The History, Physical Examination, and Cardiac …

A carefully obtained history is the cornerstone for evaluating a patient with known or suspected cardiac disease.2 A deliberate, compassionate interview forms the basis for a patientphysician relationship that can continue indefinitely. Unfortunately, the interview can result in adversarial roles for physician and patient if the interviewer appears hurried, shows impatience, fails to establish eye contact, seems to treat dreaded diseases casually, or appears to be unsympathetic. When the medical interview is unsatisfactory because of poor communication and lack of rapport, inaccurate information and often unnecessary testing will be obtained. Also, important facts not revealed during a meticulous initial history are usually not detected later because both the patient and physician become focused on high-technology studies and more aggressive therapeutic interventions.

The patients chief complaint, which requires further elaboration and investigation, may not identify his or her most serious problem. Therefore, symptoms other than the patients chief complaint must be defined. The interviewer should note all existing symptoms and establish a present illness for each of these.

A medical questionnaire given to the patient well in advance of the interview is useful and can record important data more accurately because of the time thus made available to reflect and check details.

A proper interpretation of the past history is important; the physician should not accept a past event as a fact when the evidence is not well established. Information obtained from family members about the patients symptoms and his or her response to the illness is extremely important.

Serious heart disease can occur in patients with mild or no symptoms. The physician must determine whether or not the history obtained is sufficient to support a decision-making process about the patient.2 Although many patients with severe heart disease have no symptoms, others have many symptoms associated with minor or no disease.

Some patients deny symptoms because they cannot accept the reality of the situation, and others purposely withhold information so as not to jeopardize their jobs.2 Some patients overstate their symptoms for personal gain. Elderly patients, sedentary patients, and those with other illnesses can have no symptoms because they are not physically active enough to induce them.

The past history can provide important clues to the presence of cardiovascular disease. A definite history of rheumatic fever can be useful in defining the cause of a heart murmur (see Chap. 75), but a negative history does not exclude it. A history of hypertension in a family member increases the likelihood that the patient has essential hypertension.3 Previous trauma may be the cause of constrictive pericarditis, a thoracic aortic aneurysm, an arteriovenous fistula, and other types of cardiac lesions. A detailed history of the use of medications, addicting drugs, and alcohol, each of which can cause heart disease, is essential. A past history of pulmonary embolism, thrombophlebitis, or systemic embolism should be ascertained.

A history of dental work, some other diagnostic or therapeutic procedure, or recent infection suggests infective endocarditis in a patient with valvular heart disease. Patients often give a history of a heart attack that, in fact, can have been an episode of unstable angina, heart failure, or arrhythmia. The heart attack history often becomes myocardial infarction (MI) in the patients medical record unless more information is obtained or documentation of the event is reviewed.

Many patients are referred who have had several catheterizations, percutaneous coronary interventions, and one or more coronary bypass operations in addition to multiple noninvasive tests. A thorough and often time-consuming review of records from other institutions, operative notes, cineangiographic films, and noninvasive studies will often provide an accurate assessment of the patients current status without the unnecessary repetition of expensive and potentially risky procedures.4

Past and present therapeutic regimens must be reviewed carefully. Previous treatment programs may have been inappropriate or suboptimal. Drugs used for the treatment of patients with cardiovascular diseases have potential side effects that can produce both cardiovascular and noncardiovascular symptoms (see Chap. 95).

Multiple risk factors for developing coronary heart disease (CHD) have been identified, including age, male gender, hypertension, hypercholesterolemia, a low level of high-density lipoprotein (HDL) cholesterol, cigarette smoking, diabetes, and a family history of premature atherosclerosis (see Chap. 50).

Information from previous health evaluations should be sought. Patients have often been examined for military service, athletics, or insurance, and they might have been told of a heart murmur or hypertension on those occasions5 or were rejected for medical insurance or military service. Many patients have never had a careful examination of the cardiovascular system.

The increasing hemodynamic burden of pregnancy can cause an otherwise marginally compensated cardiac patient to become symptomatic (see Chap. 97). Specific inquiry should be made about heart failure, edema, dyspnea, or prescribed prolonged periods of bedrest during pregnancy. Many normal women have had a murmur detected during pregnancy. A history of illicit parenteral drug use should raise the suspicion of infective endocarditis, especially in a febrile patient (see Chap. 86). Cocaine can cause coronary artery vasospasm and also raise myocardial oxygen demand by increasing heart rate and blood pressure. Angina, MI, and sudden cardiac death after cocaine use have been well documented (see Chap. 95).

A history of moderate to excessive alcohol consumption, an enlarged heart on a prior chest radiograph, periods of rapid weight gain or loss, and other illnesses can provide important information.

A family history of congenital heart disease indicates a higher risk of a congenital heart lesion (see Chap. 84). If the patients mother gives a history of rubella during the first few months of pregnancy, this increases the likelihood that the patient has patent ductus arteriosus, pulmonic valve stenosis, coarctation of the pulmonary arteries, or atrial septal defect (ASD).

Although many of the common cardiovascular diseases are sporadic, genetic transmission has been documented in a rapidly increasing number of disease entities. These are detailed elsewhere (see Chap. 82).

Chest pain or chest discomfort is the foremost manifestation of myocardial ischemia and results from a disparity between myocardial oxygen demand and coronary blood flow (CBF) in patients with CAD. The most common causes of myocardial ischemia are coronary atherosclerosis, coronary vasoconstriction, and coronary artery thrombosis, the latter occurring particularly in patients with acute coronary syndromes (ACS) such as acute MI and unstable angina (see Chaps. 58 and 59). An increase in myocardial oxygen consumption (MVO2) or demand ischemia, a decrease in or inadequate blood flow (supply ischemia), or their combination can be responsible for anginal chest pain (see Chap. 53).

