a LANGE medical book

CURRENT

Diagnosis & Treatment
Cardiology
THIRD EDITION
Edited by
Michael H. Crawford, MD
Professor ...
Copyright © 2009 by The McGraw-Hill Companies, Inc. All rights reserved. Except as permitted under the United States Copyr...
Contents
Authors
Preface
1. Approach to Cardiac Disease Diagnosis
Michael H. Crawford, MD
General Considerations
Common Sy...
ᮢ

iv

CONTENTS

Other Arrhythmias
Mural Thrombi
Aneurysm and Pseudo-aneurysms
Right Ventricular Infarction
Prognosis, Ris...
Physical Examination
Diagnostic Studies
Treatment
Medical
Surgical
Postoperative Management
Prognosis
Pulmonic Valve Disea...
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vi

CONTENTS

Chagas Disease, or American Trypanosomiasis
HIV
Toxoplasmosis
Cytomegalovirus
Lyme Myocarditis
Giant Cell...
Catheter Ablation and Other Modalities
Stroke Prophylaxis
Multifocal Atrial Tachycardia
General Considerations
Treatment
P...
ᮢ

viii

CONTENTS

Polymorphic VT in the Setting of
Prolonged QT Interval
Clinical Findings
Management
Polymorphic VT with...
Pulmonary Hypertension due to
Chronic Thrombotic or Embolic Disease
Prognosis

28. Congenital Heart Disease in Adults
Ian ...
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x

CONTENTS

Atrial Fibrillation
Native Valvular Heart Disease
Prosthetic Heart Valves
Left Ventricular Thrombus
Aortic...
Symptoms and Signs
Physical Examination
Diagnostic Studies
Treatment
Cushing Syndrome
General Considerations
Diagnostic Co...
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xii

CONTENTS

Diagnostic Studies
Treatment & Prognosis
Rheumatoid Coronary Artery Disease
General Considerations
Clini...
35. Thoracic Aortic Aneurysms & Dissections 516
John A. Elefteriades, MD
Aneurysms
General Considerations
Etiology
Clinica...
Authors
Cedela Abdulla, MD

Kuang-Yuh Chyu, MD, PhD

Department of Family Medicine, Memorial Hermann
Hospital System, Hous...
ᮢ

AUTHORS

xv

Nora Goldschlager, MD

Peter R. Kowey, MD

Professor of Clinical Medicine, University of California, San
F...
ᮢ

xvi

AUTHORS

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

Craig Timm, MD

UCSF School of Medicine, Robert Wood Johnson
Founda...
Preface
Current Diagnosis & Treatment: Cardiology is designed to be a concise discussion of the essential knowledge needed...
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ᮢ

Approach to Cardiac
Disease Diagnosis
Michael H. Crawford, MD

ᮣ General Considerations
The patient’s history is a crit...
ᮢ

2

CHAPTER 1
B. History

Table 1–1. Common Symptoms of
Potential Cardiac Origin.
Chest pain or pressure
Dyspnea on exer...
history of hypertension in the family might prompt a more
intensive search for a secondary cause. A history of atheroscler...
ᮢ

4

CHAPTER 1

3. Jugular venous pulse—Assessment of the jugular venous
pulse can provide information about the central ...
A third heart sound occurs during early rapid filling of
the left ventricle; it can be produced by any condition that
caus...
ᮢ

6

CHAPTER 1

exist, the method is very reliable for detecting such murmurs. Inspiration is associated with reductions ...
between the left ventricle and the aorta, allowing more
forward flow. This results in the same amount of mitral
regurgitan...
ᮢ

8

CHAPTER 1

the stratification of risk of developing sustained ventricular
arrhythmias in postmyocardial infarction p...
it is not 100% accurate. Furthermore, it is impossible to
obtain high-quality images or Doppler signals in as many as
5% o...
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Transcript of "Current diagnosis & treatment cardiology, 3rd edition"

