Clinical Electrocardiography: A Simplified Approach, 7th Edition (2006)


Chapter 11. Pericardial, Myocardial, and Pulmonary Syndromes

A wide variety of major disease processes may affect the ECG. Particularly important are conditions affecting the pericardium (pericarditis and pericardial effusion), the myocardium itself (not including ischemia and infarction, which are discussed in Chapters 8 and 9 ), and the lungs (acute pulmonary embolism and chronic obstructive pulmonary disease).


Pericarditis (inflammation of the pericardium) may be caused by a number of factors, including viral or bacterial infection, metastatic tumors, collagen vascular diseases, myocardial infarction (MI), cardiac surgery, and uremia.

As mentioned in Chapter 9 , the ECG patterns of pericarditis resemble those seen with acute MI. The early phase of acute pericarditis is usually characterized by ST segment elevations. This type of current of injury pattern results from inflammation of the heart's surface (epicardium) that often accompanies pericardial inflammation. Figure 11-1 shows an example of the ST segment elevations with acute pericarditis. A major difference between these elevations and the ones occurring with acute MI is their distribution. The ST segment elevations with acute MI are characteristically limited to the anterior or inferior leads because of the localized area of the infarct. The pericardium envelops the heart, and the ST-T changes occurring with pericarditis are therefore usually more generalized. ST elevations are typically seen in both anterior and inferior leads. For example, in Figure 11-1 , notice the elevations in leads I, II, aVL, aVF, and V2 to V6.

FIGURE 11-1  Acute pericarditis causing diffuse ST segment elevations in leads I, II, aVF, and V2 to V6, with reciprocal ST depressions in lead aVR. By contrast, a concomitant atrial current of injury causes PR segment elevations in lead aVR with reciprocal PR depressions in the left chest leads and lead II.  (From Goldberger AL: Myocardial Infarction: Electrocardiographic Differential Diagnosis, 4th ed. St. Louis, Mosby, 1991.)

Not only does acute pericarditis affect ventricular repolarization (the ST segment), it also affects repolarization of the atria, which starts during the PR segment (the end of the P wave to the beginning of the QRS complex). In particular, pericardial inflammation often causes an atrial current of injury, reflected by elevation of the PR in lead aVr and depression of the PR in other limb leads and the left chest leads (V5 and V6). Thus, with acute pericarditis, the PR and ST segments typically point in opposite directions, with the PR being elevated (often by only 1 mm, or so) in lead aVR and the ST usually being slightly depressed in that lead. Other leads may show PR depression and ST elevation.

Figure 11-1 illustrates the subtle but often helpful repolarization changes seen with acute pericarditis. The presence of PR changes may be a useful clue in the differential diagnosis of ST segment elevation, suggesting acute pericarditis as the cause.

The ST elevations seen with acute pericarditis are sometimes followed (after a variable time) by T wave inversions ( Fig. 11-2 ). This sequence of elevations and inversions is the same as that described for MI. In some cases, the T wave inversions caused by pericarditis resolve completely with time and the ECG returns to normal. In other cases, the T wave inversions persist for long periods.

FIGURE 11-2  Notice the diffuse T wave inversions in leads I, II, III, aVL, aVF, and V2 to V6.

The similarity between the ECG patterns of acute pericarditis and acute MI has been emphasized because both conditions may produce ST segment elevations followed by T wave inversions. As noted, however, the ST-T changes with pericarditis tend to be more diffuse than the localized changes of MI. Another major difference is that pericarditis does not produce abnormal Q waves, such as those seen with certain infarcts. With MI, abnormal Q waves occur because of the death of heart muscle and the consequent loss of positive depolarization voltages (see Chapter 8 ). Pericarditis, on the other hand, generally causes only a superficial inflammation and does not produce actual myocardial necrosis. Thus abnormal Q waves never result from pericarditis alone.

Pericardial effusion refers to an abnormal accumulation of fluid in the pericardial sac. In most cases, this fluid accumulates as the result of pericarditis. In some cases, however, such as myxedema (hypothyroidism) or rupture of the heart, pericardial effusion may occur in the absence of pericarditis. The major clinical significance of pericardial effusion is the danger of cardiac tamponade, in which the fluid actually “chokes off” the heart, leading to a drop in blood pressure and sometimes to cardiac arrest (see Chapter 19 ).

The most common ECG sign of pericardial effusion (with or without actual tamponade) is low voltage of the QRS complexes. In such cases, the low voltage is probably due to short-circuiting of cardiac voltages by the fluid surrounding the heart.

The criteria for high voltage were mentioned in the discussion of hypertrophy patterns (see Chapter 6 ). Low voltage is said to be present when the total amplitude of the QRS complexes in each of the six limb leads is 5 mm (0.5 mV) or less. (Low voltage in the limb leads may or may not be accompanied by low voltage in the chest leads, defined as a peak-to-peak QRS amplitude of 10 mm or less in each of leads V1 to V6.)

Figure 11-2 shows an example of low voltage. A listing of other factors that can produce low QRS voltage is presented in one of the review tables in Chapter 24 .

