Management of Patients with Chest Pain

Management of Patients with Chest Pain

 

History

 

As with diseases of most organ systems, the ability of the physician to diagnose diseases of the cardiovascular system is in large part dependent on eliciting and interpreting the patient’s clinical history. A thorough history can enable the physician to identify a patient’s symptoms as characteristic of a specific cardiovascular disorder or to suggest that symptoms are unlikely to be caused by cardiovascular disease. In addition, a complete history will reveal the presence of other systemic diseases that may have cardiovascular manifestations, identify existing risk factors that may be modified to prevent the future development of cardiovascular disease, enable the selection of appropriate further diagnostic testing, and allow the assessment of functional capacity and extent of cardiovascular disability. The patient should be asked about prior medical conditions, including childhood illnesses (e.g., rheumatic fever), as well as intravenous drug use, which may lead to the development of valvular heart disease. Several cardiovascular disorders are inherited (e.g., hypertrophic cardiomyopathy, Marfan syndrome, long QT syndrome), and a thorough family history may bring this potential to the examiner’s attention.

 

The classic symptoms of cardiac disease include precordial discomfort or pain, dyspnea, palpitations, syncope or presyncope, and edema. Although characteristic of heart disease, these symptoms are nonspecific and may also occur as a result of diseases of other organ systems (e.g., musculoskeletal, pulmonary, renal, gastrointestinal). Furthermore, some patients with established cardiovascular disease may be asymptomatic or have atypical symptoms.

 

Chest pain is a frequent symptom and may be a manifestation of cardiovascular or noncardiovascular disease (Tables 1 and 2). Full characterization of the pain with regard to quality, quantity, frequency, location, duration, radiation, aggravating or alleviating factors, and associated symptoms may help distinguish among various causes. Reversible myocardial ischemia caused by obstructive coronary artery disease commonly results in episodic chest pain or discomfort during exertion or stress (angina pectoris). Patients frequently deny having pain and, instead, describe a discomfort in their chest. Sometimes they will refer to the discomfort as a squeezing, tightening, pressing, or burning sensation or as a heavy weight on their chest, and they will sometimes clench their fist over their chest while describing the discomfort (Levine’s sign). Anginal discomfort is classically located substernally or over the left chest. It frequently radiates to the epigastrium, neck, jaw, or back and down the ulnar aspect of the left arm. Radiation to the right chest or arm is less common, whereas radiation above the jaw or below the epigastrium is not typical of cardiac disease. Angina is usually brought on by either physical or emotional stress, is mild to moderate in intensity, lasts 2 to 10 minutes, and resolves with rest or sublingual administration of nitroglycerin. It may occur more frequently in the morning, in cold weather, after a large meal, or after exposure to environmental factors, including cigarette smoke, and is frequently accompanied by other symptoms, such as dyspnea, diaphoresis, nausea, palpitations, or lightheadedness. Patients frequently report a stable pattern of angina that is predictably reproducible with a given amount of exertion. Unstable angina occurs when a patient reports a significant increase in the frequency or severity of angina or when angina occurs with progressively decreasing exertion or at rest. When anginal-type pain occurs mainly at rest, it may be of a noncardiac origin, or it may reflect true cardiac ischemia resulting from coronary spasm (Prinzmetal’s or variant angina). The pain of an acute myocardial infarction may be similar to angina, although the former is usually more severe and prolonged (>30 min).

 

 

 

The pain of acute pericarditis is usually sharper than anginal pain, is located to the left of the sternum, and may radiate to the neck or left shoulder. In contrast to angina, the pain may last hours, typically worsens with inspiration, and improves when the patient sits up and leans forward; it may be associated with a pericardial friction rub. Acute aortic dissection produces severe, sharp, tearing pain that radiates to the back and may be associated with asymmetric pulses and a murmur of aortic insufficiency. Pulmonary emboli may produce the sudden onset of sharp chest pain that is worse on inspiration, is associated with shortness of breath, and may have an associated pleural friction rub, especially if a pulmonary infarction is present. A multitude of noncardiac conditions may also produce chest pain (see Table 2). The clinical history and physical examination findings will often help distinguish these causes from ischemic chest pain.

 

Dyspnea, an uncomfortable, heightened awareness of breathing, is commonly a symptom of cardiac disease. Patients with decreased left ventricular function may exhibit significant abnormalities of the aortic or mitral valves or decreased myocardial compliance (i.e., left ventricular hypertrophy, acute ischemia), left ventricular diastolic, and/or left atrial pressure increases transmitted through the pulmonary veins to the pulmonary capillary system, producing vascular congestion. This congestion results in exudation of fluid into the alveolar space and impairs gas exchange across the alveolar-capillary membrane, producing the subjective sensation of dyspnea. Dyspnea frequently occurs on exertion; however, in patients with severe cardiac disease, it may be present at rest. Patients with heart failure commonly sleep on two or more pillows because the augmented venous return that occurs on assuming the recumbent position produces an increase in dyspnea (orthopnea). In addition, these patients report awakening 2 to 4 hours after the onset of sleep with dyspnea (paroxysmal nocturnal dyspnea), which is likely caused by the central redistribution of peripheral edema in the supine position.

 

 

 

Dyspnea may be associated with diseases of the lungs or chest wall and is also seen in anemia, obesity, deconditioning, and anxiety disorders. In addition, the sudden onset of dyspnea, with or without chest pain, may be present with pulmonary emboli. Dyspnea is frequently difficult to distinguish cardiac from pulmonary causes by history alone, because both may produce resting or exertional dyspnea, orthopnea, or cough. Wheezing and hemoptysis are classically results of pulmonary disease, although they are also frequently present in the patient with pulmonary edema resulting from left ventricular dysfunction or mitral stenosis. True paroxysmal nocturnal dyspnea is, however, more specific for cardiac disease. In patients with coronary artery disease, dyspnea may be an anginal equivalent; that is, the dyspnea is the result of ischemia and occurs in a pattern consistent with angina but in the absence of chest discomfort.

 

Palpitation refers to the subjective sensation of the heart beating. Patients may describe a fluttering or pounding in the chest or a feeling that their heart races or skips a beat. Some people feel post-extrasystolic beats as a painful or uncomfortable sensation. Common arrhythmic causes of palpitations include premature atrial or ventricular contractions, supraventricular tachycardia, ventricular tachycardia, and sinus tachycardia. Occasionally, patients report palpitations even wheo rhythm disturbance is noted during monitoring, as occurs commonly in patients with anxiety disorders. The pattern of palpitations, especially when correlated to the pulse, may help narrow the differential diagnosis: Rapid, regular palpitations are noted with supraventricular tachycardia or ventricular tachycardia; rapid, irregular palpitations are noted with atrial fibrillation; and skipped beats are noted with premature atrial or ventricular contractions.

Syncope is the transient loss of consciousness resulting from inadequate cerebral blood flow and may be the result of a variety of cardiovascular diseases. True syncope must be distinguished from primary neurologic causes of loss of consciousness (i.e., seizures) and metabolic causes of loss of consciousness (e.g., hypoglycemia, hyperventilation). Cardiac syncope occurs after an abrupt decrease in cardiac output, as may occur with acute myocardial ischemia, valvular heart disease (aortic or mitral stenosis), hypertrophic obstructive cardiomyopathy, left atrial tumors, tachyarrhythmias (ventricular, or less commonly supraventricular, tachycardias), or bradyarrhythmias (e.g., sinus arrest, atrioventricular block, Stokes-Adams attacks). Reflex vasodilation or bradycardia may also result in syncope (vasovagal syncope, carotid sinus syncope, micturition syncope, cough syncope, or neurocardiogenic syncope), as may acute pulmonary embolism and hypovolemia. Because global, or at the very least bilateral, cortical ischemia is required to produce syncope, it rarely occurs as a result of unilateral carotid artery disease. However, syncope is occasionally the result of bilateral carotid artery disease and can also occur when disease of the vertebrobasilar system results in brain-stem ischemia. In up to 50% of patients, the cause of a syncopal episode cannot be determined; however, in the cases in which a cause is determined, the most important factor in establishing the diagnosis is obtaining an accurate history of the event.

 

Edema is a nonspecific symptom that commonly accompanies cardiac disease, as well as renal disease (e.g., nephrotic syndrome), hepatic disease (e.g., cirrhosis), and local venous abnormalities (e.g., thrombophlebitis, chronic venous stasis). When edema occurs as a result of cardiac disease, it reflects an increase in venous pressure. This increased pressure alters the balance between the venous hydrostatic and oncotic forces, resulting in extravasation of fluid into the extravascular space. When this process occurs as a result of elevated left-sided heart pressure, pulmonary edema results, whereas elevated right-sided heart pressure results in peripheral edema. Characteristically, the peripheral edema of heart failure is pitting; that is, an indentation is left in the skin after pressure is applied to the edematous region. The edema is exacerbated by long periods of standing, is worse in the evening, improves after lying down, and may first be noted when a patient has difficulty in fitting into his or her shoes. The edema may shift to the sacral region after a patient lies down for several hours. When visible edema is noted, it is usually preceded by a moderate weight gain (i.e., 5 to 10 lb), indicative of volume retention. As heart failure progresses, the edema may extend to the thighs and involve the genitalia and abdominal wall, and fluid may collect in the abdominal (ascites) or thoracic (pleural effusion) cavities. Anasarca with ascites should raise suspicion for constrictive pericarditis because this disease may progress very slowly and insidiously.

 

Cyanosis is an abnormal bluish discoloration of the skin resulting from an increase in the level of reduced hemoglobin in the blood and, in general, reflects an arterial oxygen saturation of 85% or less (normal arterial oxygen saturation ≥95%). Central cyanosis exhibits as cyanosis of the lips or trunk and often reflects right-to-left shunting of blood caused by structural cardiac abnormalities (e.g., atrial or ventricular septal defects) or pulmonary parenchymal or vascular disease (e.g., chronic obstructive pulmonary disease, pulmonary embolism, pulmonary arteriovenous fistula). Peripheral cyanosis may occur because of systemic vasoconstriction in the setting of poor cardiac output or may be a localized phenomenon resulting from venous or arterial occlusive or vasospastic disease (e.g., venous or arterial thrombosis, arterial embolic disease, Raynaud’s disease). When cyanosis occurs in childhood, it usually reflects congenital heart disease with right-to-left shunting of blood.

