ACP medicine, 3rd Edition

Cardiovascular Medicine

Approach to the Cardiovascular Patient

Catherine M. Otto MD1

David M. Shavelle MD2

1Professor of Medicine and Acting Director, Division of Cardiology, and Director, Cardiology Fellowship Program, University of Washington School of Medicine

2Harbor-UCLA Medical Center

The authors have no commercial relationships with manufacturers of products or providers of services discussed in this chapter.

April 2005

The complete evaluation of the cardiovascular patient begins with a thorough history and a detailed physical examination. These two initial steps will often lead to the correct diagnosis and assist in excluding life-threatening conditions. The history and physical examination findings should be assessed in the context of the overall clinical status of the patient, including lifestyle, comorbidities, and expectations. Cardiovascular conditions that frequently require evaluation include chest pain, dyspnea, palpitations, syncope, claudication, and cardiac murmurs. Each of these conditions will be discussed separately, with an emphasis on a diagnostic algorithm and the appropriate use of invasive and noninvasive cardiac testing.

Chest Pain

BACKGROUND

Chest pain is perhaps the most common cardiovascular symptom encountered in clinical practice. Establishing a cardiac origin of chest pain in a patient with multiple cardiovascular risk factors is essential because it allows initiation of appropriate therapy, thereby reducing the risk of myocardial infarction and death. Similarly, excluding a cardiac origin of chest pain in a low-risk patient is no less essential to avoid costly and potentially risky diagnostic testing that will neither add to the care of the patient nor relieve the patient's discomfort.1 Cardiac disorders that result in chest pain include myocardial ischemia, myocardial infarction, acute pericarditis, aortic stenosis, hypertrophic cardiomyopathy, and aortic dissection. Noncardiac disorders that may result in chest pain include pulmonary embolism, pneumonia, pleural effusion, reactive airway disease, gastrointestinal and biliary disease, anxiety, and musculoskeletal disorders.

Angina most frequently is caused by atherosclerosis of the coronary arteries. Less common causes of angina include coronary artery spasm (e.g., Prinzmetal angina or spasm secondary to drug use, as with cocaine), coronary artery embolism (from aortic valve endocarditis), congenital coronary anomalies, spontaneous coronary artery dissection, coronary arteritis, and aortic dissection when the right coronary artery is involved. Angina may also occur in the presence of angiographically normal coronary arteries and is referred to as syndrome X. The underlying pathophysiology is thought to be related to microvascular dysfunction; the prognosis is generally good despite frequent episodes of chest pain.2

HISTORY AND PHYSICAL EXAMINATION

Essential features of the history include an accurate description of the chest pain, including the severity, frequency, location, radiation, quality, alleviating and aggravating factors, and duration of symptoms [see Table 1]. Anginal chest pain is often described as pressure or a heavy sensation. Symptoms may be difficult for the patient to describe and may be better characterized as discomfort, not pain. Angina typically is described as substernal with radiation to the left neck, jaw, or arm; is mild to moderate in severity; and lasts for 5 to 15 minutes. Classically, angina occurs with exercise, stress, or exposure to cold weather and is relieved with rest or use of nitroglycerin. Some of the most useful features of the patient history that help establish that chest pain is angina are (1) reproducibility of the pain with a given degree of activity, (2) brief duration, and (3) alleviation of the pain with rest or use of nitroglycerin. In patients with a history of coronary artery disease (CAD), an accurate characterization of the quality and frequency of the pain is essential to determine whether a change in the anginal pattern has occurred (i.e., a patient with chronic stable angina now has unstable angina) or if a noncardiac origin of pain is now present (e.g., a patient with chronic stable angina now has musculoskeletal pain). Elderly patients, diabetic patients, and women experiencing angina often present with atypical symptoms that may appear to be noncardiac in nature.

Table 1 Differentiating Features in the Patient's History of Chest Pain

Condition

Location

Radiation

Quality

Alleviating Factors

Aggravating Factors

Duration

Angina pectoris

Substernal

Jaw, arm

Pressure

Rest, nitroglycerin

Exercise, cold weather

5–15 minutes

Pericarditis

Left-sided, substernal

Neck, trapezius ridge

Sharp

Sitting up and leaning forward

Inspiration, supine position

Hours

Musculoskeletal

Variable over entire chest wall

None

Sharp

Rest, anti-inflamatory or analgesic medications

Movement, palpation

Variable, but usually constant

Aortic stenosis

Substernal

Occasionally to jaw, arm

Pressure

Rest, nitroglycerin

Exercise, cold weather

Minutes

Hypertrophic cardiomyopathy

Substernal

Occasionally to jaw, arm

Pressure

Rest, nitroglycerin

Exercise, cold weather

Minutes

Aortic dissection

Substernal

Back

Tearing

None

None

Minutes to hours

Anginal chest pain may also be seen in patients with aortic stenosis or hypertrophic cardiomyopathy secondary to the supply-demand imbalance caused by excessive myocardial hypertrophy. Pericarditis commonly results in a sharp type of chest pain that occurs in the substernal region and worsens on inspiration (pleuritic) when the patient is in a supine position and improves when the patient is in an upright position. The pain of aortic dissection is also substernal, but typically, it is described as a tearing or ripping sensation, radiates to the back or interscapular area, begins abruptly, and fails to improve with rest or use of nitroglycerin. Musculoskeletal pain may be located anywhere on the chest wall, is often reproducible with palpation, and frequently worsens with rotation of the thorax. If the pain is musculoskeletal in origin, recent episodes of excessive lifting or activity may be elicited in the history. Esophageal spasm and gastroesophageal reflux disease are frequent causes of noncardiac chest pain.3

Cardiovascular risk factors should be reviewed in all patients presenting with chest pain. These risk factors include (1) a history of hypertension, hyperlipidemia, diabetes mellitus, or cigarette smoking,4 and (2) a family history of CAD (i.e., a first-degree male relative with myocardial infarction or sudden death occurring before 55 years of age or a first-degree female relative with these events occurring before 65 years of age). Relatively uncommon factors that may also result in angina include prior radiation therapy, drug use (e.g., cocaine and amphetamines), and the presence of a systemic disease (e.g., lupus erythematosus, polyarteritis nodosum, or rheumatoid arthritis) that is associated with coronary arteritis.

The physical examination is usually unremarkable in patients presenting with anginal chest pain. However, certain physical findings can be very helpful in supporting the diagnosis of CAD. Elevated blood pressure by cuff sphygmomanometry and retinal abnormalities on fundoscopic examination (e.g., arteriovenous nicking, microaneurysms, arteriolar narrowing, or hemorrhages) may indicate previously undiagnosed hypertension. Xanthomas (cholesterol-filled nodules that occur subcutaneously or over tendons) indicate severe elevations in serum cholesterol levels. Femoral, carotid, or renal artery bruits and diminished peripheral pulses signify peripheral vascular disease and markedly increase the probability of CAD.5 Tenderness to palpation of the chest wall, especially at the costochondral and chondrosternal articulations, suggests a musculoskeletal etiology of chest pain. Occasionally, patients with anginal chest pain also have a component of reproducible pain with palpation. A third heart sound and a holosystolic murmur of mitral regurgitation (secondary to ischemia of a papillary muscle) may be present if a patient with CAD is examined during an episode of anginal pain.

Physical examination also is directed toward findings that suggest an alternative cause of chest pain. Asymmetrical peripheral pulses, an early diastolic murmur, and the appropriate clinical history (tearing chest pain with radiation to the back) indicate an aortic dissection. A systolic murmur that radiates to the base of the neck (aortic stenosis) or a systolic murmur that increases in intensity with the strain phase of the Valsalva maneuver (hypertrophic cardiomyopathy) are uncommon but useful findings. A so-called leatherlike or scratchy series of sounds indicates a pericardial rub and supports a diagnosis of pericarditis. The intensity of the rub may increase with inspiration, indicating associated inflammation of the pleura, or pleuritis. Examination of the lung fields may disclose diminished breath sounds associated with dullness to percussion (pleural effusion), rhonchi, and egophony (pneumonia) or expiratory wheezes (asthma).

