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InternalMed_Harrison. A midsystolic murmur begins after S1 and ends before S2; it is typically crescendo-decrescendo in configuration. AS is the most common cause of a midsystolic murmur in an adult. It is often difficult to estimate the severity of the valve lesion on the basis of the physical examination findings, especially in older hypertensive patients with stiffened carotid arteries or patients with low cardiac output in whom the intensity of the systolic heart murmur is misleadingly soft. Examination findings consistent with severe AS would include parvus et tardus carotid upstrokes, a late-peaking grade 3 or greater midsystolic murmur, a soft A2, a sustained LV apical impulse, and an S4. It is sometimes difficult to distinguish aortic sclerosis from more advanced degrees of valve stenosis. The former is defined by focal thickening and calcification of the aortic valve leaflets that is not severe enough to result in obstruction. These valve changes are associated with a Doppler jet velocity across


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InternalMed_Harrison. is defined by focal thickening and calcification of the aortic valve leaflets that is not severe enough to result in obstruction. These valve changes are associated with a Doppler jet velocity across the aortic valve of 2.5 m/s or less. Patients


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InternalMed_Harrison. FIGURE 267-5 A. Top. Graphic representation of the systolic pressure difference (green shaded area) between left ventricle and left atrium with phonocardiographic recording of a holosystolic murmur (HSM) indicative of mitral regurgitation. ECG, electrocardiogram; LAP, left atrial pressure; LVP, left ventricular pressure; S1, first heart sound; S2 second heart sound. Bottom. Graphic representation of the systolic pressure gradient (green shaded area) between left ventricle and aorta in patient with aortic stenosis. A midsystolic murmur (MSM) with a crescendo-decrescendo configuration is recorded. AOP, aortic pressure. B. Top. Graphic representation of the diastolic pressure difference between the aorta and left ventricle (blue shaded area) in a patient with aortic regurgitation, resulting in a decrescendo, early diastolic murmur (EDM) beginning with A2. Bottom. Graphic representation of the diastolic left atrial–left ventricular gradient (blue areas) in a patient with mitral stenosis


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InternalMed_Harrison. in a decrescendo, early diastolic murmur (EDM) beginning with A2. Bottom. Graphic representation of the diastolic left atrial–left ventricular gradient (blue areas) in a patient with mitral stenosis with a mid-diastolic murmur (MDM) and late presystolic murmurs (PSM).


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InternalMed_Harrison. with aortic sclerosis can have grade 2 or 3 midsystolic murmurs identical in their acoustic characteristics to the murmurs heard in patients with more advanced degrees of AS. Other causes of a midsystolic heart murmur include pulmonic valve stenosis (with or without an ejection sound), HOCM, increased pulmonary blood flow in patients with a large atrial septal defect and left-to-right shunting, and several states associated with accelerated blood flow in the absence of structural heart disease, such as fever, thyrotoxicosis, pregnancy, anemia, and normal childhood/adolescence.


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InternalMed_Harrison. The murmur of HOCM has features of both obstruction to LV outflow and MR, as would be expected from knowledge of the pathophysiology of this condition. The systolic murmur of HOCM usually can be distinguished from other causes on the basis of its response to bedside maneuvers, including Valsalva, passive leg raising, and standing/ squatting. In general, maneuvers that decrease LV preload (or increase LV contractility) will cause the murmur to intensify, whereas maneuvers that increase LV preload or afterload will cause a decrease in the intensity of the murmur. Accordingly, the systolic murmur of HOCM becomes louder during the strain phase of the Valsalva maneuver and after standing quickly from a squatting position. The murmur becomes softer with passive leg raising and when squatting. The murmur of AS is typically loudest in the second right interspace with radiation into the carotids, whereas the murmur of HOCM is best heard between the lower left sternal border and the apex. The


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InternalMed_Harrison. The murmur of AS is typically loudest in the second right interspace with radiation into the carotids, whereas the murmur of HOCM is best heard between the lower left sternal border and the apex. The murmur of PS is best heard in the second left interspace. The midsystolic murmur associated with enhanced pulmonic blood flow in the setting of a large atrial septal defect (ASD) is usually loudest at the mid-left sternal border.


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InternalMed_Harrison. is low-pitched or rumbling, and is introduced by an OS in the early stages of the rheumatic disease process. Presystolic accentuation refers to an increase in the intensity of the murmur just before the first heart sound and occurs in patients with sinus rhythm. It is absent FIGURE 267-6 Behavior of the click (C) and murmur (M) of mitral valve prolapse with in patients with atrial fibrillation. The aus changes in loading (volume, impedance) and contractility. S1, first heart sound; S2, sec cultatory findings in patients with rheumatic ond heart sound. With standing (left side of figure), volume and impedance decrease, as a tricuspid stenosis typically are obscured by result of which the click and murmur move closer to S . With squatting (right), the click and 1 left-sided events, although they are similar in murmur move away from S due to the increases in left ventricular volume and impedance 1 nature to those described in patients with MS.


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InternalMed_Harrison. (afterload). Ao, aorta; LV, left ventricle. (Adapted from RA O’Rourke, MH Crawford: Curr Prob Physical Examination of the Cardiovascular System Cardiol 1:9, 1976.) A late systolic murmur, heard best at the apex, indicates MVP. As previously noted, the murmur may or may not be introduced by a nonejection click. Differential radiation of the murmur, as previously described, may help identify the specific leaflet involved by the myxomatous process. The click-murmur complex behaves in a manner directionally similar to that demonstrated by the murmur of HOCM during the Valsalva and stand/squat maneuvers (Fig. 267-6). The murmur of MVP can be identified by the accompanying nonejection click.


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InternalMed_Harrison. Holosystolic murmurs are plateau in configuration and reflect a continuous and wide pressure gradient between the left ventricle and left atrium with chronic MR, the left ventricle and right ventricle with a ventricular septal defect (VSD), and the right ventricle and right atrium with TR. In contrast to acute MR, in chronic MR the left atrium is enlarged and its compliance is normal or increased to the extent that there is little if any further increase in left atrial pressure from any increase in regurgitant volume. The murmur of MR is best heard over the cardiac apex. The intensity of the murmur increases with maneuvers that increase LV afterload, such as sustained hand grip. The murmur of a VSD (without significant pulmonary hypertension) is holosystolic and loudest at the mid-left sternal border, where a thrill is usually present. The murmur of TR is loudest at the lower left sternal border, increases in intensity with inspiration (Carvallo’s sign), and is accompanied by visible


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InternalMed_Harrison. border, where a thrill is usually present. The murmur of TR is loudest at the lower left sternal border, increases in intensity with inspiration (Carvallo’s sign), and is accompanied by visible cv waves in the jugular venous wave form and, on occasion, by pulsatile hepatomegaly.


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InternalMed_Harrison. Diastolic Murmurs In contrast to some systolic murmurs, diastolic heart murmurs always signify structural heart disease (Fig. 267-5). The murmur associated with acute, severe AR is relatively soft and of short duration because of the rapid rise in LV diastolic pressure and the progressive diminution of the aortic-LV diastolic pressure gradient. In contrast, the murmur of chronic severe AR is classically heard as a decrescendo, blowing diastolic murmur along the left sternal border in patients with primary valve pathology and sometimes along the right sternal border in patients with primary aortic root pathology.


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InternalMed_Harrison. With chronic AR, the pulse pressure is wide 1449 and the arterial pulses are bounding in character. These signs of significant diastolic run-off are absent in the acute phase. The murmur of pulmonic regurgitation is also heard along the left sternal border. It is most commonly due to pulmonary hypertension and enlargement of the annulus of the pulmonic valve. S2 is single and loud and may be palpable. There is a right ventricular/parasternal lift that is indicative of chronic right ventricular pressure overload. A less impressive murmur of PR is present after repair of tetralogy of Fallot or pulmonic valve atresia. In this postoperative setting, the murmur is softer and lower-pitched, and the severity of the accompanying pulmonic regurgitation can be underestimated significantly.


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InternalMed_Harrison. MS is the classic cause of a midto late diastolic murmur, which is best heard over the apex in the left lateral decubitus position, to the generation of mid-diastolic murmurs that are created by increased and accelerated transvalvular diastolic flow, even in the absence of valvular obstruction, in the setting of severe MR, severe TR, or a large ASD with left-to-right shunting. The Austin Flint murmur of chronic severe AR is a low-pitched midto late apical diastolic murmur that sometimes can be confused with MS. The Austin Flint murmur typically decreases in intensity after exposure to vasodilators, whereas the murmur of MS may be accompanied by an opening snap and also may increase in intensity after vasodilators because of the associated increase in cardiac output. Unusual causes of a mid-diastolic murmur include atrial myxoma, complete heart block, and acute rheumatic mitral valvulitis.


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InternalMed_Harrison. Continuous Murmur A continuous murmur is predicated on a pressure gradient that persists between two cardiac chambers or blood vessels across systole and diastole. The murmurs typically begin in systole, envelop the second heart sound (S2), and continue through some portion of diastole. They can often be difficult to distinguish from individual systolic and diastolic murmurs in patients with mixed valvular heart disease. The classic example of a continuous murmur is that associated with a PDA, which usually is heard in the second or third interspace at a slight distance from the sternal border. Other causes of a continuous murmur include a ruptured sinus of Valsalva aneurysm with creation of an aortic–right atrial or right ventricular fistula, a coronary or great vessel arteriovenous fistula, and an arteriovenous fistula constructed to provide dialysis access. There are two types of benign continuous murmurs. The cervical venous hum is heard in children or adolescents in the


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InternalMed_Harrison. fistula, and an arteriovenous fistula constructed to provide dialysis access. There are two types of benign continuous murmurs. The cervical venous hum is heard in children or adolescents in the supraclavicular fossa. It can be obliterated with firm pressure applied to the diaphragm of the stethoscope, especially when the subject turns his or her head toward the examiner. The mammary soufflé of pregnancy relates to enhanced arterial blood flow through engorged breasts. The diastolic component of the murmur can be obliterated with firm pressure over the stethoscope.


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InternalMed_Harrison. Dynamic Auscultation Diagnostic accuracy can be enhanced by the performance of simple bedside maneuvers to identify heart murmurs and characterize their significance (Table 267-1). Except for the pulmonic Respiration Right-sided murmurs and sounds generally increase with inspiration, except for the PES. Left-sided murmurs and sounds are usually louder during expiration. Valsalva maneuver Most murmurs decrease in length and intensity. Two exceptions are the systolic murmur of HOCM, which usually becomes much louder, and that of MVP, which becomes longer and often louder. After release of the Valsalva maneuver, right-sided murmurs tend to return to control intensity earlier than do left-sided murmurs.


