Ebook Current diagnosis & treatment cardiology (3rd edition): Part 1

a LANGE medical book

CURRENT

Diagnosis & Treatment
Cardiology
THIRD EDITION
Edited by
Michael H. Crawford, MD
Professor of Medicine
Lucy Stern Chair in Cardiology
Interim Chief of Cardiology
University of California, San Francisco

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Contents
Authors
Preface
1. Approach to Cardiac Disease Diagnosis
Michael H. Crawford, MD
General Considerations
Common Symptoms
History
Physical Findings
Physical Examination
Diagnostic Studies

2. Lipid Disorders

4. Unstable Angina/Non-ST Elevation
Myocardial Infarction

xiv
xvii

Prediman K. Shah, MD & Kuang-Yuh Chyu, MD, PhD
General Considerations
38
Background
38
Clinical Spectrum
38
Pathophysiology
38
Clinical Findings
40
Symptoms and Signs
40
Physical Examination
41
Diagnostic Studies
41
Differential Diagnosis
42
Acute Myocardial Infarction
42

Acute Aortic Dissection
42
Acute Pericarditis
42
Acute Pulmonary Embolism
43
Gastrointestinal Causes of Pain
43
Other Causes of Chest Pain
43
Treatment
43
Initial Management
43
Definitive Management
49
Prognosis
50

1
1
1
2
3
3
7

14

Christian Zellner, MD

General Considerations
Lipoproteins and Apolipoproteins
Clinical Findings
History
Physical Examination
Laboratory Assessment
Treatment
LDL Goals
Non-HDL Goals and Hypertriglyceridemia
HDL and Lipoprotein(a)
Nonpharmacologic Approaches
Pharmacologic Therapy
When to Refer

3. Chronic Ischemic Heart Disease

14
14
16
16
16
17
17
17
18
19
20
21
24

5. Acute Myocardial Infarction
Andrew J. Boyle, MBBS, PhD & Allan S. Jaffe, MD
General Considerations
Pathophysiology & Etiology
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Pre-hospital Management
Emergency Department Therapy
Reperfusion Therapy
In-hospital Management
Primary PCI versus Fibrinolysis
Fibrinolytic Agents
Adverse Effects of Fibrinolytic Therapy
Complications of Myocardial Infarction
Cardiogenic Shock
Congestive Heart Failure
Acute Mitral Valve Regurgitation
Acute Ventricular Septal Rupture
Cardiac Rupture
Recurrent Ischemia
Pericarditis
Conduction Disturbances

25

Michael H. Crawford, MD
General Considerations

Pathophysiology & Etiology
Clinical Findings
Risk Factors
Symptoms
Physical Examination
Laboratory Findings
Diagnostic Studies
Choosing a Diagnostic Approach
Treatment
General Approach
Pharmacologic Therapy
Revascularization
Selection of Therapy
Prognosis

38

25
25
26
26
26
27
27
27
29
30
30
31
34

35
37

iii

51
51
51
52
52
53
53
56
56
56
57
59
60
60
63
64
64
64
65
65
65
66
66
66

ᮢ

iv

CONTENTS

Other Arrhythmias
Mural Thrombi
Aneurysm and Pseudo-aneurysms
Right Ventricular Infarction
Prognosis, Risk Stratification, & Management
Risk Predictors
Risk Assessment
Risk Management

6. Cardiogenic Shock
Edward McNulty, MD & Craig Timm, MD
General Considerations
Definition
Etiology
Pathogenesis
Cardiogenic Shock after Acute MI
Mechanical Complications of Acute MI
Right Ventricular Infarction
Arrhythmias
Other Causes of Cardiogenic Shock
Clinical Findings
History
Physical Examination

Laboratory Findings
Diagnostic Studies
Left Heart (Cardiac) Catheterization
Treatment
Acute MI
Mechanical Complications
Right Ventricular Infarction
Arrhythmias
Prognosis

7. Aortic Stenosis

67
68
69
69
70
70
70
71

73
73
73
73
74
74
74
75
75

76
76
76
76
77
77
78
78
78
80
80
81
81

82

Blase A. Carabello, MD & Michael H. Crawford, MD
General Considerations & Etiology
82
Bicuspid Aortic Valve
82
Tricuspid Aortic Valve Degeneration
82
Congenital Aortic Stenosis
82
Rheumatic Fever
82
Other Causes
83
Clinical Findings

83
Symptoms and Signs
83
Physical Examination
84
Diagnostic Studies
85
Treatment
88
Pharmacologic Therapy
88
Aortic Balloon Valvuloplasty
88
Surgical Therapy
89
Prognosis
92
Coincident Disease
93
Follow-up
93

8. Aortic Regurgitation
William A. Zoghbi, MD, FASE, FACC &
Michael H. Crawford, MD
Etiology
Pathophysiology
Chronic Aortic Regurgitation
Acute Aortic Regurgitation
Clinical Findings

Symptoms and Signs
Laboratory Findings
Diagnostic Studies
Treatment
Acute Aortic Regurgitation
Chronic Aortic Regurgitation
Prognosis

9. Mitral Stenosis
Robert J. Bryg, MD
General Considerations
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Medical Therapy
Percutaneous Mitral Balloon Valvotomy
Surgical Therapy
Prognosis

10. Mitral Regurgitation
Michael H. Crawford, MD
General Considerations
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies
Differential Diagnosis
Treatment

Pharmacologic Therapy
Surgical Treatment
Prognosis

95

95
95
95
95
96
96
97
97
102
102
103
105

106
106
107
107
107
108
110
110
110
111
112

113
113
114
114
114
116
118
119
119
119
121

11. Tricuspid & Pulmonic Valve Disease

122

Brian D. Hoit, MD & Subha L. Varahan, MD
Tricuspid Valve Disease
General Considerations
Pathophysiology & Etiology
Tricuspid Regurgitation
Tricuspid Stenosis
Clinical Findings
Symptoms and Signs

122
122
122
122

124
124
124


Physical Examination
Diagnostic Studies
Treatment
Medical
Surgical
Postoperative Management
Prognosis
Pulmonic Valve Disease
General Considerations
Pathophysiology & Etiology
Pulmonic Regurgitation
Pulmonic Stenosis
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Prognosis

12. Infective Endocarditis

124
125
133
133

133
134
134
134
134
134
134
135
135
135
135
136
136
136

137

Bruce K. Shively, MD* & Michael H. Crawford, MD
General Considerations
137
Pathophysiology & Etiology
137
Cardiac Infection—Vegetations
137
Extracardiac Disease
138
Clinical Syndromes
138
Clinical Findings
142

Diagnostic Criteria
142
Symptoms and Signs
143
Physical Examination
143
Diagnostic Studies
144
Management
147
Initial Decisions
147
Antibiotic Therapy
147
Management of Complications
149
Management of High-Risk Endocarditis
150
Surgery
151
Follow-up after Endocarditis
151

13. Systemic Hypertension
William F. Graettinger, MD, FACC, FACP, FCCP
General Considerations
Pathophysiology & Etiology
Natural History
Ethnic and Socioeconomic Factors
Clinical Findings

Initial Evaluation
Physical Examination
Diagnostic Studies
Organ Involvement
Treatment
*Deceased

153
153
153
154
154
154
155
155
155
156
157

ᮢ

CONTENTS

v

Nonpharmacologic Therapy
Pharmacologic Therapy
Management of Complicated Hypertension
Prognosis

14. Hypertrophic Cardiomyopathies
Pravin M. Shah, MD, MACC
General Considerations
Pathophysiology & Etiology
Systolic Function
Diastolic Function
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Medical Management
Surgical Myectomy
Chemical Myectomy
Pacemaker Implantation
Cardioverter Defibrillator Implantation
Prognosis
Future Prospects

15. Restrictive Cardiomyopathies
John D. Carroll, MD & Michael H. Crawford, MD
General Considerations
Definitions and Terminology
Pathophysiology
Etiology
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies
Differential Diagnosis

Treatment
Diastolic Dysfunction
Cardiac Complications
Underlying Disease
Prognosis

16. Myocarditis

157
157
161
163

164
164
164
165
165
165
165
166
167
169
169
170
170
170
170
170
171

172
172
172
172
173
174
174
174
174
176
176
176
178
178
178

179

John B. O’Connell, MD & Michael H. Crawford, MD
General Considerations
179
Pathophysiology
179
Clinical Findings
180
Symptoms and Signs
180
Physical Examination
181

Diagnostic Studies
181
Treatment
183
Prognosis
184
Specific Forms of Myocarditis
184


ᮢ

vi

CONTENTS

Chagas Disease, or American Trypanosomiasis
HIV
Toxoplasmosis
Cytomegalovirus
Lyme Myocarditis
Giant Cell Myocarditis
Sarcoidosis