The mechanism responsible for cardiac pain is not clearly understood. Nonmedullated small sympathetic nerve fibers that parallel the coronary arteries are thought to provide the afferent sensory pathway for angina; these enter the spinal cord in the C8 to T4 segments. Impulses are transmitted to corresponding spinal ganglia and then through the spinal cord to the thalamus and cerebral cortex. Angina pectoris, similar to other pain of visceral origin, is often poorly localized and is commonly referred to the corresponding segmental dermatomes.

The differential diagnosis of chest pain is extensive.4 In addition to angina pectoris and MI, other cardiovascular diseases, gastrointestinal diseases, psychogenic diseases, neuromuscular diseases, and diseases of the pulmonary system must be considered (Table 141). An accurate interpretation of the cause and significance of chest discomfort is critically dependent on a carefully taken history. Important, clinically relevant information can be missed if the overenthusiastic use of noninvasive or invasive diagnostic methods replaces rather than augments direct physicianpatient communication (See Chap. 63).

The original subjective description of angina pectoris by William Heberden3 in the late 18th century has not been surpassed. It is quoted in Chap. 63. Angina pectoris is defined as chest pain or discomfort of cardiac origin that usually results from a temporary imbalance between myocardial oxygen supply and demand.6 It can occur only with exertion or spontaneously at rest; various subtypes are defined in Chap. 63. The quality of the chest discomfort is usually described as tightness, pressure, burning, heaviness, aching, strangling, or compression. The patient is usually able to describe a deep rather than a superficial origin of the pain. Because the qualitative description of the pain is greatly influenced by the patients intelligence, education, and social and cultural background, a delineation of the other characteristics of the chest discomfort is often extremely important in evaluating the symptoms appropriately. The most important of these characteristics are the precipitating factors for the onset of pain, its mode of onset and duration, its pattern of disappearance, and its location. Classically, the discomfort is induced by exercise, emotion, eating, or cold weather.

A recognizable pattern of reproducibility of chest pain by certain activities is an important characteristic of angina. Often, patients develop pain with exertion after meals, and there is a greater tendency for arm work (a greater degree of isometric exercise) to produce distress. Occasionally, angina will dissipate despite continued exercise (the walk-through phenomenon) or will not occur when a second exercise effort is undertaken that previously produced chest discomfort (warmup phenomenon). Both circumstances can be attributed to the opening of functioning coronary arterial collaterals during the initial myocardial ischemia. This is consistent with ischemic preconditioning as described elsewhere (see Chap. 53).

Angina commonly occurs after the patient has eaten a heavy meal or when he or she is excited, angry, or tense. Whereas cold showers increase blood pressure and heart rate, hot showers cause an augmented cardiac output in response to vasodilation. Either can precipitate angina after exercise. The chest pain during any activity is often made worse by the use of tobacco. All of the hemodynamic changes caused by the use of nicotine increase myocardial oxygen demand.

Angina pectoris characteristically has a crescendo pattern at onset and builds up. Pains, often described as shooting or stabbing, that reach their maximum intensity virtually instantaneously are often not angina but are of musculoskeletal or neural origin. Angina is usually relieved within 5 to 20 minutes by rest with or without the use of vasodilator drugs such as nitroglycerin (TNG), although sublingual TNG or TNG spray characteristically hastens relief. Failure to obtain relief with rest or TNG suggests another cause of pain or actual impending MI. The reproducible relief of chest pain in an appropriate time frame (usually within 10 minutes) is strong evidence favoring ischemia. A trial of TNG can be a useful diagnostic strategy. Patients with angina pectoris are usually classified functionally from class I to class IV (Table 142), depending on the amount of activity necessary to induce chest pain.

Localizing the site of chest discomfort provides additional information as to its cause. Anginal pain is ordinarily retrosternal or felt slightly to the left of the midline beside or partly under the sternum. It is rarely isolated to the cardiac apex in the inframammary region. The chest pain of myocardial ischemia tends to radiate bilaterally across the chest into the arms (left more than right) and into the neck and lower jaw. Occasionally, radiation to the back or occiput is noted. In the arms, the pain passes down the ulnar and volar surface to the wrist and then only into the ulnar fingers, rarely into the thumb or down the outer (extensor) surface of the arm, which has a different dermatome pattern. Pain can occasionally be felt only in the arm or can start in the arm and radiate to the chest. Noting the patients gestures in characterizing and localizing the site of pain can be useful. One or two clenched fists held by the patient over the sternal area (Levine sign) is much more indicative of ischemic pain than is a finger pointed to a small, circumscribed area in the left inframammary region. The latter is likely an indicator of psychogenic pain.

The duration of chest pain can also be a useful differentiating feature. Angina pectoris rarely lasts less than 1 minute or more than 20 minutes in the absence of MI or persistent arrhythmias. Most patients with angina report prompt relief in less than 5 minutes after cessation of activity or with the use of sublingual or spray TNG. Carotid sinus massage should be performed only in the absence of extracranial occlusive cerebrovascular disease as indicated by carotid bruits or decreased carotid arterial pulsations and with careful auscultatory monitoring of the heart rate. The Valsalva maneuver can also relieve anginal pain by decreasing myocardial wall stress because of the reduced venous return and left ventricular (LV) volume accompanying the increase in intrathoracic pressure. Associated symptomssuch as nausea, vomiting, faintness, fatigue, or diaphoresisoften accompany severe episodes of myocardial ischemia. Severe myocardial ischemia often produces marked dyspnea caused by a large increase in LV diastolic filling pressure, sometimes producing an angina equivalent in the absence of chest discomfort.7,8

Linked angina is a term applied to definite episodes of angina in patients with established CAD caused by gastrointestinal factors unrelated to an increase in cardiac work. Episodes are typically induced by stooping or occur after eating; they can be mimicked by esophageal acid stimulation, which can reduce CBF.

