Cardiac Enlargement and Hypertrophy
Right atrial overload (acute or chronic) may lead to an increase in P-wave amplitude (≥2.5 mm) (Fig. 228-8). 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. 228-8). This pattern 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.
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.)
Right ventricular hypertrophy due to a pressure load (as from pulmonic valve stenosis or pulmonary artery hypertension) is characterized by a relatively tall R wave in lead V1 (R ≥ S wave), usually with right axis deviation (Fig. 228-9); 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 right ventricular volume overload, is commonly associated with an incomplete or complete right bundle branch block pattern with a rightward QRS axis.
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.
Acute cor pulmonale due to pulmonary embolism (Chap. 262), 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.
Chronic cor pulmonale due to obstructive lung disease (Chap. 234) 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.
A number of different voltage criteria for left ventricular hypertrophy (Fig. 228-9) 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 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. 229).
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. 228-10). 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 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.
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.
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 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.
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. 228-10). 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 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 elevations in the right chest leads is seen with the Brugada pattern (Chap. 233).
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, respectively). 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 conduction, particularly hyperkalemia or drugs (e.g., class 1 antiarrhythmic agents, tricyclic antidepressants, phenothiazines).
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. 233) 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.
Myocardial Ischemia and Infarction
(See also Chap. 245) 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).
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. 228-11). 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 acute ischemic ST deviations. Profound ST elevation or depression in multiple leads usually indicates very severe ischemia. From a clinical viewpoint, the division of 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.
Acute ischemia causes a current of injury. With predominant subendocardial ischemia (A), the resultant ST vector will be directed toward the inner layer of the affected ventricle and the ventricular cavity. Overlying leads therefore will record ST depression. With ischemia involving the outer ventricular layer (B) (transmural or epicardial injury), the ST vector will be directed outward. Overlying leads will record ST elevation.
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 lateral) wall ischemia is reflected by ST elevations or increased T-wave positivity in one or more of the precordial leads (V1–V6) and leads I and aVL. Inferior wall ischemia produces changes in leads II, III, and aVF. "Posterior" wall ischemia (usually associated with lateral or inferior involvement) may be indirectly recognized by reciprocal ST depressions in leads V1 to V3 (thus constituting an ST elevation "equivalent" acute coronary syndrome). Right ventricular ischemia usually produces ST elevations in right-sided chest leads (Fig. 228-5). When ischemic ST elevations occur as the earliest sign of acute infarction, they typically are followed within a period ranging from hours to days by evolving T-wave inversions and often by Q waves occurring in the same lead distribution. Reversible transmural ischemia, for example, due to coronary vasospasm (Prinzmetal's variant angina and probably the Tako-Tsubo "stress" cardiomyopathy syndrome), may cause transient ST-segment elevations without development of Q waves, as may very early reperfusion in acute coronary syndromes. Depending on the severity and duration of ischemia, the ST elevations may resolve completely in minutes or be followed by T-wave inversions that persist for hours or even days. Patients with ischemic chest pain who present with deep T-wave inversions in multiple precordial leads (e.g., V1–V4) with or without cardiac enzyme elevations typically have severe obstruction in the left anterior descending coronary artery system (Fig. 228-12). In contrast, patients whose baseline ECG already shows abnormal T-wave inversions may develop T-wave normalization (pseudonormalization) during episodes of acute transmural ischemia.
Severe anterior wall ischemia (with or without infarction) may cause prominent T-wave inversions in the precordial leads. This pattern (sometimes referred to as Wellens T waves) is usually associated with a high-grade stenosis of the left anterior descending coronary artery.
With infarction, depolarization (QRS) changes often accompany repolarization (ST-T) abnormalities. Necrosis of sufficient myocardial tissue may lead to decreased R-wave amplitude or abnormal Q waves (even in the absence of transmurality) in the anterior or inferior leads (Fig. 228-13). Previously, abnormal Q waves were considered markers of transmuralmyocardial infarction, whereas subendocardial infarcts were thought not to produce Q waves. However, careful ECG-pathology correlative studies have indicated that transmural infarcts may occur without Q waves and that subendocardial (nontransmural) infarcts sometimes may be associated with Q waves. Therefore, infarcts are more appropriately classified as "Q-wave" or "non-Q-wave." The major acute ECG changes in syndromes of ischemic heart disease are summarized schematically in Fig. 228-14. Loss of depolarization forces due to posterior or lateral infarction may cause reciprocal increases in R-wave amplitude in leads V1 and V2 without diagnostic Q waves in any of the conventional leads. Atrial infarction may be associated with PR-segment deviations due to an atrial current of injury, changes in P-wave morphology, or atrial arrhythmias.