DIAGNOSTIC TESTS

On the basis of the history, chest pain is characterized as anginal, atypical anginal (some features of angina combined with some noncharacteristic features), or nonanginal. Estimates of the pretest probability of CAD can be accurately derived from a description of the chest pain syndrome and the presence or absence of cardiovascular risk factors.6,7 The most widely used method for determining pretest likelihood of CAD is the Duke University Database formula, which considers the patient's age, sex, cardiovascular risk factor profile, description of chest pain, and information from the resting electrocardiogram.8

Although the diagnostic yield from the baseline ECG is low, it provides useful information on the advisability of pursuing additional diagnostic testing [see Figure 1]. Notable findings include Q waves consistent with a prior myocardial infarction and left ventricular hypertrophy that may be secondary to aortic stenosis, hypertrophic cardiomyopathy, or long-standing hypertension. ST segment depression, T wave abnormalities, and arrhythmias may be present if the ECG is obtained during an episode of anginal chest pain. A normal resting ECG predicts normal left ventricular function with a high degree of certainty (i.e., > 95%).

 

Figure 1. Evaluation of Patients with Chest Pain

Evaluation of patients with chest pain. (CAD—coronary artery disease; ECG—electrocardiogram)

As with the ECG, a routine chest roentgenogram is usually normal. However, the presence of cardiomegaly, a left ventricular aneurysm, significant coronary or aortic calcification, or pulmonary venous congestion would be useful information and may warrant additional diagnostic testing.

Some physicians have started to use portable or handheld echocardiographic devices to evaluate patients with chest pain. Pertinent findings by echocardiography that would assist in establishing the etiology of chest pain include a pericardial effusion (pericarditis), hypokinesis or akinesis of a left ventricular wall segment (acute coronary ischemia), a dilated right ventricle (pulmonary embolism), and calcification and impaired excursion of the aortic valve leaflets (aortic stenosis).

Noninvasive stress testing is most likely to influence clinical decision making when the pretest probability of CAD is in the intermediate range. Patients with a low risk of CAD should not undergo noninvasive cardiac stress testing, because an abnormal test result would likely be a false positive one, and a negative test result would simply confirm the low probability of CAD. However, if patient reassurance is a consideration, a normal test result may be very useful. In addition, exercise stress testing provides information regarding symptom status, exercise capacity, and the hemodynamic response to exercise if the history is unclear (e.g., the patient denies symptoms but has decreased exercise capacity for “other reasons”). Absolute and relative contraindications to exercise testing should be reviewed in all patients before testing is begun [see Table 2].8

Table 2 Absolute and Relative Contraindications to Exercise Testing7

Absolute

Relative

Recent myocardial infarction (within 48 hr)

Left main coronary stenosis

Unstable angina not previously stabilized with medical therapy

Moderate stenotic valvular heart disease

Uncontrolled cardiac arrhythmias causing symptoms or hemodynamic compromise

Electrolyte abnormalities

Symptomatic severe aortic stenosis

Severe arterial hypertension

Uncontrolled symptomatic heart failure

Tachycardia or bradyarrhythmias

Acute pulmonary embolism or pulmonary infarction

Hypertrophic cardiomyopathy and other forms of outflow tract obstruction

Acute myocarditis or pericarditis

Mental or physical impairment leading to inability to exercise adequately

Acute aortic dissection

High degree of atrioventricular block

Similarly, patients with a high risk of CAD in general should not undergo noninvasive cardiac stress testing for the purpose of diagnosing CAD, because a negative test result would likely be a false negative one, and a positive result would simply confirm the high probability of CAD. In such patients, coronary angiography should be used to establish a diagnosis of CAD. However, noninvasive cardiac stress testing in certain patients at high risk for CAD may be useful. Indications for noninvasive stress testing in these patients include (1) assessment of the effectiveness of current medical therapy, (2) objective measurement of exercise capacity, (3) evaluation of the extent and location of ischemia or infarction with nuclear or echocardiographic imaging, (4) preoperative risk assessment in patients with known CAD who are undergoing noncardiac surgery, and (5) assessment of prognosis in patients with symptoms consistent with CAD or in patients with known CAD.

To establish the diagnosis of CAD in intermediate-risk patients, a number of noninvasive testing methods are available.9 The decision whether to perform a specific test is based on various patient characteristics (e.g., body size, associated medical conditions, and ability to exercise), findings on the baseline ECG, and institutional experience with specific testing methods [see Table 3].10,11,12,13,14,15,16 The most appropriate noninvasive stress test is chosen on the basis of each of these factors, as indicated in the chest pain algorithm [see Figure 1]. For most patients who are able to exercise with a normal baseline ECG, treadmill-ECG stress testing is indicated [see Table 2].14,15,17Women have a higher incidence of false positive results; therefore, many physicians recommend that, for all women, exercise be combined with an imaging method (e.g., echocardiography or nuclear imaging).11 In general, to establish the diagnosis of CAD, exercise is preferred over pharmacologic stress agents. For patients who are unable to exercise because of physical limitations (e.g., arthritis or orthopedic problems), severe coexisting pulmonary disease, or general disability, pharmacologic stress agents such as dobutamine, adenosine, or dipyridamole can be employed. Each of these agents has specific contraindications [see Table 4].

Table 3 Diagnostic Testing Methods Available for Evaluating Chest Pain9,10,11,12,13,14

Diagnostic Test

Indications

Information Obtained

Limitations

Sensitivity

Specificity

Exercise electrocardiographic stress test (stress ECG)

  Initial test for most males with chest pain to establish diagnosis of CAD; females have higher rate of false positive test results
  Assess prognosis and functional capacity in patients with prior MI or known CAD
  Assess efficacy of current medical therapy in patients with known CAD

  Exercise duration and functional aerobic capacity
  Amount of ST segment depression as indication of extent of ischemia
  Hemodynamic response to exercise

  Normal baseline ECG
  Ability to exercise (patients who cannot attain adequate cardiopulmonary stress because of respiratory or musculoskeletal problems should receive a pharmacologic stress agent)
  Contraindications [see Table 2]
  False positives occur with left ventricular hypertrophy, bundle branch block, preexcitation syndromes, electrolyte abnormalities, and digoxin use

68%1(females, 61%2)

77%1(females, 70%2)

Thallium-201 perfusion scintigraphy

  Often used when increased diagnostic accuracy for CAD required
  Can be combined with pharmacologic stress agents such as dobutamine, adenosine, or dipyridamole

  Diagnosis of CAD with higher sensitivity and specificity than stress ECG
  Extent of ischemia
  Extent of infarction
  Left ventricular cavity size

  Higher cost and longer testing time than stress ECG
  Imaging artifacts (attenuation) from diaphragm, breast, and intestine
  Contraindications [see Table 2 if exercise; seeTable 4 if pharmacologic stress agent]

Ex thall 89%5
Ph thall 90%5
Dob thall 88%4

Ex thall 76%5
Ph thall 70%5
Dob thall 74%4

Technetium-99m perfusion scintigraphy

  Often used when increased diagnostic accuracy for CAD required
  Can be combined with pharmacologic stress agents such as dobutamine, adenosine, or dipyridamole

  Higher sensitivity and specificity for diagnosis of CAD than stress-ECG
  Extent of infarction
  Extent of ischemia
  Left ventricular cavity size
  ECG-gated SPECT allows calculation of left ventricular ejection fraction and evaluation of wall motion; evaluation of wall motion reduces false positive scans caused by imaging artifacts (attenuation)
  Used when excessive body weight precludes thallium imaging

  Higher cost and longer testing time than stress ECG
  Imaging artifacts (attentuation) from diaphragm, breast, and intestine
  Contraindications [see Table 2 if exercise; seeTable 4 if pharmacologic stress agent]

Ex tech 89%5
Ph tech 90%5
Dob tech 88%4

Ex tech 76%5
Ph tech 70%5
Dob tech 74%4

Exercise or dobutamine echocardiography

  Exercise echocardiography often used when patient can exercise and has good-quality echocardiographic images
  Dobutamine used when exercise not possible

  Higher sensitivity and specificity for diagnosis of CAD than stress ECG
  Left and right ventricular chamber size and function, presence of valve disease, and pulmonary arterial pressures

  Inadequate image quality may occur in patients with obesity, chronic obstructive pulmonary disease, and chest wall deformities
  Contraindications [see Table 2 if exercise; seeTable 4 if pharmacologic stress agent]