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InternalMed_Harrison. After VPB or AF Murmurs originating at normal or stenotic semilunar valves increase in the cardiac cycle after a VPB or in the cycle after a long cycle length in AF. By contrast, systolic murmurs due to AV valve regurgitation do not change, diminish (papillary muscle dysfunction), or become shorter (MVP). Positional changes With standing, most murmurs diminish, with two exceptions being the murmur of HOCM, which becomes louder, and that of MVP, which lengthens and often is intensified. With squatting, most murmurs become louder, but those of HOCM and MVP usually soften and may disappear. Passive leg raising usually produces the same results.


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InternalMed_Harrison. Exercise Murmurs due to blood flow across normal or obstructed valves (e.g., PS, MS) become louder with both isotonic and submaximal isometric (hand grip) exercise. Murmurs of MR, VSD, and AR also increase with hand grip exercise. However, the murmur of HOCM often decreases with nearly maximum hand grip exercise. Left-sided S4 and S3 sounds are often accentuated by exercise, particularly when due to ischemic heart disease. Abbreviations: AF, atrial fibrillation; AR, aortic regurgitation; HOCM, hypertrophic obstructive cardiomyopathy; MR, mitral regurgitation; MS, mitral stenosis; MVP, mitral valve prolapse; PES, pulmonic ejection sound; PR, pulmonic regurgitation; PS, pulmonic stenosis; TR, tricuspid regurgitation; TS, tricuspid stenosis; VPB, ventricular premature beat; VSD, ventricular septal defect.


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InternalMed_Harrison. ejection sound, right-sided events increase in intensity with inspiration and decrease with expiration; left-sided events behave oppositely (100% sensitivity, 88% specificity). As previously noted, the intensity of the murmurs associated with MR, VSD, and AR will increase in response to maneuvers that increase LV afterload, such as hand grip and vasopressors. The intensity of these murmurs will decrease after exposure to vasodilating agents. Squatting is associated with an abrupt increase in LV preload and afterload, whereas rapid standing results in a sudden decrease in preload. In patients with MVP, the click and murmur move away from the first heart sound with squatting because of the delay in onset of leaflet prolapse at higher ventricular volumes. With rapid standing, however, the click and murmur move closer to the first heart sound as prolapse occurs earlier in systole at a smaller chamber dimension. The murmur of HOCM behaves similarly, becoming softer and shorter with


InternalMed_Harrison

InternalMed_Harrison. the click and murmur move closer to the first heart sound as prolapse occurs earlier in systole at a smaller chamber dimension. The murmur of HOCM behaves similarly, becoming softer and shorter with squatting (95% sensitivity, 85% specificity) and longer and louder on rapid standing (95% sensitivity, 84% specificity). A change in the intensity of a systolic murmur in the first beat after a premature beat or in the beat after a long cycle length in patients with atrial fibrillation suggests valvular AS rather than MR, particularly in an older patient in whom the murmur of the AS may be well transmitted to the apex (Gallavardin effect). Of note, however, the systolic murmur of HOCM also increases in intensity in the beat after a premature beat. This increase in intensity of any LV outflow murmur in the beat after a premature beat relates to the combined effects of enhanced LV filling (from the longer diastolic period) and postextrasystolic potentiation of LV contractile function. In


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InternalMed_Harrison. murmur in the beat after a premature beat relates to the combined effects of enhanced LV filling (from the longer diastolic period) and postextrasystolic potentiation of LV contractile function. In either instance, forward flow will accelerate, causing an increase in the gradient across the LV outflow tract (dynamic or fixed) and a louder systolic murmur. In contrast, the intensity of the murmur of MR does not change in a postpremature beat, because there is relatively little change in the nearly constant LV to left atrial pressure gradient or further alteration in mitral valve flow. Bedside exercise can sometimes be performed to increase cardiac output and, secondarily, the intensity of both systolic and diastolic heart murmurs. Most left-sided heart murmurs decrease in intensity and duration during the strain phase of the Valsalva maneuver. The murmurs associated with MVP and HOCM are the two notable exceptions. The Valsalva maneuver also can be used to assess the integrity of the


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InternalMed_Harrison. during the strain phase of the Valsalva maneuver. The murmurs associated with MVP and HOCM are the two notable exceptions. The Valsalva maneuver also can be used to assess the integrity of the heart and vasculature in the setting of advanced heart failure.


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InternalMed_Harrison. Prosthetic Heart Valves The first clue that prosthetic valve dysfunction may contribute to recurrent symptoms is frequently a change in the quality of the heart sounds or the appearance of a new murmur. The heart sounds with a bioprosthetic valve resemble those generated by native valves. A mitral bioprosthesis usually is associated with a grade 2 or 3 midsystolic murmur along the left sternal border (created by turbulence across the valve struts as they project into the LV outflow tract) as well as by a soft mid-diastolic murmur that occurs with normal LV filling. This diastolic murmur often can be heard only in the left lateral decubitus position and after exercise. A high pitched or holosystolic apical murmur is indicative of pathologic MR due to a paravalvular leak and/or intra-annular bioprosthetic regurgitation from leaflet degeneration, for which additional imaging is usually indicated. Clinical deterioration can occur rapidly after the first expression of mitral bioprosthetic


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InternalMed_Harrison. bioprosthetic regurgitation from leaflet degeneration, for which additional imaging is usually indicated. Clinical deterioration can occur rapidly after the first expression of mitral bioprosthetic failure. A tissue valve in the aortic position is always associated with a grade 2 to 3 midsystolic murmur at the base or just below the suprasternal notch. A diastolic murmur of AR is abnormal in any circumstance. Mechanical valve dysfunction may first be suggested by a decrease in the intensity of either the opening or the closing sound. A high-pitched apical systolic murmur in patients with a mechanical mitral prosthesis and a diastolic decrescendo murmur in patients with a mechanical aortic prosthesis indicate paravalvular regurgitation. Patients with prosthetic valve thrombosis may present clinically with signs of shock, muffled heart sounds, and soft murmurs.


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InternalMed_Harrison. Pericardial Disease A pericardial friction rub is nearly 100% specific for the diagnosis of acute pericarditis, although the sensitivity of this finding is not nearly as high, because the rub may come and go over the course of an acute illness or be very difficult to elicit. The rub is heard as a leathery or scratchy three-component or two-component sound, although it may be monophasic. Classically, the three components are ventricular systole, rapid early diastolic filling, and late presystolic filling after atrial contraction in patients in sinus rhythm. It is necessary to listen to the heart in several positions. Additional clues may be present from the history and 12-lead electrocardiogram. The rub typically disappears as the volume of any pericardial effusion increases. Pericardial tamponade can be diagnosed with a sensitivity of 98%, a specificity of 83%, and a positive likelihood ratio of 5.9 (95% confidence interval 2.4–14) by a pulsus paradoxus that exceeds 12 mmHg in a


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InternalMed_Harrison. tamponade can be diagnosed with a sensitivity of 98%, a specificity of 83%, and a positive likelihood ratio of 5.9 (95% confidence interval 2.4–14) by a pulsus paradoxus that exceeds 12 mmHg in a patient with a large pericardial effusion.


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InternalMed_Harrison. The findings on physical examination are integrated with the symptoms previously elicited with a careful history to construct an appropriate differential diagnosis and proceed with indicated imaging and laboratory assessment. The physical examination is an irreplaceable component of the diagnostic algorithm and in selected patients can inform prognosis. Educational efforts to improve clinician competence eventually may result in cost saving, particularly if the indications for imaging can be influenced by the examination findings. Ary L. Goldberger An electrocardiogram (ECG or EKG) is a graphic recording of electric potentials generated by the heart. The signals are detected by means of metal electrodes attached to the extremities and chest wall and then are amplified and recorded by the electrocardiograph. ECG leads actually display the instantaneous differences in potential between the electrodes.


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InternalMed_Harrison. The clinical utility of the ECG derives from its immediate availability as a noninvasive, inexpensive, and highly versatile test. In addition to its use in detecting arrhythmias, conduction disturbances, and myocardial ischemia, electrocardiography may reveal findings related to life-threatening metabolic disturbances (e.g., hyperkalemia) or increased susceptibility to sudden cardiac death (e.g., QT prolongation syndromes). (See also Chaps. 274 and 276) Depolarization of the heart is the initiating event for cardiac contraction. The electric currents that spread through the heart are produced by three components: cardiac pacemaker cells, specialized conduction tissue, and the heart muscle itself. The ECG, however, records only the depolarization (stimulation) and repolarization (recovery) potentials generated by the “working” atrial and ventricular myocardium.


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InternalMed_Harrison. The depolarization stimulus for the normal heartbeat originates in the sinoatrial (SA) node (Fig. 268-1), or sinus node, a collection of pacemaker cells. These cells fire spontaneously; that is, they exhibit automaticity. The first phase of cardiac electrical activation is the spread of the depolarization wave through the right and left atria, followed by atrial contraction. Next, the impulse stimulates pacemaker and specialized conduction tissues in the atrioventricular (AV) nodal and His-bundle areas; together, these two regions constitute the AV junction. The bundle of His bifurcates into two main branches, the right and left bundles, which rapidly transmit depolarization wavefronts to the right and left ventricular myocardium by way of Purkinje fibers. The main left bundle bifurcates into two primary subdivisions: a left anterior fascicle and a left posterior fascicle. The depolarization wavefronts then spread through the ventricular wall, from endocardium to epicardium,


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InternalMed_Harrison. into two primary subdivisions: a left anterior fascicle and a left posterior fascicle. The depolarization wavefronts then spread through the ventricular wall, from endocardium to epicardium, triggering ventricular contraction.


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InternalMed_Harrison. Since the cardiac depolarization and repolarization waves have direction and magnitude, they can be represented by vectors. Vector analysis illustrates a central concept of electrocardiography: The ECG records the complex spatial and temporal summation of electrical potentials from multiple myocardial fibers conducted to the surface of the body. This principle accounts for inherent limitations in both ECG sensitivity (activity from certain cardiac regions may be canceled out or may be too weak to be recorded) and specificity (the same vectorial sum can result from either a selective gain or a loss of forces in opposite directions).


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InternalMed_Harrison. The ECG waveforms are labeled alphabetically, beginning with the P wave, which represents atrial depolarization (Fig. 268-2). The QRS complex represents ventricular depolarization, and the ST-T-U complex (ST segment, T wave, and U wave) represents ventricular repolarization. The J point is the junction between the end of the QRS complex and the beginning of the ST segment. Atrial repolarization (STa and T a) is usually too low in amplitude to be detected, but it may become apparent in conditions such as acute pericarditis and atrial infarction. The QRS-T waveforms of the surface ECG correspond in a general way with the different phases of simultaneously obtained ventricular action potentials, the intracellular recordings from single myocardial FIGURE 268-1 Schematic of the cardiac conduction system. FIGURE 268-2 Basic ECG waveforms and intervals. Not shown is the RR interval, the time between consecutive QRS complexes.


