^H
I ^
1 ^
^^^^^^p .. ^ ^K
>
^^H ^^^^^^. ^^^^L. ^^^^^^^^^^K^K ^ A
PIB
C
J
I ^^c^^^Hl^HSw^'J
'M
o
' 1
1 ^^^^^^^E^^
^^ ^
' 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
AORTIC RI
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-
AORTIC REGURGITATION
295
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.
AORTIC REGURGITATION
297
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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§
e
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
<rf' ^*-%ifit inAlMMMtiM petmled^ and to I4ike salicylate of soda
>^*fr>« «f»>iiT1 nta fftqmtmt doses of diKitaU& The patient subee-
^\ vtiHfd Kfe tww^fT m»d lemm to practice. Ihiring tlie
'm^ atwiitlinTil fcnml fmetke and limitLd
ht mm^ kb fteUcnce a short disunoe
simn^dttm^ vrmvMm^ to and fro on an efe-
$mi« to tlio slatiow.
After tkat attack
^iK^ f^ 9«v wmA fm Um on digitalis^
xtii »j|,a>ai4, a^ » lis had aona
^ wm AM«ki tht iatenai^
>^^cw m tho latter fwrl
^ - , ^«ddeiilir seized witk
^v#i iWrfT a patirat in ht« office, whic^
!WiM after a few daym reat at borne, witk
.,, uilf^vcertn«
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
C. B
8*
3»
3i
H
3t
3+
8*
3*
2f
3*
E. B
W. C
S. D
H. De V
R.E
E. E
S. E
F.G
G.G
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
W. V
J. W
J. W
J. W
C
C. H
8*
3i
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-
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
t
■
^/
^^s
1
1
^^^f-
B
i^^^^r ^^^^^^^1
1
pv 1
i
*
^: 1
4
|^>lV' ■
t/' 1. J
mk^ J
^'^ 9
Fui, 115.— Po»T-Mo
IIT£M SrKClMtX Uf HeaBT AjfD
tK FlUd. lis AKt
AKxruYAiiAL Sac fhom Ca«£ rioiBXO ^^^H
^^H
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
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APPLET ON AND COMPANY, Publishers
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DISEASES OF THE ANUS, RECTUM,
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SECOND REVISED AND ENLARGED EDITION.
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