Ex echo 85%6
Dob echo 82%6

Ex echo 86%6
Dob echo 82%6

Holter monitoring

Prinzmetal angina

Transient ST segment elevation during chest pain

Difficult to interpret because of baseline abnormalities

 

 

Coronary angiography

  Chest pain of unclear etiology despite noninvasive testing
  Angina not responsive to medical therapy
  Unstable and postinfarction angina
  Unclear diagnosis of CAD despite noninvasive stress testing

  Anatomic severity of CAD
  Completely exclude cardiac origin of chest pain—gold standard of diagnostic tests
  Left ventricular function if left ventricular angiography also performed

  Invasive procedure with low (< 2%) but inherent risk of MI, stroke, and death
  Represents a luminogram; does not evaluate functional significance of arterial narrowing

100%

100%

CAD—coronary artery disease  Dob tech—dobutamine technetium  Dob thall—dobutamine thallium  ECG—electrocardiogram  Ex echo—exercise echocardiography   Ex tech—exercise technetium  Ex thall—exercise thallium  MI—myocardial infarction  Ph stress—pharmacologic stress  Ph tech—pharmacologic (adenosine or dipyridamole) stress combined with technetium  Ph thall—pharmacologic (adenosine or dipyridamole) stress combined with thallium  SPECT—single-photon emission computed tomography

Table 4 Mechanism of Action, Side Effects, and Contraindications of Pharmacologic Stress Agents

Pharmacologic Stress Agent

Mechanism of Action

Side Effects

Contraindications

Dobutamine

Increase myocardial oxygen demand by increasing heart rate, blood pressure, and myocardial contractility

78% of patients experience side effects: chest pain, palpitations, headache, flushing, malaise, and dyspnea; ventricular and atrial arrhythmias may occur

Severe hypertension at baseline, recent history of ventricular and/or atrial arrhythmias, and current beta-blocker use

Dipyridamole

Coronary artery vasodilatation—indirect response by blocking adenosine uptake and degradation

Increase in heart rate (average, 5–10 beats a minute), decrease in systolic blood pressure (average, 10–15 mm Hg); approximately 50% of patients experience side effects: chest pain, flushing, dizziness, headaches, or nausea; may provoke bronchospasm

Severe reactive airway disease (not contraindicated with chronic obstructive pulmonary disease unless a significant component of reactive airway disease is present), current theophylline use; avoid caffeine use 1 day before testing

Adenosine

Coronary artery vasodilatation—direct response

79% of patients experience side effects (more than with dipyridamole); side effects are chest, throat or jaw pain, headache, flushing, malaise, nausea, and bradyarrhythmias

Similar to dipyridamole; avoid caffeine use 1 day before testing; may cause bradyarrhythmias and is therefore contraindicated with baseline second- or third-degree heart block

Coronary angiography is considered the gold standard for the diagnosis of CAD. Although the incidence of major complications is low (< 2%), coronary angiography is costly and has some risk; thus, it is reserved for (1) patients with markedly positive noninvasive tests (i.e., hypotension and significant ST segment depression on ECG stress testing on a treadmill), (2) patients at high risk for CAD in whom a course of empirical antianginal therapy has failed, (3) patients with unstable or postinfarction angina, (4) patients with a contraindication to exercise or pharmacologic stress testing, and (5) patients with equivocal results on noninvasive stress testing when the diagnosis of CAD remains unclear. Coronary angiography has certain limitations, including the inability to determine (1) the functional significance of a coronary artery stenosis and (2) which coronary plaque is likely to rupture (i.e., the so-called vulnerable plaque) and result in an acute coronary syndrome. Intravascular ultrasound studies have shown that coronary angiography may occasionally underestimate the severity of an area of narrowing, because it represents a so-called luminogram (shadow image) and not the size of the atherosclerotic plaque.18 Despite these shortcomings, the extent and severity of CAD and measurement of left ventricular function by left heart catheterization are powerful predictors of clinical outcome.14

Dyspnea

BACKGROUND

Dyspnea refers to difficulty with breathing and can occur with a wide variety of cardiac, pulmonary, and systemic conditions [see Table 5]. Dyspnea can be classified as occurring (1) at rest, (2) with exertion, (3) during the night, awakening a patient from sleep (paroxysmal nocturnal dyspnea), or (4) during episodes of recumbency (orthopnea). Paroxysmal nocturnal dyspnea and orthopnea result from similar mechanisms. Specifically, the recumbent position augments venous return to the right heart. This increase in cardiac filling further increases the pulmonary capillary pressure and results in interstitial (and possibly intra-alveolar) pulmonary edema. Patients find relief by sitting upright, which reduces venous filling and transiently decreases the pulmonary interstitial pressure.

Table 5 Causes of Dyspnea

Cardiac

  Valve disease

    Aortic stenosis

    Aortic regurgitation

    Mitral stenosis

    Mitral regurgitation

  Myocardial disease

    Dilated cardiomyopathy

    Restrictive cardiomyopathy

    Hypertrophic cardiomyopathy

  Pericardial disease

    Constrictive pericarditis

    Pericardial tamponade

    Pericardial effusion

  Coronary disease

    Myocardial infarction and ischemia

  Arrhythmia

    Ventricular and supraventricular arrhythmias

  Congenital heart disease

Pulmonary

   Reactive airway disease

   Chronic obstructive lung disease (chronic bronchitis and emphysema)

    Interstitial lung disease

    Infection (acute bronchitis and pneumonia)

    Pulmonary embolism

    Chest wall disease

    Pleural effusion

Deconditioning

Obesity

Malingering

Psychogenic

  Anxiety and panic disorders

Anemia

Dyspnea may be acute or chronic. An acute presentation suggests a pulmonary embolism, acute asthma exacerbation, pneumothorax, or rapidly developing pulmonary edema, as occurs with ischemic mitral regurgitation. Chronic dyspnea suggests heart failure resulting from systolic or diastolic dysfunction.

HISTORY AND PHYSICAL EXAMINATION

The history will often exclude less likely conditions and establish the etiology of dyspnea. A history of reactive airway disease, bronchodilator use, or corticosteroid use suggests asthma. Reactive airway disease tends to occur in children and young adults; therefore, in older patients given this diagnosis, a cardiac cause for dyspnea (e.g., new onset of congestive heart failure) should be considered. A significant history of tobacco use, wheezing, chronic cough, and sputum production suggests obstructive airway disease.19 A recent history of fever, chills, and productive cough may indicate bronchitis or pneumonia. The acute onset of dyspnea associated with pleuritic chest pain after a period of immobilization suggests pulmonary embolism. Paroxysmal nocturnal dyspnea, orthopnea, nocturia, recent weight gain, and lower extremity edema suggest a cardiac cause for dyspnea. Patients with chronic obstructive pulmonary disease may also awaken at night with dyspnea, but they usually have a history of sputum production and expectoration that improves with the patient in the upright position. Occasionally, on the basis of the history alone, it may not be possible to determine whether a cardiac or pulmonary cause of dyspnea is present.20 In up to one third of patients being evaluated, dyspnea may have more than one cause.21 In elderly patients, dyspnea may be the only symptom of a myocardial infarction. Hemoptysis may indicate the presence of severe underlying pulmonary disease (e.g., pulmonary embolism or lung cancer) but must be differentiated from hematemesis and nasopharyngeal bleeding.

Several findings on physical examination can assist in excluding a cardiac cause for dyspnea. These findings include a normal level of the jugular venous pressure, a normal point of maximal cardiac impulse, the lack of a third heart sound or cardiac murmurs, the absence of rales on lung examination, and the absence of peripheral edema. Alternatively, elevated jugular venous pressure, a displaced point of maximal cardiac impulse, a third heart sound, a holosystolic murmur of mitral regurgitation, basilar rales, and peripheral edema suggest congestive heart failure. A positive abdominojugular reflux maneuver may also identify dyspnea of cardiac origin.22

Obese patients and those with chest wall deformities may experience dyspnea secondary to the increased workload of breathing from the mechanical limitation imposed on the chest wall. Patients with emphysema frequently have an increased anteroposterior chest diameter, prolonged expiratory phase, expiratory wheezes, and diminished breath sounds. Central cyanosis, a normal anteroposterior chest diameter, and expiratory wheezes or rhonchi on lung examination suggest chronic bronchitis. Expiratory wheezing can occur in both cardiac and pulmonary conditions and is therefore not helpful in establishing an etiology. Stridor may result from an upper airway obstruction or vocal cord paralysis and at times may resemble wheezing. Tachypnea, a loud pulmonic component of the second heart sound, and calf tenderness suggest a pulmonary embolism.