A myriad of other symptoms, many of them nonspecific, may occur with cardiac disease. Fatigue frequently occurs in the setting of poor cardiac output or may occur secondary to the medical therapy of cardiac disease from overdiuresis, aggressive blood pressure lowering, or use of β-blocking agents. Nausea and vomiting frequently occur during an acute myocardial infarction and may also reflect intestinal edema in the setting of right ventricular heart failure. Anorexia and cachexia may occur in severe heart failure. Positional fluid shifts may result in polyuria and nocturia in patients with edema. In addition, epistaxis, hoarseness, hiccups, fever, and chills may reflect underlying cardiovascular disease.

 

Many patients with significant cardiac disease are asymptomatic. Patients with coronary artery disease frequently have periods of asymptomatic ischemia that can be documented with ambulatory electrocardiographic (ECG) monitoring. Furthermore, nearly one third of patients who suffer an acute myocardial infarction are unaware of the event. This silent ischemia appears to be more common in older adults and in patients with diabetes. Patients may also be asymptomatic despite having severely depressed ventricular function; this usually bespeaks a chronic, slowly progressive process. Reduced exercise capacity may only be seen during provocative testing. Similarly, recent findings show that a high percentage of episodes of atrial fibrillation are unrecognized by patients.

 

Assessment of Functional Capacity

 

In patients with cardiac disorders, their ability or inability to perform various activities (functional status) plays an important role in determining their extent of disability, deciding when to institute various therapies or interventions, and assessing their response to therapy, as well as determining their overall prognosis. The New York Heart Association Functional Classification is a standardized method for the assessment of functional status (Table 3) and relates functional capacity to the presence or absence of cardiac symptoms during the performance of usual activities. The Canadian Cardiovascular Society has provided a similar classification of functional status specifically in patients with angina pectoris. These tools are useful in that they allow a patient’s symptoms to be classified and then compared with their symptoms at a different point in time.

 

 

 

 

Physical Examination

 

EXAMINATION OF THE JUGULAR VENOUS PULSATIONS

 

The examination of the neck veins allows for estimation of the right atrial pressure and for identification of the venous waveforms. The right internal jugular vein is used for this examination because it more accurately reflects right atrial pressure than the external jugular or left jugular vein. With the patient lying at a 45-degree angle (higher in patients with elevated venous pressure, lower in patients with low venous pressure) with his or her head turned to the left, the vertical distance from the sternal angle (angle of Louis) to the top of the venous pulsation can be determined. Because the right atrium lies approximately 5 cm vertically below the sternal angle, distention of the internal jugular vein 4 cm above the sternal angle reflects a right atrial pressure of 9 cm of water (H₂O). The right atrial pressure is normally 5 to 9 cm H₂O and is increased with congestive heart failure, tricuspid insufficiency or stenosis, and restrictive or constrictive heart disease. With inspiration, negative intrathoracic pressure develops, venous blood drains into the thorax, and the normal venous pressure falls; the opposite is true with expiration. This pattern is reversed (Kussmaul’s sign) in the setting of right ventricular heart failure, constrictive pericarditis, or restrictive myocardial disease. With right ventricular heart failure, the elevated venous pressure results in passive congestion of the liver. Pressure applied over the liver for 1 to 3 minutes in this setting results in an increase in the jugular venous pressure (hepatojugular reflux).

 

The normal waveforms of the venous pulsation consist of the a, c, and v waves and the x and y descents; these waveforms are shown in Figure 1A and reflect events in the right side of the heart. The a wave results from atrial contraction. Subsequent atrial relaxation results in a decrease in the right atrial pressure, which is seen as the x descent. This descent is interrupted by the c wave, generated by the bulging of the tricuspid valve cusps into the right atrium during ventricular systole. As the atrial pressure increases owing to venous return, the v wave is generated. This wave is normally smaller than the a wave and is followed by the y descent as the tricuspid valve opens and blood flows from the right atrium to the right ventricle during diastole.

 

Abnormalities of the venous waveforms reflect underlying structural, functional, or electrical abnormalities of the heart (see Fig. 1B through G). The a wave increases in any condition in which greater resistance to right atrial emptying occurs (e.g., tricuspid stenosis, right ventricular hypertrophy or failure, pulmonary hypertension). Cannon a waves are seen when the atrium contracts against a closed tricuspid valve, as occurs with complete heart block, with junctional or ventricular rhythms, and occasionally with ventricular pacemakers. The a wave is absent in atrial fibrillation. In tricuspid regurgitation, the v wave is prominent and may merge with the c wave (cv wave), thus diminishing or eliminating the x descent altogether. The y descent is attenuated in tricuspid stenosis, owing to the impaired atrial emptying. In pericardial constriction and restrictive cardiomyopathy, as well as in right ventricular infarction, the y descent becomes rapid and deep, and the x descent may also become prominent (w waveform). In pericardial tamponade, the x descent is prominent, but the y descent is diminished or absent.

 

 

 

 

Figure 1. Normal and abnormal jugular venous pulse tracings. A, Normal jugular pulse tracing with simultaneous ECG and phonocardiogram. B, Loss of the a wave in atrial fibrillation. C, Large a wave in tricuspid stenosis. D, Large c-v wave in tricuspid regurgitation. E, Prominent x and y descents in constrictive pericarditis. F, Prominent x descent and diminutive y descent in pericardial tamponade. G, Jugular venous pulse tracing and simultaneous ECG during complete heart block demonstrating cannon a waves occurring when the atrium contracts against a closed tricuspid valve during ventricular systole.

 

The arterial blood pressure can be measured with the use of a sphygmomanometer. The cuff is applied to the upper arm, rapidly inflated to 30 mm Hg above the anticipated systolic pressure, and then slowly deflated (= 3 mm Hg/sec) while listening for the sounds produced by blood entering the previously occluded brachial artery (Korotkoff sounds). The pressure at which the first sound is heard (usually a clear, tapping sound) represents the systolic pressure. Diastolic pressure occurs at the point at which the Korotkoff sounds disappear. Normally, the pressure in both arms is the same (approximately 120/70 mm Hg), and the systolic pressure in the legs is 10 to 20 mm Hg higher. Asymmetric arm pressures can result from atherosclerotic disease of the aorta, aortic dissection, and stenosis of the innominate or subclavian arteries. Coarctation of the aorta and severe atherosclerotic disease of the aorta or the femoral or iliac arteries can result in a lower blood pressure in the legs than in the arms. Aortic insufficiency is frequently associated with a leg pressure greater than 20 mm Hg higher than the arm pressure (Hill’s sign). Use of a cuff that is too small for a patient’s arm will result in erroneously high pressure measurements. Similarly, a cuff that is too large results in erroneously low measurements.

 

The arterial examination should include assessments of the carotid, radial, brachial, femoral, popliteal, posterior tibial, and dorsalis pedis pulses, although the carotid artery pulse most accurately reflects the central aortic pulse. The rhythm, strength, contour, and symmetry of the pulses should be noted. The normal arterial pulse (Fig. 2A) rises rapidly to a peak in early systole, plateaus, and then falls. The descending pressure wave is interrupted by the dicrotic notch, related to aortic valve closure. This normal pattern is altered in a variety of cardiovascular disease states (see Fig. 2B through F). The amplitude of the pulse increases in aortic insufficiency, anemia, pregnancy, and thyrotoxicosis and decreases in conditions such as hypovolemia, tachycardia, left ventricular failure, and severe mitral stenosis. Aortic insufficiency results in a bounding pulse (Corrigan’s pulse or water-hammer pulse), owing to an increased pulse pressure (the difference between systolic and diastolic pressure), and is accompanied by a multitude of abnormalities in the peripheral pulses that reflect this increased pulse pressure. Aortic stenosis characteristically results in an attenuated carotid pulse with a delayed upstroke (pulsus parvus et tardus) and may be associated with a palpable thrill over the aortic area (the carotid shudder). A bisferious pulse is commonly felt in the presence of pure aortic regurgitation and is characterized by two systolic peaks. The first peak is the percussion wave, resulting from the rapid ejection of a large volume of blood early in systole; the second peak is the tidal wave, a reflected wave from the periphery. This bifid pulse may also be noted in hypertrophic cardiomyopathy in which the initial rapid upstroke of the pulse is cut short by the development of a left ventricular outflow tract obstruction, resulting in a fall in the pulse. The reflected wave again produces the second impulse. In severe left ventricular dysfunction, the intensity of the pulse may alternate from beat to beat (pulsus alternans), and in atrial fibrillation, the pulse intensity is variable. With inspiration, negative intrathoracic pressure is transmitted to the aorta and the systolic pressure normally decreases by up to 10 mm Hg. Pulsus paradoxus is an exaggeration of this normal inspiratory fall in systolic pressure and is characteristically seen with pericardial tamponade, although it may also occur as a result of severe obstructive lung disease, constrictive pericarditis, hypovolemic shock, and pregnancy.

 

 

Figure 2. Normal and abnormal carotid arterial pulse contours. A, Normal arterial pulse with simultaneous ECG. The dicrotic wave (D) occurs just after aortic valve closure. B, Wide pulse pressure in aortic insufficiency. C, Pulsus parvus et tardus (small amplitude with a slow upstroke) associated with aortic stenosis. D, Bisferious pulse with two systolic peaks, typical of hypertrophic obstructive cardiomyopathy or aortic insufficiency, especially if concomitant aortic stenosis is present. E, Pulsus alternans, characteristic of severe left ventricular failure. F, Paradoxic pulse (systolic pressure decrease of >10 mm Hg with inspiration), most characteristic of cardiac tamponade.