17. Pericardial Diseases
Martin M. LeWinter, MD
General Considerations
Normal Pericardial Anatomy and Physiology
Pericardial Pressure and Normal Function
Pathogenesis

Infectious Pathogens
Iatrogenic Causes
Connective Tissue Disorders
Other Causes
Acute Pericarditis
General Considerations
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Pericardial Effusion
General Considerations
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Cardiac Tamponade
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Treatment
Constrictive Pericarditis
General Considerations
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies

Differential Diagnosis
Treatment
Effusive-Constrictive Pericarditis

18. Congestive Heart Failure

184
184
185
185
185
185
185

187
187
187
187
187
187
189
190
190
192
192
192
192
192
192
194

194
194
194
194
194
195
195
195
195
195
195
196
197
197
197
198
198
198
198
200
201
201

203

Prakash C. Deedwania, MD & Enrique V. Carbajal, MD
General Considerations
203
Pathophysiology & Etiology
203

Types of Heart Failure
204
Causes
206

Clinical Findings
Symptoms and Signs
Physical Examination
Laboratory Findings
Diagnostic Studies
Differential Diagnosis
Treatment
General Measures
Pharmacologic Treatment
Nonpharmacologic Treatment
Prognosis

19. Heart Failure with Preserved
Ejection Fraction
Sanjiv J. Shah, MD
General Considerations
Pathophysiology
Diastolic Dysfunction
Left Ventricular Enlargement and
Increased Intravascular Volume
Abnormal Ventricular-Arterial Coupling
Left Ventricular Hypertrophy
Coronary Artery Disease
Clinical Findings
Risk Factors

Symptoms and Signs
Diagnostic Studies
Differential Diagnosis
Prevention
Treatment
Nonpharmacologic Therapy
Pharmacologic Therapy
Prognosis

20. Supraventricular Tachycardias
Byron K. Lee, MD & Peter R. Kowey, MD
General Considerations
Pathophysiology & Etiology
General Diagnostic Approach
Sinus Tachycardia & Sinus Node Reentry
Sinus Tachycardia
General Considerations
Treatment
Sinus Node Reentry
General Considerations
Treatment
Atrial Flutter
General Considerations
Pathophysiology
Clinical Findings
Prevention
Treatment
Conversion
Rate Control

206
206
207
208
209
209
210
210
210
218
220

221
221
222
222
222
223
223
223
223
223
224
224
228
229
229
229
229
232

233
233
233
236
236
236
236
237
237
237
238
238
238
238
238
238
239
239
239


Catheter Ablation and Other Modalities
Stroke Prophylaxis
Multifocal Atrial Tachycardia
General Considerations
Treatment
Prognosis
Atrial Tachycardia
General Considerations

Treatment
Pharmacologic Therapy
Ablation
General Considerations
Pathophysiology
Prevention
Treatment
Vagal Maneuvers
Pharmacologic Therapy
Radiofrequency Modification in
Slow–Fast AVNRT
Junctional Tachycardia (Accelerated
AV Junctional Rhythm)
General Considerations
Clinical Findings
Treatment
Bypass Tracts & the
Wolff-Parkinson-White Syndrome
General Considerations
Epidemiology
Pathophysiology
Anatomy
Cardiac Electrical Conduction
Mechanism
Treatment
Vagal Maneuvers
Pharmacologic Therapy
Radiofrequency Catheter Ablation Therapy
Surgical Ablation Therapy
Other Bypass Tracts

Sinus Node Arrhythmia
Other Supraventricular Arrhythmias
General Considerations
Treatment
Wandering Atrial Pacemaker
General Considerations
Treatment

21. Atrial Fibrillation
Melvin M. Scheinman, MD
General Considerations
Epidemiology
Clinical Findings
Symptoms and Signs
Physical Examination
Treatment

239
240
240
240
240
240
241
241
242
242
242
242
242

243
243
243
243
243
246
246
246
247

ᮢ

CONTENTS

vii

Rate Control
Long-Term Antiarrhythmic Therapy
and Elective Cardioversion
Antiarrhythmic Drug Therapy for
Atrial Fibrillation
Nonpharmacologic Treatment of
Atrial Fibrillation

260

22. Conduction Disorders & Cardiac Pacing

267

Richard H. Hongo, MD & Nora Goldschlager, MD
General Considerations
Pathophysiology & Etiology
Sinus Node Dysfunction
Atrioventricular Nodal-His Block
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Cardiac Pacing
Pacing System Malfunctions
Assessment of Pacing System Function

23. Ventricular Tachycardia
247
247
247
247
247
248
249
251
251
251
254
255
255
256
256

256
256
257
257
257

259
259
259
259
259
259
260

260
261
265

267
267
267
268
268
268
270
273
278
283
293
296

299

Nitish Badhwar, MD
Diagnostic Issues
Underdiagnosis
Misdiagnosis
Diagnostic Approach to the Patient
with Wide QRS Complex Tachycardia
Atrioventricular Relationship
QRS Complex Duration
Specific QRS Morphology
QRS Complex Axis
History, Physical Examination and 12-Lead ECG
Monomorphic VT in Association
with Idiopathic Dilated Cardiomyopathy
Monomorphic VT in Arrhythmogenic
Right Ventricular Cardiomyopathy
Monomorphic VT in Patients
with Congenital Heart Disease
Monomorphic VT in Other Forms
of Structural Heart Disease
Idiopathic Left Ventricular Tachycardia
or Fascicular VT
Outflow Tract Ventricular Tachycardia
Annular Ventricular Tachycardia
Diagnostic Studies
Immediate Termination
Prevention
Pharmacologic Therapy

Nonpharmacologic Therapy
Polymorphic Ventricular Tachycardia

299
299
299
300
301
301
301
303
303
304
305
306
306
307
307
308
308
310
310
310
311
311


ᮢ

viii

CONTENTS

Polymorphic VT in the Setting of
Prolonged QT Interval
Clinical Findings
Management
Polymorphic VT with a Normal QT Interval
Prognosis

311
311
312
313
313

Surgical or Catheter Ablation
Implantable Cardioverter Defibrillators
Identification of Patients at Risk
Risk-Assessment Studies
Primary Prevention of Sudden Death

26. Pulmonary Embolic Disease
24. Syncope
Michael H. Crawford, MD
General Considerations
Pathophysiology & Etiology
Cardiac Causes
Neurocardiogenic Causes
Orthostatic Hypotension

Psychiatric Disorders
Neuralgia
Syncope of Unknown Cause
Clinical Findings
History and Physical Examination
Noninvasive Diagnostic Studies
Invasive Electrophysiology Studies
Differential Diagnosis
Seizure
Metabolic Disorders and Hypoxia
Cerebral Vascular Insufficiency
and Extracranial Vascular Disease
Psychiatric Disorders with
Hyperventilation and Pseudoseizure
Treatment
Pharmacologic and Nonpharmacologic
Electrophysiologic Therapies
Prognosis

25. Sudden Cardiac Death
John P. DiMarco, MD, PhD
General Considerations
Pathophysiology & Etiology
Coronary Artery Disease
Hypertrophic Cardiomyopathy
Nonischemic Dilated Cardiomyopathy
Other Cardiac Diseases
Inherited Arrhythmia Syndromes
Drug-Induced Arrhythmias
Other Arrhythmias

Management of Cardiac Arrest:
Initial Resuscitation
Management of Cardiac Arrest Survivors:
In-Hospital Phase
Complications of Resuscitation
Diagnostic Studies
Treatment of Cardiac Arrest Survivors
Antiarrhythmic Drug Therapy
Revascularization

315
315
315
315
316
317
318
318
318
318
318
320
322
323
323
323
323
324
324
324

325
325

327
327
327
327
328
329
329
329
330
330
330
331
331
332
333
333
333

Rajni K. Rao, MD
General Considerations
Etiology
Thrombophilia
Women’s Health
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Prevention

Risk Stratification
Treatment
Heparin
Low-Molecular-Weight Heparin
Thrombolysis
Embolectomy
Inferior Vena Caval Filters
Warfarin
Adjunctive Measures
Venous Thromboembolism in Pregnancy
Counseling

27. Pulmonary Hypertension
David D. McManus, MD & Teresa De Marco, MD
General Considerations
Classification & Pathogenesis
Pulmonary Arterial Hypertension
Pulmonary Hypertension with
Left-Sided Heart Disease
Pulmonary Hypertension Associated
with Lung Diseases and Hypoxemia
Pulmonary Hypertension due to
Chronic Thrombotic or Embolic Diseases
Miscellaneous
Pathophysiologic Consequences of
Pulmonary Hypertension
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies

Differential Diagnosis
Treatment
Pulmonary Arterial Hypertension
Pulmonary Hypertension with
Left-Sided Heart Disease
Pulmonary Hypertension Associated
with Lung Disease or Hypoxemia

334
334
335
335
336

337
337
337
337
338
338
338
339
345
346
346
346
347
347
348
349

349
350
350
350

352
352
352
352
355
355
356
356
357
358
358
359
359
363
365
365
369
370


Pulmonary Hypertension due to
Chronic Thrombotic or Embolic Disease
Prognosis

28. Congenital Heart Disease in Adults

Ian S. Harris, MD & Elyse Foster, MD
General Considerations
Acyanotic Congenital Heart Disease
Congenital Aortic Valvular Disease
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Differential Diagnosis
Prognosis & Treatment
Pulmonary Valve Stenosis
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Prognosis & Treatment
Atrial Septal Defect
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Prognosis & Treatment
Ventricular Septal Defects
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Prognosis & Treatment
Patent Ductus Arteriosus
General Considerations

Clinical Findings
Symptoms and Signs
Diagnostic Studies
Prognosis & Treatment
Coarctation of the Aorta
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Prognosis & Treatment
Ebstein Anomaly
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Prognosis & Treatment
Congenitally Corrected Transposition of
the Great Arteries
General Considerations

370
370

371
371
400
373
373
373
373

373
375
375
376
376
377
377
377
378
379
379
380
380
381
384
384
384
385
385
386
386
388
388
389
389
389
389
390
390
391

391
391
392
393
393
394
394
394
395
396
396

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CONTENTS

ix

Clinical Findings
Symptoms and Signs
Diagnostic Studies
Prognosis & Treatment
Other Acyanotic Congenital Defects
Cyanotic Congenital Heart Disease
Tetralogy of Fallot & Pulmonary Atresia VSD
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Prognosis & Treatment

Eisenmenger Syndrome
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Prognosis & Treatment
Transposition of the Great Arteries
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Prognosis & Treatment
Tricuspid Atresia
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Prognosis & Treatment
Pulmonary Atresia with Intact Ventricular Septum
General Considerations
Clinical Findings
Prognosis & Treatment
Other Cyanotic Congenital Heart Defects
Palliative Surgical Procedures
Genetic Counseling & Pregnancy
Recommendations for Exercise &
Sports Participation
Acquired Heart Disease in Adults with
Congenital Heart Disease

29. Long-Term Anticoagulation for
Cardiac Conditions
Richard D. Taylor, MD & Richard W. Asinger, MD
General Considerations
Anticoagulants
Risks of Anticoagulant Therapy
Pathophysiology & Etiology
Pathogenesis of Intravascular Thrombi
Embolization of Thrombi
Diagnostic Studies
Treatment of Cardiac Conditions
Requiring Anticoagulation

397
397
397
399
399
400
401
402
403
403
403
403
405
405
406
406
406

406
409
409
410
410
410
410
411
411
411
411
411
412
401
413
413
414
414
415
415
415
415

417
417
417
418
418
418
419

420
421


ᮢ

x

CONTENTS

Atrial Fibrillation
Native Valvular Heart Disease
Prosthetic Heart Valves
Left Ventricular Thrombus
Aortic Atheroma
Paradoxical Emboli Associated with
Patent Foramen Ovale
Pacemakers, Implantable Cardioverter
Defibrillators, and Other Intracardiac Devices
Special Considerations

30. Cardiac Tumors

422
425
426
427
429
429
429

430

Kirsten Tolstrup, MD, FACC, FASE
General Considerations
Cardiovascular Physiology of Normal Pregnancy
Blood Volume
Cardiac Output
Intravascular Pressures and Vascular Resistance
Etiology & Symptomatology
Congenital Heart Disease
Valvular Heart Disease
Myocarditis
Cardiomyopathy
Coronary Artery Disease
Arrhythmias
Pericardial Diseases
Pulmonary Hypertension
Diseases of the Aorta
Hypertension

458
458
458
458
458
459
460
460
462
462

463

432

Bill P.C. Hsieh, MD & Rita F. Redberg, MD, MSc, FACC,
FAHA
General Considerations
432
Metastatic Cardiac Tumors
432
Primary Tumors
432
Clinical Findings
437
Symptoms and Signs
437
Physical Examination
438
Diagnostic Studies
438
Differential Diagnosis
441
Treatment
441
Pharmacologic Therapy
441
Radiation
442
Surgery
442

Pericardiocentesis
442
Cardiac Transplantation
442
Prognosis
443
Metastatic Tumors
443
Primary Tumors
443
Cardiac Toxicities from Oncologic Treatments
443
Chemotherapy
443
Radiation
444

31. Cardiovasular Disease in Pregnancy

Clinical Findings
History
Symptoms and Signs
Physical Examination
Diagnostic Difficulties
Diagnostic Studies
Treatment
Pharmacologic Treatment
Surgical Treatment
Labor and Delivery
Prognosis

446
446
446
446
446
447
447
447
450
452
452
454
455
456
456
457
458

32. Endocrinology & the Heart
B. Sylvia Vela, MD & Michael H. Crawford, MD
Thyroid & the Heart
Hyperthyroidism
General Considerations
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Prognosis

Hypothyroidism
General Considerations
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Prognosis
Effect of Heart Disease on Thyroid Function
Cardiovascular Drugs & the Thyroid
Parathyroid & the Heart
Hyperparathyroidism
General Considerations
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment & Prognosis
Hypoparathyroidism
Adrenal & the Heart
Pheochromocytoma
General Considerations
Clinical Findings
Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Prognosis
Adrenal Insufficiency
General Considerations

Clinical Findings

464
464
464
464
465
465
466
466
467
468
468
468
468
468
469
469
470
470
471
471
472
472
472
473
473
473
473
473

473
474
474
474
474
474
475
475
475
476
476
476
476


Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Cushing Syndrome
General Considerations
Diagnostic Considerations
Treatment
Primary Hyperaldosteronism
General Considerations
Diagnostic Considerations
Treatment
Acromegaly & the Heart
General Considerations
Clinical Findings

Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Growth Hormone Deficiency
Carcinoid Tumors & the Heart
General Considerations
Treatment
Diabetes Mellitus & the Heart
General Considerations
Clinical Findings
Treatment
Estrogens & the Heart
Hormone Replacement Therapy
Oral Contraceptives

476
477
477
477
477
477
478
478
478
478
478
478
479
479

479
479
479
479
480
480
480
480
481
481
481
481
481
482
482
483

33. Connective Tissue Diseases & the Heart 484
Carlos A. Roldan, MD
Systemic Lupus Erythematosus
General Considerations
Valvular Heart Disease
General Considerations
Valve Vegetations, or Libman-Sacks
Endocarditis
Valve Thickening
Valve Regurgitation
Clinical Findings
Symptoms and Signs
Physical Examination

Diagnostic Studies
Treatment
Specific Antiinflammatory Therapy
Long-Term Anticoagulation
Other Therapy
Pericarditis
General Considerations
Clinical Findings
Symptoms and Signs
Laboratory Findings

484
484
485
485
485
485
485
485
485
486
487
487
487
487
487
487
487
488
488

488

ᮢ

CONTENTS

xi

Diagnostic Studies
Treatment
Medical Therapy
Surgical Therapy
Myocarditis or Cardiomyopathy
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Treatment
Specific Antiinflammatory Therapy
Other Therapy
Thrombotic Diseases
General Considerations
Clinical Findings
Symptoms and Signs
Laboratory Findings
Diagnostic Studies
Treatment
Specific Antiinflammatory Therapy
Other Therapy
Coronary Artery Disease

General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Treatment
Specific Antiinflammatory Therapy
Other Therapy
Cardiac Arrhythmias & Conduction Disturbances
General Considerations
Treatment
Specific Antiinflammatory Therapy
Other Therapy
Prognosis
Rheumatoid Arthritis
Rheumatoid Pericarditis
General Considerations
Clinical Findings
Symptoms and Signs
Laboratory Findings
Diagnostic Studies
Treatment
Prognosis
Rheumatoid Valvular Heart Disease
General Considerations
Clinical Findings
Physical Examination
Diagnostic Studies
Treatment
Rheumatoid Myocarditis
General Considerations

Clinical Findings
Physical Examination
Laboratory Findings

488
488
488
488
488
488
489
489
489
489
489
489
489
489
489
489
490
490
490
490
490
490
490
490
490
490

491
491
491
491
491
491
491
491
491
492
492
492
492
492
492
492
493
493
493
493
493
493
493
493
494
494
494
494
494