  1. 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 New York Chicago San Francisco Lisbon London Madrid Mexico City Milan New Delhi San Juan Seoul Singapore Sydney Toronto
  2. 2. Copyright © 2009 by The McGraw-Hill Companies, Inc. All rights reserved. Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher. ISBN: 978-0-07-170199-0 MHID: 0-07-170199-0 The material in this eBook also appears in the print version of this title: ISBN: 978-0-07-144211-4, MHID: 0-07-144211-1. All trademarks are trademarks of their respective owners. Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and to the benefit of the trademark owner, with no intention of infringement of the trademark. Where such designations appear in this book, they have been printed with initial caps. McGraw-Hill eBooks are available at special quantity discounts to use as premiums and sales promotions, or for use in corporate training programs. To contact a representative please e-mail us at bulksales@mcgraw-hill.com. Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatmentand drug therapy are required. The authors and the publisher of this work have checked with sources believed to be reliable intheir efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the authors nor the publishernor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for theresults obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurateand that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. TERMS OF USE This is a copyrighted work and The McGraw-Hill Companies, Inc. (“McGraw-Hill”) and its licensors reserve all rights in and to the work. Use of this work is subject to these terms. Except as permitted under the Copyright Act of 1976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill’s prior consent. You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited. Your right to use the work may be terminated if you fail to comply with these terms. THE WORK IS PROVIDED “AS IS.” McGRAW-HILL AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS OF OR RESULTS TO BE OBTAINED FROM USING THE WORK, INCLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE WORK VIA HYPERLINK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO IMPLIED WARRANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. McGraw-Hill and its licensors do not warrant or guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free. Neither McGraw-Hill nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom. McGraw-Hill has no responsibility for the content of any information accessed through the work. Under no circumstances shall McGraw-Hill and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages. This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise.
  3. 3. 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
  4. 4. ᮢ 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
  5. 5. 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
  6. 6. ᮢ 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
  7. 7. 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
  8. 8. ᮢ 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
  9. 9. 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 ᮢ 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
  10. 10. ᮢ 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
  11. 11. 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
  12. 12. ᮢ 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
  13. 13. 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
  14. 14. Authors Cedela Abdulla, MD Kuang-Yuh Chyu, MD, PhD Department of Family Medicine, Memorial Hermann Hospital System, Houston, Texas cedela_a@yahoo.com The Athlete’s Heart Assistant Professor-in-Residence, Department of Medicine, University of California, Los Angeles, California Kuang-Yuh.Chyu@cshs.org 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 asing001@umn.edu Long-Term Anticoagulation for Cardiac Conditions Professor of Medicine, Lucy Stern Chair in Cardiology; Interim Chief of Cardiology, University of California, San Francisco, California crawfordm@medicine.ucsf.edu 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 badhwar@medicine.ucsf.edu 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 aboyle@medicine.ucsf.edu 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 demarco@medicine.ucsf.edu Pulmonary Hypertension Robert J. Bryg, MD Professor of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California nevsimbob@aol.com Mitral Stenosis Blase A. Carabello, MD John P. DiMarco MD, PhD Professor, Baylor College of Medicine, Houston, Texas blaseanthony.carabello@med.va.gov Aortic Stenosis Professor of Medicine; Director, Clinical Cardiac Electrophysiology Division of Cardiovacular Medicine University of Virginia Health System, Charlottesville, Virginia jdimarco@virginia.edu 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 enrique.carbjal@med.va.gov Congestive Heart Failure John A. Elefteriades, MD Professor & Chief, Section of Cardiothoracic Surgery, Yale University School of Medicine, New Haven, Connecticut john.elefteriades@yale.edu 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 john.carroll@uchsc.edu Restrictive Cardiomyopathies Professor of Clinical Medicine and Anesthesia, University of California, San Francisco, California foster@medicine.ucsf.edu Congenital Heart Disease in Adults xiv