 

 

 

Atherosclerotic disease of the peripheral vascular system frequently accompanies coronary atherosclerosis; therefore, the presence of peripheral vascular disease warrants a search for symptoms or signs of coronary artery disease and vice versa. When atherosclerosis occurs in a peripheral artery to the lower extremity and impairs blood flow distally, the patient may complain of intermittent cramping in the buttocks, thigh, calf, or foot (claudication). Severe peripheral vascular disease may result in digital ischemia or necrosis, without or with associated erectile dysfunction (Leriche’s syndrome). The peripheral pulses should be palpated and the abdominal aorta assessed for enlargement in all cardiac patients; a pulsatile, expansile, periumbilical mass suggests the presence of an abdominal aortic aneurysm. With significant stenosis of the peripheral vasculature, the distal pulses may be diminished or absent, and the blood flow through the stenotic artery may be audible (a bruit). With normal aging, the elastic arteries lose their compliance, and this change in physical property may obscure abnormal findings.

 

EXAMINATION OF THE PRECORDIUM

 

Inspection and palpation of the precordium may yield valuable clues as to the existence of cardiac disease. Chest wall abnormalities should be noted, such as pectus excavatum, which may be associated with Marfan syndrome or mitral valve prolapse, pectus carinatum, which may be associated with Marfan syndrome, and kyphoscoliosis (occasionally a cause of secondary pulmonary hypertension and right ventricular heart failure). The presence of visible pulsations in the aortic (second right intercostal space and suprasternal notch), pulmonic (third left intercostal space), right ventricular (left parasternal region), and left ventricular (fourth to fifth intercostal space and left midclavicular line) regions should be noted and will help direct the palpation of the heart. Retraction of the left parasternal area may be seen with severe left ventricular hypertrophy, and systolic retraction of the chest wall at the cardiac apex or left axilla (Broadbent’s sign) is characteristic of constrictive pericarditis.

 

Precordial palpation is best performed with the patient supine or in the left lateral position, with the examiner standing to the patient’s right side. In this position, firm placement of the examiner’s right hand over the patient’s lower left chest wall places the fingertips over the region of the cardiac apex and the palm over the region of the right ventricle. The normal cardiac apical impulse is a brief, discrete impulse (approximately 1 cm) located in the fourth to fifth intercostal space in the left midclavicular line generated as the left ventricle strikes the chest wall during early systole. In a patient with a structurally normal heart, the apex is the point of maximal impulse (PMI) of the heart against the chest wall. Enlargement of the left ventricle results in lateral displacement of the apical impulse, whereas chronic obstructive pulmonary disease may result in inferior displacement of the PMI. Volume overload states, such as aortic insufficiency and mitral regurgitation, produce ventricular enlargement primarily from dilation and result in a hyperdynamic apical impulse; that is, the impulse is brisk and increased in amplitude. Pressure overload states, such as aortic stenosis and long-standing hypertension, produce ventricular enlargement primarily from hypertrophy. In this setting, the apical impulse is sustained, and atrial contraction is frequently detected (a palpable S₄). Hypertrophic cardiomyopathy characteristically produces a double or triple apical impulse. Left ventricular aneurysms produce an apical impulse that is larger thaormal and dyskinetic.

 

The right ventricular impulse is not normally palpable. When an impulse is felt over the left parasternal region, it usually reflects right ventricular hypertrophy or dilation. Aortic aneurysms may be palpable (or visible) in the suprasternal notch or the second right intercostal space. Pulmonary hypertension may produce a palpable systolic impulse in the left third intercostal space and may also be associated with a palpable pulmonic component of the second heart sound (P₂). Harsh murmurs originating from valvular or congenital heart disease may be associated with palpable vibratory sensations (thrills), as can occur with aortic stenosis, hypertrophic cardiomyopathy, and ventricular septal defects.

 

Auscultation

 

TECHNIQUE

 

Auscultation of the heart should ideally be performed in a quiet room with the patient in a comfortable position and the chest fully exposed. Certain heart sounds are better heard with either the bell or diaphragm of the stethoscope. Low-frequency sounds are best heard with the bell applied to the chest wall with just enough pressure to form a seal. As more pressure is applied to the bell, low-frequency sounds are filtered out. High-frequency sounds are best heard with the diaphragm firmly applied to the chest wall. In a patient with a normally situated heart, four major zones of cardiac auscultation are assessed. Aortic valvular events are best heard in the second right intercostal space. Pulmonary valvular events are best heard in the second left interspace. The fourth left interspace is ideal for auscultating tricuspid valvular events, and mitral valvular events are best heard at the cardiac apex or PMI. Because anatomic abnormalities, both congenital and acquired, can alter the location of the heart in the chest, the auscultatory areas may vary among patients. For instance, in patients with emphysema, the heart is shifted downward, and heart sounds may be best heard in the epigastrium. In dextrocardia, the heart lies in the right hemithorax, and the auscultatory regions are reversed. Additionally, auscultation in the axilla or supraclavicular areas or over the thoracic spine may be helpful in some settings, and having the patient lean forward, exhale, or perform various maneuvers may help accentuate particular heart sounds (Table 4).

 

 

 

 

NORMAL HEART SOUNDS

 

The two major heart sounds heard during auscultation are termed S₁ and S₂. These heart sounds are high-pitched sounds originating from valve closure ( Web Sounds normal). S₁ occurs at the onset of ventricular systole and corresponds to closure of the atrioventricular valves. It is usually perceived as a single sound, although occasionally its two components, M₁ and T₁, corresponding to closure of the mitral and tricuspid valves, respectively, can be heard. M₁ occurs earlier, is the louder of the two components, and is best heard at the cardiac apex. T₁ is somewhat softer and heard at the left lower sternal border. The second heart sound results from closure of the semilunar valves. The two components, A₂ and P₂, originating from aortic and pulmonic valve closure, respectively, can be easily distinguished. A₂ is usually louder than P₂ and is best heard at the right upper sternal border. P₂ is loudest over the second left intercostal space. During expiration, the normal S₂ is perceived as a single event. However, during inspiration, the augmented venous return to the right side of the heart and the increased capacitance of the pulmonary vascular bed result in a delay in pulmonic valve closure. In addition, the slightly decreased venous return to the left ventricle results in slightly earlier aortic valve closure. Thus, physiologic splitting of the second heart sound, with A₂ preceding P₂ during inspiration, is a normal respiratory event.

 

Occasionally, additional heart sounds may be heard iormal individuals. A third heart sound (see later discussion) can be heard iormal children and young adults, in whom it is referred to as a physiologic S₃; it is rarely heard after the age of 40 years in healthy individuals ( Web Sound S₃).

 

A fourth heart sound (S₄) is generated by forceful atrial contraction and is rarely audible iormal young individuals but is fairly common in older individuals ( Web Sound S₄).

 

A murmur is an auditory vibration usually generated either by abnormally increased flow across a normal valve or by normal flow across an abnormal valve or structure. Innocent murmurs are always systolic murmurs, are usually soft and brief, and are by definitioot associated with abnormalities of the cardiovascular system. They arise from flow across the normal aortic or pulmonic outflow tracts and are present in a large proportion of children and young adults. Murmurs associated with high-flow states (e.g., pregnancy, anemia, fever, thyrotoxicosis, exercise) are not considered innocent, although they are not usually associated with structural heart disease. These are termed physiologic murmurs, owing to their association with altered physiologic states. Diastolic murmurs are never innocent or physiologic.

 

ABNORMAL HEART SOUNDS

 

Abnormalities of S₁ and S₂ relate to abnormalities in their intensity (Table 5) or abnormalities in their respiratory splitting (Table 6). As noted, splitting of the S₁ is normal but not frequently noted. This splitting becomes more apparent with right bundle branch block or with Ebstein’s anomaly of the tricuspid valve, owing to delay in closure of the tricuspid valve in these conditions ( Web Sound Ebstein). The intensity of S₁ is determined in part by the opening state of the atrioventricular valves at the onset of ventricular systole. If the valves are still widely open, as may occur with tachycardia or a short P-R interval, S₁ will be accentuated. Conversely, in the presence of a long P-R interval, the mitral valve drifts toward a closed position before the onset of ventricular systole, and the subsequent S₁ is soft. The intensity of S₁ may vary in the presence of Mobitz type I heart block, atrioventricular dissociation, and atrial fibrillation when the relationship between atrial and ventricular systole varies. In mitral stenosis with a pliable valve, the persistent pressure gradient at the end of diastole keeps the mitral valve leaflets relatively open and results in a loud S₁ at the onset of systole. In severe mitral stenosis, when the mitral valve is heavily calcified and has decreased leaflet excursion, S₁ becomes faint or absent (Figs. 3 and 4).

 

 

 

 

 

 

 

S₂ may be loud in systemic hypertension, owing to accentuated aortic valve closure (loud A₂), or in pulmonary hypertension, owing to accentuated pulmonic valve closure (loud P₂). When the aortic or pulmonary valves are stenotic, the force of valve closure is decreased, thus A₁ and P₂ become soft or inaudible. In this setting, S₂ may appear to be single; in the setting of aortic stenosis, prolonged left ventricular ejection narrows the normal splitting of S₂; and with severe aortic stenosis, S₂ may become absent altogether as prolonged ejection and its accompanying murmur obscure P₂. Wide splitting of the S₂ with normal respiratory variation occurs when either pulmonic valve closure is delayed (e.g., right bundle branch block, pulmonic stenosis) or aortic valve closure occurs earlier owing to more rapid ejection of left ventricular volume (e.g., mitral regurgitation, ventricular septal defect). Fixed splitting of S₂ without respiratory variation is characteristic of atrial septal defects and also occurs with right ventricular failure ( Web Sounds ASD). Paradoxic splitting of S₂ is a reversal of the usual closure sequence of the aortic and pulmonic valves (i.e., P₂ precedes A₂). In this setting, a single S₂ with inspiration and splitting of S₂ with expiration can be heard. This circumstance occurs most commonly when delay occurs in closure of the aortic valve resulting from either delay in electrical conduction to the left ventricle (e.g., left bundle branch block) or prolonged mechanical contraction of the left ventricle (e.g., aortic stenosis, hypertrophic cardiomyopathy).

 

 

 

 

 

Figure 3. Abnormal heart sounds can be related to abnormal intensity, abnormal presence of a gallop rhythm, or abnormal splitting of S₂ with respiration.