ᮢ

xii

CONTENTS

Diagnostic Studies
Treatment & Prognosis
Rheumatoid Coronary Artery Disease
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Treatment
Conduction Disturbances
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Treatment
Rheumatoid Pulmonary Hypertension
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Treatment & Prognosis
Scleroderma
General Considerations
Coronary Artery Disease

Pathophysiology
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Treatment
Myocarditis
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Treatment
Prognosis
Conduction Disturbances & Arrhythmias
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Treatment
Prognosis
Pericarditis
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Treatment
Prognosis
Valvular Heart Disease
Secondary Scleroderma Heart Disease
Ankylosing Spondylitis

494
495
495
495
495
495
495
495
495
495
496
496
496
496
496
496
496
496
496
496
497
497
497
497
497
497
497
498
498
498

499
499
499
499
499
499
499
499
499
499
500
500
500
500
500
500
500
500
500
500
500
501

General Considerations
Aortitis & Aortic Regurgitation
General Considerations
Clinical Findings
Physical Examination
Diagnostic Studies
Treatment

Medical Therapy
Surgical Therapy
Conduction Disturbances
Clinical Findings
Physical Examination
Diagnostic Studies
Treatment
Specific Antiinflammatory Therapy
Other Therapy
Mitral Valve Disease
Myocardial Disease, Pericardial Disease,
& Bacterial Endocarditis
Prognosis
Polymyositis/Dermatomyositis
General Considerations
Clinical Findings
Myocarditis
Arrhythmias & Conduction Disturbances
Coronary Arteritis
Valvular Heart Disease
Pericarditis
Pulmonary Hypertension, Cor Pulmonale,
& Hyperkinetic Heart Syndrome
Treatment & Prognosis
Mixed Connective Tissue Disease
General Considerations
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Treatment

Prognosis

34. The Athlete’s Heart

501
502
502
502
502
502
502
502
502
502
503
503
503
503
503
503
504
504
504
504
504
504
505
505
505
505

505
505
505
505
506
506
506
506
506
506

507

Cedela Abdulla, MD & J. V. (Ian) Nixon, MD, FACC, FAHA
General Considerations
507
Physiology of Exercise Training
507
Acute Responses to Exercise
507
Effects of Systematic Exercise Training
509
Morphologic Responses to Training
510
Electrocardiography
512
Racial Differences in Response to Training
512
Detraining
512

Sudden Death in Athletes
513
The Preparticipation Physical Examination
513


35. Thoracic Aortic Aneurysms & Dissections 516
John A. Elefteriades, MD
Aneurysms
General Considerations
Etiology
Clinical Findings
Natural History
Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Risks of Aortic Surgery
Indications and Contraindications
Surgical Techniques
Specific Clinical Scenarios and Issues
Aortic Dissection
General Considerations
Terminology
Anatomic Classification
Clinical Findings
Symptoms and Signs
Diagnostic Studies
Differential Diagnosis
Treatment

Pharmacotherapy
Surgical Treatment
Prognosis

516
516
516
520
520
524
524
524
525
525
526
526
528
529
529
529
531
531
531
531
532
533
533
534
535

ᮢ

CONTENTS
36. Evaluation & Treatment of
the Perioperative Patient

Sanjiv J. Shah, MD
Preoperative Risk Assessment
Algorithms
Intermediate Risk Patients
Understanding Cardiac Complications
Treatment to Reduce Perioperative Risk
β-Blockers
Statins
Clonidine
Calcium Channel Blockers
Maintanence of Normothermia
Deep Venous Thrombosis Prophylaxis
Endocarditis Prophylaxis
Perioperative Medication Management
Prophylactic Coronary Revascularization
Special Populations
Vascular Surgery
Aortic Stenosis
Heart Failure
Pulmonary Hypertension
Pacemakers and Defibrillators

Index

xiii

536
536
536
537
539
540
540
540
540
540
540
540
540
541
542
543
543
543
543
543
543

545


Authors
Cedela Abdulla, MD

Kuang-Yuh Chyu, MD, PhD

Department of Family Medicine, Memorial Hermann
Hospital System, Houston, Texas

The Athlete’s Heart

Assistant Professor-in-Residence, Department of Medicine,
University of California, Los Angeles, California

Unstable Angina/Non-ST Evaluation Myocardial Infarction

Richard W. Asinger, MD

Michael H. Crawford, MD

Director of Cardiology Division - HCMC, Professor of
Medicine, University of Minnesota Medical School,
Minneapolis, Minnesota

Long-Term Anticoagulation for Cardiac Conditions

Professor of Medicine, Lucy Stern Chair in Cardiology;
Interim Chief of Cardiology, University of California,
San Francisco, California

Approach to Cardiac Disease Diagnosis; Chronic Ischemic
Heart Disease; Aortic Stenosis; Aortic Regurgitation; Mitral
Regurgitation; Infective Endocarditis; Restrictive Cardiomyopathies; Myocarditis; Syncope; Endocrinology & the
Heart

Nitish Badhwar, MD
Assistant Clinical Professor of Medicine, University of
California, San Francisco, California

Ventricular Tachycardia

Prakash C. Deedwania, MD
Chief, University of California, San Francisco School of
Medicine, Cardiology Sections; Veterans Affairs Central
California Health Care System, San Francisco, California
Congestive Heart Failure

Andrew J. Boyle, MBBS, PhD
Assistant Clinical Professor of Medicine, University of
California, San Francisco, California

Acute Myocardial Infarction

Teresa De Marco, MD
Professor of Clinical Medicine and Surgery; Director, Heart
Failure and Pulmonary Hypertension; Medical Director,
Heart Transplantation, University of California, San
Francisco, California

Pulmonary Hypertension

Robert J. Bryg, MD
Professor of Medicine, David Geffen School of Medicine at
UCLA, Los Angeles, California

Mitral Stenosis

Blase A. Carabello, MD

John P. DiMarco MD, PhD

Professor, Baylor College of Medicine, Houston, Texas

Aortic Stenosis

Professor of Medicine; Director, Clinical Cardiac
Electrophysiology Division of Cardiovacular Medicine
University of Virginia Health System, Charlottesville,
Virginia

Sudden Cardiac Death

Enrique V. Carbajal, MD
Assistant Clinical Professor of Medicine, University of
California, San Francisco Medical Education Program;
Assistant Chief, Cardiology Section, Veterans Affairs
Central California Health Care System, Fresno,
California

Congestive Heart Failure

John A. Elefteriades, MD
Professor & Chief, Section of Cardiothoracic Surgery, Yale
University School of Medicine, New Haven, Connecticut

Thoracic Aortic Aneurysms & Dissections

John D. Carroll, MD

Elyse Foster, MD

Professor of Medicine, Director Cardiac and Vascular
Center; Chief, Interventional and Clinical Cardiology,
University of Colorado Hospital, Denver, Colorado

Restrictive Cardiomyopathies

Professor of Clinical Medicine and Anesthesia, University of
California, San Francisco, California

Congenital Heart Disease in Adults

xiv


ᮢ

AUTHORS

xv

Nora Goldschlager, MD

Peter R. Kowey, MD

Professor of Clinical Medicine, University of California, San
Francisco; Director, Coronary Care Unit, ECG
Department and Pacemaker Clinic, San Francisco
General Hospital, San Francisco, California

Conduction Disorders & Cardiac Pacing

Professor of Medicine, Jefferson Medical College; Chief,
Division of Cardiovascular Diseases, Lankenau Hospital,
Philadelphia, Pennsylvania

Supraventricular Tachycardias

Byron K. Lee, MD
William F. Graettinger, MD, FACC, FACP, FCCP
Professor & Vice-Chairman, Department of Internal
Medicine, Chief, Division of Cardiology, University of
Nevada School of Medicine, Reno; Chief, Cardiology
Section, VA Sierra Nevada Healthcare System, Reno,
Nevada

Systemic Hypertension

Ian S. Harris, MD
Assistant Professor of Medicine, Department of Internal
Medicine, Division of Cardiology, Adult Congenital
Heart Disease Service, University of California School of
Medicine, San Francisco, California

Congenital Heart Disease in Adults

Brian D. Hoit, MD
Professor of Medicine and Physiology and Biophysics, Case
Western Reserve University; Director of
Echocardiography, Case Medical Center, University
Hospitals of Cleveland, Ohio

Tricuspid and Pulmonic Valve Disease

Richard H. Hongo, MD
California Pacific Medical Center, San Francisco, California

Conduction Disorders & Cardiac Pacing

Bill P.C. Hsieh, MD
Instructor in Medicine, Albert Einstein College of Medicine,
Montefiori Medical Center, New York, New York
Cardiac Tumors

Allan S. Jaffe, MD
Assistant Professor of Medicine & Consultant, Divisions of
Cardiology and Laboratory Medicine, Mayo Clinic,
Rochester, Minnesota