No consideration of myocardial ischemia as a likely cause of chest discomfort is complete without carefully considering the chest pain in the context of known risk factors for CAD (see Chap. 50).

Angina pectoris should be considered a symptom and not a specific disease. Coronary arteriographic studies have demonstrated that more than 90% of patients with chest pain precipitated by exercise and relieved by rest have angiographic evidence of significant CAD.9 However, other diseases can be associated with classic angina pectoris.

Several reports have described certain patients with typical exertional chest discomfort and arteriographically normal coronary arteries. These patients are more likely to be women; have fewer coronary risk factors; and have variable responses to various antianginal agents, including TNG. Although the underlying cause of this condition remains unsettled, the life expectancy of these patients appears no different from that of an age- and gender-matched population without chest discomfort.

Some evidence suggests that abnormal function of small coronary arteries can cause limited CBF responses to stress or pharmacologic vasodilators in a subset of patients with anginal chest pain despite angiographically normal coronary arteries (microvascular angina). In the past, investigators arguing for or against the existence of this syndrome have often used the term syndrome X to describe their patient cohort. Syndrome X appears to include a heterogeneous group of patients with a wide spectrum of chest pain and a variety of hypersensitive vascular and smooth muscle constrictor responses. Multiple research studies continue in an effort to explain syndrome X. The term syndrome X is a poor substitute for chest pain in patients with normal large vessel coronary arteriography. It is likely to represent a polyglot of disorders. It must be distinguished from the metabolic syndrome (X) of insulin resistance (glucose intolerance), hypertension, hyperlipidemia, and upper body obesity. The latter is often associated with severe vascular disease and frequently abnormal coronary arteriography. Some patients with classic angina but near-normal contrast laminography and angiography fail to demonstrate areas of plaque formation because of coronary artery remodeling. Intracoronary ultrasonography often demonstrates plaque of various size, volume, and location when CHD is present.

Some patients with CAD experience angina at rest as a complication or an isolated clinical manifestation of ischemic heart disease.10 Myocardial ischemic pain at rest more likely results from an acute reduction in CBF than from an increase in MVO2. Possible causative factors include isolated coronary artery spasm or embolism, coronary artery spasm superimposed on coronary atherosclerosis (a common occurrence), and coronary thrombosis with spontaneous thrombolysis. In patients with progressive coronary atherosclerosis, however, ischemic rest pain also can result from intermittent arrhythmias that increase MVO2 or decrease CBF or from labile hypertension, with its increased systolic wall stress. Chest pain at rest can occur only as nocturnal angina. In addition, nocturnal angina (also known as angina decubitus) can be produced by the increase in LV wall stress and as a result of the redistribution of the intravascular blood volume in the recumbent position.

The relative hypercapnia and acidosis that occur during sleep can also contribute to nocturnal angina (see Chap. 73). The diagnosis of sleep apnea is often overlooked in patients with angina, heart failure, and arrhythmia. Nocturnal angina has been accompanied by concomitant rapid eye movement sleep patterns on the electroencephalogram, which can be associated with augmented sympathetic discharge increasing or causing coronary constriction11-14 (see Chap. 63).

The quality of pain with rest angina is usually similar to that of exertional angina, but the discomfort can be more severe and its duration longer. In addition, angina at rest is commonly associated with nausea, vomiting, and diaphoresis. The onset of shortness of breath during or after the beginning of chest discomfort suggests that the pain is caused by extensive myocardial ischemia and results from an acute elevation of LV filling pressure secondary to the development of a large, transiently ischemic myocardial segment. Such patients commonly have multivessel occlusive CAD on arteriography.

It is important to emphasize that a significant number of individuals with clinically important CAD will have no symptoms, minimal symptoms, or atypical symptoms. This is particularly true of the elderly population, diabetic patients, and women.7 For example, dyspnea on exertion in the absence of chest pain may be an anginal equivalent that reflects acute pulmonary venous congestion in an individual with a large area of reversible ischemia-induced LV dysfunction or transient mitral regurgitation caused by papillary muscle dysfunction.

Chest pain or discomfort resulting from MI is qualitatively similar to angina at rest. Differentiating the pain resulting from ischemia and that caused by MI is often impossible based on the history alone. Pain associated with ACS is usually more severe and longer lasting than anginal pain and is often associated with nausea, vomiting, and diaphoresis (see Chaps. 58 and 59). In addition, MI or other ACS is frequently accompanied by symptoms of sustained LV dysfunction (dyspnea, orthopnea) and evidence of autonomic nervous system hyperactivity (tachycardia, diaphoresis, bradycardia). Painless or atypical presentations of MI, however, occur in up to 40% of patients, particularly in diabetic and elderly patients. Thus, determination of serial serum enzymes, isoenzymes, and other serum biomarkers (eg, troponin I or T); providing evidence of myocardial necrosis; and serial electrocardiograms (ECGs) indicating myocardial injury are necessary to establish the diagnosis (see Chaps. 58 and 59).