DIAGNOSTIC TESTS

An ECG and a chest roentgenogram should be the initial tests in the evaluation of dyspnea. Pertinent ECG findings include Q waves (prior myocardial infarction), a bundle branch block (structural heart disease), left ventricular hypertrophy (aortic stenosis, hypertension), and evidence of atrial chamber enlargement (valvular heart disease). Notable chest roentgenogram findings include an enlarged cardiac silhouette; interstitial or alveolar edema (congestive heart failure); aortic valve calcification (valvular heart disease); lung mass (lung cancer); focal infiltrate (pneumonia); pleural effusion (congestive heart failure, infectious process); and hyperinflation, bullae, and flattened hemidiaphragms (emphysema). Screening laboratory tests may be useful to exclude anemia as a potential cause of dyspnea.

If the diagnosis of dyspnea remains unclear, additional testing can be pursued [see Figure 2]. For patients with cardiovascular risk factors, with findings on physical examination that suggest structural heart disease, or with abnormal ECGs, echocardiography is indicated to exclude valvular heart disease and assess systolic and diastolic ventricular function. Patients with a presumed pulmonary etiology for dyspnea that remains undiagnosed should undergo pulmonary function testing to exclude reactive airway and restrictive and chronic obstructive pulmonary disease. Stress-ECG may be useful to objectively evaluate the degree of limitation and may be particularly helpful for patients with presumed deconditioning, malingering, or a psychogenic cause for dyspnea. For patients who may have a component of dyspnea from both a cardiac and a pulmonary source, cardiopulmonary exercise testing can be considered. Serum brain natriuretic peptide (BNP) levels are useful in distinguishing cardiac from noncardiac causes of dyspnea; a BNP greater than 100 pg/ml has a sensitivity of 90% but a specificity of only 73% for establishing the diagnosis of heart failure.23 Other factors that affect BNP levels include renal failure, acute coronary syndrome, and female gender.

 

Figure 2. Evaluation of Patients with Dyspnea

Evaluation of patients with dyspnea. (ECG—electrocardiogram)

Palpitations

BACKGROUND

Palpitations are a nonspecific symptom associated with severity ranging from an increased awareness of the normal heartbeat to life-threatening ventricular arrhythmias [see Table 6]. Although palpitations represent one of the most common complaints requiring evaluation in the outpatient setting,24 consensus guidelines describing the appropriate evaluation have not yet been established.

Table 6 Causes of Palpitations

General Category

Prognosis

Hyperdynamic state

Anemia, thyrotoxicosis, and exercise—all leading to sinus tachycardia

Increase in cardiac stroke volume

Aortic regurgitation, patent ductus arteriosus

Arrhythmia

 

  Ventricular

Frequent ventricular premature beats, ventricular tachycardia

  Supraventricular

Frequent atrial premature beats, atrial fibrillation, atrial flutter, multifocal atrial tachycardia, atrial tachycardia, atrioventricular nodal reentry tachycardia, atrioventricular reentry tachycardia

Psychiatric

Anxiety, panic, or somatization disorder

For patients with an underlying cardiac disease associated with palpitations, long-term outcome is poor. In contrast, clinical outcome is excellent for those with a noncardiac origin for palpitations, despite a high rate of recurrent episodes.25 The key, then, in the evaluation of palpitations is to establish or exclude the presence of underlying structural heart disease. This determination can often be made by use of information from the history, physical examination, and ECG, but it may require additional evaluation with ambulatory ECG monitoring and possibly electrophysiologic testing. Psychiatric illnesses (anxiety, panic, and somatization disorders) account for a certain number of patients who seek medical attention for palpitations25; these disorders can initially be screened by use of simple and rapid patient-administered questionnaires. Although an underlying psychiatric illness should be considered in appropriate patients, it does not obviate the need for a complete evaluation to exclude a cardiac origin.26 A diagnostic algorithm is presented that utilizes a rational approach to diagnostic testing [see Figure 3].

 

Figure 3. Evaluation of Patients with Palpitations

Evaluation of patients with palpitations. Patients with a potential substrate for arrhythmias include those with prior myocardial infarction, dilated cardiomyopathy, hypertrophic cardiomyopathy, or significant valvular or congenital heart disease. (ECG—electrocardiogram; EF—ejection fraction; EP—electrophysiologic)

HISTORY AND PHYSICAL EXAMINATION

Palpitations are often described as a fluttering, a pounding, or an uncomfortable sensation in the chest. Occasionally, patients may complain only of a sensation of awareness of the heart rhythm. Patients may be able to discern whether the episodes are rapid and regular or rapid and irregular. Tapping a finger on the patient's chest in either a regular or an irregular manner may occasionally lead to an accurate description of the events.

A history of palpitations since childhood suggests a supraventricular arrhythmia and possibly an atrioventricular bypass tract, such as in the Wolff-Parkinson-White syndrome. Patients with congenital long QT syndrome typically begin to manifest symptoms in adolescence. A family history of sudden cardiac death, congestive heart failure, or syncope may suggest an inherited dilated or hypertrophic cardiomyopathy.

Knowing the circumstances in which palpitations occur may be useful in determining their origin. Palpitations associated only with strenuous physical activity are normal, whereas episodes occurring at rest or with minimal activity suggest underlying pathology. Episodes associated with a lack of food intake suggest hypoglycemia, and episodes after excessive alcohol intake suggest the toxic effects of alcohol. The resolution of symptoms with vagal maneuvers (breath-holding or the Valsalva maneuver) suggests paroxysmal supraventricular tachycardia. The onset of an episode of palpitations on assuming an upright position after bending over suggests atrioventricular nodal tachycardia.27Emotional stress and strenuous exercise may precipitate episodes in patients with long QT syndrome. Palpitations associated with anxiety or a sense of doom or panic suggest, but do not confirm, an underlying psychiatric disorder. An odds-ratio analysis found that regular palpitations, palpitations experienced at work, and those affected by sleeping were more likely to indicate cardiac origin.28

Symptoms associated with an episode of palpitations should also be explored. Syncope or presyncope after an episode suggests ventricular arrhythmias. However, patients with structural heart disease (e.g., severe left ventricular systolic dysfunction) may also experience these symptoms after supraventricular arrhythmias because of dependence on atrial filling. Additional mechanisms of syncope in patients with supraventricular arrhythmias have also been reported.29 Regardless of the mechanism, syncope and presyncope are worrisome symptoms and merit a complete cardiovascular evaluation. Occasionally, patients may experience an episode of polyuria that follows the palpitations. This condition may suggest supraventricular arrhythmias as the cause of palpitations, although studies have found this to be uncommon.30

The physical examination should focus on establishing whether underlying structural heart disease is present. Evidence of cardiac enlargement, third heart sound, and holosystolic murmur of mitral regurgitation suggest an underlying dilated cardiomyopathy. A midsystolic click, often followed by a systolic murmur, indicates mitral valve prolapse, which may be associated with both ventricular and supraventricular arrhythmias. A midsystolic murmur along the left sternal border that varies in intensity with alterations in left ventricular filling (e.g., Valsalva maneuver or changes in body position) is consistent with hypertrophic cardiomyopathy. Although atrial fibrillation is common in hypertrophic cardiomyopathy, ventricular arrhythmias may also occur.

DIAGNOSTIC TESTS

The ECG is the first step in the diagnostic evaluation of a patient with palpitations [see Figure 3]. A short PR interval and delta wave (Wolff-Parkinson-White syndrome), prolonged QT interval (long QT syndrome), and left bundle branch block (structural heart disease) are notable findings. Certain medications [see Table 7] may result in prolongation of the QT interval (i.e., acquired prolonged QT) and increase the risk of arrhythmias. Extreme voltage amplitudes and Q waves in leads I, aVL, and V4 through V6 are seen with hypertrophic cardiomyopathy. Pathologic Q waves indicate prior myocardial infarction and therefore a substrate for ventricular arrhythmias. Left ventricular hypertrophy or atrial abnormalities are nonspecific findings but suggest underlying structural heart disease. Many pertinent findings for various causes of palpitations can be obtained from the history, physical examination, and ECG [see Table 8].