 

 

Figure 4. The relationship of extra heart sounds to the normal first (S₁) and second (S₂) heart sounds. S₁ is composed of the mitral (M₁) and tricuspid (T₁) closing sounds, although it is frequently perceived as a single sound. S₂ is composed of the aortic (A₂) and pulmonic (P₂) closing sounds, which are usually easily distinguished. A fourth heart sound (S₄) is soft and low pitched and precedes S₁. A pulmonic or aortic ejection sound (ES) occurs shortly after S₁. The systolic click (C) of mitral valve prolapse may be heard in mid systole or late systole. The opening snap (OS) of mitral stenosis is high pitched and occurs shortly after S₂. A tumor plop or pericardial knock occurs at the same time and can be confused with an OS or an S₃, which is lower in pitch and occurs slightly later.

 

The third heart sound, S₃ (also called the ventricular diastolic gallop), is a low-pitched sound occurring shortly after A₂ in mid diastole and heard best at the cardiac apex with the patient in the left lateral position. A pathologic S₃ is distinguished from a physiologic S₃ by age or the presence of underlying cardiac disease. It is frequently heard with ventricular systolic dysfunction from any cause and likely results either from blood entering the ventricle during the rapid filling phase of diastole or from the impact of the ventricle against the chest wall. Maneuvers that increase venous return accentuate S₃, and maneuvers that decrease venous return make the S₃ softer. An S₃ can also be heard in hyperdynamic states, where it likely results from rapid early diastolic filling. The left ventricular S₃ is best noticed at the cardiac apex, whereas the right ventricular S₃ is heard best at the left lower sternal border and increases in intensity with inspiration. The timing of the S₃ is similar to the sound generated by atrial tumors (tumor plop) and constrictive pericarditis (pericardial knock) and can also be confused with the opening snap of a stenotic mitral valve.

 

The fourth heart sound, S₄ (also called the atrial diastolic gallop), is best heard at the cardiac apex with the bell of the stethoscope. It is a low-pitched sound originating from the active ejection of blood from the atrium into a noncompliant ventricle and is therefore not present in the setting of atrial fibrillation. S₄ is commonly heard in patients with left ventricular hypertrophy from any cause (e.g., hypertension, aortic stenosis, hypertrophic cardiomyopathy) or acute myocardial ischemia and in hyperkinetic states. Frequently, the S₄ is also palpable at the cardiac apex. S₃ and S₄ are occasionally present in the same patient. In the presence of tachycardia or a prolonged PR interval, the S₃ and S₄ may merge to produce a summation gallop.

 

The opening of normal cardiac valves is not audible. However, abnormal valves may produce opening sounds. In the presence of a bicuspid aortic valve or in aortic stenosis with pliable valve leaflets, an ejection sound is audible as the leaflets open to their maximal extent. A similar ejection sound may originate from a stenotic pulmonic valve, and in this case, the ejection sound decreases in intensity with inspiration. These ejection sounds are high pitched, occur early in systole, and are frequently followed by the typical ejection murmur of aortic or pulmonic stenosis. Ejection sounds are also heard with systemic or pulmonary hypertension, the exact mechanism of which is not clear.

 

Ejection sounds heard in mid systole to late systole are referred to as systolic clicks and are most commonly associated with mitral valve prolapse. As the redundant mitral valve prolapses and reaches its maximal superior displacement, it produces a high-pitched click. Several clicks may be heard as various parts of the redundant valve prolapse ( Web Sound MVP). Frequently, the click is followed by a mitral regurgitant murmur. Maneuvers that decrease venous return cause the clicks to occur earlier in systole and the murmur to become longer (see Table 4).

 

The opening of abnormal mitral or tricuspid valves can also be heard in the presence of rheumatic valvular stenosis, when the sound is referred to as an opening snap ( Web Sounds MS). The snap is heard only if the valve leaflets are pliable and is generated as the leaflets abruptly dome during early diastole. The interval between S₂ and the opening snap is of diagnostic importance: As the stenosis worsens and the atrial pressure increases, the mitral valve opens earlier in diastole, and the interval between the S₂ and the opening snap shortens.

 

MURMURS

 

As stated previously, murmurs are a series of auditory vibrations generated when either abnormal blood flow across a normal cardiac structure or normal flow across an abnormal cardiac structure results in turbulent flow. These sounds are longer than the individual heart sounds and can be described by their location, intensity, frequency (pitch), quality, duration, and timing in relation to systole or diastole. The intensity of a murmur is graded on a scale of 1 to 6 (Table 7). In general, murmurs of grade 4 or greater are associated with a palpable thrill. The loudness of a murmur does not necessarily correlate with the severity of the underlying abnormality. For instance, flow across a large atrial septal defect is essentially silent, whereas flow across a small ventricular septal defect is frequently associated with a loud murmur ( Web Sound VSD). Higher-frequency murmurs correlate with a higher velocity of flow at the site of turbulence. Important to note are the pattern or configuration of the murmur (e.g., crescendo, crescendo-decrescendo, decrescendo, plateau) (Fig. 5) and the quality of the murmur (e.g., harsh, blowing, rumbling), as well as the location of maximal intensity and the pattern of radiation of the murmur. Various physical maneuvers may help clarify the nature of a particular murmur (see Table 4).

 

 

 

Figure 5. Abnormal sounds and murmurs associated with valvular dysfunction displayed simultaneously with left atrial (LA), left ventricular (LV), and aortic pressure tracings. AVO = aortic valve opening; E = ejection click of the aortic valve; MVO = mitral valve opening; OS = opening snap of the mitral valve. The shaded areas represent pressure gradients across the aortic valve during systole or mitral valve during diastole, characteristic of aortic stenosis and mitral stenosis, respectively.

 

 

 

 

 

Murmurs can be divided into three categories-(1) systolic, (2) diastolic, and (3) continuous (Table 4-8)-and can result from abnormalities on the right or left side of the heart, as well as the great vessels. Right-sided murmurs may become significantly louder after inspiration, owing to the resulting augmentation of venous return, whereas left-sided murmurs are relatively unaffected by respiration. Systolic murmurs can be further divided into ejection-type murmurs and regurgitant murmurs. Ejection murmurs reflect turbulent flow across the aortic or pulmonic valve ( Web Sounds AS and PS). They begin shortly after S₁, increase in intensity as the velocity of flow increases, and subsequently decrease in intensity as the velocity falls (crescendo-decrescendo). Examples of ejection-type murmurs include innocent murmurs and the murmurs of aortic sclerosis, aortic stenosis, pulmonic stenosis, and hypertrophic cardiomyopathy. Innocent murmurs and aortic sclerotic murmurs are short in duration and do not radiate (Web Sound benign murmur). The duration of aortic or pulmonic stenotic murmurs varies depending on the severity of the stenosis (compare Web Sound AS-early and AS-late). With more severe stenosis, the murmur becomes longer, and the time to peak intensity of the murmur lengthens (i.e., early-, mid-, and late-peaking murmurs). The murmur of aortic stenosis is usually harsh, radiates to the carotid arteries, and at times may radiate to the cardiac apex (Gallavardin phenomenon). The murmur of hypertrophic cardiomyopathy may be confused with aortic stenosis, but it does not radiate to the carotids, and it is the only ejection murmur that becomes louder with decreased venous return. Mitral regurgitation associated with mitral valve prolapse may also show this response, but it is not a typical ejection murmur.

 

The classic regurgitant systolic murmurs of mitral (MR) and tricuspid regurgitation (TR) last throughout all of systole (holosystolic), are plateau in pattern, and terminate at S₂ ( Web Sound MR). With acute MR, the murmur may be limited to early systole and may be somewhat decrescendo in pattern. When MR is secondary to mitral valve prolapse, it starts in mid systole to late systole and is preceded by a mitral valve click. Ventricular septal defects may also result in holosystolic murmurs, although a small muscular ventricular septal defect may have a murmur limited to early systole.

 

Early-diastolic murmurs result from aortic or pulmonic insufficiency and are decrescendo in pattern. The duration of the murmur reflects chronicity: A short murmur is heard in acute aortic insufficiency or mild insufficiency, whereas chronic aortic insufficiency may produce a murmur throughout diastole. A Graham Steell murmur denotes a pulmonic insufficiency murmur in the setting of pulmonary hypertension. Mid-diastolic murmurs classically result from mitral or tricuspid stenosis, are low pitched, and are referred to as diastolic rumbles. Similar murmurs may be heard with obstructing atrial myxomas or in the presence of augmented diastolic flow across an unobstructed mitral or tricuspid valve, as occurs with an atrial or ventricular septal defect or with significant MR or TR. Severe, chronic aortic insufficiency may also produce a diastolic rumble, owing to premature closure of the mitral valve (Austin Flint murmur). Late-diastolic murmurs reflect presystolic accentuation of the mid-diastolic murmurs, owing to augmented mitral or tricuspid flow after atrial contraction.

 

The classic regurgitant systolic murmurs of mitral (MR) and tricuspid regurgitation (TR) last throughout all of systole (holosystolic), are plateau in pattern, and terminate at S₂ ( Web Sound MR). With acute MR, the murmur may be limited to early systole and may be somewhat decrescendo in pattern. When MR is secondary to mitral valve prolapse, it starts in mid systole to late systole and is preceded by a mitral valve click. Ventricular septal defects may also result in holosystolic murmurs, although a small muscular ventricular septal defect may have a murmur limited to early systole.

 

Continuous murmurs are murmurs that last throughout all of systole and continue into at least early diastole. These murmurs are referred to as machinery murmurs and are generated by continuous flow from a vessel or chamber with high pressure into a vessel or chamber with low pressure. A patent ductus arteriosus produces the classic continuous murmur ( Web Sound PDA).

 

OTHER CARDIAC SOUNDS

 

Pericardial rubs occur in the setting of pericarditis. These rubs produce coarse, scratching sounds heard best at the left sternal border with the patient leaning forward and holding his or her breath at end expiration. The classic rub has three components corresponding to atrial systole, ventricular systole, and ventricular diastole, although frequently only one or two of the components are audible ( Web Sound pericardial rubs). Localized irritation of the surrounding pleura may result in an associated pleural friction rub (pleuropericardial rub), which varies with respiration.