There are two groups of cardiovascular diseases causing chest pain that is not caused by coronary atherosclerosis (see Table 141). The first group consists of cardiac diseases causing myocardial ischemiarelated angina in the absence of CAD. Ischemia is caused by hemodynamic changes associated with an inadequate CBF in relation to a normal or increased myocardial oxygen demand. Among these are aortic valve stenosis (see Chap. 76), hypertrophic cardiomyopathy (HCM; see Chap. 35), and systemic arterial hypertension (see Chap. 69), in which LV systolic pressure and LV wall tension are greatly increased or LV hypertrophy is present. Chest pain caused by myocardial ischemia may also occur with severe aortic regurgitation (AR) (see Chap. 76). The large LV volume load increases LV end diastolic pressure and the reduced diastolic perfusion pressure results in a relatively inadequate CBF. Occasionally, very severe anemia or hypoxia can also produce myocardial ischemia as a result of inadequate oxygen blood supply even in the absence of associated CAD. Both also can increase angina in the presence of obstructive CAD. In addition, severe right ventricular (RV) systolic hypertension, as often occurs with pulmonic stenosis (PS), or pulmonary hypertension (PH), can cause exertional angina, presumably on the basis of RV subendocardial ischemia.

A second group of cardiac diseases causing chest pain not usually caused by myocardial ischemia includes pericarditis (see Chap. 85), aortic dissection (see Chap. 106), and mitral valve prolapse (MVP) (see Chap. 77). Pericarditis is a relatively common cause of chest pain. It is most often sharp and penetrating in quality; patients often obtain relief by sitting up and bending forward. The cardinal diagnostic feature of pericardial pain is its frequent worsening by changes in body position, during deep inspiration, and occasionally on swallowing. The chest discomfort can radiate to the shoulders, upper back, and neck because of irritation of the diaphragmatic pleura, which is innervated through the phrenic nerve by fibers originating in sympathetic ganglia C3 to C5. Therefore, the chest discomfort associated with pericarditis is caused predominantly by parietal pleural irritation. Occasionally, the pain of acute benign, presumptive viral pericarditis can mimic that observed in acute MI. Importantly, the most common cause of pericarditis in middle- aged or older people is acute MI. The pericarditis usually occurs several days after the myocardial necrosis and must be distinguished from recurrent infarction or ischemia. Pericarditis can also be a cause of chest pain after cardiac surgery and can be a complication of aortic dissection, with leakage into the pericardium.

Aortic dissection (see Chap. 106) can be misdiagnosed on initial presentation as an acute MI; indeed, MI is a recognized complication of aortic dissection. The pain with dissection, however, is usually of sudden onset compared with that of myocardial ischemia, which builds in intensity with time.11 Patients frequently characterize the pain as excruciating, having a tearing quality, and commonly localized to the interscapular area. The discomfort can radiate widely into the neck, back, abdomen, flanks, and legs and can migrate, depending on the location and progression of the aortic dissection and the amount of arterial luminal compression. Neurologic symptoms and signs may occur when dissection involves the cerebral arteries. With the exception of patients with Marfan syndrome or idiopathic cystic medial necrosis, most patients with aortic dissection have a history of long-standing systemic arterial hypertension or evidence of it on physical examination or by ECG (left ventricular hypertrophy [LVH]).

Psychogenic chest discomfort is a common recurrent chest pain that can be difficult to separate from angina pectoris, particularly when it occurs in patients with multiple risk factors for CAD or in otherwise asymptomatic patients with well-documented CAD. The most common psychogenic cause of chest discomfort is anxiety (see Chap. 96). Psychogenic chest pain is often described as sharp or stabbing, localized to the left inframammary area, and usually sharply circumscribed. Descriptors such as stabbing or lightning-like can be used to describe extremely short (<1 minute) episodes of pain. At times, the pain can persist for many hours or several days. Patients often note psychogenic pain at rest. Also, nonvocal communicationsuch as a flat or worried facial expression, retarded motor activity, and hand wringingcan indicate underlying depression. Observation of the patient during pain that occurs spontaneously or during exercise testing often provides insight into a potential psychogenic etiology. Patients with anxiety often have multiple complaints. Associated symptomssuch as air hunger, circumoral paresthesias, globus hystericus, and multiple somatic complaintsmay suggest a neurasthenic personality or hyperventilation syndrome.

Pain originating in the gastrointestinal tract, particularly that of esophageal origin, is commonly confused with ischemic chest pain.12-14 Diffuse esophageal spasm, a neuromuscular motor disorder of the esophagus characterized by chest pain, is the extracardiac condition most frequently confused with angina pectoris. Esophageal spasm can occur at any age but is more common in 50- to 60-year-old individuals. The pain is usually retrosternal; can be burning, squeezing, or aching in quality; and often radiates to the back, arms, and jaw. It usually begins during or after a meal and can last minutes or hours. The pain can be relieved by TNG, which also relaxes esophageal smooth muscle. A useful diagnostic feature in esophageal spasm is its frequent association with pain as a result of swallowing, dysphagia, and the regurgitation of gastric contents. The diagnosis of diffuse esophageal spasm is based on the history, the exclusion of cardiac and musculoskeletal causes of chest pain, and the demonstration of abnormal esophageal motility on cine-esophagograms or by esophageal manometry.