For example, obesity can cause low voltage because of the fat tissue that lies between the heart and the chest wall. Patients with emphysema have increased inflation of the lungs. This extra air acts to insulate the heart. Of the causes of low voltage listed, obesity, anasarca (generalized edema), and emphysema are among the most common. When you see low voltage (particularly with sinus tachycardia), however, you always need to consider pericardial effusion because it can lead to fatal tamponade (see also Chapter 19 ).

Electrical alternans is another very important pattern that can occur with pericardial effusion and tamponade ( Fig. 11-3 ). This pattern is characterized by a beat-to-beat shift in the QRS axis associated with mechanical swinging of the heart to and fro in a large accumulation of fluid. Electrical alternans with sinus tachycardia is virtually diagnostic of cardiac tamponade, although not every patient with tamponade shows this pattern.

FIGURE 11-3  Electrical alternans may develop in patients with pericardial effusion and cardiac tamponade. Notice the beat-to-beat alternation in the P-QRS-T axis; this is caused by the periodic swinging motion of the heart in a large pericardial effusion. Relatively low QRS voltage and sinus tachycardia are also present.

In summary, acute pericarditis causes a diffuse current of injury pattern with ST segment elevations in the anterior and inferior leads, sometimes followed by T wave inversions in those leads. Abnormal Q waves, however, are not seen with pericarditis alone. Pericardial effusion is one of the causes of low voltage on the ECG.



A variety of conditions (e.g., certain viral infections) may be associated with inflammation of the heart muscle (myocarditis). Individuals with myocarditis may have a wide range of symptoms and presentations, ranging from those who are asymptomatic to those who have severe heart failure and even sudden death. In some cases, pericarditis and myocarditis occur together.

The ECG findings with myocarditis are also quite variable, ranging from nonspecific ST-T changes to the repolarization changes that occur with acute pericarditis. Occasionally, the ECG findings of severe myocarditis may exactly simulate those of acute MI, even with ST elevations initially and the development of pathologic Q waves. Atrial or ventricular arrhythmias can occur with myocarditis, as can atrioventricular (AV) or ventricular conduction disturbances.



Congestive heart failure (CHF) is a complex syndrome that can result from multiple causes, including extensive myocardial infarction, systemic hypertension, valvular heart disease, myocarditis, and cardiomyopathy The ECG may provide helpful clues to a specific diagnosis in some of these patients:



Prominent Q waves and typical ST-T changes suggest underlying ischemic heart disease with extensive underlying infarction.



Left ventricular hypertrophy patterns (see Chapter 6 ) may occur with hypertensive heart disease, aortic valve disease (stenosis or regurgitation), or mitral regurgitation.



The combination of left atrial enlargement (or atrial fibrillation) and signs of right ventricular hypertrophy (RVH) strongly suggest mitral stenosis (see Fig. 23-1 ).



Left bundle branch block (LBBB) (see Chapter 7 ) may occur with CHF caused by ischemic heart disease, valvular abnormalities, hypertension, or cardiomyopathy.

In some patients, marked enlargement and decreased function of the left (and often the right) ventricle occur without coronary artery disease, hypertension, or significant valvular lesions. In such cases, the term dilated (“congestive”) cardiomyopathy is applied. Dilated cardiomyopathy can be idiopathic, or it can be associated with chronic excessive alcohol ingestion (alcoholic cardiomyopathy), viral infection, hereditary factors, or a variety of other etiologies.

Patients with dilated cardiomyopathy from any cause may have a distinctive ECG pattern (the ECG-CHF triad), which is characterized by the following:



Relatively low voltages in the limb leads, such that the QRS in each of the six limb leads is 8 mm or less in amplitude



Relatively prominent QRS voltages in the chest leads, such that the sum of the S wave in either lead V1 or lead V2 plus the R wave in V5 or V6 is 35 mm or more



Very slow R wave progression defined by a QS- or rS-type complex in leads V1 to V4

When the ECG-CHF triad is present ( Fig. 11-4 ), it strongly suggests underlying cardiomyopathy but does not indicate a specific etiology. The triad may occur not only with primary dilated cardiomyopathy but also with severe heart disease caused by previous infarction or significant valvular dysfunction. Furthermore, the ECG-CHF triad has only modest sensitivity; that is, its absence does not exclude underlying cardiomyopathy.

FIGURE 11-4  Severe idiopathic dilated cardiomyopathy in a 29-year-old man. The triad of (1) relatively low QRS voltages in the limb leads, (2) prominent precordial QRS voltages, and (3) very slow R wave progression in the chest leads (rS in V4) is highly suggestive of dilated cardiomyopathy. Poor precordial R wave progression simulates anterior wall infarction.  (From Goldberger AL: Myocardial Infarction: Electrocardiographic Differential Diagnosis, 4th ed. St. Louis, Mosby, 1991.)



