Acute Pericarditis

CLINICAL FEATURES The most common symptom is precordial or retrosternal chest pain, which is most frequently described as sharp or stabbing. It may be of sudden or gradual onset and radiate to the back, neck, left shoulder, or arm; referral to the left trapezial ridge (due to inflammation of the joining diaphragmatic pleura) is a particular distinguishing feature. Chest pain due to acute pericarditis may be aggravated by inspiration or movement. It may be most severe when the patient is supine and is often relieved when the patient sits up and leans forward. In most instances, these characteristics allow the pain of acute pericarditis to be distinguished from the ischemic pain of angina or acute myocardial infarction.

Associated symptoms include (1) low-grade, intermittent fever, particularly if pericarditis is infectious in origin or of the idiopathic type; (2) dyspnea, due to accentuated pain with inspiration; and (3) dysphagia, ascribed to irritation of the esophagus by the posterior pericardium.

A pericardial friction rub is the most common and important physical finding in pericarditis. A pericardial rub most closely resembles a superficial grating or scratching sound. It is best heard with the diaphragm of the stethoscope at the lower left sternal border or apex when the patient is sitting and leaning forward or in the hands-and-knees position. It may be audible only during a certain phase of respiration and characteristically is transient (e.g., heard one hour and not the next). No inference as to the amount of pericardial fluid should be drawn from the presence or absence of a pericardial friction rub.

A pericardial rub is most often triphasic in character, consisting of a systolic component, an early diastolic component occurring during the early phase of ventricular filling, and a presystolic component synchronous with atrial systole. It is less commonly biphasic, with a systolic component with either an early diastolic or presystolic component. A monophasic rub is unusual (18 percent of cases) but is most often systolic.

DIAGNOSIS Electrocardiogram Serial ECGs recorded over a number of days may be diagnostic in acute pericarditis. The evolutionary ECG changes during acute pericarditis and convalescence have been divided into four stages. During stage 1, or the acute phase, ST-segment elevation (reflecting associated subepicardial inflammation and/or injury) is prominent in the precordial leads, especially V 5 and V6, and in standard lead I. PR-segment depression may be noted in leads II, aVf, and V4 to V6 (Fig 51:1). In stage 2, the ST segment begins returning to the isoelectric line, and T-wave amplitude decreases. T-wave inversion is rarely seen until stage 3. Stage 3 is characterized by an isoelectric ST segment and T-wave inversion in those leads previously showing ST-segment elevation. Resolution of repolarization abnormalities is the hallmark of stage 4.

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FIG. 51-1. This series of ECGs was recorded in a 28-year-old male who presented complaining of pleuritic retrosternal pain, cough, and fever. The initial ECG (dated 10-20) demonstrates diffuse ST-segment elevation (stage I). The ST-segment to T-wave amplitude ratio measured in V6 is 5 mm/10 mm, or 0.50, thus meeting criteria for pericarditis rather than early repolarization (see the text). The ECG dated 10-29 demonstrates a return of the ST segment to the isoelectric point in most leads in which they had been elevated (stage II). The third tracing (dated 11-3) demonstrates resolution of ST changes and the appearance of T-wave inversion in the anterior precordial leads (stage III). These evolutionary changes are typical of and diagnostic for pericarditis and usually occur over several weeks.

If a large pericardial effusion develops during the course of acute pericarditis, additional ECG abnormalities may be noted, including low-voltage QRS complexes and electrical alternans. These phenomena are due to the "insulating" effect of pericardial fluid, which attenuates electrical signals of myocardial origin, and the pendular motion of the heart within the fluid-filled pericardial space.

Although serial ECG tracings are of diagnostic value in acute pericarditis, sequential ECG assessment is not a diagnostic luxury afforded the emergency physician. Differentiating pericarditis from the normal variant with "early repolarization" is a common problem and can be difficult when only a single 12-lead ECG is available. Acute pericarditis is a common cause of chest pain and abnormal ECGs in young adults. The ST-T-wave changes present in the early repolarization or normal variant ECG mimic those of pericarditis and have been reported in 2 percent of healthy young adults. Investigations attempting to distinguish these two conditions have yielded conflicting results. However, a simple criterion offers considerable diagnostic utility, namely, the ST-segment/T-wave amplitude ratio in leads V 5, V6, or I.19 Using the end of the PR segment as baseline, or 0 mV, the amplitude or height of the ST segment at its onset is measured in one of the aforementioned leads and recorded in millivolts. The height of the T wave in the same lead is measured from the baseline to the T-wave peak. If the ratio of ST amplitude (in millivolts) to T-wave amplitude (in millivolts) is below 0.25, a normal variant or early repolarization is most probable. If the ratio is above 0.25, acute pericarditis is likely. This criterion may allow differentiation of acute pericarditis (stage 1) from early repolarization during emergency department evaluation ( Fig, 51-1). Pericarditis alone does not cause significant cardiac rhythm disturbances.

Radiographic Assessment Conventional posteroanterior and lateral chest x-rays are of limited value. The cardiac silhouette may be of normal size and contour in acute pericarditis and, in some instances, the setting of cardiac tamponade. If previous chest x-rays are available for comparison, a recent increase in the size of the cardiac silhouette or an increase in the cardiothoracic ratio without radiographic evidence of pulmonary venous hypertension aids in distinguishing an expanding pericardial effusion from left heart failure. The epicardial "fat-pad sign" is rarely seen on the lateral chest x-ray and has been reported in only 15 percent of cases of acute pericarditis during fluoroscopy with image intensification. If acute pericarditis is suspected on the basis of history, physical examination, or ECG, posteroanterior and lateral chest x-rays, which may demonstrate a pleuropulmonary or mediastinal abnormality, may assist in establishing a cause (e.g., neoplastic or infectious).

Echocardiography Studies Echocardiography has become the procedure of choice for the detection, confirmation, and serial follow-up of patients with acute pericarditis and a pericardial effusion.18

Normally, the pericardial sac is only a "potential" space, and the myocardium is echocardiographically in direct contact with surrounding thoracic structures. The anterior RV wall is in contact with the chest wall, and the posterior LV wall is in contact with the posterior pericardium and adjacent pleura. When a pericardial effusion is present, the pericardial space fills with echo-free fluid. Echocardiographically, a separation is seen between the right ventricle and the chest wall and between the left ventricle and the posterior pericardium. Quantitation of the size of the effusion is arbitrary and is determined by where the echo-free space is seen (anterior or posterior) and when in the cardiac cycle it occurs. For example, when an echo-free space is seen only posteriorly and only during systole, a small effusion is said to present.

Ancillary Laboratory Evaluation The laboratory studies listed in T§b!e,51-Z may be of value in establishing an etiologic diagnosis. Creatine kinase and CK-MB may be elevated in acute pericarditis due to associated myocarditis.

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