Reflux esophagitis results from mucosal irritation produced by failure of the lower esophageal sphincter to prevent regurgitation of highly acidic gastric contents into the distal esophagus. The pain is usually epigastric or retrosternal, burning in quality, and frequently precipitated by the recumbent position or by bending over. Heartburn and regurgitation often occur after meals or ingestion of coffee or after postural changes. Patients are often awakened by chest discomfort caused by acid reflux occurring in the recumbent position. Dysphagia may result from stricture formation secondary to long-standing esophageal reflux. An upper gastrointestinal x-ray series can demonstrate hiatal hernia, but this does not establish the diagnosis of esophagitis or esophageal reflux. Esophagoscopy and esophageal biopsy can demonstrate mucosal lesions and are useful for assessing the severity of inflammation and for excluding malignancy. Sphincter incompetence can be documented by the use of esophageal manometry. Esophageal acid perfusion testing (Bernstein test) often provokes the patients characteristic symptoms, and distal esophageal pH monitoring will detect gastroesophageal reflux.15

Acute esophageal rupture, a serious and often rapidly lethal event, causes severe retrosternal pain secondary to the chemical mediastinitis produced by acidic gastric contents. Spontaneous rupture usually results from a prolonged bout of vomiting or retching after a heavy meal. The pain varies in location depending on the ruptures site and position. The diagnosis is based on symptoms and signs of mediastinal air after vomiting or esophageal instrumentation.

Although peptic ulcer disease and biliary colic are less commonly confused with chest pain of cardiac origin, myocardial ischemic pain can occasionally be described as burning in character and located near the epigastrium.

Diseases involving the neuromuscular and skeletal systems can cause pain affecting dermatomal patterns similar to those occurring with angina pectoris. The thoracic outlet syndromes, in which various neural and vascular structures are compressed, can produce symptoms that are sometimes confused with cardiac chest pain. Although compression of the neurovascular bundle by a cervical rib or the scalenus anterior muscle can cause discomfort radiating to the head and neck, the shoulder region, or the axilla, most patients experience pain in the upper extremity ulnar distribution resulting from somatic nerve compression. The presence of associated paresthesias and pain unrelated to physical exercise as well as the worsening of discomfort with certain body positions are useful differentiating characteristics.

Tietze syndrome, or idiopathic costochondritis, is an occasional cause of anterior chest wall pain that is aggravated by movement and deep breathing. Reproducing the chest pain syndrome by direct pressure over the involved costochondral junction or the relief of pain after local infiltration with lidocaine is a helpful diagnostic maneuver. Degenerative arthritis of the cervical and thoracic vertebrae can cause bandlike pain confined to the chest, neck, or back that often radiates to the arms. Radiologic evidence of degenerative changes involving the cervical and thoracic vertebrae is often found in asymptomatic elderly patients. The production or exacerbation of pain by various postures, movement, sneezing, or coughing is more useful in the diagnosis of chest discomfort caused by vertebral disease.

The preeruptive stage of herpes zoster can be characterized by bandlike chest pain over one or more dermatomes. The advanced age of the patient; additional symptoms of malaise, headache, and fever; the presence of hyperesthesia of the involved area on physical examination; and the eventual eruption of typical lesions 4 or 5 days after the onset of symptoms will result in the correct diagnosis. Chest wall pain and tenderness can also occur for unknown reasons. The discomfort can be reproduced by pressure over the painful area and by movements of the thorax such as bending, twisting, or turning.

The syndrome of acute massive pulmonary embolism with its associated acute PH and low cardiac output occasionally can simulate acute MI because myocardial ischemia can be present in both conditions. The quality of chest pain can be identical to that observed in patients with nonradiating ischemic chest pain or can be pleuritic. The associated signs of severe dyspnea, tachypnea, and intense cyanosis accompanied by profound anxiety and agitation, however, favor the diagnosis of pulmonary embolism9-12 (see Chap. 72). Measurements of arterial blood gases, CT angiography, or pulmonary ventilation/perfusion scans, and if needed, pulmonary arteriography will establish the correct diagnosis.

Other pulmonary conditions associated with chest discomfort, such as pneumothorax, are rarely confused with ischemic chest pain because of additional characteristic clinical features. Spontaneous pneumothorax usually occurs in otherwise healthy men in the third and fourth decades of life. The clinical presentation is usually characterized by the abrupt onset of agonizing unilateral pleuritic chest pain associated with severe shortness of breath. The plain or expiratory chest film provides the definitive diagnosis. Chest pain associated with pneumonias of various causes as well as pulmonary infarctions as a consequence of pulmonary embolus may result from pleural irritation. The discomfort is sharp, varies acutely with breathing, and is frequently accompanied by a reduced inspiratory effort. Associated signs of pulmonary parenchymal infection or infarction usually indicate the underlying diagnosis.

Intermittent claudication of the lower extremities caused by peripheral atherosclerosis (see Chap. 109) can present as discomfort during exercise in the arch of the foot, calf of the leg, thighs, hips, or gluteal region. Acute arterial occlusion in the lower extremities caused by systemic embolism can cause the sensation of hypesthesia and or pain. The pain of Raynaud disease can be noted in the fingers after exposure to cold, with pallor of the fingers before the sensation of pain. Pain and swelling of lower extremities can be caused by thrombophlebitis.

Head pain secondary to myocardial ischemia can be felt in the jaw, hard palate, and cheek and sometimes deep in the ear canals. The pain of temporal arteritis, commonly localized to the temporal area, is often associated with abnormal vision and polymyalgia rheumatica. A severe headache can be present in patients with uncontrolled hypertension (see Chap. 68).

Pain in the abdomen, often localized to the midabdomen and lower portion of the back, can be produced by an expanding or rupturing atherosclerotic abdominal aneurysm. Abdominal angina caused by vascular disease of the mesenteric arteries is discussed in Chap. 106. The liver is often painful and tender in severe right-sided heart failure, with worsening of the pain during activity.

