The History and Physical Examination
The history and physical examination should allow the clinician to establish the previous probability of
heart disease, that is, the likelihood that the symptoms reported by the
patient result from heart disease. A reasonable goal is to establish the risk
of heart disease in a patient as “low,” “intermediate,” or “high.” One
demonstration of this principle in clinical medicine is the assessment of
patients with chest pain, in which exercise stress testing to accurately
diagnose coronary heart disease (CHD) depends on the previous probability of
disease. In patients with a low risk of CHD based on clinical findings,
exercise stress testing results in a large number of false-positive test
results. Because up to 15% of exercise stress tests produce positive results in
individuals without CHD, use of this test in a low-risk population can result
in an adverse ratio of false-positive to true-positive test results and
unnecessary cardiac catheterizations. Conversely, in patients with a high risk
of CHD based on clinical findings, exercise stress testing can result in
false-negative test results, which is an equally undesirable outcome, because
patients with significant coronary artery disease (CAD) and their physicians
may be falsely reassured that no further evaluation or treatment is necessary.
Emphasis is increasing on quantifying previous probability to an even
greater degree with various mathematical models. This is a useful approach in
teaching and may be clinically feasible in some diseases. However, for most
patients with suspected heart disease, categorizing risk as low, intermediate,
and high is appropriate, reproducible, and feasible in a busy clinical
practice. Therefore obtaining the history and physical examination represents a
key step before any testing, to minimize use of inappropriate diagnostic
procedures.
A wealth of information is available to clinicians who carefully assess
the history of the patient. Key components are assessment of the chief
complaint; careful questioning for related, often subtle symptoms that may
further define the chief complaint; and determination of other factors that
help categorize the likelihood of disease. Major symptoms of heart patients
include chest discomfort, dyspnea, palpitations, and syncope or presyncope.
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| FIG 2.1 Pain of myocardial ischemia. |
Determining whether chest discomfort results from a cardiac cause is
often a challenge. The most common cause of chest discomfort is myocardial
ischemia, which produces angina pectoris. Many causes of angina exist, and the
differential diagnosis for chest discomfort is extensive (Box 2.1). Angina that
is reproducible and constant in frequency and severity is often referred to as
stable angina. For the purposes of this chapter, stable angina is a
condition that occurs when CAD is present, and coronary blood flow cannot be
increased to accommodate for increased myocardial demand. However, as discussed
in Chapters 12 through 14, there are many causes of myocardial ischemia,
including fixed coronary artery stenoses and endothelial dysfunction, which lead
to reduced vasodilatory capacity.
A description of chest discomfort can help establish whether the pain is
angina or of another origin. First, characterization of the quality and
location of the discomfort is essential (Fig. 2.1). Chest discomfort because of
myocardial ischemia may be described as pain, a tightness, a heaviness, or
simply an uncomfortable and difficult-to-describe feeling. The discomfort can
be localized to the midchest or epigastric area, or may be characterized as
pain in related areas, including the left arm, both arms, the jaw, or the back.
The radiation of chest discomfort to any of these areas increases the
likelihood of the discomfort being angina. Second, the duration of discomfort
is important because chest discomfort due to cardiac causes generally lasts
minutes. Therefore pain of short duration (“seconds” or “moments”), regardless
of how typical it may be of angina, is less likely to be of cardiac origin.
Likewise, pain that lasts for hours, on many occasions, in the absence of objective
evidence of myocardial infarction (MI), is not likely to be of coronary origin.
Third, the presence of accompanying symptoms should be considered. Chest
discomfort may be accompanied by other symptoms (including dyspnea,
diaphoresis, or nausea), any of which increase the likelihood that the pain is
cardiac in origin. However, the presence of accompanying symptoms is not needed
to define the discomfort as angina. Fourth, factors that precipitate or relieve
the discomfort should be evaluated. Angina typically occurs during physical
exertion, during emotional stress, or
in other circumstances of increased myocardial oxygen demand. When exercise precipitates
chest discomfort, relief after cessation of exercise substantiates the
diagnosis of angina. Sublingual nitroglycerin also relieves angina, generally
over a period of minutes. Instant relief or relief after longer periods lessens
the likelihood that the chest discomfort was angina.
