Ebook Manual of cardiac diagnosis Part 1
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Manual of
Cardiac Diagnosis
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Manual of
Cardiac Diagnosis
Editors
Kanu Chatterjee
MBBS
Clinical Professor of Medicine
The Carver College of Medicine
University of Iowa
United States of America
Emeritus Professor of Medicine
University of California, San Francisco
United States of America
®
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®
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© 2014, Jaypee Brothers Medical Publishers
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Manual of Cardiac Diagnosis
First Edition: 2014
ISBN 978-93-5152-194-5
Printed at
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Contributors
Abhimanyu (Manu)
Uberoi MD
Department of Cardiology
The Stanford School of Medicine
Palo Alto, California, USA
Amardeep K Singh MD
Department of Cardiology
University of California
San Francisco, USA
Andrew Boyle MD
Assistant Professor of Medicine
University of California
San Francisco, USA
Brad H Thompson MD
Professor of Medicine
The Carver College of Medicine
University of Iowa, USA
Ellen El Gordon MD
Associate Professor of Medicine
The Carver College of Medicine
University of Iowa, USA
Eric A Osborn MD PhD
Cardiology Division
Beth Israel Deaconess Medical
Center
Harvard Medical School, Boston, MA
Cardiovascular Research Center
Cardiology Division, and Center
for Molecular Imaging Research,
Massachusetts General Hospital
Harvard Medical School, Boston,
MA, USA
Farouc A Jaffer MD PhD
Associate Professor of Medicine
The Carver College of Medicine
University of Iowa, USA
Cardiovascular Research Center
Cardiology Division and Center for
Molecular Imaging Research
Massachusetts General Hospital
Harvard Medical School
Boston, MA, USA
Dipti Gupta MD MPH
Gardar Sigurdsson MD
Byron F Vandenberg MD
Cardiology Division
The Carver College of Medicine
University of Iowa, USA
Donald Brown MD
Associate Professor of Medicine
The Carver College of Medicine
University of California
San Francisco, USA
Professor of Medicine
The Carver College of Medicine
University of Iowa, USA
Isidore C Okere MBBS
Edwin JR van Beek MD
Jagat Narula MD PhD
Professor of Medicine
Chair of Clinical Radiology
Clinical Research Imaging Centre
Queen’s Medical Research Institute
University of Edinburgh, United
Kingdom
The Carver College of Medicine
University of Iowa, USA
Cardiology Division
University of California
Irvine School of Medicine
Irvin, CA
Kanu Chatterjee MBBS
Professor of Medicine and
Radiology
University of California
San Francisco, USA
Professor of Medicine
The Carver College of Medicine
University of Iowa
Emeritus Professor of Medicine
University of California
San Francisco, USA
Elaine M Demetroulis MD
Manjula V Burri MD
Elias H Botvinick MD
Associate Professor of Medicine
The Carver College of Medicine
University of Iowa, USA
Department of Cardiology
The Carver College of Medicine
University of Iowa, USA
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vi
Manual of Cardiac Diagnosis
Mohan Brar MD
Assistant Clinical Professor of
Medicine
The Carver College of Medicine
University of Iowa, USA
Nelson B Schiller MD
Professor of Medicine
University of California
San Francisco, USA
Paul Lindower MD
Professor of Medicine
The Carver College of Medicine
University of Iowa, USA
Peter J Fitzgerald MD
Professor of Medicine
The Stanford University School of
Medicine
Pala Alto, California, USA
Rakesh K Mishra MD
University of California
San Francisco, USA
Richard E Kerber MD
Professor of Medicine
The Carver College of Medicine
University of Iowa, USA
Robert M Weiss MD
Professor of Medicine
The Carver College of Medicine
University of Iowa, USA
Seyed M Hashemi MD
Division of Cardiology
The Carver College of Medicine
University of Iowa, USA
Teresa De Marco MD
Professor of Medicine
University of California
San Francisco, USA
Teruyoshi Kume MD
Stanford School of Medicine
Palo Alto, California, USA
Victor F Froelicher MD
Professor of Medicine
The Stanford University School of
Medicine
Pala Alto, California, USA
Vijay U Rao MD PhD
Department of Cardiology
University of California
San Francisco, USA
Wassef Karrowni MD
Division of Cardiology
The Carver College of Medicine
University of Iowa, USA
William Parmley MD
Emeritus Professor of Medicine
University of California, San
Francisco, USA
Yasuhiro Honda MD
Stanford School of Medicine
Palo Alto, California, USA
Yerem Yeghiazarians MD
Associate Professor of Medicine
University of California, San
Francisco, USA
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Preface
Diagnosis is the first stone, which needs to be turned in
order to discover the cure. Progress in the diagnosis and
management of patients with congenital and acquired
heart diseases has been intimately tied to technological
developments in cardiac imaging.