  15. 15. ᮢ 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 ngoldschlager@medsfgh.ucsf.edu Conduction Disorders & Cardiac Pacing Professor of Medicine, Jefferson Medical College; Chief, Division of Cardiovascular Diseases, Lankenau Hospital, Philadelphia, Pennsylvania koweypr@mlhheart.org 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 william.graettinger@med.va.gov 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 harrisi@medicine.ucsf.edu 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 bdh6@cwru.edu Tricuspid and Pulmonic Valve Disease Richard H. Hongo, MD California Pacific Medical Center, San Francisco, California rhongo@cpcmg.com 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 jaffe.allan@mayo.edu Acute Myocardial Infarction Assistant Professor of Medicine, Division of Cardiology, University of California, San Francisco, California leeb@medicine.ucsf.edu 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 martin.lewinter@vtmednet.org Pericardial Disease David D. McManus, MD Instructor in Medicine, Cardiology Division, Department of Medicine, University of Massachusetts Medical Center, Worchester, Massachusetts mcmanus.dave@gmail.com Pulmonary Hypertension Edward McNulty, MD Assistant Clinical Professor of Medicine, University of San Francisco, San Francisco, California edward.j.mcnulty@kp.org 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 jnixon@mcvh-vcu.edu The Athlete’s Heart John B. O’Connell, MD Professor & Chairman, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan joconnell@nmff.org Myocarditis Rajni K. Rao, MD Assistant Clinical Professor of Medicine, University of California, San Francisco, California rao@medicine.ucsf.edu Pulmonary Embolic Disease
  16. 16. ᮢ 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 redberg@medicine.ucsf.edu Cardiac Tumors Professor of Internal Medicine, Associate Dean of Undergraduate Medical Education, University of New Mexico Health Sciences Center, Albuquerque, New Mexico ctimm@salud.unm.edu 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 carlosroldan2@med.va.gov Connective Tissue Diseases & the Heart Assistant Director, Cardiac Noninvasive Laboratory, Cedars-Sinai Heart Institute; Associate Professor, UCLA Geffen School of Medicine, Los Angeles, California tolstrupk@cshs.org 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 scheinman@medicine.ucsf.edu Atrial Fibrillation Pravin M. Shah, MD, MACC Chair, Medical Director, Hoag Heart and Vascular Institute, Newport Beach, California pshah@hoaghospital.org 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 shahp@cshs.org 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 sanjiv.shah@northwestern.edu 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 rpkjtay@comcast.net 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 svarahan@gmail.com 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 sylvia.vela@med.va.gov Endocrinology & the Heart Christian Zellner, MD Cardiology Fellow, University of California, San Francisco, California christian.zellner@ucsf.edu 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 wzoghbi@tmhs.org Aortic Regurgitation
  17. 17. 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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  19. 19. ᮢ 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.
  20. 20. ᮢ 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
  21. 21. 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. ᮢ 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.
  22. 22. ᮢ 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.
  23. 23. 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
  24. 24. ᮢ 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.
  25. 25. between the left ventricle and the aorta, allowing more forward flow. This results in the same amount of mitral regurgitant flow as on a normal beat with a higher aortic pressure and less forward flow. The increased volume during the long pause goes out of the aorta rather than back into the left atrium. Unfortunately, there is no reliable way of inducing a premature ventricular contraction in most patients; it is fortuitous when a physician is present for one. Atrial fibrillation with markedly varying cycle lengths produces the same phenomenon and can be very helpful in determining the origin of murmurs. Various rapid-acting pharmacologic agents have been used to clarify the origin of cardiac murmurs. A oncepopular bedside pharmacologic maneuver was the inhalation of amyl nitrite. Because this produces rapid vasodilatation and decreases in blood pressure, it diminishes the murmurs of aortic and mitral regurgitation and ventricular septal defect and increases systolic flow murmurs (eg, those caused by aortic stenosis and hypertrophic obstructive cardiomyopathy). Patients never liked the unpleasant odor of amyl nitrite and its popularity has since waned. Other pharmacologic maneuvers have occasionally been used to clarify the origin of a murmur. These include the infusion of synthetic catecholamines to increase blood pressure, isoproterenol to increase the heart rate, and intravenous β-blockers to decrease the heart rate. With the ready availability of echocardiography, these more invasive interventions have also diminished in popularity. Brennan JM et al. A comparison by medicine residents of physical examination versus hand-carried ultrasound for estimation of right atrial pressure. Am J Cardiol. 2007 Jun 1;99(11):1614–6. [PMID: 17531592] Marcus GM et al. Usefulness of the third heart sound in predicting an elevated level of B-type natriuretic peptide. Am J Cardiol. 