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Symptoms of pericarditis
Last reviewed: 04.07.2025
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Some patients develop symptoms of inflammation (acute pericarditis), while others have predominantly fluid accumulation (pericardial effusion). The manifestations of the disease vary depending on the severity of the inflammation and the amount and location of the pericardial effusion.
Even a large effusion may be asymptomatic if it accumulates slowly (eg, over months).
Symptoms of acute pericarditis
Acute pericarditis often causes chest pain and a pericardial friction rub, sometimes dyspnea. The first manifestation may be tamponade with arterial hypotension, shock, or pulmonary edema.
Because the innervation of the pericardium and myocardium is similar, pericardial chest pain sometimes resembles the pain of myocardial inflammation or ischemia: dull or sharp pain in the precordium or behind the breastbone, which may radiate to the neck, trapezius muscle (especially the left), or shoulders. The pain varies from moderate to severe. Unlike ischemic chest pain, the pain of pericarditis is usually aggravated by chest movement, coughing, and breathing; it is relieved by sitting up and leaning forward. Tachypnea and nonproductive cough may be present. Fever, chills, and weakness are common. In 15% to 25% of patients with idiopathic pericarditis, symptoms occur intermittently over many months or years.
The most important physical sign is a pericardial friction rub that coincides with the contraction of the heart. However, this rub is often inconstant and short-lived. It may be present only during systole or (less commonly) diastole. A significant amount of pericardial effusion may muffle the heart sounds, increase the area of cardiac dullness, and alter the size and shape of the cardiac silhouette.
If acute pericarditis is suspected, hospitalization is sometimes necessary for primary diagnostics. An ECG and chest X-ray are performed. If signs of increased pressure in the right half of the heart, tamponade, or dilation of the cardiac contours are detected, echocardiography is performed to detect effusion and abnormal filling of the heart chambers. Leukocytosis and increased ESR are possible in blood tests, but these data are nonspecific.
Diagnosis is based on the presence of typical clinical symptoms and changes in ECG data. A series of ECGs may be required to detect changes.
The ECG in acute pericarditis may show changes (elevation) of the ST segment and T wave, usually in most leads.
The ST segment in lead II or III is elevated but subsequently returns to baseline. Unlike myocardial infarction, acute pericarditis does not cause reciprocal segment depression (except in leads aVR), nor does it produce abnormal Q waves. The PR interval may be shortened. After a few days or more, the waves may become flattened and then negative, except in lead aVR. Wave inversion occurs after the segment returns to baseline, distinguishing the findings from those of acute ischemia or MI.
Because the pain of pericarditis may resemble that of acute MI and pulmonary infarction, additional studies (eg, changes in serum cardiac markers, lung scan) may be needed if the history and ECG findings are not typical of pericarditis.
Postpericardiotomy and postinfarction syndromes can be difficult to diagnose. They must be differentiated from recent MI, pulmonary embolism, and pericardial infection after surgery. Pain, pericardial friction rub, and fever that appear 2 weeks to several months after surgery and a rapid response to aspirin, NSAIDs, or glucocorticoids are helpful in the diagnosis.
Pericardial effusion
Pericardial effusion is often painless, but when it develops in acute pericarditis, pain syndrome is possible. As a rule, heart sounds are muffled. Pericardial friction rub can be heard. With extensive effusion, in some cases, compression of the basal sections of the left lung develops, weakened breathing (near the left scapula) and fine bubbling rales (sometimes crepitation) appear. Arterial pulse, jugular venous pulse and blood pressure are normal unless intrapericardial pressure increases significantly, causing tamponade.
In post-MI syndrome, pericardial effusion may be associated with fever, pericardial friction rub, fluid accumulation, pleurisy, pleural effusion, and pain. This syndrome typically develops between 10 days and 2 months after MI. It is usually mild, but not always. Sometimes, the heart ruptures after MI, leading to hemopericardium and tamponade, usually 1-10 days after MI, more often in women.
A presumptive diagnosis is made based on clinical data, but often the suspicion of this pathology arises only after an enlarged cardiac contour is detected on a chest X-ray. The voltage of the QRS complex often decreases on the electrocardiogram, and sinus rhythm is preserved in approximately 90% of patients. With a large volume of effusion, chronic course of the disease, the electrocardiogram may show electrical alternans (the amplitude of the P wave, QRS complex, or T wave increases and decreases from contraction to contraction). Electrical alternans is associated with changes in the position of the heart. Echocardiography has a high degree of sensitivity and specificity in detecting pericardial fluid.
Patients with a normal electrocardiogram, low (< 0.5 L) fluid volume, and no suspicious history or physical examination findings may be observed with serial examinations and echocardiographs. Other patients require further evaluation to determine the etiology.
Cardiac tamponade
Clinical features are similar to those of cardiogenic shock: decreased cardiac output, low systemic arterial pressure, tachycardia, and dyspnea. The neck veins are markedly dilated. Severe cardiac tamponade is almost always accompanied by a fall of more than 10 mm Hg in systolic blood pressure during inspiration (pulsus paradoxus). In some cases, the pulse may disappear during inspiration. (However, pulsus paradoxus may also be present in COPD, asthma, pulmonary embolism, right ventricular infarction, and noncardiogenic shock.) Heart sounds are muffled if the effusion is large enough.
Low voltage and electrical alternans on the electrocardiogram suggest cardiac tamponade, but these findings are not sensitive or specific enough. If tamponade is suspected, echocardiography is performed unless a short delay is life-threatening. In the latter case, pericardiocentesis is performed immediately for diagnostic and therapeutic purposes. Echocardiographic changes in the respiration-dependent transvalvular and venous flows and compression or collapse of the right heart chambers in the presence of pericardial effusion confirm the diagnosis.
If tamponade is suspected, right heart catheterization (Swan-Ganz) may be performed. In cardiac tamponade, the early diastolic decline in ventricular pressure is absent. In the atrial pressure curve, the x-segment of the pressure curve is preserved, but the y-segment is lost. In contrast, in severe failure due to dilated cardiomyopathy or pulmonary artery occlusion, the left ventricular diastolic pressure usually exceeds the right atrial pressure, and the mean right ventricular pressure is 4 mmHg or more.
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Symptoms of constrictive pericarditis
Fibrosis or calcification rarely causes symptoms unless constrictive pericarditis develops. The only early changes are increased ventricular, atrial, pulmonary, and systemic venous pressures. Signs of peripheral venous congestion (eg, peripheral edema, neck vein distension, hepatomegaly) may appear with an early diastolic murmur (pericardial click), often heard best on inspiration. This sound is due to abrupt limitation of diastolic ventricular filling by the dense pericardium. Ventricular systolic function (as measured by ejection fraction) is usually preserved. Prolonged elevation of pulmonary venous pressures results in dyspnea (especially during exertion) and orthopnea. Weakness may be marked. Tension of the neck veins with increased venous pressure on inspiration (Kussmaul's sign) is detected; it disappears with tamponade. Pulsus paradoxus is rarely detected, and is usually less pronounced than with tamponade. The lungs are not full-blooded unless significant compression of the left ventricle develops.