We have witnessed the development of newer diagnostic
techniques and the refinement of older methods for detection
of cardiovascular pathology. Molecular imaging, threedimensional echocardiography, and intravascular ultrasound
imaging have been introduced. Advances have occurred
in cardiovascular nuclear, computerized tomographic, and
magnetic resonance imaging.
In this book, the advancements in these diagnostic
techniques and their clinical applications in the practice of
cardiology have been extensively discussed. The role of resting
and stress electrocardiography and echocardiography has also
been elaborated upon.
The success of cardiac angiography stimulated the
continued development of selective catheter coronary
arteriography, which is the driving force in the progress and
increased effectiveness of coronary artery bypass surgery,
prosthetic valve replacement, and valve repair.
With contributions from nationally and internationally
recognized experts, an effort has been made to bring forth a
book that will serve as a useful diagnostic manual for students
and practitioners, whole-heartedly involved in the field of
cardiology.
Kanu Chatterjee
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Contents
1.History
Kanu Chatterjee
The History 1
References 17
2.Physical Examination
Kanu Chatterjee
137
Introduction 137
Before the Test 138
Methodology of Exercise Testing 142
During the Test 147
After the Test 160
Screening 166
6. Left Ventricle
Rakesh K Mishra, Nelson B Schiller
96
Introduction 96
Basis of Electrocardiography 96
Component Parts of the Electrocardiogram 100
Lead Systems Used to Record the Electrocardiogram 100
Common Electrode Misplacements 103
Other Lead Systems 107
Identification of Atrial Activity 107
Characterization of QRS Complex 121
ST–T Wave Abnormalities 131
“U” Wave 134
QT Interval 134
5. ECG Exercise Testing
Abhimanyu (Manu) Uberoi, Victor F Froelicher
71
Introduction 71
Chest Film Technique 71
Overview of Cardiomediastinal Anatomy 73
Cardiac Anatomy on Chest Radiographs 75
Cardiac Chamber Enlargement 76
Radiographic Manifestations of Congestive Heart Failure 80
Cardiac Calcifications 86
Acquired Valvular Heart Disease 88
Pericardial Disorders 92
4.Electrocardiogram
Donald Brown
18
General Appearance 18
Measurement of Arterial Pressure 23
Auscultation 40
References 68
3.Plain Film Imaging of Adult Cardiovascular Disease
Brad H Thompson, Edwin JR van Beek
1
177
Introduction 177
Systolic Function 178
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Manual of Cardiac Diagnosis
Contrast-Enhanced Echocardiography 197
Other Echo-Derived Indices of LV Systolic Function 197
Strain-Derived Indices 199
Recognizing the Etiology of Cardiac Dysfunction 199
Dilated Cardiomyopathy 200
Hypertrophic Cardiomyopathy 201
Restrictive Cardiomyopathy 203
Left Ventricular Noncompaction 205
Visual Qualitative Indicators of Systolic Dysfunction 205
Diastolic Function 210
7.Ventricular Function—Assessment and
Clinical Application
Kanu Chatterjee, Wassef Karrowni, William Parmley
Introduction 233
Determinants of Left Ventricular Performance 233
Left Ventricular Pump Function 240
Heart Rate 247
Diastolic Function 249
Right Ventricular Function 251
8.Transthoracic Echocardiography
Byron F Vandenberg, Richard E Kerber
316
Introduction 316
Using Stress Echocardiography in Clinical Decisions 317
Future of Stress Echo 348
10. Transesophageal Echocardiography
Seyed M Hashemi, Paul Lindower, Richard E Kerber
261
Introduction 261
Chamber Quantitation 261
Doppler Echo 271
Diastolic Function 272
Pulmonary Hypertension 277
Pericardial Disease 279
Valvular Heart Disease 285
Infective Endocarditis 303
Intracardiac Masses 304
Contrast Echocardiography 305
Cardiac Resynchronization Therapy 307
9Stress Echocardiography
Ellen El Gordon, Richard E Kerber
233
357
Introduction 357
History 357
Guidelines 358
Performance 358
Safety 359
Views 359
Major Clinical Applications 360
Structural Valve Assessment 366
Acute Aortic Dissection 371
Procedural Adjunct or Intraoperative Transesophageal
Echocardiography (TEE) 372
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Contents
11. Real-time Three-dimensional Echocardiography
Manjula V Burri, Richard E Kerber
377
Introduction 377
Technique 379
Clinical Applications 387
Future Directions 420
Limitations 423
12.Intravascular Coronary Ultrasound and Beyond
Teruyoshi Kume, Yasuhiro Honda, Peter J Fitzgerald
xi
433
Introduction 433
Intravascular Ultrasound 433
Optical Coherence Tomography 464
Angioscopy 475
Spectroscopy 482
13.Cardiovascular Nuclear Medicine—Nuclear Cardiology 497
Elias H Botvinick
Introduction 497