Sequence of depolarization and repolarization changes with (A) acute anterior and (B) acute inferior wall Q-wave infarctions. 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 Goldberger.)
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 Goldberger, 2006.)
In the weeks and months after infarction, these ECG changes may persist or begin to resolve. Complete normalization of the ECG after Q-wave infarction is uncommon but may occur, particularly with smaller infarcts. In contrast, ST-segment elevations that persist for several weeks or more after a Q-wave infarct usually correlate with a severe underlying wall motion disorder (akinetic or dyskinetic zone), although not necessarily a frank ventricular aneurysm. ECG changes due to ischemia may occur spontaneously or may be provoked by various exercise protocols (stress electrocardiography; Chap. 243).
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. 12). 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 overdiagnose 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 a normal variant (including the typical "early repolarization" pattern), or in a variety of other conditions (Table 228-1). 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.
Table 228–1. Differential Diagnosis of ST-Segment Elevations
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Table 228–1. Differential Diagnosis of ST-Segment Elevations
|Noninfarction, transmural ischemia (Prinzmetal's angina, and probably Tako-Tsubo syndrome, which may also exactly simulate classical acute infarction)|
|Acute myocardial infarction|
|Postmyocardial infarction (ventricular aneurysm pattern)|
|Normal variants (including "early repolarization" patterns)|
|Left ventricular hypertrophy/left bundle branch blocka|
|Acute pulmonary embolisma|
|Brugada patterns (right bundle branch block–like pattern with ST elevations in right precordial leads)a|
|Class 1C antiarrhythmic drugsa|
|Hypothermia [J (Osborn) waves]|
|Nonischemic myocardial injury|
|Tumor invading left ventricle|
|Trauma to ventricles|
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.
Metabolic Factors and Drug Effects
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. 228-15), 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 eventually causes cardiac arrest with a slow sinusoidal type of mechanism ("sine-wave" pattern) followed by asystole. Hypokalemia(Fig. 228-16) 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. 228-16), 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. 228-16). 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. 228-17). Digitalis glycosides also shorten the QT interval, often with a characteristic "scooping" of the ST–T-wave complex (digitalis effect).
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 Goldberger.)
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. 233). 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.
Prolongation of the Q-T interval (ST-segment portion) is typical of hypocalcemia. Hypercalcemia may cause abbreviation of the ST segment and shortening of the QT interval.
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 variety 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.
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 perturbations. Total electrical alternans (P-QRS-T) with sinus tachycardia is a relatively specific sign of pericardial effusion, usually with cardiac tamponade. The mechanism relates to a periodic swinging motion of the heart in the effusion at a frequency exactly one-half the heart rate. Repolarization (ST-T or U wave) alternans is a sign of electrical instability and may precede ventricular tachyarrhythmias.
Clinical Interpretation of the ECG
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 points should be analyzed carefully in every ECG: (1) standardization (calibration) and technical features (including lead placement and artifacts), (2) rhythm, (3) heart rate, (4) PR interval/AV conduction, (5) QRS interval, (6) QT/QTc interval, (7) mean QRS electrical axis, (8) P waves, (9) QRS voltages, (10) precordial R-wave progression, (11) abnormal Q waves, (12) ST segments, (13) T waves, (14) U waves.
Only after analyzing all these points should the interpretation be formulated. Where appropriate, important clinical correlates or inferences should be mentioned. For example, sinus tachycardia with QRS and QT-(U) prolongation, especially in the context of changes in mental status, suggests tricyclic antidepressant overdose (Fig. 228-16). The triad of peaked T waves (hyperkalemia), a long QT due to ST-segment lengthening (hypocalcemia), and left ventricular hypertrophy (systemic hypertension) suggests chronic renal failure. Comparison with any previous ECGs is invaluable. The diagnosis and management of specific cardiac arrhythmias and conduction disturbances are discussed in Chaps. 232 and 233.
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.