Various types of joint pain can be associated with heart disease (see Chaps. 75 and 89). Rheumatic fever, rheumatoid arthritis, lupus erythematosus, psoriatic arthritis, ankylosing spondylitis, gonococcal arthritis, Reiter syndrome, and Lyme disease can be associated with valvular, myocardial, or pericardial disease.

Dyspnea is defined as difficult or labored respiration or the unpleasant awareness of ones breathing. A clue to the cause is obtained from the factors that precipitate or relieve it. Chronic dyspnea may be caused by heart failure, pulmonary disease, anxiety, obesity, poor physical fitness, pleural effusions, and asthma. Acute dyspnea may occur with acute pulmonary edema, hyperventilation, pneumothorax, pulmonary embolism, pneumonia, and airway obstruction.

Dyspnea on effort, a frequent symptom, is usually caused by congestive heart failure, chronic pulmonary disease, or physical deconditioning (see Chap. 31). A recent or dramatic increase in dyspnea is more likely to be caused by the development of heart failure than by lung disease. When heart and lung disease coexist, however, determination of the relative contribution of pulmonary and cardiac dysfunction to dyspnea can be very difficult.

Cheyne-Stokes respiration is a form of periodic breathing characterized by cycles beginning with shallow respirations that increase in rate and depth to significant hyperpnea followed by decreasing rate and depth of respiration and then a period of apnea that can last 15 seconds or longer. This form of respiration occurs in advanced congestive heart failure and in some forms of central nervous system disease. Cheyne-Stokes respiration often occurs during sleep without the patients awareness and is often reported by others.

Orthopnea results from an increase in hydrostatic pressure in the lungs that occurs with assumption of the supine position. It consists of cough and dyspnea in some patients with LV failure or mitral valve (MV) disease and necessitates the use of two or more pillows on lying down. Patients with severe obstructive lung disease, especially acute asthma, also cannot lie flat comfortably.

Paroxysmal nocturnal dyspnea (PND) is the occurrence of dyspnea during sleep, commonly 2 to 3 hours after going to bed, which is relieved by assuming the upright position. Episodes can be mild, or they can be severe with wheezing, coughing, gasping, and apprehension.1 Some episodes progress to pulmonary edema. The probable mechanism for this relatively specific symptom of left-sided heart failure is the increase in central blood volume in the supine position.

A dry, unproductive cough occurring with effort or at rest may be related to the pulmonary congestion associated with heart failure (see Chap. 27). Although dyspnea is usually present, cough can dominate the clinical picture. Whereas the cough that accompanies acute pulmonary edema is often associated with frothy, pink-tinged sputum, the sputum associated with chronic bronchitis is usually white and mucoid. Sputum associated with pneumonia is often thick and yellow and because of pulmonary infarction can be bloody, as can the sputum associated with cancer of the lung or bronchiectasis. Cough can also be caused by angiotensin-converting enzyme inhibitors or much less commonly angiotensin receptor blockers.

Recurrent coughing caused by heart failure is often thought to be caused by bronchitis, and patients with chronic bronchitis can cough more when heart failure ensues. Patients with a high pulmonary blood flow caused by congenital left-to-right shunts are subject to pulmonary infection. Patients with a high pulmonary venous pressure (eg, mitral stenosis [MS]) are more vulnerable to pulmonary edema when they have viral pneumonitis than are patients with normal pulmonary venous pressure.

Hemoptysis occurs in many cardiac disorders. Posterior epistaxis as a result of systemic hypertension can cause blood-streaked sputum; patients on anticoagulants can have epistaxis that mimics hemoptysis. Bright red pulmonary venous blood from rupture of submucosal pulmonary venules can be expectorated by patients with pulmonary venous hypertension caused by MS or severe LV failure. Darker blood or clots often occur with pulmonary emboli.

Pink, frothy sputum can be produced during acute pulmonary edema. Blood-streaked sputum is a feature of the winter bronchitis of MS. Massive hemoptysis with exsanguination can follow rupture of an aortic aneurysm or one of the cardiac chambers into the bronchial tree. Rupture of a pulmonary artery by the balloon of an indwelling pulmonary artery catheter can cause abrupt, severe hemoptysis in hospitalized patients.

Wheezing associated with dyspnea can be caused by lung or heart disease. If the symptoms have developed recently in an adult older than 40 years of age, other clues indicating heart disease (cardiac asthma) should be sought.

Edema is a common symptom or finding in patients with right-or left-sided heart failure. Fluid retention in heart failure results from increased venous pressure and abnormal activity of salt-retaining hormones (see Chap. 30). In an average-sized person, 5 to 10 lb (2.3-4.5 kg) of excess fluid is required for edema to become apparent; a history of recent weight gain will often correlate with deterioration in clinical status. The amount of weight loss in response to treatment for heart failure in the past will relate to the severity of the problem. Minor degrees of edema are evident only after a period of dependency of the legs and decrease after rest. Presacral edema can be most obvious when the patient has been on bedrest. Although edema of cardiac origin can progress to anasarca, cardiac edema rarely involves the face or upper extremities. Persistent edema in the legs from which veins were harvested at the time of bypass surgery is common. Other causes of edemasuch as varicosities, obesity, tight girdle, renal insufficiency, or cirrhosis with hypoproteinemiamust be considered. A patient with chronic congestive heart failure can detect edema of the ankles and lower legs during the day and note that it diminishes during the night. It is important to ascertain whether edema of the extremities preceded or followed dyspnea on effort. The calcium antagonists can produce bilateral edema of the lower legs. Edema may occur in one or both legs after the harvesting of veins for conduits in patients undergoing coronary artery bypass grafting (CABG) surgery.