The ECG is not a sensitive test for pulmonary embolism. In some cases, the obstruction produced by an embolus in the pulmonary artery system can lead to ECG changes, but generally no single pattern is always diagnostic. All of the following patterns may be seen ( Fig. 11-5 ):



Sinus tachycardia (Arrhythmias such as ventricular ectopy and atrial fibrillation also occur.)



A right ventricular overload (formerly called “strain”) pattern (inverted T waves in leads V1 to V4)



The so-called S1QIIITIII pattern, with an S wave in lead I and a new Q wave in lead III with T wave inversion in that lead (This pattern, which may simulate that produced by acute inferior wall MI, is probably due to acute right ventricular dilation.)



Shifting of the QRS axis to the right



ST segment depressions indicative of subendocardial ischemia



An incomplete or complete right bundle branch block (RBBB) pattern (wide rSR′ in lead V1)

FIGURE 11-5  Features occasionally seen with pulmonary embolism include sinus tachycardia, S waves in lead I with Q waves and T wave inversions in lead III (SIQIIITIII pattern), and slow R wave progression with T wave inversions in chest leads V1 to V4 resulting from acute right ventricular overload.

The appearance of these changes, particularly in combination, is suggestive but not diagnostic of pulmonary embolism. Some patients with even massive pulmonary embolism have only minor, relatively nonspecific changes on their ECG. Thus both the diagnostic sensitivity and the specificity of the ECG with pulmonary embolism are limited. Figure 11-5 shows a classic example of the changes seen with pulmonary embolism. These findings may also be due to other causes of acute or subacute right ventricular overload (cor pulmonale, due, for example, to severe pneumonia or extensive pulmonary malignancy).



Patients with severe chronic obstructive lung disease from emphysema often have a relatively characteristic constellation of ECG findings ( Fig. 11-6 ), including low QRS voltage, slow R wave progression in the chest leads, and a vertical or rightward QRS axis in the frontal plane. Excessive pulmonary air trapping causes the low voltage. The slow R wave progression results, in part, from the downward displacement of the diaphragm. Thus the chest leads are actually placed relatively higher than usual. In addition, right ventricular dilation may contribute to the delayed chest lead transition zone. Finally, the anatomically vertical position of the heart in the chest of a patient with emphysema (and sometimes right ventricular enlargement) causes the mean QRS axis to be vertical or even rightward (greater than +100°). Tall, relatively narrow P waves caused by right atrial overload (see Fig. 11-6 ) may also be present, with a vertical or rightward P wave axis (+90° or so).

FIGURE 11-6  Notice the characteristic combination of relatively low voltages in the limb leads, right axis deviation, right atrial overload pattern (“P pulmonale”), and slow R wave progression. The P wave axis is also more rightward than usual (almost +90°).



Pericarditis often produces diffuse ST segment elevations, usually in one or more of the chest leads and also in leads I, aVL, II, and aVF. PR segment elevation in lead aVr with PR depression in other leads may be caused by an atrial current of injury. Abnormal Q waves do not develop. After a variable period, the ST segment elevations may be followed by T wave inversions.

Pericardial effusion often produces low voltage of the QRS complex (amplitude of 5 mm or less in all six limb leads). Low voltage is not specific for pericardial effusion because it may also occur with obesity, emphysema, and diffuse myocardial injury or infiltration. In addition, low voltage may occur as a normal variant.

Pericardial effusion complicated by cardiac tamponade is usually associated with sinus tachycardia and low-voltage complexes. Some of these patients also have electrical alternans, a pattern characterized by a beat-to-beat shift in the QRS axis.

Myocarditis can produce ST-T changes that are nonspecific or that resemble the changes of pericarditis or myocardial infarction (MI). It may also be associated with serious atrial or ventricular arrhythmias.

The ECG may provide important clues to the etiology of congestive heart failure, including evidence of extensive myocardial infarction and ventricular hypertrophy. Patients with dilated cardiomyopathyfrom any cause may have a distinctive ECG pattern (the ECG-CHF triad):



Relatively low voltages in the limb leads, such that the QRS in each of the six limb leads is 8 mm or less in amplitude



Relatively prominent QRS voltages in the chest leads, such that the sum of the S wave in either lead V1 or lead V2 plus the R wave in V5 or V6 is 35 mm or more



Very slow R wave progression defined by a QS- or rS-type complex in leads V1 to V4

Pulmonary embolism may produce any of the following patterns:



Sinus tachycardia and various arrhythmias



Right ventricular strain T wave inversions






Right axis shift



ST depressions resulting from subendocardial ischemia



Acute right bundle branch block

Chronic obstructive lung disease from emphysema often produces a relatively characteristic combination of ECG findings, including low QRS voltage, slow R wave progression in the chest leads, and a vertical or rightward QRS axis in the frontal plane. Peaked P waves (right atrial overload pattern) may also be present.





Sinus tachycardia with electrical alternans is most indicative of which one of the following life-threatening conditions?



Pericardial effusion with cardiac tamponade



Acute myocardial infarction



Acute pulmonary embolism



Emphysema with respiratory failure



Acute myocarditis



True or false: The ECG is a highly sensitive and specific test for acute pulmonary embolism.

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