Pathophysiologic Considerations 498
Myocardial Perfusion Imaging 505
Risk Assessment of General and Specific Patient Populations 521
Positron Emission Tomography Perfusion and Metabolism 524
Imaging Myocardial Viability 526
Imaging Perfusion 530
Quantitation of Regional Coronary Flow and Flow Reserve 532
Blood Pool Imaging—Equilibrium Radionuclide Angiography
and First Pass Radionuclide Angiography 533
First Pass Curve Analysis 535
Equilibrium Gated Imaging—Erna 538
The Value of Functional Imaging 540
Phase Analysis 545
Imaging Myocardial Sympathetic Innervation 545
Radiation Concerns 547
14. Cardiac Computed Tomography
Isidore C Okere, Gardar Sigurdsson
Introduction 557
Technical Aspects 558
Coronary Artery Disease 569
Myocardium and Chambers 575
Pulmonary Veins 578
Cardiac Veins 580
Valvular Disease 580
Pericardium 582
Masses 584
Incidental Findings 587
Future 588
15.Cardiovascular Magnetic Resonance
Robert M Weiss
557
602
Introduction 602
Diagnosis of Epicardial Coronary Artery Stenosis 603
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Assessment of Global and Regional Left Ventricular Function at
Rest and During Inotropic Stress 604
Myocardial Perfusion Imaging 605
Cardiovascular Magnetic Resonance Coronary Angiography 606
Unrecognized Myocardial Infarction 607
Dilated Cardiomyopathy 607
Hypertrophic Cardiomyopathy 612
Restrictive Cardiomyopathy 616
Cardiovascular Magnetic Resonance-Guided Therapy 618
Valvular Heart Disease 618
Diseases With Right Ventricular Predominance 620
Miscellaneous Conditions 624
16.Molecular Imaging of Vascular Disease
Eric A Osborn, Jagat Narula, Farouc A Jaffer
Introduction 637
Molecular Imaging Fundamentals 637
Molecular Imaging Modalities 643
Molecular Imaging of Vascular Disease Processes 646
17Cardiac Hemodynamics and Coronary Physiology
Amardeep K Singh, Andrew Boyle, Yerem Yeghiazarians
709
Introduction 709
History and Devices 709
Techniques 711
Safety and Complications 713
Analysis of EMB Tissue 714
Indications 716
Disease States 724
Cardiac Transplantation 737
19Swan-Ganz Catheters: Clinical Applications
Dipti Gupta, Wassef Karrowni, Kanu Chatterjee
676
Introduction 676
Cardiac Catheterization—The Basics 676
Catheterization Computations 680
Cardiac Cycle Pressure Waveforms 684
Hemodynamics In Valvular Heart Disease 686
Hemodynamics In Cardiomyopathy 695
Hemodynamics In Pericardial Disease 700
Coronary Hemodynamics 703
References 707
18. Cardiac Biopsy
Vijay U Rao, Teresa De Marco
637
750
Introduction 750
Historical Perspective and Evolution of Catheter Designs 750
Placement of Balloon Flotation Catheters 751
Normal Pressures and Waveforms 754
Abnormal Pressures and Waveforms 758
Clinical Applications 759
Indications for Pulmonary Artery Catheterization 768
Complications 769
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Contents
xiii
20.Coronary Angiography and Catheter-based Coronary
Intervention776
Elaine M Demetroulis, Mohan Brar
Introduction 777
Indications for Coronary Angiography 778
Contraindications for Coronary Angiography 780
Patient Preparation 781
Sites and Techniques of Vascular Access 782
Catheters for Coronary Angiography 786
Catheters for Bypass Grafts 788
Arterial Nomenclature and Extent Of Disease 790
Angiographic Projections 792
Normal Coronary Anatomy 793
Congenital Anomalies of the Coronary Circulation 801
General Principles for Coronary and/or Graft Cannulation 806
The Fluoroscopic Imaging System 814
Characteristics of Contrast Media 816
Contrast-Induced Renal Failure 817
Access Site Hemostasis 819
Complications of Cardiac Catheterization 821
Lesion Quantification 824
Degenerated Saphenous Vein Grafts 828
Lesion Calcification 828
Physiologic Assessment of Angiographically Indeterminate
Coronary Lesions 829
Clinical Use of Translesional Physiologic Measurements 830
Non-Atherosclerotic Coronary Artery Disease and Transplant
Vasculopathy 831
Potential Errors In Interpretation of the Coronary
Angiogram 834
Percutaneous Coronary Intervention 838
Pharmacotherapy for PCI 839
Parenteral Anticoagulant Therapy 846
Equipment for Coronary Interventions 848
Percutaneous Transluminal Coronary Angioplasty 851
Coronary Stents 852
Types of Stents 852
Stent Deployment 853
Adjunctive Coronary Interventional Devices 854
Embolic Protection Devices for Venous Bypass Graft PCI 856
Clinical Outcomes 857
Procedural Success and Complications Related to Coronary
Intervention 862
Complications Specific to PCI 862
Index881
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CHAPTER
History
1
Kanu Chatterjee
Chapter Outline
• The History
–– General Approach
–– Analysis of Symptoms