Patients will be aware of ascites because of increased abdominal girth. Previously comfortable trousers or skirts can no longer fit. Bending at the waist is uncomfortable, with ill-defined abdominal fullness. Patients with severe edema caused by congestive heart failure may develop ascites; however, ascites is particularly common in patients with constrictive pericardial disease, sometimes occurring before peripheral edema becomes obvious (see Chap. 85). Ascitic fluid is formed when elevated venous pressure leads to transudation of fluids from the serosal surfaces.

Fatigue and weakness can be caused by many conditions and therefore are not specific symptoms for heart disease. The most common cause of these symptoms when isolated is anxiety and depression. Anemia, thyrotoxicosis, and other chronic disease states can be associated with fatigue and weakness.

When a patient with heart disease is volume overloaded or when there is pulmonary congestion caused by heart disease, the patient is likely to complain of dyspnea. With vigorous diuretic therapy, this complaint can be replaced by symptoms of fatigue and weakness, probably related to inadequate cardiac output (see Chap. 28). As congestive heart failure worsens, fatigue can replace dyspnea as the major symptom. -Blockers used to treat angina or hypertension and LV dysfunction often cause fatigue and lethargy. When starting -blockers to treat heart failure, start low and go slow. Hypotension or hypokalemia caused by diuretics can result in fatigue and weakness, as can relative hypovolemia caused by the use of angiotensin-converting enzyme inhibitors.

Most normal individuals are intermittently aware of their heart action, particularly at times of physical and emotional stress. When the heart action is more vigorous than usual or its perception is unpleasant, the term palpitation is appropriate. The patient may complain of a pounding, stopping, jumping, or racing in the chest. Palpitation is frequently a benign symptom without any serious cardiac disease present; at other times, it can indicate a potentially life-threatening condition. Simple premature beats can be perceived as a floating or flopping sensation in the chest caused by the more forceful beat that occurs after the pause following the premature beat. Sometimes a transient feeling of fullness in the neck (caused by cannon A waves) is perceived with premature beats. Certain patients perceive almost every premature beat, but others are totally unaware of frequent or advanced arrhythmias. A report of skips or irregularity during uninterrupted sinus rhythm is common. Generally, thin, tense individuals are likely to be more aware of their cardiac activity than others. Individuals with and without arrhythmias often are aware of their cardiac activity when they first lie down to sleep, especially if they lie on their left side.

Rapid heart action of a paroxysmal tachycardia usually begins and terminates abruptly and causes a pounding sensation in the chest. Patients often indicate whether the tachycardia is regular or irregular and can be able to tap out the rate and rhythm of the episode (see Chap. 39). Chest pressure suggesting angina can occur with an episode of tachycardia even in young, healthy patients without CAD. Patients with CAD, however, often develop severe angina with a sustained arrhythmia because of increased Depending on the rate and mechanism of the arrhythmia, faintness and syncope can be described during questioning. Nevertheless, sustained ventricular tachycardia may occur in the setting of serious underlying cardiac disease without a significant compromise in hemodynamics (see Chap. 41). Syncope caused by tachyarrhythmias may occur without the patient being aware of palpitations.

Cardiac syncope (fainting) is defined as the transient loss of consciousness caused by inadequate cerebral blood flow secondary to an abrupt decrease in cardiac output (see Chap. 5). Near syncope refers to the clinical situation in which the patient feels dizzy and weak and tends to lose postural tone but does not lose consciousness. In assessing a patient with syncope, one determines if there were precipitating factors, premonitory symptoms, injury with the episode, seizure activity or incontinence, or a postictal state. Injury during an episode suggests a sudden profound loss of body tone and increases the likelihood of more serious causes. Brief, unsustained seizure activity can occur with syncope caused by a cardiac arrhythmia.

The patient can be incontinent during cardiogenic syncope, but an aura, sustained tonic-clonic movements, tongue biting, and confusion or drowsiness after the event are more characteristic of syncope caused by central nervous system disease. In contrast, return of consciousness to the alert state is prompt after reversal of the arrhythmia causing cardiac syncope. The common faint (vasovagal syncope) results from bradycardia and hypotension caused by excessive vagal discharge. It is often associated with some precipitating event such as a heavy meal in a warm room and has brief premonitory signs and symptoms such as nausea, yawning, diaphoresis, and sometimes the feeling of decreased hearing or vision. The results of head-up, tilt-table testing indicate a vasovagal mechanism in some patients with syncope who do not have premonitory symptoms. After a fainting episode, the patient may be pale and diaphoretic and have a slow heart rate. A history of similar episodes during the preceding several years is common in patients with vagal syncope.

A hypersensitive carotid sinus can cause syncope. A history of episodes during an activity such as shaving, wearing a tight collar, or extreme turning of the head can occur but is unusual even when a sensitive carotid sinus is shown to be the cause of syncope. Syncope after urination (micturition syncope) can occur at the time of rapid decompression of a distended bladder, which typically occurs after a period of sleep. Paroxysms of coughing, usually in patients with underlying pulmonary disease, can result in syncope. Very fast or slow arrhythmias can decrease the cardiac output enough to cause alterations in consciousness, ranging from abrupt profound syncope to mild lightheadedness. Stokes-Adams syncope is caused by intermittent complete heart block, sinus arrest, or ventricular tachyarrhythmias. It is characterized by an abrupt loss of consciousness without warning, a variable period of unconsciousness (seconds to minutes), and then a rapid return of normal mental status without amnesia or a postictal state.