Although the presence of symptoms during exertion is important in assessing
CHD risk, individuals, especially sedentary ones, may have angina-like symptoms
that are not related to exertion. These include postprandial and nocturnal
angina, or angina that occurs while the individual is at rest. As described
herein, “rest-induced angina,” or the new onset of angina, connotes a
pathophysiology different from effortinduced angina. Angina can also occur in
persons with fixed CAD and increased
myocardial oxygen demand due to anemia, hyperthyroidism,bor similar conditions (Box
2.2). Angina occurring at rest, or with minimal exertion, may denote a
different pathophysiology, one that involves platelet aggregation, which is
clinically termed “unstable angina” or “acute coronary syndrome” (see Chapters
20 and 21).
Patients with heart disease need not present with chest pain at all.
Anginal equivalents include dyspnea during exertion, abdominal dis- comfort,
fatigue, or decreased exercise tolerance. Clinicians must be alert to and
specifically ask about these symptoms. Often, a patient’s family member or
spouse notices subtle changes in the endurance of the patient or that the
individual no longer performs functions that require substantial physical
effort. Sometimes, patients may be unable to exert themselves due to
comorbidities. For instance, the symptoms of myocardial ischemia may be absent
in patients with severe peripheral vascular disease who have limiting
claudication. One should also be attuned to subtle or absent symptoms in
individuals with diabetes mellitus (including type 1 and type 2 diabetes),
which is a coronary risk equivalent as defined by the Framingham Risk
Calculator.
When the likelihood that CHD accounts for a patient presenting with chest
discomfort or any of the aforementioned variants is considered, assessment of
the cardiac risk factor profile is important. The Framingham Study first
codified the concept of cardiac risk factors, and over time, quantification of
risk using these factors has become an increasingly useful tool in clinical
medicine. Cardiac risk factors deter- mined by the Framingham Study include a
history of cigarette smoking, diabetes mellitus, hypertension, or
hypercholesterolemia; a family history of CHD (including MI, sudden cardiac
death, and first-degree relatives having undergone coronary revascularization);
age; and sex (male). Although an attempt has been made to rank these risk
factors, all are important, with a history of diabetes mellitus being perhaps
the single most important factor. Subsequently, a much longer list of potential
predictors of cardiac risk has been made (Box 2.3). Multiple risk calculators
have since been created, such as the atherosclerotic cardiovascular disease
algorithm used by the American College of Cardiology, the American Heart
Association cholesterol guidelines, and the Multi-Ethnic Study of
Atherosclerosis (MESA), which uses classic risk factors with the addition of a
coronary artery calcium score to predict a 10-year risk of CHD.
Symptoms suggestive of vascular disease require special attention.
Peripheral vascular disease may mask CHD because the individual may not be able
to exercise sufficiently to provoke angina. A history of stroke, transient
ischemic attack, or atheroembolism in any vascular distribution is usually
evidence of significant vascular disease. Sexual dysfunction in men is not an
uncommon presentation of peripheral vascular disease. The presence of
Raynaud-type symptoms should also be elicited because such symptoms suggest
abnormal vascular tone and function, and increase
the risk that CHD is present.
Determining whether the patient has stable or unstable angina is as important as making the diagnosis of
angina. Stable angina is important to evaluate and treat but does not
necessitate emergent intervention. However, unstable angina or acute coronary
syndrome carries a significant risk of MI or death in the immediate future. The
types of symptoms reported by patients with stable and unstable angina differ
little, and the risk factors for both are identical. The severity of symptoms
is not necessarily greater in patients with unstable angina, just as a lack of
chest discomfort does not rule out significant CHD. The important distinction
between stable and unstable coronary syndromes is whether the onset is new or
recent, and/or progressive (e.g., occurring more
frequently or with less exertion). The initial presentation of angina is, by definition, unstable angina,
although for a high percentage of individuals this may merely represent the
first recognizable episode of angina. For those with unstable angina, the risk
of MI in the near future is markedly increased. Likewise, when the patient
experiences angina in response to decreased levels of exertion or when
exertional angina has begun to occur at rest, these urgent circumstances require
immediate therapy. The treatment of stable angina and acute coronary syndrome
is discussed in Chapters 19 to 21.