The history and physical examination are essential, not only
for the diagnosis of cardiovascular disorders but also to assess
its severity to establish a plan of its management and to assess
the prognosis. Appropriate history and physical examination are
also essential to decide what tests are necessary for a patient as
presently a plethora of tests is available for the diagnosis and
management of the same cardiac disorder. For example, for the
diagnosis of the etiology of chest pain due to coronary artery
disease, one can perform many noninvasive, semiinvasive and
invasive tests to establish or exclude the presence of obstructive
coronary artery disease. It should also be appreciated that “history
and physical examination” are cost-effective. Many tests that
are frequently performed today are unnecessary and are much
more expensive. During examination of the patient, the physician
can gain the confidence of the patient and of the family and can
establish a good rapport that is necessary for the appropriate
management of the problem of the patient. During examination,
the physician has the opportunity to demonstrate sincerity, which
facilitates to gain trust of the patient and the family.
In today’s electronic age, the patients and their relatives
are often more familiar than the physicians about the recent
developments in the diagnostic techniques and therapies. It
is thus preferable (but sometimes impossible) to have this
knowledge before examining the patient. In today’s health care
environment, there are severe constraints on time available
for taking appropriate history and to do adequate physical
examination.1 Frequently, the physicians have to order the
“tests” because of time constraints even before examining
the patient. Furthermore, there is a growing concern about
malpractice suits and the medical and paramedical personnels
are frequently forced to perform the investigations, which are
otherwise would not have been necessary.
THE HISTORY
General Approach
During taking history, it is desirable to allow the patient to present
the symptoms without interruption. Frequent interruptions give
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Manual of Cardiac Diagnosis
the impression that the physician is in hurry and impatient and
disinterested. While taking history, the physician can observe
the manner in which the patient describes the symptoms and
the patient’s emotional state and mood.
After the patient describes the symptoms, it is appropriate
to discuss with the patient and the family to ascertain the
chronology of symptoms and their severity. The patient
may present with many symptoms. It is pertinent to inquire
about each symptom. The major symptoms associated with
cardiovascular disorders are chest pain or discomfort, dyspnea,
palpitations, dizziness, and syncope.
Analysis of Symptoms
Chest Pain or Discomfort
Chest pain is one of the very common presenting symptoms that
patients present to the cardiologists for their expert views for
the diagnosis of its etiology and management. The chest pain
or discomfort can be caused by various cardiac and noncardiac
causes that are summarized in Tables 1 to 4.
“Cardiac pain” may be due to myocardial ischemia or it
can be nonischemic in origin. The cardiac pain resulting from
myocardial ischemia is called “Angina pectoris”. The precise
mechanism of cardiac pain due to myocardial ischemia has not
been elucidated. It has been postulated that small nonmedullated
sympathetic nerve fibers, which are present in the epicardium
along the coronary arteries, serve as the afferent pathways for
angina pectoris. The afferent impulses enter the spinal cord in C8
TABLE 1
Cardiac chest pain
•
•
•
•
•
•
•
Coronary artery disease
cute coronary syndromes
A
Stable angina
Ischemic cardiomyopathy
Noncoronary artery disease
Aortic dissection
Acute pulmonary embolism
TABLE 2
Noncardiac chest pain (pulmonary)
•
•
•
•
•
•
leuritis
P
Pneumonia
Tracheobronchitis
Pneumothorax
Mediastinitis
Tumor
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History
3
TABLE 3
Cardiac causes of chest discomfort
•
•
•
•
•
ortic stenosis
A
Aortic regurgitations
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Pulmonary hypertension
TABLE 4
Noncardiac chest pain
Musculoskeletal
• Costochondritis
• Intercostal muscle cramps
• Cervical disk disease
Other causes
• Herpes zoster
• Emotional
• Chest wall tumor
• Disorders of breast
to T4 segments and are transmitted to the sympathetic ganglia of
the same segments. The impulses then travel by spinothalamic
tract to the thalamus. The pain perception requires activation
of the specific cortical centers.