Table 7 Medications Associated with Prolongation of the QT Interval

Antibiotics

  Tetracycline

  Erythromycin

  Trimethoprim and sulfamethoxazole

  Pentamidine

Antihistamines

  Terfenadine

  Astemizole

  Diphenhydramine

Antiarrhythmic agents

  Quinidine

  Procainamide

  Disopyramide

  Sotalol

  Amiodarone

  Dofetilide

Other cardiac drugs

  Bepridil

Gastrointestinal

  Cisapride

Antifungal drugs

  Ketoconazole

  Fluconazole

  Itraconazole

Psychotropic drugs

  Tricyclic antidepressants

  Phenothiazines

  Haloperidol

  Resperidone

Diuretics

  Indapamide

Table 8 Diagnosis of the Underlying Etiology of Palpitations

Condition

History

Physical Examination

ECG

Underlying Etiology of Palpitations

Congenital long QT syndrome

Symptom onset in adolescence; episodes may be triggered by emotional stress and strenuous exercise

Normal

Prolonged QT interval

Ventricular arrhythmias

Atrioventricular bypass tract (e.g., Wolf-Parkinson-White syndrome)

Childhood episodes of palpitations

Normal

Short PR interval, delta wave

Supraventricular arrhythmias

Inherited dilated cardiomyopathy

Family history of cardiomyopathy, syncope, or sudden cardiac death

Abnormal cardiac impulse, systolic murmur (MR), third heart sound

Atrial enlargement, IVCD, LBBB, ventricular ectopic beats, or Q waves

Supraventricular or ventricular arrhythmias

Hypertrophic cardiomyopathy

Family history of cardiomyopathy, syncope, or sudden cardiac death

Systolic murmur

Increased voltage amplitude (LVH), Q waves in V4-V6, I, aVL

Supraventricular or ventricular arrhythmias

Anxiety, panic, or somatization disorder

Sense of doom, panic, or anxiety associated with episodes; coexisting psychiatric illness

Normal

Normal

Psychiatric

Mitral valve prolapse

Associated fatigue, dyspnea

Midsystolic click, systolic murmur (MR)

Normal or left atrial enlargement

Supraventricular arrhythmias

IVCD—interventricular conduction defect  LBBB—left bundle branch block  LVH—left ventricular hypertrophy  MR—mitral regurgitation

If the cause of palpitations is not apparent after the initial evaluation (history, physical examination, and ECG), additional diagnostic testing is indicated for certain patients [see Figure 3].27 Such patients include those with presumed arrhythmias that remain undiagnosed and those with prior myocardial infarction, dilated cardiomyopathy, hypertrophic cardiomyopathy, or significant valvular or congenital heart disease. In addition, patients who desire a specific diagnosis should be considered for additional testing.

Ambulatory ECG devices include Holter monitoring and continuous-loop event recorders. Holter monitors continuously record the heart rhythm for 24 or 48 hours. Patients are asked to maintain a diary documenting the time and describing the symptoms during the monitoring period. The key is to correlate patient symptoms with documented rhythm abnormalities. Patients with significant complaints of palpitations that correlate with periods of normal sinus rhythm should be further evaluated for underlying psychiatric disorders. Event monitors also continuously record the heart rhythm but require the patient to trigger the device to save the information. These devices can be kept by patients for several weeks and are especially useful when symptoms are infrequent. Event monitors are more cost-effective than Holter monitors for evaluating palpitations.31,32 For patients with underlying structural heart disease and documented ventricular arrhythmias on ambulatory ECG monitoring, additional evaluation is warranted, including determination of left ventricular function and, occasionally, electrophysiologic testing.

Syncope

BACKGROUND

Syncope refers to a transient loss of consciousness accompanied by loss of postural tone. Roughly one third of all persons have an episode of syncope during their lifetime. It is a particularly common problem encountered in emergency departments and accounts for approximately 6% of all hospital admissions.33 Determining which patients require hospital admission is difficult, given the large number of potential causes of syncope. Although many conditions that result in syncope are life threatening, other common etiologies, such as medication side effects, orthostatic hypotension, and psychiatric disorders, are benign.

Syncope is classified on the basis of the underlying etiology [see Table 9]. In elderly patients, the etiology may be multifactorial and related to medication side effects (particularly antihypertensives and antidepressants),34 orthostatic hypotension, and bradyarrhythmias. Various medications are associated with prolongation of the QT interval and the development of ventricular arrhythmias and resulting syncope [seeTable 7]. Vasovagal syncope is particularly common in otherwise healthy patients and has a benign prognosis. Episodes often occur in response to injury and are characterized by a sudden decline in blood pressure with or without associated bradycardia.

Table 9 Classification of Syncope Based on Etiology

Cardiac

  Blood flow obstruction

    Aortic stenosis

    Pulmonic stenosis

    Left atrial myxoma

    Hypertrophic cardiomyopathy

    Massive pulmonary embolism

   Reduction in forward cardiac output

     Pericardial tamponade

     Severe pump failure

   Arrhythmia

     Tachyarrhythmias

Ventricular tachycardia

Supraventricular tachycardia

     Bradyarrhythmias

      Sinus bradycardia

      Sick sinus syndrome

      Atrioventricular block

      Carotid sinus hypersensitivity (can also be considered neurologic cause)

Neurologic

  Vasovagal

  Situational (micturition)

  Seizures

  Cerebrovascular accident

  Cerebrovascular insufficiency

  Orthostatic hypotension—autonomic dysfunction

Other

  Volume depletion

  Drugs

  Hypoglycemia

  Anxiety attack

  Psychogenic

Establishing the presence of structural heart disease in the evaluation of patients with syncope is essential because such patients may have a 1-year mortality as high as 30%.35,36 Structural heart disease is usually apparent on the basis of history, physical examination, and information from the baseline ECG. Occasionally, additional diagnostic testing with echocardiography, tilt-table testing, or electrophysiologic testing may be required.

HISTORY AND PHYSICAL EXAMINATION

The first step in establishing the presence of structural heart disease is to obtain an accurate description of the episode of syncope. Key elements of the history include the presence of postural or exertional symptoms; associated chest pain, shortness of breath, or palpitations; and the situation in which the episode occurred (e.g., during micturition). Neurologic symptoms such as focal motor weakness, arm or leg movement, tongue biting, or a postictal state suggest a neurologic rather than cardiac event. However, seizures can occur from cardiac causes if a patient is kept upright during an episode (usually the result of a well-meaning bystander) because of cerebral hypoperfusion. A witness to the episode of syncope may provide a clear description of the event and should be questioned if possible. Medications associated with QT prolongation [see Table 7], blood pressure lowering (antihypertensives), and volume depletion (diuretics) should be reviewed. A family history of sudden cardiac death, syncope, or heart failure suggests hypertrophic cardiomyopathy, an inherited dilated cardiomyopathy, or long QT syndrome. A history of myocardial infarction or congestive heart failure raises the possibility of ventricular arrhythmias.