The Canadian Cardiovascular Society Functional Classification of Angina
Pectoris is a useful guide for everyday patient assessment (Box 2.4).
Categorizing patients according to their class of symptoms is rapid and precise
and can be used in follow-up. Class IV describes the typical patient with acute
coronary syndrome.
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| FIG 2.2 Physical examination. CHF, Congestive heart failure. |
Finally, it is important to distinguish those patients who have noncoronary
causes of chest discomfort from those with CHD. Patients with gastroesophageal
reflux disease (GERD) often present with symptoms that are impossible to
distinguish from angina. In numerous studies, GERD was the most common
diagnosis in patients who underwent diagnostic testing for angina and were
found not to have CHD. The characteristics of the pain can be identical.
Because exercise can increase intraabdominal pressure, GERD may be exacerbated
with exercise, especially after meals. Symptoms from GERD can also be relieved
with use of sublingual nitroglycerin. GERD can also result in early morning
awakening (as can unstable angina) but tends to awaken individuals 2 to 4 hours
after going to sleep, rather than 1 to 2 hours before arising, as is the case
with unstable angina. Other causes (see Box 2.1) of angina like pain can be
benign or suggestive of other high-risk syndromes, such as aortic dissection or
pulmonary embolus. Many of these “coronary mimics” can be ruled out by patient
history, but others, such as valvular aortic stenosis, can be confirmed or
excluded by physical examination.
The goal of taking the history is to alert the clinician to entities that
can be confirmed or excluded by physical examination or that necessitate
further diagnostic testing.
Dyspnea can accompany angina pectoris or it can be an angina! equivalent.
Dyspnea can also reflect congestive heart failure (CHF) or occur because of
noncardiac causes. The key to understanding the etiology of dyspnea is a clear
patient history, which is then confirmed by a targeted physical examination.
Dyspnea during exertion that quickly resolves at rest or with use of
nitroglycerin may be a result of myocardial ischemia. It is impottant to
establish the amount of activity necessary to provoke dyspnea, the
reproducibility of these symptoms, and the duration of recovery. As with
angina, dyspnea, as an angina! equivalent or a aecompanying symptom, tends to
occur at a given workload or stress e el; dyspnea that occurs one day at low
levels of exertion but not pro pted by vigorous exertion on another day is less
likel}I to be an angina! equivalent.
In patients with CHF, dyspnea generally reflects i creased left
ventricular (LV) filling pressures (Fig. 2.2 ).
Although V systolic dysfunction is the most common cause of the dyspnea,
dyspnea also occurs in individuals with preserved LV systolic function and
severe diastolic dysfunction. However, these two entities present differently,
and physical examination can distinguish them. With LV systolic dysfunction,
dyspnea tends to gradually worsen, and its exacerbation is more variable than
that of exertional dyspnea resulting from myocardial ischemia, although both
are due to fluctuations in pulmonary arterial volume and left atrial filling
pressures. Typically, patients with LV systolic dysfunction do not recover
immediately after exercise cessation or use of sublingual nitroglycerin, and
the dyspnea may linger for longer periods. Orthopnea, the occurrence of dyspnea
when recumbent, or paroxysmal nocturnal edema provides further support for a
presumptive diagnosis of LV systolic dysfunction. Patients with LV diastolic
dysfunction tend to present abruptly with severe dyspnea that resolves more
rapidly in response to diuretic therapy than does dyspnea caused by LV systolic
dysfunction. The New York Heart Association (NYHA) functional classification
for CHF ( Table2.1 ) is extremely useful in following patients with CHF and
provides a simple and rapid means for longitudinal assessment. The NYHA
functional classification also correlates well with prognosis. Patients who are in NYHA functional class I have a
low risk of death or hospital
admission within the following year. In contrast, the annual mortality rate of
those with NYHA functional class IV symptoms exceeds 30%.