Angina pectoris is a symptom of both of chronic coronary
artery disease and of acute coronary syndromes. For the
diagnosis of angina pectoris, it is imperative to inquire about the
character, location, site of radiation, duration, and precipitating
and relieving factors of the chest discomfort.
The character of the discomfort is usually not severe pain.
More frequently, it is described as “heaviness”, “pressure”,
“tightness”, “squeezing” or “band across the chest”. Sometimes
the patients have difficulty describing precisely the character
of the chest discomfort. The character of angina pectoris is
usually “dull and deep” and not “sharp and superficial”. The
“elephant sitting on the chest” is a typical textbook description,
and frequently a knowledgeable patient uses this phrase to
describe the character of the chest discomfort. However, such
description is rather infrequently associated with coronary artery
disease.
The location of the chest discomfort can be retrosternal,
epigastric or left pectoral. It is infrequently located in the left
axilla. Occasionally, the initial location of angina can be left
arm and hands, interscapular or left infrascapular area. When the
character of pain is stabbing and pleuritic, and it is positional or
reproducible with palpation, it is unlikely to be angina and the
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Manual of Cardiac Diagnosis
likelihood ratio is 0.2:0.3.2 When chest pain is much localized
and can be indicated by one or two finger tips, it is unlikely
to be angina pectoris.
The radiation of angina pain may be to one or both shoulders,
one or both arms and hands, one or both sides of the neck,
lower jaw and interscapular area. The radiation can also occur
to armpits, epigastrium, and subcostal areas. The radiation is
usually from the center to the periphery (centripetal) and rarely
from the periphery to center (centrifugal). The radiation to one
or both shoulders is associated with the likelihood ratios of
2.3:4.7.2
Patient’s gestures during describing the chest discomfort
have been thought to be useful in the diagnosis of its etiology.
The prevalences, specificities, and positive predictive values of
the Levine sign, the palm sign, the arm sign and the pointing
sign (Figs 1A to D) have been assessed in a prospective obser
vational study.3 The prevalence of the Levine, palm, arm and
pointing signs was 11%, 35%, 16% and 4%, respectively. The
specificities of Levine sign and arm sign were 78% and 86%,
respectively, but the positive predictive values were only 50%
and 55%, respectively. The pointing sign had a specificity of
98% for nonischemic chest discomfort.
The intensity of angina increases slowly and reaches its
peak in minutes, not instantaneously. Similarly, it is relieved
gradually, not abruptly. Analysis of the duration of chest
discomfort is also helpful to decide whether it is ischemic or
FIGURES 1A TO D: Illustrations of (A) the Levine aign, (B) the palm
sign, (C) the arm sign, (D) the pointing sign [Source: Marcus GM, et
al. Am J Med. 2007;120:83-9 (Ref 3)]
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History
5
FIGURE 2: Description of effort angina by Sir William Heberden in
1768 (Ref 4)
nonischemic pain. When the duration is extremely short, only
1–2 seconds, it cannot be angina pectoris. Similarly, if the chest
pain lasts continuously without remission for several hours and
without evidence for myocardial necrosis, it is unlikely to be
angina.
The precipitating and relieving factors of the chest
discomfort should be analyzed to determine its etiology. The
classic angina (Heberden’s angina) is precipitated by exercise
or by emotional stress and is relieved when the exercise is
discontinued. It tends to occur often after meals. The original
description of classic angina pectoris by William Heberden is
shown in Figure 2.4
The effort angina is also relieved by sublingual nitroglycerin.
The time for relief after using nitroglycerin sublingually is
not instantaneous. It takes a few seconds (usually 30 seconds
or longer). It should be appreciated that chest pain due to
esophageal spasm is also relieved by nitroglycerin.
Exposure to cold weather precipitates angina more easily in
patients with classic angina. Similarly, carrying heavy objects
and heavy meals are also frequent precipitating factors. The
character, location and radiation of chest discomfort are similar
in the different clinical subsets of angina. However, some
distinctive features can be recognized in various subsets.
In patients with vasospastic angina, angina occurs at rest
and usually not during exercise. The duration is variable. It
tends to have cyclic phenomenon, and in the individual patient,
it tends to occur more or less at the same time.
In patients with acute coronary syndromes, the duration is
usually longer. In patients with ST segment elevation myocardial
infarction (STEMI), the relief of chest pain may not occur until
reperfusion therapy is established.
