Atlas of pathophysiology, 2 Edition
Part II - Disorders
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.
· Bacterial, fungal, or viral infection
· High-dose radiation to the chest
· Hypersensitivity or autoimmune disease
· Previous cardiac injury, such as myocardial infarction, trauma, or surgery
· Drugs, such as hydralazine or procainamide
· Idiopathic factors
· Aortic aneurysm
Pericarditis most commonly affects men ages 20 to 50, generally following respiratory illness. It can also occur in children.
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)
The pain in pericarditis is commonly pleuritic, increasing with deep inspiration and decreasing when the patient sits up and leans forward, pulling the heart away from the diaphragmatic pleurae of the lungs.
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.
· 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
TISSUE CHANGES IN PERICARDITIS