Pericardial, Myocardial, and Pulmonary Syndromes

Acute Pericarditis

Acute pericarditis (inflammation of the pericardium) may be caused by multiple factors, including viral or bacterial infection (e.g., staphylococcus, streptococcus, haemophilus, tuberculosis), metastatic tumors, collagen vascular diseases (e.g., systemic lupus erythematosus), cardiac surgery, uremia, and myocardial infarction (MI). In clinical practice, the cause is often undetermined (idiopathic) and presumed viral. COVID-19 infection causing acute pericarditis or myocarditis is discussed below.

As mentioned in Chapter 10 , the ECG patterns of acute pericarditis resemble those seen with acute ST elevation MI. The early phase of acute pericarditis is also usually characterized by ST segment elevations. This type of current of injury pattern results from inflammation of the heart’s surface (epicardial layer), which often accompanies inflammation of the overlying pericardium ( Fig. 12.1 ).

One major difference between the ST elevations occurring with acute MI and acute pericarditis is their distribution. The ST segment elevations with acute MI are characteristically localized to the area of the infarct. The pericardium, in contrast, envelops nearly the entire heart. Therefore the ST-T changes occurring with pericarditis are usually more generalized and seen in both anterior and inferior lead distributions. For example, in Fig. 12.1 note the elevations in leads I, II, aVL, aVF, and V ₂ to V ₆ . Reciprocal ST depressions in pericarditis are usually limited to lead aVR, and sometimes V ₁ .

A second important difference is that the ST elevations seen with acute pericarditis tend to be less prominent than those with STEMI; however, multiple exceptions occur. The morphology of ST elevations with pericarditis is usually associated with maintenance of upward concavity, whereas those with STEMI can be concave or convex. However, here again, multiple exceptions occur, precluding the application of “hard and fast” rules in differential diagnosis based primarily on ST-T morphology alone.

Third, acute pericarditis may not only affect ventricular repolarization (the ST segment). Pericarditis also often affects repolarization of the atria, which starts during the PR segment, or the short period between the end of one P wave and the beginning of the next QRS complex (see Fig. 12.1 ). 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 (V ₅ and V ₆ ).

PR segment deviations may also be useful in distinguishing the ECG of acute pericarditis from that of benign early repolarization . In younger adults, the two patterns may coexist, causing further diagnostic confusion.

The ST segment elevations seen with acute pericarditis are sometimes followed (after a variable time) by T wave inversions ( Fig. 12.2 ). The general sequence of ST elevations and T wave inversions is similar to 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. Furthermore, very prominent T wave inversions (i.e., 5 mm or more in depth) are rare with pericarditis. Some patients with acute pericarditis never manifest evolving T wave inversions.

Another major difference between infarction and pericarditis is that pericarditis does not produce abnormal Q waves, such as those seen with certain infarcts. With MI, abnormal Q waves may occur because of the necrosis of heart muscle and the consequent loss of positive depolarization voltages (see Chapter 9 ). Pericarditis, on the other hand, generally causes only a superficial inflammation and does not produce actual myocardial necrosis.

Some patients have recurrent or relapsing episodes of pericarditis, which may occur intermittently or 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 or constrictive changes develop (see the following sections).

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, in extreme cases, to cardiac arrest with pulseless electrical activity (PEA; see Chapter 21 ).

The most common ECG sign of pericardial effusion (with or without actual tamponade) is low voltage (or relatively low voltage) of the QRS complexes. The mechanism of the low voltage in this setting has not been established with certainty.

Different sets of criteria for high voltage were mentioned in the discussion of hypertrophy patterns (see Chapter 7 ). Low voltage (see Chapter 11 ) is strictly considered to be present when the total amplitude of the QRS complexes in each of the six extremity leads is 5 mm (0.5 mV) or less. Low voltage in the extremity leads may or may not be accompanied by low voltage in the chest leads, defined as a peak-to-trough QRS amplitude (total range) of 10 mm or less in each of leads V ₁ to V ₆ . Clinicians should be aware that pericardial effusion may produce relatively low voltage (especially compared with previous), without meeting absolute criteria just defined.

Fig. 12.2 shows an example of low voltage. A listing of other factors that can produce low QRS voltage is presented in one of the Instant Replay boxes in Chapter 25 . One class of causes of low voltages includes myocardial deposition syndromes, in which the heart muscle gets infiltrated, and eventually replaced, with substances like amyloid or iron (iron in hemochromatosis).

The mechanism of the low voltage QRS complexes differs based on the context. For example, obesity can cause low voltage because of the insulating effect of fat tissue that lies between the heart and the chest wall. Patients with emphysema have increased inflation of the lungs. This extra air also acts to insulate the heart. Replacement of, or damage to, ventricular heart muscle tissue by fibrosis or amyloid can also cause low QRS voltages. Of the causes of low voltage, obesity, anasarca (generalized edema), pleural effusions, and emphysema are among the most common. However, when you see low voltage (particularly with unexplained sinus tachycardia), you need to consider the possibility of pericardial effusion because it can lead to fatal tamponade with pulseless electrical activity (see also Chapter 21 ).

Electrical alternans is a very distinctive finding that can occur with pericardial effusion especially when it is associated with tamponade or severe hemodynamic compromise ( Fig. 12.3 ). This pattern is characterized by a periodic, beat-to-beat shift in the QRS axis associated with mechanical swinging of the heart to-and-fro in a relatively large accumulation of fluid. The finding is usually most apparent in the mid-chest leads. The triad of sinus tachycardia, electrical alternans, and low QRS voltage is virtually diagnostic of cardiac tamponade, although not every patient with tamponade shows this pattern (i.e., it has high specificity, but only modest sensitivity). ^a

a Note that “electrical alternans” is a general term for alternation of one or more ECG waveforms on a beat-to-beat basis. The type of “total” electrical alternans (which usually affects the entire P-QRS-T) associated with pericardial effusion/tamponade is seen with sinus rhythm, and usually with sinus tachycardia. Practitioners should be aware that other forms of electrical alternans have nothing to do with pericardial disease. Probably the most common setting of QRS electrical alternans is (non-sinus) paroxysmal supraventricular tachycardia (PSVT). The ventricular rate is usually very fast (>200 beats/min) in such cases and the alternans is thought to result from a subtle change in conduction patterns on a beat-to-beat basis. QRS alternans may also occur with monomorphic ventricular tachycardias (see 14 , 16 ).

Electrical alternans is most likely to occur with larger effusions, and therefore, has been associated with metastatic malignancy (e.g., breast or lung). However, alternans per se is not a unique marker for pericardial effusion due to any specific cause.