The physical examination focuses on determining whether structural heart disease is present and excluding common causes of syncope. Orthostatic vital signs should be obtained in all patients. Focal neurologic findings such as a motor deficit or a visual-field defect may indicate a neurologic cause for syncope. Pertinent findings on cardiovascular examination include a delayed carotid upstroke (aortic stenosis), an abnormal point of maximal cardiac impulse (cardiomyopathy), an irregular or bradycardiac rhythm (arrhythmias), a third heart sound (cardiomyopathy), a midsystolic murmur (aortic stenosis, hypertrophic cardiomyopathy), and a holosystolic murmur (mitral regurgitation secondary to left ventricular dilatation). Less common findings include an early diastolic sound (so-called tumor plop, indicating a left atrial myxoma), asymmetrical peripheral pulses (aortic dissection), and a loud second heart sound (pulmonary hypertension secondary to pulmonary embolism). Information from the history and physical examination yields a cause for syncope in approximately 45% of patients.37

DIAGNOSTIC TESTS

An ECG is the initial diagnostic test for all patients with syncope. Although the yield of the baseline ECG is low (approximately 5%), a number of potential findings are useful,37 including bundle branch block, Q waves indicating prior myocardial infarction, left ventricular hypertrophy, prolonged QT interval, or evidence of atrioventricular block. The presence of sinus bradycardia, first-degree atrioventricular block, and bundle branch block suggests bradyarrhythmias as the cause of syncope. Extreme voltage amplitudes and Q waves in leads I, aVL, and V4 through V6 suggest hypertrophic cardiomyopathy and therefore the possibility of ventricular arrhythmias. An uncommon but unique ECG abnormality is the combination of a right bundle branch block, T wave inversions in leads V1 through V3, and an epsilon wave (a positive wave on the terminal portion of the QRS complex)—findings that indicate right ventricular dysplasia, which is associated with ventricular arrhythmias. Ventricular arrhythmias are also seen in the Brugada syndrome, which can be identified on the ECG by an incomplete right bundle branch block and ST segment elevation in leads V1 through V3.38 A short PR interval and slurring of the initial portion of the QRS complex (the delta wave) suggests preexcitation (i.e., Wolff-Parkinson-White syndrome), with the possibility of rapid antegrade conduction via the accessory pathway.

If the etiology of syncope remains unclear after reviewing the history, physical examination, and ECG, additional diagnostic testing should be pursued. For patients with findings suggestive of an underlying cardiac cause, echocardiography and coronary angiography can be performed; for those with a possible neurologic cause, brain imaging (computed tomography or magnetic resonance imaging), neurovascular studies (carotid and transcranial Doppler ultrasound studies), and electroencephalography can be performed; and for those with a presumed pulmonary cause, lung scanning can be considered [see Figure 4]. If the diagnosis remains uncertain despite these tests, one of three pathways can be followed.39

 

Figure 4. Evaluation of Patients with Syncope

Evaluation of patients with syncope.37,38,39 (ECG—electrocardiogram; OHD—organic heart disease)

The first pathway is for patients with structural heart disease or an abnormal ECG, who therefore have an increased likelihood for underlying arrhythmias or valve disease as a cause for syncope. Echocardiography, noninvasive stress testing, and ambulatory ECG monitoring using either a Holter monitor or continuous-loop event recorder should be considered for these patients. Event recorders have been found to be more accurate than Holter monitors in the diagnosis of syncope and presyncope; however, some patients find event recorders difficult to operate correctly.40 If ambulatory ECG monitoring documents normal sinus rhythm in the setting of reported syncope, psychiatric evaluation and possibly tilt-table testing are warranted.

The second pathway is for patients older than 60 years, who are more likely to have valve disease (aortic stenosis), ischemic heart disease, carotid sinus syncope, cerebrovascular disease (transient ischemic attacks), and situational events (micturition, defecation, postural) as a basis for syncope. Carotid sinus massage (in the absence of carotid bruits, recent myocardial infarction, or stroke) should be the initial diagnostic test for these patients.41,42 A positive test is defined as asystolic arrest lasting 3 seconds or longer and may identify those with cardioinhibitory hypersensitivity of the carotid sinus who will benefit from pacemaker placement. For those with a negative test result, echocardiography, noninvasive stress testing, and ambulatory ECG monitoring can be performed.

The third pathway is for patients with unexplained syncope and no suspected structural heart disease. For those who have had a single episode, additional evaluation can be deferred until a second episode occurs. In patients with more than one episode, ambulatory ECG monitoring or tilt-table testing and, possibly, psychiatric evaluation should be considered.

Tilt-table testing was initially developed in the 1980s to evaluate patients with presumed vasovagal syncope. The passive portion of the test involves quickly raising a patient from the supine position to an angle of 60° (the tilt angle) for approximately 45 minutes, which causes pooling of venous blood in the lower extremities, a decrease in venous return, compensatory tachycardia, and enhanced ventricular contraction. For individuals with vasovagal syncope, augmented ventricular contraction causes activation of vasodepressor reflexes that result in hypotension, bradycardia, or both. Approximately 49% of patients referred for evaluation of vasovagal syncope have positive responses, compared with 9% of control patients.43 The active portion of tilt-table testing uses an isoproterenol infusion to enhance the vasodepressor reflex.

Claudication

BACKGROUND

Claudication is a condition of muscle pain or weakness associated with compromised blood flow to the extremities. It is a common complaint of patients who have peripheral vascular disease (PVD). Claudication is also a common symptom of CAD, a disease that shares risk factors with PVD. PVD is associated with an increased risk of stroke, cardiovascular death, and all-cause mortality44; it is most frequently caused by atherosclerosis. Studies suggest that PVD is infrequently diagnosed and often undertreated in the primary care setting.45

Intermittent claudication associated with PVD is a reproducible discomfort of a muscle group that is induced by exercise and relieved by rest. It is frequently manifested during ambulation as pain in the buttocks, upper thighs, and calves. The differential diagnosis of claudication [see Table 10] can be challenging and requires a detailed history and physical examination supplemented with diagnostic testing.

Table 10 Differential Diagnosis of Claudication

Condition

History

Physical Examination

Diagnostic Tests

Comments

Peripheral vascular disease

Symptoms occur with exercise and are relieved by rest

Diminished or absent peripheral pulses

ABI, arterial duplex ultrasound

Angiography reserved for those with severe disease who are considering surgical or percutaneous revascularization

Lumbar spinal stenosis

Paresthesias occur with standing and walking

 

 

 

Symptoms are relieved by sitting and/or leaning forward

Normal peripheral pulses

Computed tomography or magnetic resonance imaging of the lumbar spine

Referred to as pseudoclaudication

History may include chronic low back pain and prior lumbar surgery

Arthritis

Pain localized to the joint area as opposed to adjacent muscles

Normal peripheral pulses

Radiograph of affected joint

 

Myalgia

Pain within a muscle group at rest and with exertion

Tenderness to palpation of the affected muscle group; reduced muscle strength

Laboratory evaluation of muscle inflammation with CPK, aldolase

Associated with hypothyroidism and end-stage renal disease; may be related to drug side effect (e.g., HMG-CoA reductase inhibitors)

No relief with rest

ABI—ankle-brachial index  CPK—creatinine phosphokinase

HISTORY AND PHYSICAL EXAMINATION

Claudication is described by patients as pain or cramping in the buttocks, thighs, and calf muscles. Symptoms typically occur during ambulation and are relieved by rest. Patients may also describe generalized weakness or a tired sensation within the legs. Depending on the extent of disease, men may experience impotence. Patients with severe disease may experience pain at rest. Patients with pain originating from compression of a nerve root describe an electric shock-like discomfort that frequently involves both legs and may be relieved by sitting down and leaning forward. More than one cause for leg symptoms may exist in a given patient, necessitating careful and clear delineation of each individual patient. Lumbar stenosis is another common cause of these symptoms (i.e., pseudoclaudication). The pain of pseudoclaudication is often poorly localized and may affect the leg from thigh to calf. Additional information that should be elicited from the history include the presence of a nonhealing ulcer or wound and previous manifestations of PVD, such as prior carotid endarterectomy. Risk factors associated with PVD are similar to those associated with CAD and include older age, cigarette smoking, diabetes mellitus, hypertension, and hyperlipidemia.

Physical examination should focus on assessment of all peripheral pulses, including the carotid, femoral, popliteal, dorsal pedis, and posterior tibial. Peripheral pulses should be described as normal, diminished, or absent, and the presence or absence of a bruit should be noted. For patients with severe PVD, the skin distal to the area of occlusion may be cold, and elevation of the legs may result in pallor of the soles of the feet. The presence and location of ulcers, skin wounds, and gangrene should be noted. Auscultation over the neck and abdomen may reveal bruits suggesting carotid artery stenosis and renal artery stenosis, repectively.