The atypical presentations frequently called “anginal
equivalents” are dyspnea, indigestion and belching, and
dizziness and syncope without chest pain. The atypical
presentations are more common in diabetics, women, and the
elderly. A few clinical features of angina are summarized in
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Manual of Cardiac Diagnosis
Tables 5 and 6. The chest pain due to acute pericarditis, acute
pulmonary embolism, or acute aortic dissection may be similar
to that of acute coronary syndromes.
The pericardial pain is usually superficial and sharp and
may have a pleuritic quality. It can radiate to both shoulders
and infraspinatus areas. Generally, pericardial pain is worse in
supine position and less severe in sitting and leaning forward
position. Occasionally pericardial pain waxes and wanes with
cardiac systole and diastole.
The location of pain of acute pulmonary embolism can be
retrosternal and may not have a pleuritic quality. It is frequently
associated with tachypnea.
The chest pain resulting from acute aortic dissection is
usually severe. The location can be anterior chest. Radiation to
the back is common. The downward radiation along the spine
is very suggestive of aortic dissection. The onset of pain is
frequently instantaneous and the maximal severity may occur
at the onset. The character of the pain is “shearing or tearing”.
A few clinical features of pain of acute pericarditis, pulmonary
embolism, and acute aortic dissection are summarized in
Table 7.
The severity of angina is assessed by the Canadian Cardio
vascular Society (CCS) functional classification5 (Table 8)
TABLE 5
Clinical features of stable angina
Location
• Usually retrosternal, can be epigastric, interscapular
Localization
• Usually diffuse, difficult to localize
• When is very localized (point sign)—unlikely to be angina
Quality
• Pressure, heaviness, squeezing, indigestion
Radiation
• One or both arms, upper back, neck, epigastrium, shoulder
• Lower jaw (upper jaw, head, lower back, lower abdomen or lower
extremities radiation is not feature of angina )
Duration
• Usually 1–10 minutes (not a few seconds or hours)
Precipitating factors
• Physical activity, emotional stress, sexual intercourse
Aggravating factors
• Cold weather, heavy meals
Relieving factors
• Cessation of activity, nitroglycerin (if relief is instantaneous, it is
unlikely to be angina)
Associated symptoms
• Usually none, occasionally dyspnea
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History
7
TABLE 6
Clinical features of chest pain in acute coronary syndromes
Location
• Same as stable angina
Quality
• Same as stable angina
Duration
• Usually longer than stable angina
Relieving factors
• Usually unrelieved by rest or nitroglycerin
Associated symptoms
• Dyspnea, sweating, weakness, nausea, vomiting presyncope, or
syncope
TABLE 7
Clinical features of chest pain due to acute pericarditis, acute
pulmonary embolism, and acute aortic dissection
Acute pericarditis
Location
• Anterior chest, superficial
Character
• Sharp, can be pleuritic
Radiation
• Supraspinatus areas, shoulders, back
Relieving factors
• Worse in supine position, less severe in sitting and leaning forward position, relieved by analgesics, nonsteroidals and steroids
Acute pulmonary embolism
Location
• Usually retrosternal
Quality
• Deep, may be similar to acute coronary syndromes
Associated symptoms
• Tachypnea and dyspnea
Acute aortic dissection
Location
• Chest, back
Quality
• Shearing, tearing
Onset
• Instantaneous
Radiation
• Downwards along the spine
or Specific Activity Scale6 (Table 9). The CCS functional
classification is most frequently used to assess the severity of
angina and has been proven to be useful to assess its prognosis.7
The Specific Activity Scale, which is a more quantitative assess
ment of the severity of angina, is not used in the clinical trials.
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Manual of Cardiac Diagnosis
TABLE 8
Canadian Cardiovascular Society (CCS) functional classification
Class I
• O
rdinary physical activity, such as walking and climbing stairs, does
not cause angina
• A
ngina with strenuous or rapid or prolonged exertion at work or
recreation
Class II
• S
light limitation of ordinary activity. Walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in cold, in
wind or when under emotional stress, or only during the few hours
after awakening
• W
alking more than two blocks on the level, and climbing more than
one flight of ordinary stairs at a normal pace and in normal conditions
Class III
• Marked limitation of ordinary physical activity
• W
alking 1–2 blocks on the level and climbing more than one flight
in normal conditions
Class IV
• Inability to carry out any physical activity without discomfort—anginal
syndrome may be present at rest
TABLE 9
Specific activity scale
Class I
• Patients can perform to completion any activity requiring <7 metabolic equivalents [e.g. can carry 24 lbs up eight steps; carry objects
that weigh 80 lbs, do outdoor work (shovel snow, spade soil); do
recreational activities (skiing, basketball, squash, handball, jog/
walk 5 mph)]
Class II
• Patients can perform to completion any activity requiring <5 metabolic equivalents (e.g. have sexual intercourse without stopping,
garden, rake, weed, roller skate, dance fox trot, walk 4 mph on
level ground), but cannot and do not perform to completion activities
requiring >7 metabolic equivalents
Class III
• Patients can perform to completion any activity requiring >2 metabolic equivalents (e.g. shower without stopping, strip and make
bed, clean windows, walk 2.5 mph, bowl, play golf, dress without
stopping), but cannot and do not perform to completion any activities
requiring >5 metabolic equivalents
Class IV
• Patients cannot or do not perform to completion activities requiring
>2 metabolic equivalents. Cannot carry out activities listed above
(Specific Activity Scale Class III)
In patients with suspected or documented coronary artery
disease, inquiries should be made about the risk factors.