Acute Myocardial Infarction

Assistant Professor of Medicine, Division of Cardiology,
University of California, San Francisco, California

Supraventricular Tachycardias

Martin M. LeWinter, MD
Professor of Medicine & Molecular Physiology and
Biophysics, University of Vermont College of Medicine,
Attending Cardiologist and Director, Heart Failure
Program, Fletcher Allen Health Care, Burlington,
Vermont

Pericardial Disease

David D. McManus, MD
Instructor in Medicine, Cardiology Division, Department of
Medicine, University of Massachusetts Medical Center,
Worchester, Massachusetts

Pulmonary Hypertension

Edward McNulty, MD
Assistant Clinical Professor of Medicine, University of San
Francisco, San Francisco, California

Cardiogenic Shock

J. V. (Ian) Nixon, MD, FACC, FAHA
Professor of Internal Medicine & Cardiology, Virginia
Commonwealth University School of Medicine Director,
Noninvasive Cardiology Services, Pauley Heart Center,
VCU Health System, Richmond, Virginia

The Athlete’s Heart

John B. O’Connell, MD
Professor & Chairman, Department of Internal Medicine,
Wayne State University School of Medicine, Detroit,
Michigan

Myocarditis

Rajni K. Rao, MD
Assistant Clinical Professor of Medicine, University of
California, San Francisco, California

Pulmonary Embolic Disease


ᮢ

xvi

AUTHORS

Rita F. Redberg, MD, MSc, FACC, FAHA

Craig Timm, MD

UCSF School of Medicine, Robert Wood Johnson
Foundation Health Policy Fellow, Professor of Medicine,
University of California, San Francisco Medical Center,
San Francisco, California

Cardiac Tumors

Professor of Internal Medicine, Associate Dean of
Undergraduate Medical Education, University of New
Mexico Health Sciences Center, Albuquerque, New
Mexico

Cardiogenic Shock

Carlos A. Roldan, MD

Kristen Tolstrup, MD, FACC, FASE

Associate Professor of Medicine, Cardiology Division,
Veterans Affairs Medical Center and University of New
Mexico, Albuquerque, New Mexico

Connective Tissue Diseases & the Heart

Assistant Director, Cardiac Noninvasive Laboratory,
Cedars-Sinai Heart Institute; Associate Professor, UCLA
Geffen School of Medicine, Los Angeles, California

Cardiovascular Disease in Pregnancy

Melvin M. Scheinman, MD

Subha L. Varahan, MD

Professor of Medicine, Emeritus, Walter H., Shorenstein
Endowed Chair in Cardiology, University of California,
San Francisco, California

Atrial Fibrillation

Pravin M. Shah, MD, MACC
Chair, Medical Director, Hoag Heart and Vascular Institute,
Newport Beach, California

Hypertrophic Cardiomyopathies

Prediman K. Shah, MD
Shapell and Webb Chair & Director, Division of Cardiology
and Oppenheimer Atherosclerosis Research Center,
Cedar-Sinai Medical Center; Professor of Medicine,
University of California, Los Angeles, California

Unstable Angina/Non-ST Evaluation Myocardial Infarction

Sanjiv J. Shah, MD
Assistant Professor of Medicine, Division of Cardiology,
Department of Medicine; Director, Heart Failure with
Preserved Ejection Fraction, Bluhm Cardiovascular
Institute, Northwestern University Feinberg School of
Medicine, Chicago, Illinois

Heart Failure with Preserved Ejection Fraction; Evaluation &
Treatment of the Perioperative Patient

Richard D. Taylor, MD
Director, Arrhythmia Management Program, Hennepin
County Medical Center; Assistant Professor of Medicine,
Minneapolis, Minnesota

Long-Term Anticoagulation for Cardiac Conditions

Fellow Division of Cardiovascular Medicine, University
Hospitals Case Medical Center, Division of
Cardiovascular Medicine, Department of Medicine,
Cleveland, Ohio

Tricuspid and Pulmonic Valve Disease

B. Sylvia Vela, MD
Associate Professor of Clinical Medicine, University of
Arizona College of Medicine; Associate Chief of Staff,
Education, Phoenix VA Health Care System, Phoenix,
Arizona

Endocrinology & the Heart

Christian Zellner, MD
Cardiology Fellow, University of California, San Francisco,
California

Lipid Disorders

William A. Zoghbi, MD, FASE, FACC
William L. Winters Endowed Chair in CV Imaging;

Professor of Medicine, Weill Cornell Medical College;
Director, Cardiovascular Imaging Institute, The
Methodist DeBakey Heart & Vascular Center, Houston,
Texas

Aortic Regurgitation


Preface
Current Diagnosis & Treatment: Cardiology is designed to be a concise discussion of the essential knowledge needed to diagnose
and manage cardiovascular diseases. Current Diagnosis & Treatment: Cardiology cannot be considered a condensed textbook
because detailed pathophysiologic discussions are omitted; there are no chapters on diagnostic techniques; and rare or obscure
entities are not included. Also, it is not a cardiac therapeutics text because diagnostic techniques, prevention strategies, and
prognosis are fully discussed.

INTENDED AUDIENCE
Current Diagnosis & Treatment: Cardiology is designed to be a quick reference source in the clinic or on the ward for the
experienced physician. Cardiology fellows will find that it is an excellent review for Board examinations. Also, students and
residents will find it useful to review the essentials of specific conditions and to check the current references included in each
section for further study. Nurses, technicians, and other health care workers who provide care for cardiology patients will find
Current Diagnosis & Treatment: Cardiology a useful resource for all aspects of heart disease care.

COVERAGE
The 36 chapters in Current Diagnosis & Treatment: Cardiology cover the major disease entities and therapeutic challenges in
cardiology. There are chapters on major management issues in cardiology such as pregnancy and heart disease, the use of
anticoagulants in heart disease, and the perioperative evaluation of heart disease patients. Each section is written by experts in
the particular area, but has been extensively edited to ensure a consistent approach throughout the book and the kind of
readability found in single-author texts.
Since the second edition the book has changed somewhat. Each chapter has been thoroughly revised and the references
updated, often by new authors. A new chapter has been added on heart failure with preserved ejection fraction and the chapters

covering thoracic aortic diseases have been combined into one. My hope is that the book is found useful and improves patient
care. Also, I hope it is an educational tool that improves knowledge of cardiac diseases. Finally, I hope it stimulates clinical
research in areas where our knowledge is incomplete.
Michael H. Crawford, MD

xvii


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ᮢ

Approach to Cardiac
Disease Diagnosis
Michael H. Crawford, MD

ᮣ General Considerations
The patient’s history is a critical feature in the evaluation of
suspected or overt heart disease. It includes information
about the present illness, past illnesses, and the patient’s
family. From this information, a chronology of the patient’s
disease process should be constructed. Determining what
information in the history is useful requires a detailed
knowledge of the pathophysiology of cardiac disease. The
effort spent on listening to the patient is time well invested
because the cause of cardiac disease is often discernible from
the history.

A. Common Symptoms

1

1

asleep or recumbent for an hour or more. This symptom is
caused by the redistribution of body fluids from the lower
extremities into the vascular space and back to the heart,
resulting in volume overload; it suggests a more severe
condition. Third is orthopnea, a dyspnea that occurs immediately on assuming the recumbent position. The mild
increase in venous return (caused by lying down) before any
fluid is mobilized from interstitial spaces in the lower
extremities is responsible for the symptom, which suggests
even more severe disease. Finally, dyspnea at rest suggests
severe cardiac disease.
Dyspnea is not specific for heart disease, however. Exertional dyspnea, for example, can be due to pulmonary
disease, anemia, or deconditioning. Orthopnea is a frequent
complaint in patients with chronic obstructive pulmonary
disease and postnasal drip. A history of “two-pillow orthopnea” is of little value unless the reason for the use of two
pillows is discerned. Resting dyspnea is also a sign of pulmonary disease. Paroxysmal nocturnal dyspnea is perhaps the
most specific for cardiac disease because few other conditions cause this symptom.

1. Chest pain—Chest pain is one of the cardinal symptoms
(Table 1–1) of ischemic heart disease, but it can also occur
with other forms of heart disease. The five characteristics of
ischemic chest pain, or angina pectoris, are
• Anginal pain usually has a substernal location but may
extend to the left or right chest, the shoulders, the neck,
jaw, arms, epigastrium, and, occasionally, the upper back.
• The pain is deep, visceral, and intense; it makes the patient

pay attention but is not excruciating. Many patients
describe it as a pressure-like sensation or a tightness.
• The duration of the pain is minutes, not seconds.
• The pain tends to be precipitated by exercise or emotional stress.
• The pain is relieved by resting or taking sublingual
nitroglycerin.