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InternalMed_Harrison. FIGURE 268-1 Schematic of the cardiac conduction system. FIGURE 268-2 Basic ECG waveforms and intervals. Not shown is the RR interval, the time between consecutive QRS complexes. fibers (Chap. 274). The rapid upstroke (phase 0) of the action potential corresponds to the onset of QRS. The plateau (phase 2) corresponds to the isoelectric ST segment, and active repolarization (phase 3) corresponds to the inscription of the T wave. Factors that decrease the slope of phase 0 by impairing the influx of Na+ (e.g., hyperkalemia and drugs such as flecainide) tend to increase QRS duration. Conditions that prolong phase 2 (amiodarone, hypocalcemia) increase the QT interval. In contrast, shortening of ventricular repolarization (phase 2), such as by digitalis administration or hypercalcemia, abbreviates the ST segment.


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InternalMed_Harrison. The ECG ordinarily is recorded on special graph paper that is divided into 1-mm2 gridlike boxes. Since the usual ECG paper speed is 25 mm/s, the smallest (1 mm) horizontal divisions correspond to 0.04 (40 ms), with heavier lines at intervals of 0.20 s (200 ms). Vertically, the ECG graph measures the amplitude of a specific wave or deflection (1 mV = 10 mm with standard calibration; the voltage criteria for hypertrophy mentioned below are given in millimeters). There are four major ECG intervals: RR, PR, QRS, and QT (Fig. 268-2). The heart rate (beats per minute) can be computed readily from the interbeat (RR) interval by dividing the number of large (0.20 s) time units between consecutive R waves into 300 or the number of small (0.04 s) units into 1500. The PR interval measures the time (normally 120–200 ms) between atrial and ventricular depolarization, which includes the physiologic delay imposed by stimulation of cells in the AV junction area. The QRS interval (normally 100–110 ms


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InternalMed_Harrison. 120–200 ms) between atrial and ventricular depolarization, which includes the physiologic delay imposed by stimulation of cells in the AV junction area. The QRS interval (normally 100–110 ms or less) reflects the duration of ventricular depolarization. The QT interval includes both ventricular depolarization and repolarization times and varies inversely with the heart rate. A rate-related (“corrected”) QT interval, QTc, can be calculated as QT/√RR and normally is ≤0.44 s. (Some references give QTc upper normal limits as 0.43 s in men and 0.45 s in women. Also, a number of different formulas have been proposed, without consensus, for calculating the QTc.)


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InternalMed_Harrison. The QRS complex is subdivided into specific deflections or waves. If the initial QRS deflection in a particular lead is negative, it is termed a Q wave; the first positive deflection is termed an R wave. A negative deflection after an R wave is an S wave. Subsequent positive or negative waves are labeled R′ and S′, respectively. Lowercase letters (qrs) are used for waves of relatively small amplitude. An entirely negative QRS complex is termed a QS wave. The 12 conventional ECG leads record the difference in potential between electrodes placed on the surface of the body. These leads are divided into two groups: six limb (extremity) leads and six chest (precordial) leads. The limb leads record potentials transmitted onto the frontal plane (Fig. 268-3A), and the chest leads record potentials transmitted onto the horizontal plane (Fig. 268-3B). + V4 deflection will be recorded.


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InternalMed_Harrison. + V4 deflection will be recorded. FIGURE 268-3 The six frontal plane (A) and six horizontal plane (B) leads provide a P WAVE ambulatory ECG (Holter) recordings usually employ only one or two modified leads. Intracardiac electrocardiography and electrophysiologic testing are discussed in Chaps. 274 and 276. The ECG leads are configured so that a positive (upright) deflection is recorded in a lead if a wave of depolarization spreads toward the positive pole of that + lead, and a negative deflection is recorded if the wave spreads toward the negative pole. If the mean orientation + of the depolarization vector is at right angles to a particu lar lead axis, a biphasic (equally positive and negative) three-dimensional representation of cardiac electrical activity.


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InternalMed_Harrison. The spatial orientation and polarity of the six frontal plane leads is represented on the hexaxial diagram (Fig. 268-4). The six chest leads (Fig. 268-5) are unipolar recordings obtained by electrodes in the following positions: lead V1, fourth intercostal space, just to the right of the sternum; lead V2, fourth intercostal space, just to the left of the sternum; lead V3, midway between V2 and V4; lead V4, midclavicular line, fifth intercostal space; lead V5, anterior axillary line, same level as V4; and lead V6, midaxillary line, same level as V4 and V5. Additional posterior leads are sometimes placed on the same horizontal plane as V4 to facilitate detection of acute posterolateral infarction (V7, midaxillary line; V8 posterior axillary line; and V9, posterior scapular line).


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InternalMed_Harrison. Together, the frontal and horizontal plane electrodes provide a three-dimensional representation of cardiac electrical activity. Each lead can be likened to a different video camera angle “looking” at the same events—atrial and ventricular depolarization and repolarization— from different spatial orientations. The conventional 12-lead ECG can be supplemented with additional leads in special circumstances. For example, right precordial leads V3R, V4R, etc., are useful in detecting evidence of acute right ventricular ischemia. Bedside monitors and The normal atrial depolarization vector is oriented down


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InternalMed_Harrison. Rightaxisdeviation Normalaxis Leftaxisdeviation –90° –aVF –60° –III –30° +aVL 0° +I +30° –aVR +60° +II +90° +aVF +120° +III +150° – aVL 180° –I –150° +aVR –120° –II Extremeaxisdeviation FIGURE 268-4 The frontal plane (limb or extremity) leads are rep-resented on a hexaxial diagram. Each ECG lead has a specific spatial orientation and polarity. The positive pole of each lead axis (solid line) and the negative pole (hatched line) are designated by their angular position relative to the positive pole of lead I (0°). The mean electrical axis of the QRS complex is measured with respect to this display.


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InternalMed_Harrison. ward and toward the subject’s left, reflecting the spread of depolarization from the sinus node to the right and then the left atrial myocardium. Since this vector points toward the positive pole of lead II and toward the negative pole of lead aVR, the normal P wave will be positive in lead II and negative in lead aVR. By contrast, activation of the atria from an ectopic pacemaker in the lower part of either atrium or in the AV junction region may produce retrograde P waves (negative in lead II, positive in lead aVR). The normal P wave in lead V1 may be biphasic with a positive component reflecting right atrial depolarization, followed by a small (<1 mm2) negative component reflecting left atrial depolarization.


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InternalMed_Harrison. Normal ventricular depolarization proceeds as a rapid, continuous spread of activation wave fronts. This complex process can be divided into two major sequential phases, and each phase can be represented by a mean vector (Fig. 268-6). The first phase is depolarization of the interventricular septum from the left to the right and anteriorly (vector 1). The second results from the simultaneous depolarization of the right and left ventricles; it normally is dominated by the more massive left ventricle, so that vector 2 points leftward and posteriorly. Therefore, a right precordial lead (V1) will record this biphasic depolarization process with a small positive deflection (septal r wave) followed by a larger negative deflection (S wave). A left precordial lead, e.g., V6, will record the same sequence with a small negative deflection (septal q wave) followed by a relatively tall positive deflection (R wave). Intermediate leads show a relative increase in R-wave amplitude (normal R-wave


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InternalMed_Harrison. sequence with a small negative deflection (septal q wave) followed by a relatively tall positive deflection (R wave). Intermediate leads show a relative increase in R-wave amplitude (normal R-wave progression) and a decrease in S-wave amplitude progressing across the chest from right to left. The precordial lead where


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InternalMed_Harrison. V1V3RV4RV2V3V4V5V6FIGURE 268-5 The horizontal plane (chest or precordial) leads are obtained with electrodes in the locations shown. major phases, each represented by a vector. A. The first phase (arrow 1) denotes depolarization of the ventricular septum, beginning on the left side and spreading to the right. This process is represented by a small “septal” r wave in lead V1 and a small septal q wave in lead V6. B. Simultaneous depolarization of the left and right ventricles (LV and RV) constitutes the second phase. Vector 2 is oriented to the left and posteriorly, reflecting the electrical predominance of the LV. C. Vectors (arrows) representing these two phases are shown in reference to the horizontal plane leads. (After AL Goldberger et al: Goldberger’s Clinical Electrocardiography: A Simplified Approach, 8th ed. Philadelphia, Elsevier/Saunders, 2013.) the R and S waves are of approximately equal amplitude is referred to as the transition zone (usually V3 or V4) (Fig. 268-7).


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InternalMed_Harrison. The QRS pattern in the extremity leads may vary considerably from one normal subject to another depending on the electrical axis of the QRS, which describes the mean orientation of the QRS vector with reference to the six frontal plane leads. Normally, the QRS axis ranges from –30° to +100° (Fig. 268-4). An axis more negative than –30° is referred to as left axis deviation, and an axis more positive than +100° is referred to as right axis deviation. Left axis deviation may occur as a normal variant but is more commonly associated with left ventricular hypertrophy, also may occur as a normal variant (particularly in children and young 1453 adults), as a spurious finding due to reversal of the left and right arm electrodes, or in conditions such as right ventricular overload (acute or chronic), infarction of the lateral wall of the left ventricle, dextrocardia, left pneumothorax, and left posterior fascicular block.


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InternalMed_Harrison. Normally, the mean T-wave vector is oriented roughly concordant with the mean QRS vector (within about 45° in the frontal plane). Since depolarization and repolarization are electrically opposite processes, this normal QRS–T-wave vector concordance indicates that repolarization normally must proceed in the reverse direction from depolarization (i.e., from ventricular epicardium to endocardium). The normal U wave is a small, rounded deflection (≤1 mm) that follows the T wave and usually has the same polarity as the T wave. An abnormal increase in U-wave amplitude is most commonly due to drugs (e.g., dofetilide, amiodarone, sotalol, quinidine) or to hypokalemia. Very prominent U waves are a marker of increased susceptibility to the torsades de pointes type of ventricular tachycardia (Chap. 276). Inversion of the U wave in the precordial leads is abnormal and may be a subtle sign of ischemia.


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InternalMed_Harrison. Right atrial overload (acute or chronic) may lead to an increase in P-wave amplitude (≥2.5 mm) (Fig. 268-8), sometimes referred to as “P-pulmonale.” Left atrial overload typically produces a biphasic P wave in V1 with a broad negative component or a broad (≥120 ms), often notched P wave in one or more limb leads (Fig. 268-8). This pattern, previously referred to as “P-mitrale,” may also occur with left atrial conduction delays in the absence of actual atrial enlargement, leading to the more general designation of left atrial abnormality.