 

Continuous venous murmurs, or venous hums, are almost universally present in children. They are also frequent in adults, especially during pregnancy or in the setting of thyrotoxicosis or anemia. These murmurs are best heard at the base of the neck with the patient’s head turned to the opposite direction and can be eliminated by gentle pressure over the vein.

 

PROSTHETIC HEART SOUNDS

 

Prosthetic valves produce characteristic auscultatory findings. Porcine or bovine bioprosthetic valves produce heart sounds that are similar to native valve sounds; however, because these valves are smaller than the native valves that they replace, they almost always have an associated murmur (systolic ejection murmur when placed in the aortic position and diastolic rumble when placed in the mitral position). Mechanical valves result in crisp, high-pitched sounds related to valvular opening and closure. With ball-in-cage valves (e.g., Starr-Edwards valves, the opening sound is louder than the closure sound. With all other mechanical valves (e.g., Björk-Shiley valves, St. Jude valves), the closure sound is louder. These valves also produce an ejection-type murmur. Listening for all of the expected prosthetic sounds in patients with prosthetic valves is important because dysfunction of these valves may first be suggested by a change in the intensity or quality of the heart sounds or the development of a new or changing murmur.

 

Diagnostic Tests and Procedures

Chest Radiography

 

The chest radiograph is an integral part of the cardiac evaluation and gives valuable information regarding structure and function of the heart, lungs, and great vessels. A routine examination includes posteroanterior and lateral projections (Fig. 6).

 

 

Figure 6. Schematic illustration of the parts of the heart, whose outlines can be identified on a routine chest radiograph. A, Posteroanterior chest radiograph. B, Lateral chest radiograph. Ao = aorta; LA = left atrium; LV = left ventricle; PA = pulmonary artery; RA = right atrium; RV = right ventricle.

 

 

In the posteroanterior view, cardiac enlargement may be present when the transverse diameter of the cardiac silhouette is greater than one half of the transverse diameter of the thorax. The heart may appear falsely enlarged when it is displaced horizontally, such as with poor inflation of the lungs, and if the film is an anteroposterior projection, which magnifies the heart shadow. Left atrial enlargement is suggested when the left-sided heart border is straightened or bulges toward the left. In addition, the main bronchi may be widely splayed, and a circular opacity or double density within the cardiac silhouette may be seen. Right atrial enlargement may be present when the right-sided heart border bulges toward the right. Left ventricular enlargement results in downward and lateral displacement of the apex. A rounding of the displaced apex suggests ventricular hypertrophy. Right ventricular enlargement is best assessed in the lateral view and may be present when the right ventricular border occupies more than one third of the retrosternal space between the diaphragm and thoracic apex.

 

The aortic arch and thoracic aorta may become dilated and tortuous in patients with severe atherosclerosis, long-standing hypertension, and aortic dissection. Dilation of the proximal pulmonary arteries may occur when pulmonary pressures are elevated and pulmonary vascular resistance is increased. Disease states associated with increased pulmonary artery flow and normal vascular resistance, such as atrial or ventricular septal defects, may result in dilation of the proximal and distal pulmonary arteries.

 

Pulmonary venous congestion secondary to elevated left ventricular heart pressures results in redistribution of blood flow in the lungs and prominence of the apical vessels. Transudation of fluid into the interstitial space may result in fluid in the fissures and along the horizontal periphery of the lower lung fields (Kerley’s B lines). As venous pressures further increase, fluid collects within the alveolar space, which early on collects preferentially in the inner two thirds of the lung fields, resulting in a characteristic butterfly appearance.

 

Fluoroscopy or plain films may identify abnormal calcification involving the pericardium, coronary arteries, aorta, and valves. In addition, fluoroscopy can be instrumental in evaluating the function of mechanical prosthetic valves.

 

Electrocardiography

 

The electrocardiogram (ECG) represents the electrical activity of the heart recorded by skin electrodes. This wave of electrical activity is represented as a sequence of deflections on the ECG (Fig. 7). The horizontal scale represents time such that, at a standard paper speed of 25 mm/sec, each small box (1 mm) represents 0.04 seconds and each large box (5 mm) represents 0.20 seconds. The vertical scale represents amplitude (10 mm = 1 mV). The heart rate can be estimated by dividing the number of large boxes between complexes (R-R interval) into 300.

 

In the normal heart, the electrical impulse originates in the sinoatrial (SA) node and is conducted through the atria. Given that depolarization of the SA node is too weak to be detected on the surface ECG, the first, low-amplitude deflection on the surface ECG reflects atrial activation and is termed the P wave. The interval between the onset of the P wave and the next rapid deflection (QRS complex) is known as the PR interval and primarily represents the time taken for the impulse to travel through the atrioventricular (AV) node. The normal PR segment ranges from 0.12 to 0.20 seconds. A PR interval greater than 0.20 seconds defines AV nodal block.

 

Figure 7. Normal electrocardiographic (ECG) complex with labeling of waves and intervals.

 

Once the wave of depolarization has moved through the AV node, the ventricular myocardium is depolarized in a sequence of four phases. First, the interventricular septum depolarizes from left to right. This phase is followed by depolarization of the right ventricle and inferior wall of the left ventricle, then the apex and central portions of the left ventricle, and, finally, the base and the posterior wall of the left ventricle. Ventricular depolarization results in a high-amplitude complex on the surface ECG known as the QRS complex. The first downward deflection of this complex is the Q wave, the first upward deflection is the R wave, and the subsequent downward deflection is the S wave. In some individuals, a second upward deflection may be present after the S wave and is termed R prime (R’). Normal duration of the QRS complex is less than 0.10 seconds. Complexes greater than 0.12 seconds are usually secondary to some form of interventricular conduction delay.

 

The isoelectric segment after the QRS complex is the ST segment and represents a brief period during which relatively little electrical activity occurs in the heart. The junction between the end of the QRS complex and the beginning of the ST segment is the J point. The upward deflection after the ST segment is the T wave and represents ventricular repolarization. The QT interval, which reflects the duration and transmural gradient of ventricular depolarization and repolarization, is measured from the onset of the QRS complex to the end of the T wave. The QT interval varies with heart rate, but, for rates between 60 and 100 beats/min, the normal QT interval ranges from 0.35 to 0.44 seconds. For heart rates outside this range, the QT interval can be corrected by the formula:

 

 

 

In some individuals, a U wave (of varying amplitude) may be noted after the T wave, the cause of which is unknown.

 

The standard ECG consists of 12 leads: six limb leads (I, II, III, aVR, aVL, and aVF) and six chest or precordial leads (V₁ to V₆) (Fig. 8).

 

 

Figure 8. Normal 12-lead electrocardiogram.

 

The electrical activity recorded in each lead represents the direction and magnitude (vector) of the electrical force as seen from that particular lead position. Electrical activity directed toward a particular lead is represented as an upward deflection, and an electrical impulse directed away from a particular lead is represented as a downward deflection. Although the overall direction of electrical activity can be determined for any of the waveforms previously described, the mean QRS axis is the most clinically useful and is determined by examining the six limb leads.

Figure 9.  Hexaxial reference figure for frontal plane axis determination, indicating values for abnormal left and right QRS axis deviations.

 

 

Figure 9 illustrates Einthoven’s triangle and the polarity of each of the six limb leads of the standard ECG. Skin electrodes are attached to both arms and legs, with the right leg serving as the ground. Leads I, II, and III are bipolar leads and represent electrical activity between two leads: Lead I represents electrical activity between the right and left arms (left arm positive), lead II between the right arm and left leg (left leg positive), and lead III between the left arm and left leg (left leg positive). Leads aVR, aVL, and aVF are designated the augmented leads. With these leads, the QRS will be positive or have a predominant upward deflection when the electrical forces are directed toward the right arm for aVR, left arm for aVL, and left leg for aVF. These six leads form a hexaxial frontal plane of 30-degree arc intervals. The normal QRS axis ranges from -30 to +90 degrees. An axis more negative than -30 defines left-axis deviation, and an axis greater than +90 defines right-axis deviation. In general, a positive QRS complex in leads I and aVF suggests a normal QRS axis between 0 and 90 degrees.

 

 The six precordial leads (V₁ to V₆) are attached to the anterior chest wall. Electrical activity directed toward these leads results in a positive deflection on the ECG tracing. Leads V₁ and V₂ are closest to the right ventricle and interventricular septum, and leads V₅ and V₆ are closest to the anterior and anterolateral walls of the left ventricle. Normally, a small R wave occurs in lead V₁ reflecting septal depolarization and a deep S wave reflecting predominantly left ventricular activation. From V₁ to V₆, the R wave becomes larger (and the S wave smaller) because the predominant forces directed at these leads originate from the left ventricle. The transition from a predominant S wave to a predominant R wave usually occurs between leads V₃ and V₄. Right-sided chest leads are used to look for evidence of right ventricular infarction. ST segment elevation in V_4R has the best sensitivity and specificity for making this diagnosis. Some groups have advocated the use of posterior leads to increase the sensitivity for diagnosing lateral and posterior wall infarction or ischemia (areas that are often deemed to be electrically silent on traditional 12-lead ECGs).

 

Abnormal Electrocardiographic Patterns

 

CHAMBER ABNORMALITIES AND VENTRICULAR HYPERTROPHY

 

The P wave is normally upright in leads I, II, and F; inverted in aVR; and biphasic in V₁. Left atrial abnormality (defined as enlargement, hypertrophy, or increased wall stress) is characterized by a wide P wave in lead II (0.12 second) and a deeply inverted terminal component in lead V₁ (l mm). Right atrial abnormality is present when the P waves in the limb leads are peaked and 2.5 mm or more in height.

 

Left ventricular hypertrophy may result in increased QRS voltage, slight widening of the QRS complex, late intrinsicoid deflection, left-axis deviation, and abnormalities of the ST-T segments (Fig. 10).

 

Figure 10. Left ventricular hypertrophy as seen on an electrocardiographic (ECG) recording. Characteristic findings include increased QRS voltage in precordial leads (deep S in lead V₂ and tall R in lead V₅) and down-sloping ST depression and T wave inversion in lateral precordial leads (strain pattern) and leftward axis.

 

 

Multiple criteria with variable sensitivity and specificity for detecting left ventricular hypertrophy are available. The most frequently used criteria are given in Table 9.