The modifiable and nonmodifiable risk factors for atherosclerotic
coronary artery diseases are summarized in Table 10.
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History
9
TABLE 10
Cardiac and pulmonary causes of dyspnea: Differential diagnosis
of dyspnea
Cardiac
Pulmonary
CHF
COPD
CAD
Asthma
Cardiomyopathy
Restrictive lung diseases
Valvular dysfunction
Hereditary lung diseases
LVH
Pneumothorax
Pericardial diseases
Arrhythmias
Congenital HD
(Abbreviations: CHF: Congestive heart disease; HD: Heart disease;
CAD: Coronary heart disease; LVH: Left ventricular hypertrophy
Smoking, hypertension, diabetes, obesity, metabolic
syndrome, hyperlipidemia, and physical inactivity are risk
factors for coronary artery disease. History of peripheral vascular
and cerebrovascular disease and stroke is also associated with
a higher risk of coronary artery disease. These risk factors are
modifiable.
Older age, male gender, and family history of atherosclerotic
cardiovascular disease are also risk factors for coronary artery
disease, but these risk factors are not modifiable.
Dyspnea
Dyspnea is an uncomfortable sensation of breathing. It is also
defined as “labored” breathing. The precise mechanism of dyspnea
has not been established. It has been suggested that activation of
the mechanoreceptors in the lungs, pulmonary artery and heart
and activation of the chemoreceptors are involved in inducing
dyspnea. Dyspnea can occur during exertion (exertional), during
recumbency (orthopnea), or even with standing (platypnea).
There are both cardiac and noncardiac (Table 10) causes of
dyspnea. Pulmonary disease, such as chronic obstructive lung
disease, is one of the common noncardiac causes of dyspnea.
Many patients have both cardiac and pulmonary disease. It
is not uncommon in clinical practice to encounter patients
who have coronary artery disease and chronic obstructive
pulmonary disease. In such patients, to determine the cause
of dyspnea, appropriate history and physical examination
are essential. To distinguish between cardiac and noncardiac
dyspnea, the measurements of serum B-type Natriuretic
Peptide (BNP) or N-Terminal ProBNP (NTBNP) is helpful. In
noncardiac dyspnea, the natriuretic peptide levels are normal,
and in patients with heart failure, they are substantially
elevated.
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Exertional dyspnea can be caused by both cardiac and
nonc ardiac causes. Exertional dyspnea is an important
symptom of chronic heart failure. However, it is also a
symptom of chronic pulmonary diseases and of metabolic
disorders, such as obesity and hyperthyroidism. Dyspnea is
also a common symptom of anxiety disorders. Cardiac dyspnea
gets worse with physical activity. Dyspnea of functional origin
frequently improves after exercise.
Orthopnea is defined when patients develop dyspnea lying
flat and feel better when the upper part of the torso is elevated.
Although orthopnea is a symptom of heart failure, it also occurs
in patients with pulmonary disease, such as emphysema and
chronic obstructive pulmonary disease.
Paroxysmal nocturnal dyspnea is virtually diagnostic of
cardiac cause. After being in the recumbent position for about
15 minutes to 2 hours, the patient develops shortness of breath
and has to sit or stand up to get relief. The hemodynamic
mechanism is that after assuming the recumbent position, there
is an increase in the intravascular and intracardiac volumes,
which is associated with an increase in pulmonary venous
pressure and transient hemodynamic pulmonary edema. The
sitting and/or upright position is associated with a reduction of
intravascular and intracardiac volumes due to decreased venous
return and reduction of pulmonary venous pressure and relief
of dyspnea. Left ventricular systolic and diastolic heart failure
and aortic and mitral valve diseases are the common causes of
paroxysmal nocturnal dyspnea.
Sleep-disordered breathing, which may be associated with
dyspnea, can occur in cardiac patients. Cheyne–Stokes respiration
is a specific type of periodic breathing that is characterized by
alternating periods of apnea and hyperpnea. During hyperpneic
phases, there is a progressive decrease in PCO2 with increased
pH, which inhibits the respiratory drive; during apneic phase,
CO2 accumulates with an increase in respiratory acidosis, and
the respiratory center is stimulated and breathing is initiated.