3. Syncope and presyncope—Lightheadedness, dizziness,
presyncope, and syncope are important indications of a
reduction in cerebral blood flow. These symptoms are nonspecific and can be due to primary central nervous system
disease, metabolic conditions, dehydration, or inner-ear
problems. Because bradyarrhythmias and tachyarrhythmias
are important cardiac causes, a history of palpitations preceding the event is significant.

2. Dyspnea—A frequent complaint of patients with a variety of cardiac diseases, dyspnea is ordinarily one of four
types. The most common is exertional dyspnea, which usually means that the underlying condition is mild because it
requires the increased demand of exertion to precipitate
symptoms. The next most common is paroxysmal nocturnal
dyspnea, characterized by the patient awakening after being

4. Transient central nervous system deficits—Deficits
such as transient ischemic attacks (TIAs) suggest emboli
from the heart or great vessels or, rarely, from the venous
circulation through an intracardiac shunt. A TIA should
prompt the search for cardiovascular disease. Any sudden
loss of blood flow to a limb also suggests a cardioembolic
event.


ᮢ

2

CHAPTER 1
B. History

Table 1–1. Common Symptoms of
Potential Cardiac Origin.
Chest pain or pressure
Dyspnea on exertion
Paroxysmal nocturnal dyspnea
Orthopnea
Syncope or near syncope
Transient neurologic defects
Edema
Palpitation
Cough

5. Fluid retention—These symptoms are not specific for
heart disease but may be due to reduced cardiac function.
Typical symptoms are peripheral edema, bloating, weight
gain, and abdominal pain from an enlarged liver or spleen.
Decreased appetite, diarrhea, jaundice, and nausea and vomiting can also occur from gut and hepatic dysfunction due to
fluid engorgement.
6. Palpitation—Normal resting cardiac activity usually
cannot be appreciated by the individual. Awareness of
heart activity is often referred to by patients as palpitation.
Among patients there is no standard definition for the type
of sensation represented by palpitation, so the physician
must explore the sensation further with the patient. It is

frequently useful to have the patient tap the perceived
heartbeat out by hand. Commonly, unusually forceful
heart activity at a normal rate (60–100 bpm) is perceived as
palpitation. More forceful contractions are usually the
result of endogenous catecholamine excretion that does
not elevate the heart rate out of the normal range. A
common cause of this phenomenon is anxiety. Another
common sensation is that of the heart stopping transiently
or of the occurrence of isolated forceful beats or both. This
sensation is usually caused by premature ventricular contractions, and the patient either feels the compensatory
pause or the resultant more forceful subsequent beat or
both. Occasionally, the individual feels the ectopic beat and
refers to this phenomenon as “skipped” beats. The least
common sensation reported by individuals, but the one
most linked to the term “palpitation” is rapid heart rate
that may be regular or irregular and is usually supraventricular in origin.
7. Cough—Although cough is usually associated with pulmonary disease processes, cardiac conditions that lead to
pulmonary abnormalities may be the root cause of the
cough. A cardiac cough is usually dry or nonproductive.
Pulmonary fluid engorgement from conditions such as heart
failure may present as cough. Pulmonary hypertension from
any cause can result in cough. Finally, angiotensin-converting enzyme inhibitors, which are frequently used in cardiac
conditions, can cause cough.

1. The present illness—This is a chronology of the events
leading up to the patient’s current complaints. Usually physicians start with the chief complaint and explore the
patient’s symptoms. It is especially important to determine
the frequency, intensity, severity, and duration of all symptoms; their precipitating causes; what relieves them; and
what aggravates them. Although information about previous
related diseases and opinions from other physicians are often

valuable, it is essential to explore the basis of any prior
diagnosis and ask the patient about objective testing and the
results of such testing. A history of prior treatment is often
revealing because medications or surgery may indicate the
nature of the original problem. A list should be made of all
the patient’s current medications, detailing the dosages, the
frequency of administration, whether they are helping the
patient, any side effects, and their cost.
2. Antecedent conditions—Several systemic diseases may
have cardiac involvement. It is therefore useful to search for
a history of rheumatic fever, which may manifest as Sydenham chorea, joint pain and swelling, or merely frequent sore
throats. Other important diseases that affect the heart
include metastatic cancer, thyroid disorders, diabetes mellitus, and inflammatory diseases such as rheumatoid arthritis
and systemic lupus erythematosus. Certain events during
childhood are suggestive of congenital or acquired heart
disease; these include a history of cyanosis, reduced exercise
tolerance, or long periods of restricted activities or school
absence. Exposure to toxins, infectious agents, and other
noxious substances may also be relevant.
3. Atherosclerotic risk factors—Atherosclerotic cardiovascular disease is the most common form of heart disease in
industrialized nations. The presenting symptoms of this
ubiquitous disorder may be unimpressive and minimal, or as
impressive as sudden death. It is therefore important to
determine from the history whether any risk factors for this
disease are present. The most important are a family history
of atherosclerotic disease, especially at a young age; diabetes
mellitus; lipid disorders such as a high cholesterol level;
hypertension; and smoking. Less important factors include a
lack of exercise, high stress levels, the type-A personality, and
truncal obesity.

4. Family history—A family history is important for determining the risk for not only atherosclerotic cardiovascular
disease but for many other cardiac diseases as well. Congenital heart disease, for example, is more common in the
offspring of parents with this condition, and a history of the
disorder in the antecedent family or siblings is significant.
Other genetic diseases, such as neuromuscular disorders or
connective tissue disorders (eg, Marfan syndrome) can affect
the heart. Acquired diseases, such as rheumatic valve disease,
can cluster in families because of the spread of the streptococcal infection among family members. The lack of a


history of hypertension in the family might prompt a more
intensive search for a secondary cause. A history of atherosclerotic disease sequelae, such as limb loss, strokes, and
heart attacks, may provide a clue to the aggressiveness of an
atherosclerotic tendency in a particular family group.

ᮣ Physical Findings
A. Physical Examination
The physical examination is less important than the history
in patients with ischemic heart disease, but it is of critical
value in patients with congenital and valvular heart disease.
In the latter two categories, the physician can often make
specific anatomic and etiologic diagnoses based on the physical examination. Certain abnormal murmurs and heart
sounds are specific for structural abnormalities of the heart.
The physical examination is also important for confirming
the diagnosis and establishing the severity of heart failure,
and it is the only way to diagnose systemic hypertension
because this diagnosis is based on elevated blood pressure
recordings.
1. Blood pressure—Proper measurement of the systemic
arterial pressure by cuff sphygmomanometry is one of the

keystones of the cardiovascular physical examination. It is
recommended that the brachial artery be palpated and the
diaphragm of the stethoscope be placed over it, rather than
merely sticking the stethoscope in the antecubital fossa.
Current methodologic standards dictate that the onset and
disappearance of the Korotkoff sounds define the systolic
and diastolic pressures, respectively. Although this is the best
approach in most cases, there are exceptions. For example, in
patients in whom the diastolic pressure drops to near zero,
the point of muffling of the sounds is usually recorded as the
diastolic pressure. Because the diagnosis of systemic hypertension involves repeated measures under the same conditions, the operator should record the arm used and the
position of the patient to allow reproducible measurements
to be made on serial visits.
If the blood pressure is to be taken a second time, the
patient should be in another position, such as standing, to
determine any orthostatic changes in blood pressure. Orthostatic changes are a very important physical finding, especially in patients complaining of transient central nervous
system symptoms, weakness, or unstable gait. The technique
involves having the patient assume the upright position for
at least 90 seconds before taking the pressure to be sure that
the maximum orthostatic effect is measured. Although measuring the pressure in other extremities may be of value in
certain vascular diseases, it provides little information in a
routine examination beyond palpating pulses in all the
extremities. Keep in mind, in general, that the pulse pressure
(the difference between systolic and diastolic blood pressures) is a crude measure of left ventricular stroke volume. A
widened pulse pressure suggests that the stroke volume is
large; a narrowed pressure, that the stroke volume is small.