2004 May 15:93(10):1312–3. [PMID: 15135714] B. Diagnostic Studies 1. Electrocardiography—Electrocardiography is perhaps the least expensive of all cardiac diagnostic tests, providing considerable value for the money. Modern ECG-reading computers do an excellent job of measuring the various intervals between waveforms and calculating the heart rate and the left ventricular axis. These programs fall considerably short, however, when it comes to diagnosing complex ECG patterns and rhythm disturbances, and the test results must be read by a physician skilled at ECG interpretation. Analysis of cardiac rhythm is perhaps the ECG’s most widely used feature; it is used to clarify the mechanism of an irregular heart rhythm detected on physical examination or that of an extremely rapid or slow rhythm. The ECG is also used to monitor cardiac rate and rhythm; Holter monitoring and other continuous ECG monitoring devices allow assessment of cardiac rate and rhythm on an ambulatory basis. ECG radio telemetry is also often used on hospital wards and ᮢ APPROACH TO CARDIAC DISEASE DIAGNOSIS 7 between ambulances and emergency departments to assess and monitor rhythm disturbances. There are two types of ambulatory ECG recorders: continuous recorders that record all heart beats over 24 or more hours and intermittent recorders that can be attached to the patient or implanted subcutaneously for weeks or months and then activated to provide brief recordings of infrequent events. In addition to analysis of cardiac rhythm, ambulatory ECG recordings can be used to detect ST-wave transients indicative of myocardial ischemia and certain electrophysiologic parameters of diagnostic and prognostic value. The most common use of ambulatory ECG monitoring is the evaluation of symptoms such as syncope, near-syncope, or palpitation for which there is no obvious cause and cardiac rhythm disturbances are suspected. The ECG is an important tool for rapidly assessing metabolic and toxic disorders of the heart. Characteristic changes in the ST-T waves indicate imbalances of potassium and calcium. Drugs such as tricyclic antidepressants have characteristic effects on the QT and QRS intervals at toxic levels. Such observations on the ECG can be life-saving in emergency situations with comatose patients or cardiac arrest victims. Chamber enlargement can be assessed through the characteristic changes of left or right ventricular and atrial enlargement. Occasionally, isolated signs of left atrial enlargement on the ECG may be the only diagnostic clue to mitral stenosis. Evidence of chamber enlargement on the ECG usually signifies an advanced stage of disease with a poorer prognosis than that of patients with the same disease but no discernible enlargement. The ECG is an important tool in managing acute myocardial infarction. In patients with chest pain that is compatible with myocardial ischemia, the characteristic ST-Twave elevations that do not resolve with nitroglycerin (and are unlikely to be the result of an old infarction) become the basis for thrombolytic therapy or primary angioplasty. Rapid resolution of the ECG changes of myocardial infarction after reperfusion therapy has prognostic value and identifies patients with reperfused coronary arteries. Evidence of conduction abnormalities may help explain the mechanism of bradyarrhythmias and the likelihood of the need for a pacemaker. Conduction abnormalities may also aid in determining the cause of heart disease. For example, right bundle branch block and left anterior fascicular block are often seen in Chagas cardiomyopathy, and left-axis deviation occurs in patients with a primum atrial septal defect. A newer form of electrocardiography is the signal-averaged, or high-resolution, ECG. This device markedly accentuates the QRS complex so that low-amplitude afterpotentials, which correlate with a propensity toward ventricular arrhythmias and sudden death, can be detected. The signal-averaged ECG permits a more accurate measurement of QRS duration, which also has prognostic significance of established value in
  26. 26. ᮢ 8 CHAPTER 1 the stratification of risk of developing sustained ventricular arrhythmias in postmyocardial infarction patients, patients with coronary artery disease and unexplained syncope, and patients with nonischemic cardiomyopathy. 2. Echocardiography—Another frequently ordered cardiac diagnostic test, echocardiography is based on the use of ultrasound directed at the heart to create images of cardiac anatomy and display them in real time on a television screen. Two-dimensional echocardiography is usually accomplished by placing an ultrasound transducer in various positions on the anterior chest and obtaining cross-sectional images of the heart and great vessels in a variety of standard planes. In general, two-dimensional echocardiography is excellent for detecting any anatomic abnormality of the heart and great vessels. In addition, because the heart is seen in real time, this modality can assess the function of cardiac chambers and valves throughout the cardiac cycle. Transesophageal echocardiography (TEE) involves the placement of smaller ultrasound probes on a gastroscopic device for placement in the esophagus behind the heart; it produces much higher resolution images of posterior cardiac structures. Transesophageal echocardiography has made it possible to detect left atrial thrombi, small mitral