It appears that chemoreceptors-mediated stimulation of the
respiratory centers is blunted in patients with Cheyne–Stokes
respiration. Patients feel shortness of breath during the hyperpneic
phase. Central, obstructive, and mixed types of sleep apnea are
observed in patients with heart failure. The hemodynamic causes
of sleep-disordered breathing in heart failure have not been
clearly elucidated. Initially, the Cheyne–Stokes respiration was
thought to be due to low cardiac output;8 however, there does
not appear to be a good correlation between any hemodynamic
changes of systolic heart failure and Cheyne–Stokes respiration.
History of sleep-disordered breathing should be inquired, as it is
associated with worsening heart failure, pulmonary hypertension,
and increased risks of arrhythmias, and sudden cardiac death.
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History
11
Wheezing due to constriction of the bronchial smooth
muscles associated with dyspnea does not always imply
pulmonary diseases. It may be caused by hemodynamic
pulmonary edema in patients with systolic and diastolic heart
failure and valvular heart diseases (cardiac asthma).
There are many cardiac conditions, which can be associated
with episodic severe dyspnea. In between the episodes of
dyspnea, these patients are relatively asymptomatic and may
have good exercise tolerance. In patients with episodic dyspnea,
intermittent severe mitral regurgitation due to papillary muscle
dysfunction should be considered in the differential diagnosis.
Intermittent mitral valve obstruction due to left atrial myxoma
or ball valve thrombus is a rare cause of this syndrome. In
patients with left atrial myxoma, dyspnea may be positional
and may be associated with syncope. Another cause of episodic
severe dyspnea is “stiff heart syndrome”.9 These patients usually
have normal left ventricular ejection fraction and have history
of hypertension and coronary artery disease (diastolic heart
failure). Fluid retention, either from the increased salt intake
or from the lack of use of the diuretics, precedes the onset of
dyspnea.
Atrial or ventricular tachyarrhythmias usually do not produce
episodic severe dyspnea in absence of valvular or myocardial
disease. However, it can occur in patients with left ventricular
dysfunction and in patients with mild-to-moderate mitral
stenosis.
In patients with massive or submassive pulmonary
embolism, tachypnea and dyspnea are common presenting
symptoms. There may be associated chest pain and wheezing.
Patients with pulmonary embolism prefer the supine position
as opposed to patients with hemodynamic pulmonary edema
who prefer the upright position. Arterial desaturation may be
present in both conditions. A plain chest X-ray may be useful
to establish the diagnosis. In patients with pulmonary embolism,
the chest X-ray is clear and does not demonstrate radiologic
evidences of pulmonary venous hypertension. In patients with
hemodynamic pulmonary edema, prominent upper lobe vessels,
perihilar haziness, and Kerley lines and frank pulmonary edema
may be present (Fig. 3).
A careful cardiovascular examination may also reveal the
etiology of dyspnea. For example, evidence of valvular and
myocardial heart diseases suggests cardiac cause of dyspnea
(Table 11). The presence of S3 gallop usually indicates increased
left ventricular diastolic pressures except in young people and
patients with chronic primary mitral regurgitation. In patients
with heart failure, presence of S3 is also associated with the
increased levels of B-type natriuretic peptides. The presence
of characteristic physical findings of significant valvular heart
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FIGURE 3: A plain chest X-ray of a patient with acute severe mitral
regurgitation showing florid hemodynamic pulmonary edema
TABLE 11
Diagnosis of causes of cardiac dyspnea
Dyspnea
Cardiac or noncardiac dyspnea
Physical examination:
Signs of heart failure—diagnostic of cardiac cause, e.g. S3,
elevated JVP, positive HJR
Presence of cardiac pathology:
Very suggestive of cardiac cause
Chest X-ray:
Very helpful when findings of pulmonary venous congestion
or pulmonary hypertension are present
ECG:
Normal electrocardiogram
A negative predictive value has over 90%
(Abbreviations: JVP: Jugular venous pressure; HJR: Hepatojugular
refulx
disease also suggests cardiac dyspnea. The absence of these
signs, however, does not exclude cardiac dyspnea.
Palpitation
Palpitation is perceived as an uncomfortable sensation in the
chest associated with heartbeats. The most frequent cause of
palpitation is premature atrial or ventricular contractions. The
premature beat itself is not felt; the normal beat following the
compensatory pause is felt as a strong beat. The patients usually
describe this uncomfortable sensation as “a thump”, “skipped
beat”, “the heart is coming out of chest”, “heart stops” and
“heart stops beating”.
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