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APPROACH TO CARDIAC DISEASE DIAGNOSIS

3

2. Peripheral pulses—When examining the peripheral
pulses, the physician is really conducting three examinations. The first is an examination of the cardiac rate and
rhythm, the second is an assessment of the characteristics of
the pulse as a reflection of cardiac activity, and the third is
an assessment of the adequacy of the arterial conduit being
examined. The pulse rate and rhythm are usually determined in a convenient peripheral artery, such as the radial.
If a pulse is irregular, it is better to auscultate the heart;
some cardiac contractions during rhythm disturbances do
not generate a stroke volume sufficient to cause a palpable
peripheral pulse. In many ways, the heart rate reflects the
health of the circulatory system. A rapid pulse suggests
increased catecholamine levels, which may be due to cardiac
disease, such as heart failure; a slow pulse represents an
excess of vagal tone, which may be due to disease or athletic
training.
To assess the characteristics of the cardiac contraction
through the pulse, it is usually best to select an artery close to
the heart, such as the carotid. Bounding high-amplitude
carotid pulses suggest an increase in stroke volume and
should be accompanied by a wide pulse pressure on the
blood pressure measurement. A weak carotid pulse suggests
a reduced stroke volume. Usually the strength of the pulse is
graded on a scale of 1 to 4, where 2 is a normal pulse
amplitude, 3 or 4 is a hyperdynamic pulse, and 1 is a weak
pulse. A low-amplitude, slow-rising pulse, which may be
associated with a palpable vibration (thrill), suggests aortic
stenosis. A bifid pulse (beating twice in systole) can be a sign

of hypertrophic obstructive cardiomyopathy, severe aortic
regurgitation, or the combination of moderately severe aortic stenosis and regurgitation. A dicrotic pulse (an exaggerated, early, diastolic wave) is found in severe heart failure.
Pulsus alternans (alternate strong and weak pulses) is also a
sign of severe heart failure. When evaluating the adequacy of
the arterial conduits, all palpable pulses can be assessed and
graded on a scale of 0 to 4, where 4 is a fully normal conduit,
and anything below that is reduced, including 0—which
indicates an absent pulse. The major pulses routinely palpated on physical examination are the radial, brachial,
carotid, femoral, dorsalis pedis, and posterior tibial. In
special situations, the abdominal aorta and the ulnar, subclavian, popliteal, axillary, temporal, and intercostal arteries are
palpated. In assessing the abdominal aorta, it is important to
make note of the width of the aorta because an increase
suggests an abdominal aortic aneurysm. It is particularly
important to palpate the abdominal aorta in older individuals because abdominal aortic aneurysms are more prevalent
in those older than 70. An audible bruit is a clue to significantly obstructed large arteries. During a routine examination, bruits are sought with the bell of the stethoscope placed
over the carotids, abdominal aorta, and femorals at the
groin. Other arteries may be auscultated under special circumstances, such as suspected temporal arteritis or vertebrobasilar insufficiency.


ᮢ

4

CHAPTER 1

3. Jugular venous pulse—Assessment of the jugular venous
pulse can provide information about the central venous pressure and right-heart function. Examination of the right internal jugular vein is ideal for assessing central venous pressure
because it is attached directly to the superior vena cava
without intervening valves. The patient is positioned into the
semiupright posture that permits visualization of the top of

the right internal jugular venous blood column. The height of
this column of blood, vertically from the sternal angle, is
added to 5 cm of blood (the presumed distance to the center
of the right atrium from the sternal angle) to obtain an
estimate of central venous pressure in centimeters of blood.
This can be converted to millimeters of mercury (mm Hg)
with the formula:

mm Hg = cm blood × 0.736.
Examining the characteristics of the right internal jugular
pulse is valuable for assessing right-heart function and
rhythm disturbances. The normal jugular venous pulse has
two distinct waves: a and v; the former coincides with atrial
contraction and the latter with late ventricular systole. An
absent a wave and an irregular pulse suggest atrial fibrillation. A large and early v wave suggests tricuspid regurgitation. The dips after the a and v waves are the x and y
descents; the former coincide with atrial relaxation and the
latter with early ventricular filling. In tricuspid stenosis the y
descent is prolonged. Other applications of the jugular pulse
examination are discussed in the chapters dealing with
specific disorders.
4. Lungs—Evaluation of the lungs is an important part of
the physical examination: Diseases of the lung can affect the
heart, just as diseases of the heart can affect the lungs. The
major finding of importance is rales at the pulmonary bases,
indicating alveolar fluid collection. Although this is a significant finding in patients with congestive heart failure, it is
not always possible to distinguish rales caused by heart
failure from those caused by pulmonary disease. The presence of pleural fluid, although useful in the diagnosis of heart
failure, can be due to other causes. Heart failure most
commonly causes a right pleural effusion; it can cause
effusions on both sides but is least likely to cause isolated left

pleural effusion. The specific constellation of dullness at the
left base with bronchial breath sounds suggests an increase in
heart size from pericardial effusion (Ewart sign) or another
cause of cardiac enlargement; it is thought to be due to
compression by the heart of a left lower lobe bronchus.
When right-heart failure develops or venous return is
restricted from entering the heart, venous pressure in the
abdomen increases, leading to hepatosplenomegaly and
eventually ascites. None of these physical findings is specific
for heart disease; they do, however, help establish the diagnosis. Heart failure also leads to generalized fluid retention,
usually manifested as lower extremity edema or, in severe
heart failure, anasarca.

5. Cardiac auscultation—Heart sounds are caused by the
acceleration and deceleration of blood and the subsequent
vibration of the cardiac structures during the phases of the
cardiac cycle. To hear cardiac sounds, use a stethoscope with
a bell and a tight diaphragm. Low-frequency sounds are
associated with ventricular filling and are heard best with the
bell. Medium-frequency sounds are associated with valve
opening and closing; they are heard best with the diaphragm.
Cardiac murmurs are due to turbulent blood flow, are
usually high-to-medium frequency, and are heard best with
the diaphragm. Low-frequency atrioventricular valve inflow
murmurs, such as that produced by mitral stenosis, are best
heard with the bell, however. Auscultation should take place
in areas that correspond to the location of the heart and great
vessels. Such placement will, of course, need to be modified
for patients with unusual body habitus or an unusual cardiac
position. When no cardiac sounds can be heard over the

precordium, they can often be heard in either the subxiphoid
area or the right supraclavicular area.
Auscultation in various positions is recommended
because low-frequency filling sounds are best heard with the
patient in the left lateral decubitus position, and highfrequency murmurs, such as that of aortic regurgitation, are
best heard with the patient sitting.
A. Heart sounds—The first heart sound is coincident with
mitral and tricuspid valve closure and has two components
in up to 40% of normal individuals. There is little change in
the intensity of this sound with respiration or position. The
major determinant of the intensity of the first heart sound is
the electrocardiographic (ECG) PR interval, which determines the time delay between atrial and ventricular contraction and thus the position of the mitral valve when ventricular systole begins. With a short PR interval, the mitral valve
is widely open when systole begins, and its closure increases
the intensity of the first sound, as compared to a long PRinterval beat when the valve partially closes prior to the onset
of ventricular systole. Certain disease states, such as mitral
stenosis, also can increase the intensity of the first sound.
The second heart sound is coincident with closure of the
aortic and pulmonic valves. Normally, this sound is single in
expiration and split during inspiration, permitting the aortic
and pulmonic components to be distinguished. The inspiratory split is due to a delay in the occurrence of the pulmonic
component because of a decrease in pulmonary vascular
resistance, which prolongs pulmonary flow beyond the end
of right ventricular systole. Variations in this normal splitting of the second heart sound are useful in determining
certain disease states. For example, in atrial septal defect, the
second sound is usually split throughout the respiratory
cycle because of the constant increase in pulmonary flow. In
patients with left bundle branch block, a delay occurs in the
aortic component of the second heart sound, which results
in reversed respiratory splitting; single with inspiration, split
with expiration.

A third heart sound occurs during early rapid filling of
the left ventricle; it can be produced by any condition that
causes left ventricular volume overload or dilatation. It can
therefore be heard in such disparate conditions as congestive
heart failure and normal pregnancy. A fourth heart sound is
due to a vigorous atrial contraction into a stiffened left
ventricle and can be heard in left ventricular hypertrophy of
any cause or in diseases that reduce compliance of the left
ventricle, such as myocardial infarction.
Although third and fourth heart sounds can occasionally
occur in normal individuals, all other extra sounds are signs
of cardiac disease. Early ejection sounds are due to abnormalities of the semilunar valves, from restriction of their
motion, thickening, or both (eg, a bicuspid aortic valve,
pulmonic or aortic stenosis). A midsystolic click is often due
to mitral valve prolapse and is caused by sudden tensing in
midsystole of the redundant prolapsing segment of the
mitral leaflet. The opening of a thickened atrioventricular
valve leaflet, as in mitral stenosis, will cause a loud opening
sound (snap) in early diastole. A lower frequency (more of a
knock) sound at the time of rapid filling may be an indication of constrictive pericarditis. These early diastolic sounds
must be distinguished from a third heart sound.
B. Murmurs—Systolic murmurs are very common and do
not always imply cardiac disease. They are usually rated on a
scale of 1 to 6, where grade 1 is barely audible, grade 4 is
associated with palpable vibrations (thrill), grade 5 can be
heard with the edge of the stethoscope, and grade 6 can be
heard without a stethoscope. Most murmurs fall in the 1–3
range, and murmurs in the 4–6 range are almost always due