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InternalMed_Harrison. Right ventricular hypertrophy due to a sustained, severe pressure load (e.g., due to tight pulmonic valve stenosis or certain pulmonary artery hypertension syndromes) is characterized by a relatively tall R wave in lead V1 (R ≥ S wave), usually with right axis deviation (Fig. 268-9); alternatively, there may be a qR pattern in V1 or V3R. ST depression and T-wave inversion in the right-to-midprecordial leads are also often present. This pattern, formerly called right ventricular “strain,” is attributed to repolarization abnormalities in acutely or chronically overloaded muscle. Prominent S waves may occur in the left lateral precordial leads. Right ventricular hypertrophy due to ostium secundum–type atrial septal defects, with the accompanying a block in the anterior fascicle of the left FIGURE 268-7 Normal electrocardiogram from a healthy subject. Sinus rhythm is present with bundle system (left anterior fascicular a heart rate of 75 beats per minute. PR interval is 0.16 s; QRS


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InternalMed_Harrison. left FIGURE 268-7 Normal electrocardiogram from a healthy subject. Sinus rhythm is present with bundle system (left anterior fascicular a heart rate of 75 beats per minute. PR interval is 0.16 s; QRS interval (duration) is 0.08 s; QT interval block or hemiblock), or inferior myo-is 0.36 s; QTc is 0.40 s; the mean QRS axis is about +70°. The precordial leads show normal R-wave cardial infarction. Right axis deviation progression with the transition zone (R wave = S wave) in lead V3.


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InternalMed_Harrison. FIGURE 268-8 Right atrial (RA) overload may cause tall, peaked P waves in the limb or precordial leads. Left atrial (LA) abnormality may cause broad, often notched P waves in the limb leads and a biphasic P wave in lead V1 with a prominent negative component representing delayed depolarization of the LA. (After MK Park, WG Guntheroth: How to Read Pediatric ECGs, 4th ed. St. Louis, Mosby/ Elsevier, 2006.) FIGURE 268-9 Left ventricular hypertrophy (LVH) increases the amplitude of electrical forces directed to the left and posteriorly. In addition, repolarization abnormalities may cause ST-segment depression and T-wave inversion in leads with a prominent R wave. Right ventricular hypertrophy (RVH) may shift the QRS vector to the right; this effect usually is associated with an R, RS, or qR complex in lead V1. T-wave inversions may be present in right precordial leads.


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InternalMed_Harrison. right ventricular volume overload, is commonly associated with an incomplete or complete right bundle branch block pattern with a rightward QRS axis. Acute cor pulmonale due to pulmonary embolism (Chap. 300), for example, may be associated with a normal ECG or a variety of abnormalities. Sinus tachycardia is the most common arrhythmia, although other tachyarrhythmias, such as atrial fibrillation or flutter, may occur. The QRS axis may shift to the right, sometimes in concert with the so-called S1Q3T3 pattern (prominence of the S wave in lead I and the Q wave in lead III, with T-wave inversion in lead III). Acute right ventricular dilation also may be associated with slow R-wave progression and ST-T abnormalities in V1 to V4 simulating acute anterior infarction. A right ventricular conduction disturbance may appear.


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InternalMed_Harrison. Chronic cor pulmonale due to obstructive lung disease (Chap. 279) usually does not produce the classic ECG patterns of right ventricular hypertrophy noted above. Instead of tall right precordial R waves, chronic lung disease more typically is associated with small R waves in right-to-midprecordial leads (slow R-wave progression) due in part to downward displacement of the diaphragm and the heart. Low-voltage complexes are commonly present, owing to hyperaeration of the lungs.


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InternalMed_Harrison. A number of different voltage criteria for left ventricular hypertrophy (Fig. 268-9) have been proposed on the basis of the presence of tall left precordial R waves and deep right precordial S waves (e.g., SV1 + [RV5 or RV6] >35 mm). Repolarization abnormalities (ST depression with T-wave inversions, formerly called the left ventricular “strain” pattern) also may appear in leads with prominent R waves. However, prominent precordial voltages may occur as a normal variant, especially in athletic or young individuals. Left ventricular hypertrophy may increase limb lead voltage with or without increased precordial voltage (e.g., RaVL + SV3 >20 mm in women and >28 mm in men). The presence of left atrial abnormality increases the likelihood of underlying left ventricular hypertrophy in cases with borderline voltage criteria. Left ventricular hypertrophy often progresses to incomplete or complete left bundle branch block. The sensitivity of conventional voltage criteria for left ventricular


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InternalMed_Harrison. borderline voltage criteria. Left ventricular hypertrophy often progresses to incomplete or complete left bundle branch block. The sensitivity of conventional voltage criteria for left ventricular hypertrophy is decreased in obese persons and smokers. ECG evidence for left ventricular hypertrophy is a major noninvasive marker of increased risk of cardiovascular morbidity and mortality rates, including sudden cardiac death. However, because of false-positive and false-negative diagnoses, the ECG is of limited utility in diagnosing atrial or ventricular enlargement. More definitive information is provided by echocardiography (Chap. 270e).


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InternalMed_Harrison. Intrinsic impairment of conduction in either the right or the left bundle system (intraventricular conduction disturbances) leads to prolongation of the QRS interval. With complete bundle branch blocks, the QRS interval is ≥120 ms in duration; with incomplete blocks, the QRS interval is between 100 and 120 ms. The QRS vector usually is oriented in the direction of the myocardial region where depolarization is delayed (Fig. 268-10). Thus, with right bundle branch block, the terminal QRS vector is oriented to the right and anteriorly (rSR′ in V1 and qRS in V6, typically). Left bundle branch block alters both early and later phases of ventricular depolarization. The major QRS vector is directed to the left and posteriorly. In addition, the normal early left-to-right pattern of septal activation is disrupted such that septal depolarization proceeds from right to left as well. As a result, left bundle branch block generates wide, predominantly negative (QS) complexes in lead V1 and


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InternalMed_Harrison. activation is disrupted such that septal depolarization proceeds from right to left as well. As a result, left bundle branch block generates wide, predominantly negative (QS) complexes in lead V1 and entirely positive (R) complexes in lead V6. A pattern identical to that of left bundle branch block, preceded by a sharp spike, is seen in most cases of electronic right ventricular pacing because of the relative delay in left ventricular activation.


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InternalMed_Harrison. Bundle branch block may occur in a variety of conditions. In subjects without structural heart disease, right bundle branch block is seen more commonly than left bundle branch block. Right bundle branch block also occurs with heart disease, both congenital (e.g., atrial septal defect) and acquired (e.g., valvular, ischemic). Left bundle branch block is often a marker of one of four underlying conditions associated with increased risk of cardiovascular morbidity and mortality rates: coronary heart disease (frequently with impaired left ventricular FIGURE 268-10 Comparison of typical QRS-T patterns in right bundle branch block (RBBB) and left bundle branch block (LBBB) with the normal pattern in leads V1 and V6. Note the secondary T-wave inversions (arrows) in leads with an rSR′ complex with RBBB and in leads with a wide R wave with LBBB.


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InternalMed_Harrison. function), hypertensive heart disease, aortic valve disease, and cardiomyopathy. Bundle branch blocks may be chronic or intermittent. A bundle branch block may be rate-related; for example, it often occurs when the heart rate exceeds some critical value.


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InternalMed_Harrison. Bundle branch blocks and depolarization abnormalities secondary to artificial pacemakers not only affect ventricular depolarization (QRS) but also are characteristically associated with secondary repolarization (ST-T) abnormalities. With bundle branch blocks, the T wave is typically opposite in polarity to the last deflection of the QRS (Fig. 268-10). This discordance of the QRS–T-wave vectors is caused by the altered sequence of repolarization that occurs secondary to altered depolarization. In contrast, primary repolarization abnormalities are independent of QRS changes and are related instead to actual alterations in the electrical properties of the myocardial fibers themselves (e.g., in the resting membrane potential or action potential duration), not just to changes in the sequence of repolarization. Ischemia, electrolyte imbalance, and drugs such as digitalis all cause such primary ST–T-wave changes. Primary and secondary T-wave changes may coexist. For example, T-wave


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InternalMed_Harrison. of repolarization. Ischemia, electrolyte imbalance, and drugs such as digitalis all cause such primary ST–T-wave changes. Primary and secondary T-wave changes may coexist. For example, T-wave inversions in the right precordial leads with left bundle branch block or in the left precordial leads with right bundle branch block may be important markers of underlying ischemia or other abnormalities. A distinctive abnormality simulating right bundle branch block with ST-segment elevarightward than +110–120°) is extremely rare as an isolated finding 1455 and requires exclusion of other factors causing right axis deviation mentioned earlier.


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InternalMed_Harrison. More complex combinations of fascicular and bundle branch blocks may occur that involve the left and right bundle system. Examples of bifascicular block include right bundle branch block and left posterior fascicular block, right bundle branch block with left anterior fascicular block, and complete left bundle branch block. Chronic bifascicular block in an asymptomatic individual is associated with a relatively low risk of progression to high-degree AV heart block. In contrast, new bifascicular block with acute anterior myocardial infarction carries a much greater risk of complete heart block. Alternation of right and left bundle branch block is a sign of trifascicular disease. However, the presence of a prolonged PR interval and bifascicular block does not necessarily indicate trifascicular involvement, since this combination may arise with AV node disease and bifascicular block. Intraventricular conduction delays also can be caused by extrinsic (toxic) factors that slow ventricular


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InternalMed_Harrison. involvement, since this combination may arise with AV node disease and bifascicular block. Intraventricular conduction delays also can be caused by extrinsic (toxic) factors that slow ventricular conduction, particularly hyperkalemia or drugs (e.g., class 1 antiarrhythmic agents, tricyclic antidepressants, phenothiazines).


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InternalMed_Harrison. Prolongation of QRS duration does not necessarily indicate a conduction delay but may be due to preexcitation of the ventricles via a bypass tract, as in Wolff-Parkinson-White (WPW) patterns (Chap. 276) and related variants. The diagnostic triad of WPW consists of a wide QRS complex associated with a relatively short PR interval and slurring of the initial part of the QRS (delta wave), with the latter effect being due to aberrant activation of ventricular myocardium. The presence of a bypass tract predisposes to reentrant supraventricular tachyarrhythmias.


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InternalMed_Harrison. (See also Chap. 295) The ECG is a cornerstone in the diagnosis of acute and chronic ischemic heart disease. The findings depend on several key factors: the nature of the process (reversible [i.e., ischemia] versus irreversible [i.e., infarction]), the duration (acute versus chronic), the extent (transmural versus subendocardial), and localization (anterior versus inferoposterior), as well as the presence of other underlying abnormalities (ventricular hypertrophy, conduction defects).