In the presence of severe LV outflow obstruction (aortic stenosis or HCM), loss of consciousness with effort can occur. Syncope can be caused either by the hearts inability to increase its output in response to the peripheral vasodilatation that occurs during exercise or by a tachyarrhythmia. Intermittent obstruction of a cardiac valve by an intracavitary tumor or thrombus is a rare cause of syncope that can occasionally be precipitated when the patient changes position.

Many normal subjects experience transient lightheadedness with rapid changes in position. This is more common in older patients because the ability of the peripheral vasculature to respond is attenuated with aging. Postural hypotension is a well-defined cause of fainting or dizziness that usually occurs when the individual is upright and often just after rising from a supine or sitting position. Possible causes include peripheral neuropathy, autonomic dysfunction, volume depletion, or drug side effects.

Patients with decreased cardiac output secondary to heart failure can become mentally confused and disoriented. Such symptoms also can be caused by hypoxia, drugs that are invariably prescribed for such patients, and renal or hepatic failure.2 A completed stroke can be caused by a lacunar infarct, cerebral hemorrhage, cerebral arterial thrombosis, or a cerebral embolus (see Chap. 107). A transient cerebral ischemic attack is commonly caused by an embolus. The embolus can originate in an atheromatous ulcer in the carotid artery system or the aortic arch; be related to infective endocarditis, a recent MI, atrial fibrillation, or clots on a prosthetic valve; or originate in the leg veins and pass through a patent foramen ovale to the brain.

A patient with cardiogenic shock or with a severe tachyarrhythmia who also has considerable intracranial or extracranial vascular disease can develop such severe cerebral hypoxia that coma occurs. Hypoxic encephalopathy can follow cardiac resuscitation and occasionally occurs after cardiopulmonary bypass for cardiac surgery. A cerebral abscess can occur in patients with congenital heart disease and a right-to-left shunt.2

Fever with chills is common in patients with infective endocarditis. Symptoms of fever, chills, or sweats in any patient with a heart murmur should lead one to suspect infective endocarditis (see Chap. 86). A history of valvular heart disease is not a prerequisite because previously normal valves become infected. A history of recent dental work, genitourinary surgery, or illicit drug use increases the suspicion of infective endocarditis. Fever can accompany rheumatic fever or pericarditis. An intracardiac tumor (myxoma) can produce systemic symptoms in the absence of infection. Low-grade fever in a patient with heart failure can be a sign of pulmonary emboli. Excessive sweating can occur in patients with severe AR or acute MI. Diaphoresis is often a sign of congestive heart failure in infants.

Hoarseness can occur in patients with an aortic aneurysm that involves the left recurrent laryngeal nerve. MS can occasionally produce hoarseness caused by the pressure of a large pulmonary artery on the recurrent laryngeal nerve. Pericardial effusion can be related to myxedema, which can be associated with a coarse, low-pitched voice. Hoarseness and loss of voice can occur after the use of an endotracheal tube during cardiac surgery.

Many patients with angina pectoris caused by CAD erroneously attribute their symptoms to indigestion or heartburn. Also, patients with heartburn, esophageal reflux, and esophageal spasm may believe they have angina pectoris. Hiccups occasionally occur in patients with MI and during the postoperative period after cardiac surgery. Dysphagia can occur in patients with progressive systemic sclerosis, an aortic arch anomaly, or an extremely large left atrium (LA).

Anorexia, nausea, and vomiting can occur as a result of cardiac glycoside excess or inferior MI Hepatomegaly associated with tricuspid valve disease or severe right-sided heart failure can cause right upper quadrant epigastric pain and fullness as well as anorexia. Abdominal pain caused by visceral ischemia or infarction can occur in a patient who has had a period of very low cardiac output.

Although cyanosis is a sign rather than a symptom, patients or family members may describe cyanosis during the history. Cyanosis is a bluish color of the skin or mucous membranes caused by excess amounts of reduced hemoglobin. Approximately 4 g of reduced hemoglobin is required for cyanosis to be apparent (see Chap. 83). Severely anemic patients will not exhibit cyanosis. A distribution of cyanosis involving the mucous membranes as well as the periphery (central cyanosis) is caused by the admixture of venous blood at the level of the heart or great vessels. A patient or a family member can detect that the cyanosis is more intense in the feet than in the hands. This differential cyanosis suggests a right-to-left shunt through a patent ductus arteriosus in a patient with Eisenmenger physiology. Peripheral cyanosis does not involve the mucous membranes but is the result of slow peripheral flow with accumulation of excess reduced hemoglobin in the setting of circulatory failure, shock, or peripheral vasospasm.

Jaundice can be detected by a patient or by a member of the family. As a rule, hepatic congestion caused by heart failure will not produce jaundice. Hemolysis of red blood cells can occur in patients with prosthetic valves and can produce jaundice.

A history of flush of face and trunk, sometimes accentuated by alcohol, should lead one to search for the other signs and symptoms of carcinoid heart disease (see Chap. 86). Cardiomyopathies caused by hemochromatosis should be considered in a patient with diabetes whose skin color has changed from normal to bronze. A slate-like color of the skin, hands, and nose can develop in patients who take amiodarone.

The most common causes of insomnia are mental conflict, emotional disturbances, and depression. Heart failure, however, can also cause insomnia. Patients with Cheyne-Stokes respirations (see preceding section on Respiratory Symptoms) can sleep during the apneic phase and wake during the hyperpneic phase of the condition. Occasionally, patients with pulmonary congestion caused by heart failure have insomnia before they develop nocturnal dyspnea. Central and obstructive sleep apnea are discussed elsewhere (see Chap. 73).

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The History, Physical Examination, and Cardiac ...