to pathologic conditions; severe disease can exist with grades
1–3 or no cardiac murmurs, however. The most common
systolic murmur is the crescendo/decrescendo murmur that
increases in intensity as blood flows early in systole and
diminishes in intensity through the second half of systole.
This murmur can be due to vigorous flow in a normal heart
or to obstructions in flow, as occurs with aortic stenosis,
pulmonic stenosis, or hypertrophic cardiomyopathy. The socalled innocent flow murmurs are usually grades 1–2 and
occur very early in systole; they may have a vibratory quality
and are usually less apparent when the patient is in the sitting
position (when venous return is less). If an ejection sound is
heard, there is usually some abnormality of the semilunar
valves. Although louder murmurs may be due to pathologic
cardiac conditions, this is not always so. Distinguishing
benign from pathologic systolic flow murmurs is one of the
major challenges of clinical cardiology. Benign flow murmurs can be heard in 80% of children; the incidence declines
with age, but may be prominent during pregnancy or in
adults who are thin or physically well trained. The murmur
is usually benign in a patient with a soft flow murmur that
diminishes in intensity in the sitting position and neither a
history of cardiovascular disease nor other cardiac findings.
The holosystolic, or pansystolic, murmur is almost
always associated with cardiac pathology. The most common

ᮢ

APPROACH TO CARDIAC DISEASE DIAGNOSIS

5

cause of this murmur is atrioventricular valve regurgitation,
but it can also be observed in conditions such as ventricular
septal defect, in which an abnormal communication exists
between two chambers of markedly different systolic pressures. Although it is relatively easy to determine that these
murmurs represent an abnormality, it is more of a challenge
to determine their origins. Keep in mind that such conditions as mitral regurgitation, which usually produce holosystolic murmurs, may produce crescendo/decrescendo murmurs, adding to the difficulty in differentiating benign from
pathologic systolic flow murmurs.
Diastolic murmurs are always abnormal. The most frequently heard diastolic murmur is the high-frequency decrescendo early diastolic murmur of aortic regurgitation. This is
usually heard best at the upper left sternal border or in the
aortic area (upper right sternal border) and may radiate to
the lower left sternal border and the apex. This murmur is
usually very high frequency and may be difficult to hear.
Although the murmur of pulmonic regurgitation may sound
like that of aortic regurgitation when pulmonary artery
pressures are high, it is usually best heard in the pulmonic
area (left second intercostal space parasternally). If structural
disease of the valve is present with normal pulmonary
pressures, the murmur usually has a midrange frequency and
begins with a slight delay after the pulmonic second heart
sound. Mitral stenosis produces a low-frequency rumbling
diastolic murmur that is decrescendo in early diastole, but
may become crescendo up to the first heart sound with
moderately severe mitral stenosis and sinus rhythm. The
murmur is best heard at the apex in the left lateral decubitus
position with the bell of the stethoscope. Similar findings are
heard in tricuspid stenosis, but the murmur is loudest at the
lower left sternal border.
A continuous murmur implies a connection between a
high- and a low-pressure chamber throughout the cardiac
cycle, such as occurs with a fistula between the aorta and the

pulmonary artery. If the connection is a patent ductus
arteriosus, the murmur is heard best under the left clavicle;
it has a machine-like quality. Continuous murmurs must be
distinguished from the combination of systolic and diastolic
murmurs in patients with combined lesions (eg, aortic stenosis and regurgitation).
Traditionally, the origin of heart murmurs was based on
five factors: (1) their timing in the cardiac cycle, (2) where on
the chest they were heard, (3) their characteristics, (4) their
intensity, and (5) their duration. Unfortunately, this traditional classification system is unreliable in predicting the
underlying pathology. A more accurate method, dynamic
auscultation, changes the intensity, duration, and characteristics of the murmur by bedside maneuvers that alter hemodynamics.
The simplest of these maneuvers is observation of any
changes in murmur intensity with normal respiration
because all right-sided cardiac murmurs should increase in
intensity with normal inspiration. Although some exceptions


ᮢ

6

CHAPTER 1

exist, the method is very reliable for detecting such murmurs. Inspiration is associated with reductions in intrathoracic pressure that increase venous return from the abdomen
and the head, leading to an increased flow through the right
heart chambers. The consequent increase in pressure
increases the intensity of right-sided murmurs. These
changes are best observed in the sitting position, where
venous return is smallest, and changes in intrathoracic pressure can produce their greatest effect on venous return. In a
patient in the supine position, when venous return is near

maximum, there may be little change observed with respiration. The ejection sound caused by pulmonic stenosis does
not routinely increase in intensity with inspiration. The
increased blood in the right heart accentuates atrial contraction, which increases late diastolic pressure in the right
ventricle, partially opening the stenotic pulmonary valve and
thus diminishing the opening sound of this valve with the
subsequent systole.
Changes in position are an important part of normal
auscultation; they can also be of great value in determining
the origin of cardiac murmurs (Table 1–2). Murmurs dependent on venous return, such as innocent flow murmurs, are
softer or absent in upright positions; others, such as the
murmur associated with hypertrophic obstructive cardiomyopathy, are accentuated by reduced left ventricular volume
associated with the upright position. In physically capable
individuals, a rapid squat from the standing position is often
diagnostically valuable because it suddenly increases venous
return and left ventricular volume and accentuates flow
murmurs but diminishes the murmur of hypertrophic
obstructive cardiomyopathy. The stand-squat maneuver is
also useful for altering the timing of the midsystolic click
caused by mitral valve prolapse during systole. When the
ventricle is small during standing, the prolapse occurs earlier
in systole, moving the midsystolic click to early systole.
During squatting, the ventricle dilates and the prolapse is
delayed in systole, resulting in a late midsystolic click.

Valsalva maneuver is also frequently used. The patient
bears down and expires against a closed glottis, increasing
intrathoracic pressure and markedly reducing venous return
to the heart. Although almost all cardiac murmurs decrease
in intensity during this maneuver, there are two exceptions:
(1) The murmur of hypertrophic obstructive cardiomyopathy may become louder because of the diminished left

ventricular volume. (2) The murmur associated with mitral
regurgitation from mitral valve prolapse may become longer
and louder because of the earlier occurrence of prolapse
during systole. When the maneuver is very vigorous and
prolonged, even these two murmurs may eventually diminish in intensity. Therefore, the Valsalva maneuver should be
held for only about 10 seconds, so as not to cause prolonged
diminution of the cerebral and coronary blood flow.
Isometric hand grip exercises have been used to increase
arterial and left ventricular pressure. These maneuvers
increase the flow gradient for mitral regurgitation, ventricular septal defect, and aortic regurgitation; the murmurs
should then increase in intensity. Increasing arterial and left
ventricular pressure increases left ventricular volume,
thereby decreasing the murmur of hypertrophic obstructive
cardiomyopathy. If the patient is unable to perform isometric exercises, transient arterial occlusion of both upper
extremities with sphygmomanometers can achieve the same
increases in left-sided pressure.
Noting the changes in murmur intensity in the heart beat
following a premature ventricular contraction, and comparing these to a beat that does not, can be extremely useful. The
premature ventricular contraction interrupts the cardiac
cycle, and during the subsequent compensatory pause, an
extra-long diastole occurs, leading to increased left ventricular filling. Therefore, murmurs caused by the flow of blood
out of the left ventricle (eg, aortic stenosis) increase in
intensity. There is usually no change in the intensity of the
murmur of typical mitral regurgitation because blood pressure falls during the long pause and increases the gradient

Table 1–2. Differentiation of Systolic Murmurs Based on Changes in Their Intensity from Physiologic Maneuvers.
Origin of Murmur
Maneuver

Flow

TR

AS

MR/VSD

MVP

HOCM

– or ↑

↑

–

–

–

–

Stand

↓

–

–

–

↑

↑

Squat

↑

–

–

–

↓

↓

Valsalva

↓

↓

↓

↓

↑

↑

Handgrip/TAO

↓

–

–

↑

↑

↓

Post–PVC

↑

–

↑

–

–

↑

Inspiration

AS, aortic stenosis; Flow, innocent flow murmur; HOCM, hypertrophic obstructive cardiomyopathy; MR, mitral regurgitation; MVP, mitral valve prolapse;
PVC, premature ventricular contraction; TAO, transient arterial occlusion; TR, tricuspid regurgitation; VSD, ventricular septal defect; ↑ or ↓, change in intensity
of murmur; –, no consistent change.