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InternalMed_Harrison. Ischemia exerts complex time-dependent effects on the electrical properties of myocardial cells. Severe, acute ischemia lowers the resting membrane potential and shortens the duration of the action potential. Such changes cause a voltage gradient between normal and ischemic zones. As a consequence, current flows between those regions. These currents of injury are represented on the surface ECG by deviation of the ST segment (Fig. 268-11). When the acute ischemia is transmural, the ST vector usually is shifted in the direction of the outer (epicardial) layers, producing ST elevations and sometimes, in the earliest stages of ischemia, tall, positive so-called hyperacute T waves over the ischemic zone. With ischemia confined primarily to the subendocardium, the ST vector typically shifts toward the subendocardium and ventricular cavity, so that overlying (e.g., anterior precordial) leads show ST-segment depression (with ST elevation in lead aVR). Multiple factors affect the amplitude of


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InternalMed_Harrison. the subendocardium and ventricular cavity, so that overlying (e.g., anterior precordial) leads show ST-segment depression (with ST elevation in lead aVR). Multiple factors affect the amplitude of acute ischemic ST deviations. Profound ST elevation or depression in multiple leads usually indicates very severe ischemia.


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InternalMed_Harrison. tions in the right chest leads is seen with the A


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InternalMed_Harrison. Brugada pattern (Chap. 276). Partial blocks (fascicular or “hemiblocks”) in the left bundle system (left anterior or posterior fascicular blocks) generally do not prolong the QRS duration substantially but instead are associated with shifts in the frontal plane QRS axis (leftward or rightward, ST respectively). Left anterior fascicular block FIGURE 268-11 Acute ischemia causes a current of injury. With predominant subendocar(QRS axis more negative than –45°) is prob-dial ischemia (A), the resultant ST vector will be directed toward the inner layer of the affected ably the most common cause of marked ventricle and the ventricular cavity. Overlying leads therefore will record ST depression. With left axis deviation in adults. In contrast, left ischemia involving the outer ventricular layer (B) (transmural or epicardial injury), the ST vector posterior fascicular block (QRS axis more will be directed outward. Overlying leads will record ST elevation.


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InternalMed_Harrison. 1456 From a clinical viewpoint, the division of V1 V2 V3 V4 V5 V6 acute myocardial infarction into ST-segment elevation and non-ST elevation types is useful since the efficacy of acute reperfusion therapy is limited to the former group. The ECG leads are usually more helpful in localizing regions of ST elevation than non-ST elevation ischemia. For example, acute transmural anterior (including apical and FIGURE 268-12 Severe anterior wall ischemia (with or without infarction) may cause promilateral) wall ischemia is reflected by ST eleva-nent T-wave inversions in the precordial leads. This pattern (sometimes referred to as Wellens tions or increased T-wave positivity in one T waves) is usually associated with a high-grade stenosis of the left anterior descending or more of the precordial leads (V1–V6) and coronary artery. leads I and aVL. Inferior wall ischemia produces changes in leads II, III, and aVF. “Posterior” wall ischemia (usu-tissue may lead to decreased R-wave amplitude or


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InternalMed_Harrison. leads (V1–V6) and coronary artery. leads I and aVL. Inferior wall ischemia produces changes in leads II, III, and aVF. “Posterior” wall ischemia (usu-tissue may lead to decreased R-wave amplitude or abnormal Q waves ally associated with lateral or inferior involvement) may be indirectly (even in the absence of transmurality) in the anterior or inferior leads recognized by reciprocal ST depressions in leads V1 to V3 (thus consti-(Fig. 268-13). Previously, abnormal Q waves were considered marktuting an ST elevation “equivalent” acute coronary syndrome). Right ers of transmural myocardial infarction, whereas subendocardial ventricular ischemia usually produces ST elevations in right-sided infarcts were thought not to produce Q waves. However, careful ECG-chest leads (Fig. 268-5). When ischemic ST elevations occur as the ear-pathology correlative studies have indicated that transmural infarcts liest sign of acute infarction, they typically are followed within a period may occur without Q


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InternalMed_Harrison. ST elevations occur as the ear-pathology correlative studies have indicated that transmural infarcts liest sign of acute infarction, they typically are followed within a period may occur without Q waves and that subendocardial (nontransmural) ranging from hours to days by evolving T-wave inversions and often infarcts sometimes may be associated with Q waves. Therefore, infarcts by Q waves occurring in the same lead distribution. Reversible trans-are more appropriately classified as “Q-wave” or “non-Q-wave.” The mural ischemia, for example, due to coronary vasospasm (Prinzmetal’s major acute ECG changes in syndromes of ischemic heart disease variant angina and possibly the Tako-tsubo “stress” cardiomyopathy are summarized schematically in Fig. 268-14. Loss of depolarizasyndrome), may cause transient ST-segment elevations without devel-tion forces due to posterior or lateral infarction may cause reciprocal opment of Q waves, as may very early reperfusion in acute coronary increases in


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InternalMed_Harrison. transient ST-segment elevations without devel-tion forces due to posterior or lateral infarction may cause reciprocal opment of Q waves, as may very early reperfusion in acute coronary increases in R-wave amplitude in leads V1 and V2 without diagnostic Q syndromes. Depending on the severity and duration of ischemia, the waves in any of the conventional leads. Atrial infarction may be asso-ST elevations may resolve completely in minutes or be followed by ciated with PR-segment deviations due to an atrial current of injury, T-wave inversions that persist for hours or even days. Patients with changes in P-wave morphology, or atrial arrhythmias. In the weeks ischemic chest pain who present with deep T-wave inversions in mul-and months after infarction, these ECG changes may persist or begin tiple precordial leads (e.g., V1–V4,, I, and aVL) with or without cardiac to resolve. Complete normalization of the ECG after Q-wave infarcenzyme elevations typically have severe obstruction in the


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InternalMed_Harrison. tiple precordial leads (e.g., V1–V4,, I, and aVL) with or without cardiac to resolve. Complete normalization of the ECG after Q-wave infarcenzyme elevations typically have severe obstruction in the left anterior tion is uncommon but may occur, particularly with smaller infarcts. In descending coronary artery system (Fig. 268-12). In contrast, patients contrast, ST-segment elevations that persist for several weeks or more whose baseline ECG already shows abnormal T-wave inversions may after a Q-wave infarct usually correlate with a severe underlying wall develop T-wave normalization (pseudonormalization) during episodes motion disorder (akinetic or dyskinetic zone), although not necessarof acute transmural ischemia. ily a frank ventricular aneurysm. ECG changes due to ischemia may


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InternalMed_Harrison. With infarction, depolarization (QRS) changes often accompany occur spontaneously or may be provoked by various exercise protocols repolarization (ST-T) abnormalities. Necrosis of sufficient myocardial (stress electrocardiography; Chap. 293). A ECG sequence with anterior Q-wave infarction FIGURE 268-13 Sequence of depolarization and repolarization changes with (A) acute anterior and (B) acute inferior wall Q-wave infarc-tions. With anterior infarcts, ST elevation in leads I and aVL and the precordial leads may be accompanied by reciprocal ST depressions in leads II, III, and aVF. Conversely, acute inferior (or posterolateral) infarcts may be associated with reciprocal ST depressions in leads V1 to V3. (After AL Goldberger et al: Goldberger’s Clinical Electrocardiography: A Simplified Approach, 8th ed. Philadelphia, Elsevier/Saunders, 2013.)


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InternalMed_Harrison. Noninfarction subendocardial ischemia (classic angina) Transient ST depressions Noninfarction transmural ischemia Transient ST elevations or paradoxical T wave normalization, sometimes followed by T wave inversions Non-Q wave (Non-ST elevation) infarction ST depressions or T wave inversions without Q waves MYOCARDIAL ISCHEMIA ST elevation/ Q wave infarction New Q waves preceded by hyperacute T waves/ST elevations and followed by T wave inversions FIGURE 268-14 Variability of ECG patterns with acute myocardial ischemia. The ECG also may be normal or nonspecifically abnormal. Furthermore, these categorizations are not mutually exclusive. (After AL Goldberger et al: Goldberger’s Clinical Electrocardiography: A Simplified Approach, 8th ed. Philadelphia, Elsevier/Saunders, 2013.)


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InternalMed_Harrison. The ECG has important limitations in both sensitivity and specificity in the diagnosis of ischemic heart disease. Although a single normal ECG does not exclude ischemia or even acute infarction, a normal ECG throughout the course of an acute infarct is distinctly uncommon. Prolonged chest pain without diagnostic ECG changes therefore should always prompt a careful search for other noncoronary causes of chest pain (Chap. 19). Furthermore, the diagnostic changes of acute or evolving ischemia are often masked by the presence of left bundle branch block, electronic ventricular pacemaker patterns, and Wolff-Parkinson-White preexcitation. However, clinicians continue to over-diagnose ischemia or infarction based on the presence of ST-segment elevations or depressions; T-wave inversions; tall, positive T waves; or Q waves not related to ischemic heart disease (pseudoinfarct patterns). For example, ST-segment elevations simulating ischemia may occur with acute pericarditis or myocarditis, as


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InternalMed_Harrison. T waves; or Q waves not related to ischemic heart disease (pseudoinfarct patterns). For example, ST-segment elevations simulating ischemia may occur with acute pericarditis or myocarditis, as a normal variant (including the typical “early repolarization” pattern), or in a variety of other conditions (Table 268-1). Similarly, tall, positive T waves do not invariably represent hyperacute ischemic changes but may also be caused by normal variants, hyperkalemia, cerebrovascular injury, and left ventricular volume overload due to mitral or aortic regurgitation, among other causes.


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InternalMed_Harrison. ST-segment elevations and tall, positive T waves are common findings in leads V1 and V2 in left bundle branch block or left ventricular hypertrophy in the absence of ischemia. The differential diagnosis of Q waves includes physiologic or positional variants, ventricular hypertrophy, acute or chronic noncoronary myocardial injury, hypertrophic cardiomyopathy, and ventricular conduction disorders. Digoxin, ventricular hypertrophy, hypokalemia, and a variety of other factors may cause ST-segment depression mimicking subendocardial ischemia. Prominent T-wave inversion may occur with ventricular hypertrophy, cardiomyopathies, myocarditis, and cerebrovascular injury (particularly intracranial bleeds), among many other conditions.


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InternalMed_Harrison. A variety of metabolic and pharmacologic agents alter the ECG and, in particular, cause changes in repolarization (ST-T-U) and sometimes QRS prolongation. Certain life-threatening electrolyte disturbances may be diagnosed initially and monitored from the ECG. Hyperkalemia produces a sequence of changes (Fig. 268-15), usually beginning with narrowing and peaking (tenting) of the T waves. Further elevation of extracellular K+ leads to AV conduction disturbances, diminution in P-wave amplitude, and widening of the QRS interval. Severe hyperkalemia Noninfarction, transmural ischemia (Prinzmetal’s angina, and probably Tako-tsubo syndrome, which may also exactly simulate classical acute infarction) Brugada patterns (right bundle branch block–like pattern with ST elevations in right precordial leads)a Trauma to ventricles aUsually localized to V1–V2 or V3.