valve vegetations, and thoracic aortic dissection with a high degree of accuracy. The older analog echocardiographic display referred to as M-mode, motion-mode, or time-motion mode, is currently used for its high axial and temporal resolution. It is superior to two-dimensional echocardiography for measuring the size of structures in its axial direction, and its 1/1000-s sampling rate allows for the resolution of complex cardiac motion patterns. Its many disadvantages, including poor lateral resolution and the inability to distinguish whole heart motion from the motion of individual cardiac structures, have relegated it to a supporting role. Doppler ultrasound can be combined with two-dimensional imaging to investigate blood flow in the heart and great vessels. It is based on determining the change in frequency (caused by the movement of blood in the given structure) of the reflected ultrasound compared with the transmitted ultrasound, and converting this difference into flow velocity. Color-flow Doppler echocardiography is most frequently used. In this technique, frequency shifts in each pixel of a selected area of the two-dimensional image are measured and converted into a color, depending on the direction of flow, the velocity, and the presence or absence of turbulence. When these color images are superimposed on the two-dimensional echocardiographic image, a moving color image of blood flow in the heart is created in real time. This is extremely useful for detecting regurgitant blood flow across cardiac valves and any abnormal communications in the heart. Tissue Doppler imaging is similar to color-flow Doppler except that myocardial tissue movement velocity is interrogated. This allows for the quantitation of the rate of tissue contraction and relaxation which is a measure of myocardial performance that can be applied to systole and diastole. Regional differences in myocardial performance can be assessed and used to guide biventricular pacemaker resynchronization therapy. Because color-flow imaging cannot resolve very high velocities, another Doppler mode must be used to quantitate the exact velocity and estimate the pressure gradient of the flow when high velocities are suspected. Continuous wave Doppler, which almost continuously sends and receives ultrasound along a beam that can be aligned through the heart, is extremely accurate at resolving very high velocities such as those encountered with valvular aortic stenosis. The disadvantage of this technique is that the source of the high velocity within the beam cannot always be determined but must be assumed, based on the anatomy through which the beam passes. When there is ambiguity about the source of the high velocity, pulsed wave Doppler is more useful. This technique is range-gated such that specific areas along the beam (sample volumes) can be investigated. One or more sample volumes can be examined and determinations made concerning the exact location of areas of high-velocity flow. Two-dimensional echocardiographic imaging of dynamic left ventricular cross-sectional anatomy and the superimposition of a Doppler color-flow map provide more information than the traditional left ventricular cine-angiogram can. Ventricular wall motion can be interrogated in multiple planes, and left ventricular wall thickening during systole (an important measure of myocardial viability) can be assessed. In addition to demonstrating segmental wall motion abnormalities, echocardiography can estimate left ventricular volumes and ejection fraction. In addition, valvular regurgitation can be assessed at all four valves with the accuracy of the estimated severity equivalent to contrast angiography. Doppler echocardiography has now largely replaced cardiac catheterization for deriving hemodynamics to estimate the severity of valve stenosis. Recorded Doppler velocities across a valve can be converted to pressure gradients by use of the simplified Bernoulli equation (pressure gradient = 4 × velocity2). Cardiac output can be measured by Doppler from the velocity recorded at cardiac anatomic sites of known size visualized on the two-dimensional echocardiographic image. Cardiac output and pressure gradient data can be used to calculate the stenotic valve area with remarkable accuracy. A complete echocardiographic examination including twodimensional and M-mode anatomic and functional visualization, and color, pulsed, and continuous wave Doppler examination of blood flow provides a considerable amount of information about cardiac structure and function. A full discussion of the usefulness of this technique is beyond the scope of this chapter, but individual uses of echocardiography will be discussed in later chapters. Unfortunately, echocardiography is not without its technical difficulties and pitfalls. Like any noninvasive technique,