DIAGNOSTIC TESTS

The key diagnostic test in the evaluation of claudication is the ankle-to-brachial systolic pressure index (ABI). This involves measuring the systolic blood pressure in the ankle and the upper arm (brachial artery) in the supine position. The ankle systolic pressure is measured with a standard blood pressure cuff placed around the ankle, with the lower edge of the cuff situated above the malleoli. The blood pressure cuff is inflated to approximately 30 mm Hg above the systolic pressure to temporarily occlude flow. As the cuff is slowly deflated, a Doppler probe is used to monitor the signal; the pressure at which the Doppler flow signal is heard is recorded as the systolic pressure. A normal ABI is greater than 1.0; a value of less than 1.0 indicates the presence of PVD [see Table 11]. In addition to establishing the diagnosis of PVD, the ABI gives an assessment of disease severity and has prognostic implications for future cardiovascular and cerebrovascular events.46,47 Additional noninvasive imaging to evaluate the extent and severity of PVD may include an arterial duplex ultrasound. The vasculature from the abdominal aorta to the distal tibial arteries can be imaged to localize the area of stenosis and assess hemodynamic significance using the Doppler flow signals or Doppler velocity spectra.

Table 11 Ankle-Brachial Index (ABI) Values and Accompanying Findings in Peripheral Vascular Disease (PVD)

Condition

Symptoms

Physical Findings

ABI

Normal

None

None

> 1.0

Mild PVD

Mild claudication on exertion

Diminished pulses

0.8–0.9

Moderate PVD

Moderate or severe claudication on exertion

Diminished or absent pulses; nonhealing ulcers or skin wounds

0.5–0.8

Severe PVD

Severe claudication; symptoms may occur at rest

Absent pulses; nonhealing ulcers or skin wounds

< 0.5

Diagnostic angiography involves the use of cineangiographic imaging and radiographic contrast to image the peripheral vessels. Because angiography is an invasive procedure that carries a 1% risk of vascular complications, it is usually reserved for patients being considered for surgical or percutaneous (angioplasty and stenting) revascularization procedures; such procedures are undertaken to relieve limiting claudication, nonhealing ulcers, and severe ischemia [see Figure 5]. Magnetic resonance angiography is potentially useful in the initial evaluation of patients with renal insufficiency.

 

Figure 5. Peripheral Runoff

Abdominal aortogram showing peripheral runoff. (a) Mild irregularities of the peripheral vessels are present, but there is no evidence of severe disease. The arrow indicates mild irregularities of the right superficial femoral artery. (b) Severe peripheral vascular disease with occlusion of proximal right superficial femoral artery (arrowhead) is evident. The midportion of the right superficial femoral artery is reconstituted from collateral vessels supplied by the right profunda femoralis artery (circle).

A normal ABI excludes PVD as the cause of claudication and prompts investigation of alternative conditions as the underlying disorder [seeFigure 6].

 

Figure 6. Evaluation of Patients with Claudication

Evaluation of patients with claudication.

For patients with an abnormal ABI and mild symptoms, medical therapy can be initiated and risk factors modified.48 Patients with moderate to severe symptoms should undergo additional noninvasive testing using arterial Duplex ultrasound. Patients with limiting symptoms or threatened limb loss should undergo angiography in anticipation of surgical or percutaneous revascularization.

Cardiac Murmurs

BACKGROUND

The increased access to health care and the widespread use and availability of echocardiography have resulted in a large number of patients being diagnosed and evaluated for various cardiac murmurs. A cardiac murmur may indicate underlying valvular, congenital, or myocardial disease, but it may also be caused by systemic illnesses and occur in the setting of a structurally normal heart.

Cardiac murmurs result from disturbed or turbulent blood flow, often through diseased cardiac valves or intracardiac structures. The presence of a cardiac murmur, however, does not always indicate underlying cardiac pathology. Hyperthyroidism, anemia, and a febrile illness may all result in increased blood flow through the aortic valve and produce a soft, crescendo-decrescendo, systolic murmur over the aortic area. In this setting, the aortic valve is structurally normal, and the murmur is the result of augmented blood flow (i.e., a flow murmur) caused by the systemic illness. Another common cause of a systolic murmur is calcification of the aortic valve, which is referred to as aortic sclerosis when there is no obstruction to left ventricular outflow. Aortic sclerosis is a common finding in elderly patients; 25% of those older than 65 years are affected.49 This condition is often diagnosed when a systolic murmur is detected in an otherwise asymptomatic patient during a routine physical examination. In addition to being caused by diseases of the cardiac valves, murmurs may result from intracardiac communications (atrial and ventricular septal defects), congenital abnormalities (patent ductus arteriosus), and disease of the myocardium (hypertrophic cardiomyopathy).

A thorough history and physical examination can often provide the etiology of a murmur. Additional diagnostic tests, such as the ECG, chest roentgenogram, and echocardiogram, are used to confirm the diagnosis and establish the severity of the abnormality.

HISTORY AND PHYSICAL EXAMINATION

A history of a childhood murmur may indicate a congenital abnormality of a cardiac valve, such as a bicuspid or unicuspid aortic valve. A febrile illness occurring in childhood should raise the suspicion of rheumatic fever, possibly resulting in rheumatic mitral stenosis. Although rheumatic fever is uncommon in the United States, it may still be seen in immigrants from Asia, Latin America, and the Caribbean.

Establishing the presence or absence of cardiovascular symptoms is essential in the evaluation of a cardiac murmur. Otherwise healthy young adults without cardiac symptoms, with a systolic flow murmur and no other cardiac findings on examination, often require no additional evaluation.50 In contrast, the finding of a cardiac murmur in patients with cardiovascular symptoms must be further explored and a diagnosis established.

Aortic stenosis may result in the triad of angina, syncope, and impaired exercise tolerance or dyspnea on exertion. Patients with hypertrophic cardiomyopathy experience similar symptoms but may also complain of palpitations from associated atrial or ventricular arrhythmias. Hypertrophic cardiomyopathy is most commonly familial, with an autosomal dominant inheritance pattern; therefore, the patient should be questioned about a family history of sudden cardiac death, heart failure, and syncope. Symptoms of mitral stenosis include shortness of breath, impaired exercise tolerance, palpitations (from associated atrial fibrillation), and hemoptysis. These symptoms may occur during episodes of tachycardia, volume overload, or both as mitral valve flow is increased and the stenotic mitral valve impairs filling of the left ventricle. Asymptomatic women with mitral stenosis may develop symptoms during pregnancy. Mitral and aortic regurgitation cause a volume overload to the left atrium and left ventricle, respectively, and may result in shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, and impaired exercise capacity. A ventricular septal defect is either congenital or ischemic (e.g., occurring after a myocardial infarction). The congenital form often becomes apparent during adolescence; the ischemic form presents several days after a myocardial infarction as a new holosystolic murmur associated with significant respiratory distress.

The physical examination begins with determining the timing of the murmur in the cardiac cycle—systolic, diastolic, or continuous [see Table 12]. The grade, quality, location, area of radiation, and change in intensity with maneuvers should then be described. Murmurs are graded on a scale of 1 to 6. Grade 1 is a soft intermittent murmur, grade 4 is a palpable murmur, and grade 6 is a murmur that can be appreciated without a stethoscope. Thus, most murmurs are classified as grade 2 or 3. Midsystolic murmurs are derived from the aortic or pulmonic valves or occur in association with hypertrophic cardiomyopathy. In contrast, holosystolic murmurs are the result of regurgitant blood flow through either the mitral or the tricuspid valves or a ventricular septal defect. The murmur of a ventricular septal defect is usually well localized to the fourth left intercostal space, does not radiate significantly, and is often associated with a thrill (i.e., grade 4 or higher). Late systolic murmurs occur from mitral regurgitation that is secondary to (1) ischemia or infarction to the papillary muscles (ischemic mitral regurgitation), (2) left ventricular dilatation with functional mitral regurgitation, or (3) mitral valve prolapse. Additional findings on cardiac auscultation, such as a fixed, split second heart sound or an ejection sound, may be helpful in determining the etiology of a systolic murmur [see Table 13]. Electronic stethoscopes and handheld ultrasound devices have begun to supplement the bedside evaluation of cardiac murmurs.