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InternalMed_Harrison. Brugada patterns (right bundle branch block–like pattern with ST elevations in right precordial leads)a Trauma to ventricles aUsually localized to V1–V2 or V3. Source: Modified from AL Goldberger et al: Goldberger’s Clinical Electrocardiography: A Simplified Approach, 8th ed. Philadelphia, Elsevier/Saunders, 2013.


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InternalMed_Harrison. eventually causes cardiac arrest with a slow sinusoidal type of mechanism (“sine-wave” pattern) followed by asystole. Hypokalemia (Fig. 268-16) prolongs ventricular repolarization, often with prominent U waves. Prolongation of the QT interval is also seen with drugs that increase the duration of the ventricular action potential: class 1A antiarrhythmic agents and related drugs (e.g., quinidine, disopyramide, procainamide, tricyclic antidepressants, phenothiazines) and class III agents (e.g., amiodarone [Fig. 268-16], dofetilide, dronedarone, sotalol, ibutilide). Marked QT prolongation, sometimes with deep, wide T-wave inversions, may occur with intracranial bleeds, particularly subarachnoid hemorrhage (“CVA T-wave” pattern) (Fig. 268-16). Systemic hypothermia also prolongs repolarization, usually with a distinctive convex elevation of the J point (Osborn wave). Hypocalcemia typically prolongs the QT interval (ST portion), whereas hypercalcemia shortens it (Fig. 268-17). Digitalis


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InternalMed_Harrison. usually with a distinctive convex elevation of the J point (Osborn wave). Hypocalcemia typically prolongs the QT interval (ST portion), whereas hypercalcemia shortens it (Fig. 268-17). Digitalis glycosides also shorten the QT interval, often with a characteristic “scooping” of the ST–T-wave complex (digitalis effect).


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InternalMed_Harrison. Many other factors are associated with ECG changes, particularly alterations in ventricular repolarization. T-wave flattening, minimal T-wave inversions, or slight ST-segment depression (“nonspecific ST–T-wave changes”) may occur with a variety of electrolyte and acid-base disturbances, a number of infectious processes, central nervous system disorders, endocrine abnormalities, many drugs, ischemia, hypoxia, and virtually any type of cardiopulmonary abnormality. Although subtle ST–T-wave changes may be markers of ischemia, transient nonspecific repolarization changes may also occur after a meal or with postural (orthostatic) change, hyperventilation, or exercise in healthy individuals.


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InternalMed_Harrison. Low QRS voltage is arbitrarily defined as peak-to-trough QRS amplitudes of ≤5 mm in the six limb leads and/or ≤10 mm in the chest leads. Multiple factors may be responsible. Among the most serious include pericardial (Fig. 268-18) or pleural effusions, chronic obstructive pulmonary disease, infiltrative cardiomyopathies, and anasarca. Electrical alternans—a beat-to-beat alternation in one or more components of the ECG signal—is a common type of nonlinear cardiovascular response to a variety of hemodynamic and electrophysiologic


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InternalMed_Harrison. FIGURE 268-15 The earliest ECG change with hyperkalemia is usually peaking (“tenting”) of the T waves. With further increases in the serum potassium concentration, the QRS complexes widen, the P waves decrease in amplitude and may disappear, and finally a sine-wave pattern leads to asystole unless emergency therapy is given. (After AL Goldberger et al: Goldberger’s Clinical Electrocardiography: A Simplified Approach, 8th ed. Philadelphia, Elsevier/Saunders, 2013.) perturbations. Total electrical alternans (P-QRS-T) with sinus tachy-Hypocalcemia Normal Hypercalcemia cardia is a relatively specific sign of pericardial effusion, usually with cardiac tamponade (Fig. 268-18). The mechanism relates to a periodic II swinging motion of the heart in the effusion at a frequency exactly one-half the heart rate. In contrast, pure repolarization (ST-T or U wave) alternans is a sign of electrical instability and may precede ventricular tachyarrhythmias.


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InternalMed_Harrison. Accurate analysis of ECGs requires thoroughness and care. The patient’s age, gender, and clinical status should always be taken into account. Many mistakes in ECG interpretation are errors of omission. Therefore, a systematic approach is essential. The following 14 QT 0.48 s QT 0.36 s QT 0.26 s points should be analyzed carefully in every ECG: (1) standardization QT 0.52 QT 0.41 QT 0.36 (calibration) and technical features (including lead placement and artifacts), (2) rhythm, (3) heart rate, (4) PR interval/AV conduction, FIGURE 268-17 Prolongation of the Q-T interval (ST-segment QRS interval, (6) QT/QTc intervals, (7) mean QRS electrical axis, portion) is typical of hypocalcemia. Hypercalcemia may cause abbre P waves, (9) QRS voltages, (10) precordial R-wave progression, viation of the ST segment and shortening of the QT interval.


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InternalMed_Harrison. P waves, (9) QRS voltages, (10) precordial R-wave progression, viation of the ST segment and shortening of the QT interval. FIGURE 268-16 A variety of metabolic derangements, drug effects, and other factors may prolong ventricular repolarization with QT prolongation or prominent U waves. Prominent repolarization prolongation, particularly if due to hypokalemia, inherited “channelopathies,” or certain pharmacologic agents, indicates increased susceptibility to torsades des pointes–type ventricular tachycardia (Chap. 277). Marked systemic hypothermia is associated with a distinctive convex “hump” at the J point (Osborn wave, arrow) due to altered ventricular action potential characteristics. Note QRS and QT prolongation along with sinus tachycardia in the case of tricyclic antidepressant overdose.


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InternalMed_Harrison. FIgURE 268-18 Classic triad of findings for pericardial effusion with cardiac tamponade: (1) sinus tachycardia; (2) low QRS voltages; and (3) electrical alternans (best seen in leads V3 and V4 in this case; arrows). This triad is highly specific for pericardial effusion, usually with tamponade physiology, but of limited sensitivity. (Adapted from LA Nathanson et al: ECG Wave-Maven. http://ecg.bidmc.harvard.edu.) (11) abnormal Q waves, (12) ST segments, (13) T waves, and (14) U waves. Comparison with any previous ECGs is invaluable. The diagnosis and management of specific cardiac arrhythmias and conduction disturbances are discussed in Chaps. 274 and 276.


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InternalMed_Harrison. Computerized ECG systems are widely used for immediate retrieval of thousands of ECG records. Computer interpretation of ECGs still has major limitations. Incomplete or inaccurate readings are most likely with arrhythmias and complex abnormalities. Therefore, computerized interpretation (including measurements of basic ECG intervals) should not be accepted without careful clinician review. Atlas of Electrocardiography Ary L. Goldberger The electrocardiograms (ECGs) in this atlas supplement those illustrated in Chap. 268. The interpretations emphasize findings of specific teaching value. All of the figures are from ECG Wave-Maven, Copyright 2003, Beth Israel Deaconess Medical Center, http://ecg.bidmc.harvard.edu. The abbreviations used in this chapter are as follows: CHAPTER 269e Atlas of Electrocardiography FIguRE 269e-1 Anterior wall ischemia (deep T-wave inversions and ST-segment depressions in I, aVL, V3–V6) in a patient with LVH (increased voltage in V2–V5).


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InternalMed_Harrison. FIguRE 269e-1 Anterior wall ischemia (deep T-wave inversions and ST-segment depressions in I, aVL, V3–V6) in a patient with LVH (increased voltage in V2–V5). PART 10 Disorders of the Cardiovascular System FIguRE 269e-2 Acute anterolateral wall ischemia with ST elevations in V4–V6. Probable prior inferior MI with Q waves in leads II, III, and aVF. FIguRE 269e-3 Acute lateral ischemia with ST elevations in I and aVL with probable reciprocal ST depressions inferiorly (II, III, and aVF). Ischemic ST depressions also in V3 and V4. Left atrial abnormality. FIguRE 269e-4 Sinus tachycardia. Marked ischemic ST-segment elevations in inferior limb leads (II, III, aVF) and laterally (V6) suggestive of acute inferolateral MI, and prominent ST-segment depressions with upright T waves in V1–V4 are consistent with associated acute posterior MI.


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InternalMed_Harrison. FIguRE 269e-5 Acute, extensive anterior MI with marked ST elevations in I, aVL, V1–V6 and low amplitude pathologic Q waves in V3–V6. Marked reciprocal ST-segment depressions in III and aVF. CHAPTER 269e Atlas of Electrocardiography PART 10 Disorders of the Cardiovascular System FIguRE 269e-6 Acute anterior wall MI with ST elevations and Q waves in V1–V4 and aVL and reciprocal inferior ST depressions. FIguRE 269e-7 SR with premature atrial complexes. RBBB; pathologic Q waves and ST elevation due to acute anterior/septal MI in V1–V3. FIguRE 269e-8 Acute anteroseptal MI (Q waves and ST elevations in V1–V4) with RBBB (note terminal R waves in V1). CHAPTER 269e Atlas of Electrocardiography FIguRE 269e-9 Extensive prior MI involving inferior-posterior-lateral wall (Q waves in leads II, III, aVF, tall R waves in V1, V2, and Q waves in V5, V6). T-wave abnormalities in leads I and aVL, V5, and V6. PART 10 Disorders of the Cardiovascular System


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InternalMed_Harrison. PART 10 Disorders of the Cardiovascular System FIguRE 269e-10 SR with PR prolongation (“first-degree AV block”), left atrial abnormality, LVH, and RBBB. Pathologic Q waves in V1–V5 and aVL with ST elevations (a chronic finding in this patient). Findings compatible with prior anterolateral MI and left ventricular aneurysm. FIguRE 269e-11 Prior inferior-posterior MI. Wide (0.04 s) Q waves in the inferior leads (II, III, aVF); broad R wave in V1 (a Q wave “equivalent” here). Absence of right-axis deviation and the presence of upright T waves in V1–V2 are also against RVH. FIguRE 269e-12 SR with RBBB (broad terminal R wave in V1) and left anterior fascicular block (hemiblock) and pathologic anterior Q waves in V1–V3. Patient had severe multivessel coronary artery disease, with echocardiogram showing septal dyskinesis and apical akinesis. CHAPTER 269e Atlas of Electrocardiography


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InternalMed_Harrison. CHAPTER 269e Atlas of Electrocardiography FIguRE 269e-13 Acute pericarditis with diffuse ST elevations in I, II, III, aVF, V3–V6, without T-wave inversions. Also note concomitant PR-segment elevation in aVR and PR depression in the inferolateral leads. PART 10 Disorders of the Cardiovascular System FIguRE 269e-14 SR; diffuse ST elevations (I, II, aVL, aVF, V2–V6) with associated PR deviations (elevated PR in aVR; depressed in V4–V6); borderline low voltage. Q-wave and T-wave inversions in II, III, and aVF. Diagnosis: acute pericarditis with inferior Q-wave MI. FIguRE 269e-15 SR, prominent left atrial abnormality (see I, II, V1), right-axis deviation, and RVH (tall, relatively narrow R wave in V1) in a patient with mitral stenosis.