As with chest discomfort, the differential diagnosis of dyspnea is broad,
encompassing many cardiac and noncardiac causes (Box 2.5). Congenital heart
disease, with or without pulmonary hypertension, can cause exertional dyspnea.
Patients with significant intracardiac or extracardiac shunts and irreversible
pulmonary hypertension (Eisenmenger syndrome) are dyspneic during minimal
exertion and often at rest. It is also possible to have dyspnea because of
acquired valvular heart disease, usually from aortic or mitral valve stenosis
or regurgitation. All of these causes should be easily distinguished from CHD
or CHF by physical examination. Primary pulmonary causes of dyspnea must be
considered, with chronic obstructive pulmonary disease and reactive airways
disease (asthma) being the most common causes. Again, a careful history for
risk factors (e.g., cigarette smoking, industrial exposure, allergens)
associated with these entities and an accurate physical examination should
distinguish primary pulmonary causes from dyspnea due to CHD or CHF.
Peripheral edema and ascites are physical examination findings consistent with pulmonary hypertension
and/or right ventricular (RV) failure. These findings are included in the
history because they may be part of the presentation. Although patients often
comment on peripheral edema, with careful questioning, they may also identify
increasing abdominal girth consistent with ascites. Important questions on
lower extremity edema include determination of whether the edema is symmetrical
(unilateral edema suggests alternate diagnoses) and whether the edema improves
or resolves with elevation of the lower extremities. The finding of “no
resolution overnight” argues against RV failure as an etiology. In addition,
for peripheral edema and ascites, it is important to ask questions directed
toward determining the presence of anemia, hypoproteinemia, or other causes.
The differential diagnosis of edema is broad and beyond the scope of this
chapter.
It is normal to be aware of the sensation of the heart beating,
particularly during or immediately after exertion or emotional stress.
Palpitations refer to an increased awareness of the heart beating. Patients use
many different descriptions, including a “pounding or racing of the heart,” the
feeling that their heart is “jumping” or “thumping” in their chest, the feeling
that the heart “skips beats” or “races,” or countless other descriptions. A
history that shows that palpitations began to occur during or immediately after
exertion, and not at other times, raises the concern that these sensations
reflect ventricular ectopy associated with myocardial ischemia. It is more
difficult to assess the significance of palpitations occurring at other times.
Supraventricular and ventricular ectopy may occur at any time and may be benign
or morbid. As discussed in Chapters 41 and 42, ventricular ectopy is worrisome
in patients with a history of MI or cardiomyopathy. Lacking this information,
clinicians should be most concerned if lightheadedness or presyncope
accompanies palpitations.
Syncope generally indicates an increased risk for sudden cardiac death and is usually a result of
cardiovascular disease and arrhythmias. If a syncopal episode is a presenting complaint, the patient should
be admitted for further assessment. In approximately 85% of patients, the cause
of syncope is cardiovascular. In patients with syncope, assessment for CHD,
cardiomyopathy, and congenital or valvular heart disease should be performed.
In addition, neurocardiogenic causes represent a relatively common and
important possible etiology for syncope. Box 2.6 shows
the differential diagnosis for syncope. It is critical to determine whether
syncope really occurred. A witness to the episode and documentation of an
intervening period are helpful. In addition, with true syncope, injuries
related to the sudden loss of consciousness are common. However, individuals
who report recurrent syncope (witnessed or unwitnessed) but has never injured
themselves may not be experiencing syncope. This is not to lessen the concern
that a serious underlying medical condition exists but, instead, to reaffirm
that the symptoms fall short of syncope, with its need for immediate evaluation.