Table 12 Differential Diagnosis of a Cardiac Murmur Based on Timing of Cardiac Cycle

Systolic

  Midsystolic

    Innocent flow murmur

    Aortic stenosis

    Pulmonic stenosis

    Atrial septal defect

  Holosystolic

    Ventricular septal defect

    Tricuspid regurgitation

    Hypertrophic cardiomyopathy

    Mitral regurgitation

Diastolic

  Early diastolic

    Aortic regurgitation

    Pulmonic regurgitation

  Middiastolic

    Mitral stenosis

    Tricuspid stenosis

    Austin Flint murmur associated with chronic aortic regurgitation

    Severe mitral regurgitation (augmented antegrade mitral valve flow)

Continuous

  Patent ductus arteriosus

Table 13 Physical Findings Useful for Evaluating a Cardiac Murmur

Condition

Timing

Location

Radiation

Characteristics

Effects of Maneuvers

Associated Findings

Innocent flow murmur

Midsystolic

Base

Variable or none

Soft, ejection

No change

None

Aortic stenosis

Systolic

Base (right second ICS)

Carotid arteries

Crescendo-decrescendo

Decrease with handgrip or standing

Single S2, delayed and decreased carotid upstroke, ES if mobile valve leaflets

Mitral regurgitation

Systolic

Apex

Axilla (sometimes back)

Holosystolic

Increase with handgrip

Hyperdynamic apical impulse

Ventricular septal defect

Systolic

Left sternal border

None

Holosystolic

No change

Palpable thrill

Atrial septal defect

Systolic

Left second ICS

None

Crescendo-decrescendo

Possible increase with inspiration

Fixed split S2

Hypertrophic cardiomyopathy

Systolic

Base

Carotid arteries

Late-peaking crescendo

Increase with standing and strain phase of Valsalva maneuver

Brisk carotid upstroke

Tricuspid regurgitation

Systolic

Left lower sternal border

Right lower sternal border

Holosystolic

Increase with inspiration

Prominent v waves in JVP, pulsatile liver

Pulmonic stenosis

Systolic

Left second ICS

None

Crescendo-decrescendo

No change

ES if mobile valve leaflets

Aortic regurgitation

Diastolic

Left sternal border

None

Decrescendo, high-pitched

Increase with handgrip

Wide pulse pressure, displaced and enlarged apical impulse

Mitral stenosis

Diastolic

Apex

None

Low-pitched rumble, presystolic accentuation

Best heard in left lateral decubitus position

Loud S1, opening snap

Pulmonic regurgitation

Diastolic

Left second ICS

Left sternal border

Decrescendo

May increase with inspiration

Tricuspid stenosis

Diastolic

Right lower sternal border

Right upper abdomen

Low-pitched rumble

Increase with inspiration

Right ventricular heave

Patent ductus arteriosus

Continuous

Left second ICS

Back

Machinery-like

None

Wide pulse pressure, bounding pulses

ES—ejection sound  ICS—intercostal space  JVP—jugular venous pulse  S1, S2—first, second heart sounds

Diastolic murmurs always indicate underlying cardiac pathology and commonly occur in either early diastole or middiastole. Early diastolic murmurs begin at the onset of diastole (i.e., with the second heart sound) and originate from regurgitant flow across the pulmonic and aortic valves. Aortic regurgitation occurs because of failure of the aortic valve leaflets to adequately coadapt during diastole and may be the result of disease processes affecting the aortic valve (e.g., endocarditis) or the aortic root (e.g., aortic dissection). Pulmonary regurgitation is most commonly seen in patients with pulmonary hypertension and is therefore associated with a loud second heart sound. Middiastolic murmurs occur from either mitral or tricuspid stenosis; the Austin Flint murmur associated with chronic aortic regurgitation or occurring in the setting of severe mitral regurgitation arises from augmented antegrade flow across the mitral valve in diastole.

In adults, continuous murmurs are usually from a previously undiagnosed patent ductus arteriosus. Occasionally, a patient with chronic aortic regurgitation may have a prominent systolic murmur in addition to the early diastolic murmur, thus simulating a continuous murmur. The systolic murmur in this case is the result of enhanced stroke volume from increased diastolic filling of the left ventricle. Whereas both conditions are associated with a widened pulse pressure and murmurs that occur during both systole and diastole, the murmur of a patent ductus arteriosus is continuous and peaks on the second heart sound; with chronic aortic regurgitation, there is a so-called silent period at the end of systole as the systolic murmur fades, before the beginning of the diastolic murmur.

Additional findings on physical examination can assist in determining the severity of the valve lesion and in excluding other conditions that result in similar murmurs. For patients with a midsystolic murmur presumed to be aortic stenosis, the carotid upstroke and splitting of the second heart sound should be carefully evaluated. A delayed carotid upstroke and single splitting of the second heart sound indicate hemodynamically severe aortic stenosis. However, physical examination has a low sensitivity for diagnosis of severe aortic stenosis, and overreliance on examination findings can lead to serious errors. The threshold for diagnostic imaging should be low in a patient with possible aortic valve stenosis. In contrast, hypertrophic cardiomyopathy results in a brisk carotid upstroke (the so-called spike-and-dome configuration) and normal splitting of the second heart sound. Severe mitral regurgitation can be identified by a holosystolic murmur associated with a third heart sound and a middiastolic murmur that results from the increased blood flow crossing antegrade across the mitral valve in diastole.

Several bedside maneuvers may also be useful in the evaluation of cardiac murmurs.51 Right-sided murmurs (e.g., tricuspid regurgitation) increase in intensity during inspiration because of augmented right heart filling. The murmur of hypertrophic cardiomyopathy is extremely dependent on left ventricular filling, such that both the strain phase of the Valsalva maneuver and moving from squatting to the standing position augment the intensity of the murmur.

DIAGNOSTIC EVALUATION

An ECG should be obtained to evaluate for the presence of cardiac chamber enlargement and hypertrophy. Aortic stenosis imposes a pressure overload to the left ventricle, resulting in left ventricular hypertrophy by ECG in approximately 50% of patients. Hypertrophic cardiomyopathy is characterized by increased ventricular muscle mass, which is usually apparent on the ECG with extreme voltage amplitudes and small Q waves in leads I, aVL, and V4 through V6, referred to as septal Q waves. Mitral stenosis results in left atrial enlargement and occasionally right axis deviation and right ventricular hypertrophy.

A chest roentgenogram should be reviewed for chamber enlargement and the presence of calcification. Chronic aortic and mitral insufficiency cause a volume overload to the left ventricle and left atrium, respectively. Left atrial enlargement, without enlargement of the left ventricle, and mitral valve calcification suggest mitral stenosis. Calcification of the aortic valve frequently occurs with valvular aortic stenosis but is rarely apparent on the chest roentgenogram.

In the absence of cardiovascular symptoms and other physical findings, a grade 1 or grade 2 midsystolic murmur does not require additional evaluation [see Figure 7].50 Midsystolic murmurs of grade 3 and higher, holosystolic murmurs, or late systolic murmurs should be further evaluated by echocardiography. All patients with a diastolic or continuous murmur should be referred for echocardiography because these murmurs always indicate underlying cardiac pathology. In addition to confirming the etiology of a cardiac murmur, echocardiography provides evaluation of left ventricular systolic and diastolic function, wall motion abnormalities (that may indicate associated CAD), and estimation of pulmonary arterial pressures. For patients with valvular, congenital, or myocardial diseases, echocardiography provides a baseline from which additional studies can be obtained and used to follow disease progression over time.

 

Figure 7. Evaluation of Patients with Cardiac Murmurs

Evaluation of patients with cardiac murmurs.45

Cardiovascular Information on the Internet

There are numerous sources of cardiovascular information on the Internet. The most useful general information sites are listed [see Sidebar Pertinent Web Sites].

Pertinent Web Sites

http://www.americanheart.org

The American Heart Association maintains this site with information on recent cardiovascular trials, local and national meetings, information for patients, and clinical guidelines.

http://www.acc.org

The American College of Cardiology maintains this site with information on recent cardiovascular trials, local and national meetings, and clinical guidelines.

http://www.theheart.org

This excellent site has current information on clinical trials, pertinent articles, clinical cases, discussion forums, cybersessions, and links to other cardiovascular sites. It frequently has summaries of clinical trials recently reported at the major cardiology meetings.

http://www.vssgbi.org

The Vascular Surgical Society of Great Britain and Ireland maintains this site, which provides patient information.

http://www.tasc-pad.org

The Trans-Atlantic Inter-Society Consensus on the Management of Peripheral Arterial Disease offers management recommendations for intermittent claudication, acute limb ischemia, and critical limb ischemia.

References

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Editors: Dale, David C.; Federman, Daniel D.