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InternalMed_Harrison. FIguRE 269e-15 SR, prominent left atrial abnormality (see I, II, V1), right-axis deviation, and RVH (tall, relatively narrow R wave in V1) in a patient with mitral stenosis. FIguRE 269e-16 SR, left atrial abnormality, and LVH by voltage criteria with borderline right-axis deviation in a patient with mixed mitral stenosis (left atrial abnormality and right-axis deviation) and mitral regurgitation (LVH). Prominent precordial T-wave inversions and QT prolongation also present. CHAPTER 269e Atlas of Electrocardiography FIguRE 269e-17 Coarse AF, tall R in V2 with vertical QRS axis (positive R in aVF) indicating RVH. Tall R in V4 may be due to concomitant LVH. Patient had severe mitral stenosis with moderate mitral regurgitation. PART 10 Disorders of the Cardiovascular System


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InternalMed_Harrison. PART 10 Disorders of the Cardiovascular System FIguRE 269e-18 SR; first-degree AV “block” (PR prolongation); LVH (tall R in aVL); RBBB (wide multiphasic R wave in V1) and left anterior fascicular block in a patient with HCM. Deep Q waves in I and aVL are consistent with septal hypertrophy. FIguRE 269e-19 LVH with deep T-wave inversions in limb leads and precordial leads. Striking T-wave inversions in mid-precordial leads suggest apical HCM (Yamaguchi’s syndrome). FIguRE 269e-20 Sinus tachycardia with S1Q3T3 pattern (T-wave inversion in III), incomplete RBBB, and right precordial T-wave inversions consistent with acute RV overload in a patient with pulmonary emboli. CHAPTER 269e Atlas of Electrocardiography FIguRE 269e-21 Sinus tachycardia, right-axis deviation, RVH with tall R in V1 and deep S in V6, and inverted T waves in II, III, aVF, and V1–V5 in a patient with atrial septal defect and severe pulmonary hypertension. PART 10 Disorders of the Cardiovascular System


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InternalMed_Harrison. PART 10 Disorders of the Cardiovascular System FIguRE 269e-22 Signs of right atrial/RV overload in a patient with chronic obstructive lung disease: (1) peaked P waves in II; (2) QR in V1 with narrow QRS; (3) delayed precordial transition, with terminal S waves in V /V ; (4) superior axis deviation with an S -S -S pattern. FIguRE 269e-23 (1) Low voltage; (2) incomplete RBBB (rsr′ in V1–V3); (3) borderline peaked P waves in lead II with vertical P-wave axis (probable right atrial overload); (4) slow R-wave progression in V1–V3; (5) prominent S waves in V6; and (6) atrial premature beats. This combination is seen typically in severe chronic obstructive lung disease. FIguRE 269e-24 Prominent U waves (II, III, and V4–V6) with ventricular repolarization prolongation in a patient with severe hypokalemia. CHAPTER 269e Atlas of Electrocardiography


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InternalMed_Harrison. FIguRE 269e-24 Prominent U waves (II, III, and V4–V6) with ventricular repolarization prolongation in a patient with severe hypokalemia. CHAPTER 269e Atlas of Electrocardiography FIguRE 269e-25 Abbreviated ST segment such that the T wave looks like it takes off directly from QRS in some leads (I, V4, aVL, and V5) in a patient with severe hypercalcemia. Note also high takeoff of ST segment in V2/V3 simulating acute ischemia. PART 10 Disorders of the Cardiovascular System FIguRE 269e-26 SR with LVH, left atrial abnormality, and tall peaked T waves in the precordial leads with inferolateral ST depressions (II, III, aVF, and V6); left anterior fascicular block and borderline prolonged QT interval in a patient with renal failure, hypertension, and hyperkalemia; prolonged QT is secondary to associated hypocalcemia.


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InternalMed_Harrison. FIguRE 269e-27 Normal ECG in an 11-year-old male. T-wave inversions in V1–V2. Vertical QRS axis (+90°) and early precordial transition between V2 and V3 are normal findings in children. FIguRE 269e-28 Left atrial abnormality and LVH in a patient with long-standing hypertension. FIguRE 269e-29 Normal variant ST-segment elevations in a healthy 21-year-old male (commonly referred to asbenign early repolarization pattern). ST elevations exhibit upward concavity and are most apparent in V3 and V4, and less than 1 mm in the limb leads. Precordial QRS voltages are prominent, but within normal limits for a young adult. No evidence of left atrial abnormality or ST depression/T-wave inversions to go along with LVH. CHAPTER 269e Atlas of Electrocardiography PART 10 Disorders of the Cardiovascular System FIguRE 269e-30 SR with first-degree AV “block” (PR interval = 0.24 s) and complete LBBB.


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InternalMed_Harrison. CHAPTER 269e Atlas of Electrocardiography PART 10 Disorders of the Cardiovascular System FIguRE 269e-30 SR with first-degree AV “block” (PR interval = 0.24 s) and complete LBBB. FIguRE 269e-31 Dextrocardia with: (1) inverted P waves in I and aVL; (2) negative QRS complex and T wave in I; and (3) progressively decreasing voltage across the precordium. FIguRE 269e-32 Sinus tachycardia; intraventricular conduction delay (IVCD) with a rightward QRS axis. QT interval is prolonged for the rate. The triad of sinus tachycardia, a wide QRS complex, and a long QT in appropriate clinical context suggests tricyclic antidepressant overdose. Terminal S wave (rS) in I and terminal R wave (qR) in aVR are also noted as part of this IVCD variant. CHAPTER 269e Atlas of Electrocardiography ECG Wave-Maven http://ecg.bidmc.harvard.edu Copyright, 2007 Beth Israel Deaconess Med Ctr


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InternalMed_Harrison. CHAPTER 269e Atlas of Electrocardiography ECG Wave-Maven http://ecg.bidmc.harvard.edu Copyright, 2007 Beth Israel Deaconess Med Ctr FIguRE 269e-33 Borderline sinus bradycardia (59 beats/min), prolonged PR interval (250 ms), and RBBB are present with marked right-axis deviation (RAD), the latter consistent with left posterior fascicular block (LPFB). LPFB is a diagnosis of exclusion, which requires ruling out lead reversal, normal variant, RV overload syndromes, or lateral MI, in particular, as causes of the RAD. This ECG also shows nondiagnostic Q waves in the inferior leads. In concert with RBBB, the LPFB indicates bifascicular block. (From LA Nathanson et al: ECG Wave-Maven. http://ecg.bidmc.harvard.edu.)


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InternalMed_Harrison. The ability to image the heart and blood vessels noninvasively has been one of the greatest advances in cardiovascular medicine since the development of the electrocardiogram. Cardiac imaging complements history taking and physical examination, blood and laboratory testing, and exercise testing in the diagnosis and management of most diseases of the cardiovascular system. Modern cardiovascular imaging consists of echocardiography (cardiac ultrasound), nuclear scintigraphy including positron emission tomography (PET) imaging, magnetic resonance imaging (MRI), and computed tomography (CT). These studies, often used in conjunction with exercise testing, can be used independently or in concert depending on the specific diagnostic needs. In this chapter, we review the principles of each of these modalities and the utility and relative benefits of each for the most common cardiovascular diseases.


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InternalMed_Harrison. Echocardiography uses high-frequency sound waves (ultrasound) to penetrate the body, reflect from relevant structures, and generate an image. The basic physical principles of echocardiography are identical to other types of ultrasound imaging, although the hardware and software are optimized for evaluation of cardiac structure and function. Early echocardiography machines displayed “M-mode” echo-cardiograms in which a single ultrasound beam was displayed over time on a moving sheet of paper (Fig. 270e-1, left panel). Modern Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging


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InternalMed_Harrison. Marcelo F. Di Carli, Raymond Y. Kwong, Scott D. Solomon echocardiographic machinery uses phased array transducers that 270e-1 contain up to 512 elements and emit ultrasound in sequence. The reflected ultrasound is then sensed by the receiving elements. A “scan converter” uses information about the timing and magnitude of the reflected ultrasound to generate an image (Fig. 270e-1, right panel). This sequence happens repeatedly in “real time” to generate moving images with frame rates that are typically greater than 30 frames per second, but can exceed 100 frames per second. The gray scale of the image features indicates the intensity of the reflected ultrasound; fluid or blood appears black, and highly reflective structures, such as calcifications on cardiac valves or the pericardium, appear white. Tissues such as myocardium appear more gray, and tissues such as muscle display a unique speckle pattern. Although M-mode echocardiography has largely been supplanted by two-dimensional


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InternalMed_Harrison. appear white. Tissues such as myocardium appear more gray, and tissues such as muscle display a unique speckle pattern. Although M-mode echocardiography has largely been supplanted by two-dimensional echocardiography, it is still used because of its high temporal resolution and accuracy for making linear measurements.


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InternalMed_Harrison. The spatial resolution of ultrasound is dependent on the wavelength: the smaller the wavelength and the higher the frequency of the ultrasound beam, the greater are the spatial resolution and ability to discern small structures. Increasing the frequency of ultrasound will increase resolution but at the expense of reduced penetration. Higher frequencies can be used in pediatric imaging or transesophageal echocardiography where the transducer can be much closer to the structures being interrogated, and this is a rationale for using trans-esophageal echocardiography to obtain higher quality images. Three-dimensional ultrasound transducers use a waffle-like matrix array transducer and receive a pyramidal data sector. Three-dimensional echocardiography is being increasingly used for assessment of congenital heart disease and valves, although current image quality lags behind two-dimensional ultrasound (Fig. 270e-2).


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InternalMed_Harrison. In addition to the generation of two-dimensional images that provide information about cardiac structure and function, echocardiography can be used to interrogate blood flow within the heart and blood vessels by using the Doppler principle to ascertain the velocity of blood flow. When ultrasound emitted from a transducer reflects off red blood cells that are moving toward the transducer, the reflected ultrasound will return at a slightly higher frequency than emitted; the opposite is true when flow is away from the transducer. That frequency difference, termed the Doppler shift, is directly related to the velocity CHAPTER 270e Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging


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InternalMed_Harrison. CHAPTER 270e Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging FIGURE 270e-1 Principle of image generation in two-dimensional (2D) echocardiography. An electronically steerable phased-array transducer emits ultrasound from piezoelectric elements, and returning echoes are used to generate a 2D image (right) using a scan converter. Early echocardiography machines used a single ultrasound beam to generate an “M-mode” echocardiogram (see text), although modern equipment generates M-mode echocardiograms digitally from the 2D data. LV, left ventricle. PART 10 Disorders of the Cardiovascular System FIGURE 270e-2 Three-dimensional (3D) probe and 3D image.