 

 

 

 

 

Right ventricular hypertrophy is characterized by tall R waves in leads V₁ through V₃; deep S waves in leads I, aVL, V₅, and V₆; and right-axis deviation. In patients with chronically elevated pulmonary pressures, such as with chronic lung disease, a combination of ECG abnormalities reflecting a right-sided pathologic condition may be present and include right atrial abnormality, right ventricular hypertrophy, and right-axis deviation. In patients with acute pulmonary embolus, ECG changes may suggest right ventricular strain and include right-axis deviation; incomplete or complete right bundle branch block; S waves in leads I, II, and III; and T wave inversions in leads V₁ through V₃.

 

INTRAVENTRICULAR CONDUCTION DELAYS

 

The ventricular conduction system consists of two main branches, the right and left bundles. The left bundle further divides into the anterior and posterior fascicles. Conduction block can occur in either of the major branches or in the fascicles (Table 10).

 

 

 

 

 

Fascicular block results in a change in the sequence of ventricular activation but does not prolong overall conduction time (QRS duration remains <0.10 second). Left anterior fascicular block is a relatively common ECG abnormality and is sometimes associated with right bundle branch block. This conduction abnormality is present when extreme left-axis deviation occurs (more negative than -45 degrees); when the R wave is greater than the Q wave in leads I and aVL; and when the S wave is greater than the R wave in leads II, III, and aVF. Left posterior fascicular block is uncommon but is associated with right-axis deviation (>90 degrees); small Q waves in leads II, III, and aVF; and small R waves in leads I and aVL. The ECG findings associated with fascicular blocks can be confused with myocardial infarction. For example, with left anterior fascicular block, the prominent QS deflection in leads V₁ and V₂ can mimic an anteroseptal myocardial infarction, and the rS deflection in leads II, III, and aVF can be confused with an inferior myocardial infarction. Similarly, the rS deflection in leads I and aVL in left posterior fascicular block may be confused with a high lateral infarct. The presence of abnormal ST and T wave segments and pathologic Q waves are helpful findings to differentiate myocardial infarction from a fascicular block.

 

In left bundle branch block, depolarization proceeds down the right bundle, across the interventricular septum from right to left, and then to the left ventricle. Characteristic ECG findings include a wide QRS complex (0.12 second); a broad R wave in leads I, aVL, V₅, and V₆; a deep QS wave in leads V₁ and V₂; and ST depression and T wave inversion opposite the QRS deflection (Fig. 11).

Figure 11. A, Left bundle branch block. B, Right bundle branch block. Criteria for bundle branch block are summarized in Table 10.

 

Given the abnormal sequence of ventricular activation with left bundle branch block, many ECG abnormalities, such as Q wave myocardial infarction and left ventricular hypertrophy, cannot be interpreted. However, left bundle branch block almost always indicates the presence of underlying myocardial disease. With right bundle branch block, the interventricular septum depolarizes normally from left to right, and therefore the initial QRS deflection remains unchanged. As a result, ECG abnormalities such as Q wave myocardial infarction can still be interpreted. After septal activation, the left ventricle depolarizes, followed by the right ventricle. The ECG is characterized by a wide QRS complex; a large R’ wave in lead V₁ (R-S-R’); and deep S waves in leads I, aVL, and V₆, representing delayed right ventricular activation (see Fig. 11). Although right bundle branch block may be associated with underlying cardiac disease, it may also appear as a normal variant.

 

MYOCARDIAL ISCHEMIA AND INFARCTION

 

Myocardial ischemia and infarction may be associated with abnormalities of the ST segment, T wave, and QRS complex. Myocardial ischemia primarily affects repolarization of the myocardium and is often associated with horizontal or down-sloping ST segment depression and T wave inversion. These changes may be transient, such as during an anginal episode or an exercise stress test, or may be long lasting in the setting of unstable angina or myocardial infarction. T wave inversion without ST segment depression is a nonspecific finding and must be correlated with the clinical setting. Localized ST segment elevation suggests more extensive myocardial injury and is often associated with acute myocardial infarction (Fig. 12).

Figure 12. Evolutionary changes in a posteroinferior myocardial infarction. Control tracing is normal. The tracing recorded 2 hours after onset of chest pain demonstrated development of early Q waves, marked ST segment elevation, and hyperacute T waves in leads II, III, and aVF. In addition, a larger R wave, ST segment depression, and negative T waves have developed in leads V₁ and V₂. These are early changes indicating acute posteroinferior myocardial infarction. The 24-hour tracing demonstrates evolutionary changes. In leads II, III, and aVF, the Q wave is larger, the ST segments have almost returned to baseline, and the T wave has begun to invert. In leads V₁ to V₂, the duration of the R wave now exceeds 0.04 seconds, the ST segment is depressed, and the T wave is upright. (In this example, ECG changes of true posterior involvement extend past lead V₂; ordinarily, only leads V₁ and V₂ may be involved.) Only minor further changes occur through the 8-day tracing. Finally, 6 months later, the ECG illustrates large Q waves, isoelectric ST segments, and inverted T waves in leads II, III, and aVF and large R waves, isoelectric ST segment, and upright T waves in leads V₁ and V₂, indicative of an old posteroinferior myocardial infarction.

 

Vasospastic or Prinzmetal’s angina may be associated with reversible ST segment elevation without myocardial infarction. ST elevation may occur in other settings not related to acute ischemia or infarction. Persistent, localized ST segment elevation in the same leads as pathologic Q waves is consistent with a ventricular aneurysm. Acute pericarditis is associated with diffuse ST segment elevation and PR depression. Diffuse J point elevation in association with upward-coving ST segments is a normal variant common among young men and is often referred to as early repolarization.

 

The presence of a Q wave is one of the diagnostic criteria used to verify a myocardial infarction. Infarcted myocardium is unable to conduct electrical activity, and therefore electrical forces will be directed away from the surface electrode overlying the infarcted region, resulting in a Q wave on the surface ECG. Knowing which region of the myocardium each lead represents enables the examiner to localize the area of infarction (Table 11). A pathologic Q wave has a duration of greater than or equal to 0.04 seconds and/or a depth one fourth or more the height of the corresponding R wave.

 

 

 

 

 

Not all myocardial infarctions will result in the formation of Q waves. In addition, small R waves can return many weeks to months after a myocardial infarction.

 

Abnormal Q waves, or pseudoinfarction, may also be associated with nonischemic cardiac disease, such as ventricular pre-excitation, cardiac amyloidosis, sarcoidosis, idiopathic or hypertrophic cardiomyopathy, myocarditis, and chronic lung disease.

 

ABNORMALITIES OF THE ST SEGMENT AND T WAVE

 

A number of drugs and metabolic abnormalities may affect the ST segment and T wave (Fig. 13).

 

 

Figure 13. Metabolic and drug influences on the electrocardiographic (ECG) recording

 

Hypokalemia may result in prominent U waves in the precordial leads and prolongation of the QT interval. Hyperkalemia may result in tall, peaked T waves. Hypocalcemia typically lengthens the QT interval, whereas hypercalcemia shortens it. A commonly used cardiac medication, digoxin, often results in diffuse, scooped ST segment depression. Minor or nonspecific ST segment and T wave abnormalities may be present in many patients and have no definable cause. In these instances, the physician must determine the significance of the abnormalities based on the clinical setting.

 

Several excellent websites [1], [2], [3] containing examples of normal and abnormal ECGs are available.

 

Long-Term Ambulatory Electrocardiographic Recording

 

Ambulatory ECG (Holter monitoring) is a widely used, noninvasive method to evaluate cardiac arrhythmias and conduction disturbances over an extended period and to detect electrical abnormalities that may be brief or transient. With this approach, ECG data from two to three surface leads are stored on a tape recorder that the patient wears for a minimum of 24 to 48 hours. The recorders have both patient-activated event markers and time markers so that any abnormalities can be correlated with the patient’s symptoms or time of day. These data can then be printed in a standard, real-time ECG format for review.

 

For patients with intermittent or rare symptoms, an event recorder, which can be worn for several weeks, may be helpful in identifying the arrhythmia. The simplest device is a small, hand-held monitor that is applied to the chest wall when symptoms occur. The ECG data are recorded and can be transmitted later by telephone to a monitoring center for analysis. A more sophisticated system uses a wrist recorder that allows continuous loop storage of 4 to 5 minutes of ECG data from one lead. When the patient activates the system, ECG data preceding the event and for 1 to 2 minutes after the event are recorded and stored for further analysis. With both of these devices, the patient must be physically able to activate the recorder during the episode to store the ECG data. Implantable recording devices (subcutaneous) are sometimes used to diagnose infrequent events.

 

STRESS TESTING

 

Stress testing is an important noninvasive tool for evaluating patients with known or suggested coronary artery disease (CAD). During exercise, the increased demand for oxygen by the working skeletal muscles is met by increases in heart rate and cardiac output. In patients with significant CAD, the increase in myocardial oxygen demand cannot be met by an increase in coronary blood flow. As a result, myocardial ischemia may occur, resulting in chest pain and characteristic ECG abnormalities. These changes, combined with the hemodynamic response to exercise, can give useful diagnostic and prognostic information in the patient with cardiac abnormalities. The most frequent indications for stress testing include establishing a diagnosis of CAD in patients with chest pain, assessing prognosis and functional capacity in patients with chronic stable angina or after a myocardial infarction, evaluating exercise-induced arrhythmias, and assessing for ischemia after a revascularization procedure.

 

The most common form of stress testing uses continuous ECG monitoring while the patient walks on a treadmill. With each advancing stage, the speed and incline of the belt increases, thus increasing the amount of work the patient performs. Exercise testing may also be performed using a bicycle or arm ergometer. The stress test is deemed adequate if the patient achieves 85% of his or her maximal heart rate, which is equal to 220 minus the patient’s age. Indications for stopping the test include fatigue, severe hypertension (>220 mm Hg systolic), developing worsening angina during exercise, developing marked or widespread ischemic ECG changes, significant arrhythmias, or hypotension. The diagnostic accuracy of stress testing is improved with adjunctive echocardiography or radionuclide imaging. Contraindications to stress testing include unstable angina, acute myocardial infarction, poorly controlled hypertension (blood pressure >220/110 mm Hg), severe aortic stenosis (valve area <1.0 cm²), and decompensated congestive heart failure. In the era of reperfusion therapy (thrombolytic and/or percutaneous interventions), for acute coronary syndromes or acute MI, little role exists for the predischarge submaximal stress test that was commonly used in the past.