  27. 27. it is not 100% accurate. Furthermore, it is impossible to obtain high-quality images or Doppler signals in as many as 5% of patients—especially those with emphysema, chest wall deformities, and obesity. Although TEE has made the examination of such patients easier, it does not solve all the problems of echocardiography. Despite these limitations, the technique is so powerful that it has moved out of the noninvasive laboratory and is now frequently being used in the operating room, the clinic, the emergency department, and even the cardiac catheterization laboratory, to help guide procedures without the use of fluoroscopy. 3. Nuclear cardiac imaging—Nuclear cardiac imaging involves the injection of tracer amounts of radioactive elements attached to larger molecules or to the patient’s own blood cells. The tracer-labeled blood is concentrated in certain areas of the heart, and a gamma ray detection camera is used to detect the radioactive emissions and form an image of the deployment of the tracer in the particular area. The single-crystal gamma camera produces planar images of the heart, depending on the relationship of the camera to the body. Multiple-head gamma cameras, which rotate around the patient, can produce single-photon emission computed tomography (SPECT) images, displaying the cardiac anatomy in slices, each about 1-cm thick. A. Myocardial perfusion imaging—The most common tracers used for imaging regional myocardial blood-flow distribution are thallium-201 and the technetium-99mbased agents, such as sestamibi. Thallium-201, a potassium analog that is efficiently extracted from the bloodstream by viable myocardial cells, is concentrated in the myocardium in areas of adequate blood flow and living myocardial cells. Thallium perfusion images show defects (a lower tracer concentration) in areas where blood flow is relatively reduced and in areas of damaged myocardial cells. If the damage is from frank necrosis or scar tissue formation, very little thallium will be taken up; ischemic cells may take up thallium more slowly or incompletely, producing relative defects in the image. Myocardial perfusion problems are separated from nonviable myocardium by the fact that thallium eventually washes out of the myocardial cells and back into the circulation. If a defect detected on initial thallium imaging disappears over a period of 3–24 hours, the area is presumably viable. A persistent defect suggests a myocardial scar. In addition to detecting viable myocardium and assessing the extent of new and old myocardial infarctions, thallium-201 imaging can also be used to detect myocardial ischemia during stress testing (see section on Stress testing below) as well as marked enlargement of the heart or dysfunction. The major problem with thallium imaging is photon attenuation because of chest wall structures, which can give an artifactual appearance of defects in the myocardium. The technetium-99m-based agents take advantage of the shorter half-life of technetium (6 hours; thallium 201’s is 73 ᮢ APPROACH TO CARDIAC DISEASE DIAGNOSIS 9 hours); this allows for use of a larger dose, which results in higher energy emissions and higher quality images. Technetium-99m’s higher energy emissions scatter less and are attenuated less by chest wall structures, reducing the number of artifacts. Because sestamibi undergoes considerably less washout after the initial myocardial uptake than thallium does, the evaluation of perfusion versus tissue damage requires two separate injections. In addition to detecting perfusion deficits, myocardial imaging with the SPECT system allows for a three-dimensional reconstruction of the heart, which can be displayed in any projection on a monitor screen. Such images can be formed at intervals during the cardiac cycle to create an image of the beating heart, which can be used to detect wall motion abnormalities and derive left ventricular volumes and ejection fraction. Matching wall motion abnormalities with perfusion defects provides additional confirmation that the perfusion defects visualized are true and not artifacts of photon attenuation. Also, extensive perfusion defects and wall motion abnormalities should be accompanied by decreases in ejection fraction. B. Radionuclide angiography—Radionuclide angiography is based on visualizing radioactive tracers in the cavities of the heart over time. Radionuclide angiography is usually done with a single gamma camera in a single plane, and only one view of the heart is obtained. The most common technique is to record the amount of radioactivity received by the gamma camera over time. Although volume estimates by radionuclide angiography are not as accurate as those obtained by other methods, the ejection fraction is quite accurate. Wall motion can be assessed in the one plane imaged, but the technique is not as sensitive as other imaging modalities for detecting wall motion abnormalities. 4. Other cardiac imaging A. Chest radiography—Chest radiography is used infrequently now for evaluating cardiac structural abnormalities because of the superiority of echocardiography in this regard. The chest radiograph, however, is a rapid, inexpensive way to assess pulmonary anatomy and is very useful for evaluating pulmonary venous congestion and hypoperfusion or hyperperfusion. In addition, abnormalities of the thoracic skeleton are found in certain cardiac disorders and radiographic corroboration may help with the diagnosis. Detection of intracardiac calcium deposits by the radiograph or fluoroscopy is of some value in finding coronary artery, valvular, or pericardial disease. B. Computed tomographic scanning—Computed tomography (CT) has been applied to cardiac imaging by using ECG gating to account for the motion of the heart. The major application of this technology has been the detection of small amounts of coronary artery calcium as an indicator of atherosclerosis in the coronary arterial tree. With the development of multidetector CT and using intravenous

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