Acute Pericarditis

Acute 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 8, 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), which often accompanies inflammation of the overlying pericardium (Fig. 11-1).

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.

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 segment 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.

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) (see Fig. 11-1). In particular, pericardial inflammation often causes an atrial current of injury, reflected by elevation of the PR segment in lead aVR and depression of the PR segment in other extremity leads and the left chest leads (V₅ and V₆).

The ST segment 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 Note 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.

Some patients have recurrent or relapsing episodes of pericarditis, which may occur intermittently or may persist for sustained periods. The ECG findings are variable and may resemble those of acute or evolving pericarditis. Low voltage may occur if pericardial effusion is present (see following discussion).

Pericardial Effusion

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 with pulseless electrical activity (see Chapter 19).