 

The diagnostic accuracy of the exercise test is dependent on the pre-test likelihood of CAD in a given patient, the sensitivity and specificity of the test results in that patient population, and the ECG criteria used to define a positive test. Clinical features that are most useful at predicting important angiographic coronary disease before exercise testing include advanced age, male sex, and the presence of typical (vs. atypical) anginal chest pain. The diagnostic accuracy and cost effectiveness of exercise testing is best in patients with an intermediate risk for CAD (30% to 70%) and when ischemic ECG changes are accompanied by chest pain during exercise. Exercise testing is less cost effective in diagnosing CAD in a patient with classic symptoms of angina because a positive test will not significantly increase the post-test probability of CAD, and a negative test would likely represent a false-negative result. Nonetheless, prognostic information and objective information about the efficacy of pharmacologic therapy may still be obtained. Similarly, exercise testing in young patients with atypical chest pain may not be diagnostically useful, given that an abnormal test result will likely represent a false-positive test and will not significantly increase the post-test probability of CAD.

 

The normal physiologic response to exercise is an increase in heart rate and systolic and diastolic blood pressures. The ECG will maintaiormal T wave polarity, and the ST segment will remain unchanged or, if depressed, will have a rapid upstroke back to baseline. An ischemic ECG response to exercise is defined as (1) 1.5 mm of up-sloping ST depression measured 0.08 seconds past the J point, (2) at least 1 mm of horizontal ST depression, or (3) 1 mm of down-sloping ST segment depression measured at the J point. Given the large amount of artifact on the ECG that may occur with exercise, these changes must be present in at least three consecutive depolarizations. Other findings suggestive of more extensive CAD include early onset of ST depression (6 minutes); marked, down-sloping ST depression (2 mm), especially if present in more than five leads; ST changes persisting into recovery for more than 5 minutes; and failure to increase systolic blood pressure to 120 mm Hg or more or a sustained decrease of 10 mm Hg or more below baseline.

 

The ECG is not diagnostically useful in the presence of left ventricular hypertrophy, left bundle branch block, Wolff-Parkinson-White syndrome, or chronic digoxin therapy. In these instances, nuclear or echocardiographic imaging may be helpful in demonstrating signs of ischemia. In patients who are unable to exercise, pharmacologic stress testing with myocardial imaging has been shown to have sensitivity and specificity for detecting CAD equal to those of exercise stress imaging. Intravenous dipyridamole and adenosine are coronary vasodilators that result in increased blood flow iormal arteries without significantly changing flow in diseased vessels. The resulting heterogeneity in blood flow can be detected by nuclear imaging techniques and the regions of myocardium supplied by diseased vessels identified. Another commonly used technique to evaluate for ischemia is dobutamine-stress echocardiography. Dobutamine is an inotropic agent that increases myocardial oxygen demand by increasing heart rate and contractility. The echocardiogram is used to monitor for ischemia, which is defined as new or worsening wall motion abnormalities during the infusion. Demonstrating improvement in wall thickening with low-dose dobutamine can also assess myocardial viability of abnormal segments (i.e., segments that are hypokinetic or akinetic at baseline).

 

ECHOCARDIOGRAPHY

 

Echocardiography is a widely used, noninvasive technique in which sound waves are used to image cardiac structures and evaluate blood flow. A piezoelectric crystal housed in a transducer placed on the patient’s chest wall produces ultrasound waves. As the sound waves encounter structures with different acoustic properties, some of the ultrasound waves are reflected back to the transducer and recorded. Ultrasound waves emitted from a single, stationary crystal produce an image of a thin slice of the heart (M-mode), which can then be followed through time. Steering the ultrasound beam across a 90-degree arc multiple times per second creates two-dimensional imaging (Fig. 14).

 

 

Figure 14. Portions of standard two-dimensional echocardiograms (A, parasternal long-axis view; B, apical four-chamber view) showing the major cardiac structures. Ao = aorta; IVS = interventricular septum; LA = left atrium; LV = left ventricle; MV = mitral valve; PE = pericardial effusion; PW = posterior LV wall; RV = right ventricle.

 

Transthoracic echocardiography is safe, simple, fast, and relatively inexpensive. Hence it is the most commonly used test to assess cardiac size, structure, and function. The development of three-dimensional echocardiographic imaging techniques offers great promise for more accurate measurements of chamber volumes and mass, as well as the assessment of geometrically complex anatomy and valvular lesions.

 

Doppler echocardiography allows assessment of both direction and velocity of blood flow within the heart and great vessels. When ultrasound waves encounter moving red blood cells, the energy reflected back to the transducer is altered. The magnitude of this change (Doppler shift) is represented as velocity on the echocardiographic display and can be used to determine if the blood flow is normal or abnormal (Fig. 15).

 

 

Figure 15. Doppler tracing in a patient with aortic stenosis and regurgitation. The velocity of systolic flow is related to the severity of obstruction.

 

In addition, the velocity of a particular jet of blood can be converted to pressure using the modified Bernoulli equation (ΔP ≅ 4v²). This process allows for the assessment of pressure gradients across valves or between chambers. Color Doppler imaging allows visualization of blood flow through the heart by assigning a color to the red blood cells based on their velocity and direction (Fig. 16).

 

 

Figure 16. Color Doppler recording demonstrating severe mitral regurgitation. The regurgitant jet seen in the left atrium (LA) is represented in blue because blood flow is directed away from the transducer. The yellow components are the mosaic pattern traditionally assigned to turbulent or high velocity flow. The arrow points to the hemisphere of blood accelerating proximal to the regurgitant orifice (proximal isovelocity surface area [PISA]). The size of the PISA can be used to help grade the severity of regurgitation. LA = left atrium; LV = left ventricle.

 

 

By convention, blood moving away from the transducer is represented in shades of blue, and blood moving toward the transducer is represented in red. Color Doppler imaging is particularly useful in identifying valvular insufficiency and abnormal shunt flow between chambers. Recently, the use of Doppler techniques to record myocardial velocities or strain rates has provided a great deal of insight into myocardial function and hemodynamics.

 

Two-dimensional echocardiography and Doppler echocardiography are often used in conjunction with exercise or pharmacologic stress testing. Although variability occurs among studies, the sensitivity of stress echocardiography is apparently slightly lower, but the specificity is slightly higher, compared with myocardial perfusion imaging with nuclear tracers. The overall cost effectiveness of stress echocardiography is estimated to be significantly better thauclear perfusion imaging because of the lower cost.

 

Transesophageal echocardiography (TEE) allows two-dimensional and Doppler imaging of the heart through the esophagus by having the patient swallow a gastroscope mounted with an ultrasound crystal within its tip. Given the close proximity of the esophagus to the heart, high-resolution images can be obtained, especially of the left atrium, mitral valve apparatus, and aorta. TEE is particularly useful in diagnosing aortic dissection, endocarditis, prosthetic valve dysfunction, and left atrial masses.

 

MAGNETIC RESONANCE IMAGING

 

Magnetic resonance angiography and or imaging (MRI) is an increasingly used noninvasive method of studying the heart and vasculature, especially in patients who have contraindications to standard contrast angiography (Fig. 17). Magnetic resonance angiography has become particularly popular in the evaluation of cerebral, renovascular, and lower extremity arterial disease. MRI offers significant advantages over other imaging techniques for the characterization of different tissues (e.g., muscle, fat, scar). The presence of delayed gadolinium contrast enhancement within the myocardium is characteristic of scar or permanently damaged tissue

 

Figure 17. Cardiac magnetic resonance imaging (MRI) showing short axis views of the left ventricle (LV) and right ventricle (RV) in diastole (A) and systole (B). Excellent spatial resolution and clear distinction between myocardial tissue and blood are evident.

 

NUCLEAR CARDIOLOGY

 

Radionuclide imaging of the heart allows quantification of left ventricular size and systolic function, as well as myocardial perfusion. With radionuclide ventriculography, the patient’s red blood cells are labeled with a small amount of a radioactive tracer (usually technetium-99m). Left ventricular function can then be assessed by one of two methods. With the first-pass technique, radiation emitted by the tagged red blood cells as they initially flow though the heart is detected by a gamma camera positioned over the patient’s chest. With the gated equilibrium method, or multigated acquisition (MUGA) method, the tracer is allowed to achieve an equilibrium distribution throughout the blood pool before count acquisition begins. This second method improves the resolution of the ventriculogram. For both techniques, the gamma camera can be gated to the ECG, allowing for determination of the total emitted end-diastole counts (EDC) and end-systole counts (ESC). Left ventricular ejection fraction (LVEF) can then be calculated as:

 

 

 

If scintigraphic information is collected throughout the cardiac cycle, then a computer-generated image of the heart can be displayed in a cinematic fashion, allowing for the assessment of wall motion.

 

Myocardial perfusion imaging is usually performed in conjunction with exercise or pharmacologic (vasodilator) stress testing. Persantine, or more commonly adenosine, is used as the coronary vasodilator. Each agent can increase myocardial blood flow by four- to fivefold. Adenosine is more expensive, but has the advantage over persantine of a very short half-life. Newer adenosine-like agents with reduced side effect profiles are being investigated. Technetium-99m sestamibi is the most frequently used radionuclide and is usually injected just before completion of the stress test. Tomographic (single-photon emission computed tomography [SPECT]) images of the heart are obtained for qualitative and quantitative analyses at rest and after stress. In the normal heart, radioisotope is relatively equally distributed throughout the myocardium. In patients with ischemia, a localized area of decreased uptake will occur after exercise but partially or completely fill in at rest (redistribution). A persistent defect at peak exercise and rest (fixed defect) is consistent with myocardial infarction or scarring. However, in some patients with apparently fixed defects, repeat rest imaging at 24 hours or after re-injection of a smaller quantity of isotope will demonstrate improved uptake, indicating the presence of viable, but severely ischemic, myocardium. The use of new approaches such as combined low-level exercise and vasodilators, prone imaging, attenuation correction, and computerized data analysis has improved the quality and reproducibility of the data from these studies.

