Summary
Highlights
The pericardium, composed of fibrous and serous layers (parietal and visceral), forms a sac around the heart. The pericardial cavity between these layers typically contains less than 50 ml of fluid, allowing for free heart movement. In response to injury, the pericardium increases fluid production, which can contain fibrin and inflammatory cells, and can distend to a certain point.
Pericarditis is inflammation of the pericardium, presenting with sharp chest pain radiating to the shoulder, relieved by sitting or leaning forward. A pericardial friction rub (squeaking/scratching sound) is often audible. Elevated biomarkers include WBC count, ESR, CRP, and sometimes cardiac troponin. ECG often shows diffuse concave ST segment elevation and PR segment depression (Stage 1), followed by ST/PR normalization and T wave flattening (Stage 2), T wave inversion (Stage 3), and T wave normalization or persistent inversion (Stage 4). Treatment includes aspirin, NSAIDs, and colchicine; corticosteroids are considered if other treatments fail.
Causes of pericarditis vary, often being idiopathic but commonly viral (e.g., HIV, coxsackievirus). Other causes include metabolic disorders (kidney failure), autoimmune diseases (rheumatoid arthritis, lupus), cancers (breast, lung, Hodgkin's lymphoma), drugs (penicillin, anticoagulants), and events like myocardial infarction, cardiac surgery, trauma, or radiation therapy. Tuberculosis is a significant cause in poorer countries. Chronic inflammation can lead to constrictive pericarditis, where fibrosis or calcification forms a tough, inelastic shell around the heart, impairing diastolic filling. This can result in peripheral venous congestion and Kussmaul sign (increased jugular venous pressure during inspiration).
Pericardial effusion is the presence of excessive fluid (hundreds of milliliters) in the pericardial cavity. Causes are similar to pericarditis, as increased fluid production is a pericardial response to injury. Hemorrhagic effusions can result from trauma, myocardial infarctions, and vessel rupture. Diagnosis involves echocardiogram, CT, or MRI to assess fluid quantity and location. If pericarditis is absent, patients may be asymptomatic, though a pericardial friction rub can still be heard. ECG changes include tachycardia, electrical alternans, and low QRS voltage.
Cardiac tamponade is a life-threatening condition where pressure from pericardial effusion impedes heart filling, occurring when the pericardium's elastic limit is surpassed by rapidly accumulating or large volumes of fluid. This pressure on the heart can lead to shock. Key signs include tachycardia, high jugular venous pressure, and pulsus paradoxus (a drop of 10 mmHg or more in arterial blood pressure during inspiration). Treatment involves draining the excess fluid from the pericardial cavity.