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Pericarditis Pericarditis is inflammation of the pericardium—the fibroserous sac that envelops, supports, and protects the heart. Acute pericarditis can be fibrinous or effusive, with purulent, serous, or hemorrhagic exudate. Chronic constrictive pericarditis is characterized by dense fibrous pericardial thickening. The prognosis depends on the underlying cause but is generally good in acute pericarditis, unless constriction occurs. Causes Bacterial, fungal, or viral infection Neoplasm High-dose radiation to the chest Uremia Hypersensitivity or autoimmune disease Previous cardiac injury, such as myocardial infarction, trauma, or surgery Drugs, such as hydralazine or procainamide Idiopathic factors Aortic aneurysm Myxedema Pathophysiology Pericardial tissue damaged by bacteria or other substances releases chemical mediators of inflammation (prostaglandins, histamines, bradykinins, and serotonin) into the surrounding tissue, thereby initiating the inflammatory process. Friction occurs as the inflamed pericardial layers rub against each other. Histamines and other chemical mediators dilate vessels and increase vessel permeability. Vessel walls then leak fluids and protein (including fibrinogen) into tissues, causing extracellular edema. Macrophages already present in the tissue begin to phagocytize the invading bacteria and are joined by neutrophils and monocytes. After several days, the area fills with an exudate composed of necrotic tissue and dead and dying bacteria, neutrophils, and macrophages. If the cause of pericarditis isn’t infection, the exudate may be serous (as with autoimmune disease) or hemorrhagic (as seen with trauma or surgery). Eventually, the contents of the cavity autolyze and are gradually reabsorbed into healthy tissue. Chronic constrictive pericarditis develops if the chronic or recurrent pericarditis makes the pericardium thick and stiff, encasing the heart in a stiff shell and preventing proper filling during diastole. Consequently, left- and right-side filling pressures rise as stroke volume and cardiac output fall. Signs and symptoms Pericardial friction rub Sharp and (commonly) sudden pain, usually starting over the sternum and radiating to the neck, shoulders, back, and arms Shallow, rapid respirations Mild fever Dyspnea, orthopnea, tachycardia Heart failure Muffled, distant heart sounds Pallor, clammy skin, hypotension, pulsus paradoxus, jugular vein distention Possible progression to cardiovascular collapse Fluid retention, ascites, hepatomegaly Pericardial knock in early diastole along the left sternal border produced by restricted ventricular filling Kussmaul’s sign (increased jugular vein distention on inspiration caused by restricted right-sided filling) Diagnostic test results Twelve-lead electrocardiography reveals diffuse ST-segment elevation in the limb leads and most precordial leads that reflect the inflammatory process. Downsloping PR segments and upright T waves are present in most leads. QRS segments may be diminished when pericardial effusion exists. Arrhythmias, such as atrial fibrillation and sinus arrhythmias, may occur. In chronic constrictive pericarditis, there may be low-voltage QRS complexes, T-wave inversion or flattening, and P mitral (wide P waves) in leads I, II, and V6. Blood testing reveals an elevated erythrocyte sedimentation rate as a result of the inflammatory process and a normal or elevated white blood cell count, especially in infectious pericarditis. C-reactive protein may be elevated. Blood cultures identify an infectious cause. Antistreptolysin-O titers are positive if pericarditis is caused by rheumatic fever. Purified protein derivative skin tests are positive if pericarditis is caused by tuberculosis. Echocardiography shows an echo-free space between the ventricular wall and the pericardium and reduced pumping action of the heart. Chest X-rays show an enlarged cardiac silhouette with a water bottle shape caused by fluid accumulation if pleural effusion is present. Chest or heart magnetic resonance imaging shows enlargement of the heart and signs of inflammation. Treatment Bed rest as long as fever and pain persist Treatment of the underlying cause, if it can be identified Nonsteroidal anti-inflammatory drugs, corticosteroids Antibacterial, antifungal, or antiviral therapy Partial or total pericardectomy Diuretics Pericardiocentesis
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