 

Myocardial perfusion imaging may also be combined with ECG-gated image acquisition to allow for simultaneous assessment of ventricular function and perfusion. Not only can LVEF be quantitated with this technique, but also regional wall motion can be assessed to help rule out artifactual perfusion defects.

 

Positron-emission tomography (PET) is a noninvasive method of detecting myocardial viability by the use of both perfusion and metabolic tracers. In patients with left ventricular dysfunction, the presence of metabolic activity in a region of myocardium supplied by a severely stenotic coronary artery suggests viable tissue that may regain more normal function after revascularization (Fig. 18). PET is less widely available than conventional SPECT imaging; however, PET offers improved spatial resolution because of the higher energy of the isotopes used for this type of imaging.

 

 

Figure 18. Resting myocardial perfusion (obtained with [¹³N]-ammonia) and metabolism (obtained with [¹⁸F]-deoxyglucose) PET images of a patient with ischemic cardiomyopathy. The study demonstrates a perfusion-metabolic mismatch (reflecting hibernating myocardium) in which large areas of hypoperfused (solid arrows) but metabolically viable myocardium (open arrows) are involving the anterior, septal, and inferior walls and the left ventricular apex.

 

CARDIAC CATHETERIZATION

 

Cardiac catheterization is an invasive technique in which fluid-filled catheters are introduced percutaneously into the arterial and venous circulation. This method allows for the direct measurement of intracardiac pressures and oxygen saturation and, with the injection of a contrast agent, visualization of the coronary arteries, cardiac chambers, and great vessels. Cardiac catheterization is generally indicated when a clinically suggested cardiac abnormality requires confirmation and its anatomic and physiologic importance needs to be quantified. In the current era, coronary angiography for the diagnosis of CAD is the most common indication for this test. Noninvasive testing compared with catheterization is safer, cheaper, and equally effective in the evaluation of most valvular and hemodynamic questions. Most often, catheterization will precede some type of beneficial intervention, such as coronary artery angioplasty, coronary bypass surgery, or valvular surgery. Although cardiac catheterization is generally safe (0.1% to 0.2% overall mortality rate), procedure-related complications such as vascular injury, renal failure, stroke, and myocardial infarction can occur.

 

Left ventricular size, wall motion, and ejection fraction can be accurately assessed by injecting contrast into the left ventricle (left ventriculography). Aortic and mitral valve insufficiency can be qualitatively assessed during angiography by observing the reflux of contrast medium into the left ventricle and left atrium, respectively. The degree of valvular stenosis can be determined by measuring pressure gradients across the valve and determination of cardiac output (Gorlin formula).

 

The coronary anatomy can be defined by injecting contrast medium into the coronary tree. Atherosclerotic lesions appear as narrowings of the internal diameter (lumen) of the vessel. A hemodynamically important stenosis is defined as 70% or more narrowing of the luminal diameter. However, the hemodynamic significance of a lesion can be underestimated by coronary angiography, particularly in settings in which the atherosclerotic plaque is eccentric or elongated.

 

Biopsy of the ventricular endomyocardium can be performed during cardiac catheterization. With this technique, a bioptome is introduced into the venous system through the right internal jugular vein and guided into the right ventricle by fluoroscopy. Small samples of the endocardium are then taken for histologic evaluation. The primary indication for endomyocardial biopsy is the diagnosis of rejection after cardiac transplantation and documentation of cardiac amyloidosis; however, endomyocardial biopsy may have some use in diagnosing specific etiologic agents responsible for myocarditis.

 

 

 

 

OTHER DIAGNOSTIC PROCEDURES

 

Similar to MRI, new applications of computed tomography (CT) have greatly advanced our ability to diagnose cardiovascular disease noninvasively. Great vessel morphology and chamber size can be accurately assessed with both of these methods and, in contrast to echocardiography, they are not limited by the presence of lung disease or chest wall deformity. However, obesity and the presence of prosthetic materials (i.e., mechanical valves) will still affect image quality with these modalities. These tests are most frequently used to diagnose aortic aneurysm and acute aortic dissection and pulmonary embolism. They are also sensitive methods for defining congenital abnormalities and detecting pericardial thickening associated with constrictive pericarditis.

Ultrafast CT

(contrast medium-enhanced electron beam CT) provides complete cardiac imaging in real time and is a highly accurate noninvasive method for quantifying left ventricular volume and ejection fraction. MRI offers similar accuracy without radiation exposure . However, the presence of permanent cardiac pacemakers is a contraindication to MRI. Given the radiation exposure, lack of portability and expense, cardiac CT is not yet routinely used in clinical practice for the purposes of assessing left ventricular function. Electron beam and multidetector CT can visualize and quantitate the extent of coronary artery calcification. Although coronary artery calcification is a sensitive marker for the presence of significant CAD in some individuals, many older patients have such calcification without significant stenoses. In contrast, young patients may have high-grade noncalcified (soft) plaques that are missed by calcium scoring alone. Very recently, both ultrafast CT and MRI have also been shown to be useful methods of assessing the extent of CAD (Fig. 19). However, at the current time, coronary angiography remains the gold standard for localizing and quantifying the severity of CAD. Rapid improvements in both MRI and CT technology may lead to major shifts in diagnostic testing strategies in the near future. Some advocates of cardiac CT have proposed the use of this test for the triple rule out in patients with acute chest pain–namely, the ability to diagnose pulmonary embolism, aortic dissection, and coronary artery disease with one imaging study. Formal evaluation of this hypothesis still needs to be performed.

 

Figure 19. Computed tomographic (CT) coronary angiography compared with conventional x-ray contrast angiography. A and B, volume-rendering technique demonstrating stenosis of the right coronary artery and normal left coronary artery; C and D, Maximum intensity projection of the same arteries demonstrating severe soft plaque in the right coronary artery with superficial calcified plaque; E and F, Invasive angiography of the same arteries.

 

Assessment for the presence and severity of peripheral vascular disease is an important component of the cardiovascular evaluation. Comparison of the systolic blood pressure in the upper and lower extremities is one of the simplest tests to detect the presence of hemodynamically important arterial disease. Normally, the systolic pressure in the thigh is similar to that in the brachial artery. An ankle-to-brachial pressure ratio (ankle-brachial index) of less than or equal to 0.9 is abnormal. Patients with claudication usually have an index ranging from 0.5 to 0.8, and patients with rest pain have an index less than 0.5. In some patients, measuring the ankle-brachial index after treadmill exercise may be helpful in identifying the importance of borderline lesions. During normal exercise, blood flow increases to the upper and lower extremities and decreases in peripheral vascular resistance, whereas the ankle-brachial index remains unchanged. In the presence of a hemodynamically significant lesion, the increase in systolic blood pressure in the arm is not matched by an increase in blood pressure in the leg. As a result, the ankle-brachial index will decrease, the magnitude of which is proportional to the severity of the stenosis.

 

Once significant vascular disease in the extremities has been identified, plethysmography can be used to determine the location and severity of the disease. With this method, a pneumatic cuff is positioned on the leg or thigh and, when inflated, temporarily obstructs venous return. Volume changes in the limb segment below the cuff are converted to a pressure waveform, which can then be analyzed. The degree of amplitude reduction in the pressure waveform corresponds to the severity of arterial disease at that level.

 

Doppler ultrasound uses reflected sound waves to identify and localize stenotic lesions in the peripheral arteries. This test is particularly useful in patients with severely calcified arteries, in whom pneumatic compression is not possible and ankle-brachial indices are inaccurate. In combination with real-time imaging (duplex imaging), this technique is useful in assessing specific arterial segments and bypass grafts for stenotic or occlusive lesions.

 

Prospectus for the Future

Multidisciplinary teams consisting of cardiologists, cardiac surgeons, vascular surgeons, and radiologists will replace existing and traditional approaches for the evaluation and management of patients with cardiac disease. Such collaboration will foster efficiency and rapid advances for improvements for patient care, education, and research within a seamless, integrated environment. Career opportunities within organizations with the supporting infrastructure for cardiac imaging will likely realize the promise for patient-oriented, team-based cardiovascular medicine.

 

 

References.

A – Basic:

1. Davidson’s Principles and practice of medicine (21^st revised ed.) / by Colledge N.R., Walker B.R., and Ralston S.H., eds. – Churchill Livingstone, 2010. – 1376 p.

2. Harrison’s principles of internal medicine (18^th edition) / by Longo D.L., Kasper D.L., Jameson J.L. et al. (eds.). – McGraw-Hill Professional, 2012. – 4012 p.

3. The Merck Manual of Diagnosis and Therapy (nineteenth Edition)/ Robert Berkow, Andrew J. Fletcher and others. – published by Merck Research Laboratories, 2011.

4. Web -sites:

a)http://emedicine.medscape.com/

b) http://meded.ucsd.edu/clinicalmed/introduction.htm

 

B – Additional:

1. Braunwald’s Heart Disease: a textbook of cardiovascular medicine (9^th ed.) / by Bonow R.O., Mann D.L., and Zipes D.P., and Libby P. eds. – Saunders, 2012. – 2048 p.

2. Braunwald’s Heart Disease: review and assessment (9^th ed.) / Lilly L.S., editor. – Saunders, 2012. – 320 p.

3. Cardiology Intensive Board Review. Question Book (2^nd ed.) / by Cho L., Griffin B.P., Topol E.J., eds. – Lippincott Williams & Wilkins, 2009. – 385 p.

4. Cleveland Clinic Cardiology Board Review / Griffin B.P., Kapadia S.R., Rimmerman C.M., eds. – Lippincott Williams & Wilkins, 2012. – 952 p.

5. Hurst’s the Heart (13^th ed.) / by Fuster V., Walsh R.A., Harrington R., eds. – McGraw-Hill, 2010. – 2500 p.

5. Oxford Handbook of Cardiology (2^nd ed.) / by Ramrakha P., Hill J., eds. – Oxford University Press, 2012. – 851 p.