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InternalMed_Harrison. PART 10 Disorders of the Cardiovascular System FIGURE 270e-2 Three-dimensional (3D) probe and 3D image. of the flow of the red blood cells. The velocity of blood flow between two chambers will be directly related to the pressure gradient between those chambers. A modified form of the Bernoulli equation, where p = the pressure gradient and v = the velocity of blood flow in meters per second, can be used to calculate this pressure gradient in the majority of clinical circumstances. This principle can be used to determine the pressure gradient between chambers and across valves and has become central to the quantitative assessment of valvular heart disease.


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InternalMed_Harrison. There are three types of Doppler ultrasound that are typically used in standard echocardiographic examinations: spectral Doppler, which consists of both pulsed wave Doppler and continuous wave Doppler, and color flow Doppler. Both types of spectral Doppler will display a waveform representing the velocity of blood flow, with time on the horizontal axis and velocity on the vertical axis. Pulsed wave Doppler is used to interrogate relatively low velocity flow and has the ability to determine blood flow velocity at a particular location within the heart. Continuous wave Doppler is used to assess high-velocity flow but can only identify the highest velocity in a particular direction and cannot interrogate the velocity at a specific depth location. Both of these techniques can only accurately assess velocities that are in the direction of the ultrasound scan lines, and velocities that are at an angle to the direction of the ultrasound beam will be underestimated. Color flow Doppler is a


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InternalMed_Harrison. assess velocities that are in the direction of the ultrasound scan lines, and velocities that are at an angle to the direction of the ultrasound beam will be underestimated. Color flow Doppler is a form of pulsed wave Doppler in which the velocity of blood flow is color encoded according to a scale and superimposed on a two-dimensional grayscale image in real time, giving the appearance of real-time flow within the heart. The Doppler principle can also be used to assess the velocity of myocardial motion, which is a sensitive way to assess myocardial function (Fig. 270e-3). A standard full transthoracic echocardiographic examination consists of a series of two-dimensional views made up of different imaging planes from various scanning locations and spectral and color flow Doppler assessment.


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InternalMed_Harrison. Transesophageal echocardiography is a form of echocardiography in which the transducer is located on the tip of an endoscope that can be inserted into the esophagus. This procedure allows closer, less obstructed views of cardiac structures, without having to penetrate through chest wall, muscle, and ribs. Because less penetration is needed, a higher frequency probe can be used, and image quality and spatial resolution are generally higher than with standard trans-thoracic imaging, particularly for structures that are more posterior. Transesophageal echocardiography has become the test of choice for assessment of small lesions in the heart such as valvular vegetations, especially in the setting of a prosthetic valve disease, and intracardiac thrombi, including assessment of the left atrial appendage, which is difficult to visualize with standard transthoracic imaging, and for assessment of congenital abnormalities. Transesophageal echocardiography requires both topical and systemic


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InternalMed_Harrison. appendage, which is difficult to visualize with standard transthoracic imaging, and for assessment of congenital abnormalities. Transesophageal echocardiography requires both topical and systemic anesthesia, generally conscious sedation, and carries additional risks such as potential damage to the esophagus, including the rare possibility of perforation, aspiration, and anesthesia-related complications. Patients generally need to give consent for transesophageal echocardiography and be monitored during and subsequent to the procedure. Transesophageal echocardiography can be carried out in intubated patients and is routinely used for intraoperative monitoring during cardiac surgery.


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InternalMed_Harrison. Stress echocardiography is routinely used to assess cardiac function during exercise and can be used to identify myocardial ischemia or to assess valvular function under exercise conditions. Stress echocardiography is typically performed in conjunction with treadmill or bicycle exercise testing, but can also be performed using pharmacologic stress most typically with an intravenous infusion of dobutamine (see section on stress imaging below).


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InternalMed_Harrison. Whereas typical echocardiographic equipment is large, bulky, and expensive, small hand-held ultrasound equipment developed over the last decade now offers diagnostic quality imaging in a package small enough to be carried on rounds (Fig. 270e-4). These relatively inexpensive point-of-care devices currently lack full diagnostic capabilities but represent an excellent screening tool if used by an experienced operator. As these units become even smaller and less expensive, they are being increasingly used not just by cardiologists, but also by emergency medicine physicians, intensivists, anesthesiologists, and internists. Radionuclide imaging techniques are commonly used for the evaluation of patients with known or suspected coronary artery disease (CAD),


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InternalMed_Harrison. Radionuclide imaging techniques are commonly used for the evaluation of patients with known or suspected coronary artery disease (CAD), FIGURE 270e-3 Three types of Doppler ultrasound. A and B. Pulsed and continuous wave Doppler waveforms with time on horizontal axis and velocity of blood flow on vertical axis. C. Color flow Doppler, where velocities are encoded by colors according to scale on right side of screen and superimposed on a two-dimensional grayscale image.


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InternalMed_Harrison. including for initial diagnosis and risk stratification as well as the assessment of myocardial viability. These techniques use small amounts of radiopharmaceuticals (Table 270e-1), which are injected intravenously and trapped in the heart and/or vascular cells. Radioactivity within the heart and vasculature decays by emitting gamma rays. The interaction between these gamma rays and the detectors in specialized scanners (single-photon emission computed tomography [SPECT] and PET) creates a scintillation event or light output, which can be captured by digital recording equipment to form an image of the heart and vasculature. Like CT and MRI, radionuclide images also generate tomographic (three-dimensional) views of the heart and vasculature. Radiopharmaceuticals Used in Clinical Imaging Table 270e-1 summarizes the most commonly used radiopharmaceuticals in clinical SPECT and PET imaging.


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InternalMed_Harrison. Protocols for Stress Myocardial Perfusion Imaging Both exercise and pharmacologic stress can be used for myocardial perfusion imaging. Exercise stress is generally preferred because it is physiologic and provides additional clinically important information (i.e., clinical and hemodynamic responses, ST-segment changes, exercise duration, and functional status). However, submaximal effort will lower the sensitivity of the test and should be avoided, especially if the test is requested for initial diagnosis of CAD. In patients who are unable to exercise or who exercise submaximally, pharmacologic stress offers an adequate alternative to exercise stress testing. Pharmacologic stress can be accomplished either with coronary vasodilators, such as adenosine, dipyridamole, or regadenoson, or β1-receptor agonists, such as dobutamine. For patients unable to exercise, vasodilators are the most commonly used stressors in combination with myocardial perfusion imaging. Dobutamine is a potent


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InternalMed_Harrison. β1-receptor agonists, such as dobutamine. For patients unable to exercise, vasodilators are the most commonly used stressors in combination with myocardial perfusion imaging. Dobutamine is a potent β1-receptor agonist that increases myocardial oxygen demand by augmenting contractility, heart rate, and blood pressure similar to exercise. It is generally used as an alternative to vasodilator stress in patients with chronic pulmonary disease, in whom vasodilators may be contraindicated. Dobutamine is also commonly used as a pharmacologic alternative to stress 270e-3 testing in stress echocardiography.


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InternalMed_Harrison. FIGURE 270e-4 Two examples of hand-held ultrasound equipment: V-Scan (General Electric, left) and Sonosite (right). Imaging protocols are tailored to the individual patient based on the clinical question, patient’s risk, ability to exercise, body mass index, and other factors.


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InternalMed_Harrison. For SPECT imaging, technetium-99m (99mTc)-labeled tracers are the most commonly used imaging agents because they are associated with the best image quality and the lowest radiation dose to the patient (Fig. 270e-5). Selection of the protocol (stress-only, single-day, or 2-day) depends on the patient and clinical question. After intravenous injection, myocardial uptake of 99mTc-labeled tracers is rapid (1–2 min). After uptake, these tracers become trapped intracellularly in mitochondria and show minimal change over time. This is why 99mTc tracers can be helpful in patients with chest pain of unclear etiology occurring at rest, because patients can be injected while having chest pain and imaged some time later after symptoms subside. Because the radiotracer is trapped at the time of injection, the images provide a snapshot of myocardial perfusion at the time of injection, even if the acquisition is delayed. Indeed, a normal myocardial perfusion study following a rest injection in a


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InternalMed_Harrison. the images provide a snapshot of myocardial perfusion at the time of injection, even if the acquisition is delayed. Indeed, a normal myocardial perfusion study following a rest injection in a patient with active chest pain effectively excludes myocardial ischemia as the cause of chest pain (high negative predictive value). While used commonly in the past for perfusion imaging, thallium-201 protocols are now rarely used because they are typically associated with a higher radiation dose to the patient.


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InternalMed_Harrison. PET myocardial perfusion imaging is an alternative to SPECT and is associated with improved diagnostic accuracy and lower radiation dose to patients due to the fact that radiotracers are typically short lived (Table 270e-1). The ultra-short half-life of some PET radiopharmaceuticals in clinical use (e.g., rubidium-82) is the primary reason why imaging is generally combined with pharmacologic stress, as opposed to exercise, because this allows for faster imaging of these rapidly decaying radiopharmaceuticals. However, exercise is possible for relatively longer lived radiotracers (e.g., 13N-ammonia). PET imaging protocols are typically faster than SPECT, but more expensive. For myocardial perfusion imaging, rubidium-82 does not require an on-site medical cyclotron (it is available from a strontium-82/rubidium-82 generator) and, thus, is the most commonly used radiopharmaceutical. 13N-ammonia has better flow characteristics (higher myocardial extraction) and imaging properties than


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InternalMed_Harrison. a strontium-82/rubidium-82 generator) and, thus, is the most commonly used radiopharmaceutical. 13N-ammonia has better flow characteristics (higher myocardial extraction) and imaging properties than rubidium-82, but it does require an on-site medical cyclotron. In comparison to SPECT, PET has improved spatial and contrast resolution and provides absolute measures of myocardial perfusion (in mL/min per gram of tissue), thereby providing the patients’ regional and global coronary flow reserve. The latter helps improve diagnostic accuracy and risk stratification, especially in obese patients, women, and higher risk individuals (e.g., diabetes mellitus) (Fig. 270e-6). Contemporary PET and SPECT scanners are combined with a CT scanner (so-called hybrid PET/CT and SPECT/CT). CT is used primarily to guide patient positioning in the field of view and for correcting inhomogeneities in radiotracer distribution due to attenuation by soft tissues (so-called attenuation


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InternalMed_Harrison. CHAPTER 270e Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging Abbreviations: PET, positron emission tomography; SPECT, single-photon emission computed tomography. PART 10 Disorders of the Cardiovascular System Perfusion Defect blackout map 506.0 100.0% 0.0 0.0% Perfusion Defect blackout map 145.0 100.0% 0.0 0.0% Perfusion Defect blackout map 50.0% 100.0% 0.0% 0.0%