Pericarditis
Pericarditis: Excerpt from Professional Guide to Diseases (Eighth Edition)
Pericarditis is an inflammation of the pericardium, the fibroserous sac that envelops, supports, and protects the heart. It occurs in both acute and chronic forms. 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 and incidence
Common causes of this disease include:
❑ bacterial, fungal, or viral infection (infectious pericarditis)
❑ neoplasms (primary or metastatic from lungs, breasts, or other organs)
❑ high-dose radiation to the chest
❑ uremia
❑ hypersensitivity or autoimmune disease, such as acute rheumatic fever (most common cause of pericarditis in children), systemic lupus erythematosus, and rheumatoid arthritis
❑ postcardiac injury such as myocardial infarction (MI), which later causes an autoimmune reaction (Dressler’s syndrome) in the pericardium; trauma; or surgery that leaves the pericardium intact but causes blood to leak into the pericardial cavity
❑ drugs, such as hydralazine or procainamide
❑ idiopathic factors (most common in acute pericarditis).
Less common causes include aortic aneurysm with pericardial leakage, and myxedema with cholesterol deposits in the pericardium.
Pericarditis most commonly affects men ages 20 to 50, but it can also occur in children following infection with an adenovirus or coxsackievirus.
Signs and symptoms
Acute pericarditis typically produces a sharp and often sudden pain that usually starts over the sternum and radiates to the neck, shoulders, back, and arms. However, unlike the pain of MI, pericardial pain is often 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.
Pericardial effusion, the major complication of acute pericarditis, may produce effects of heart failure (such as dyspnea, orthopnea, and tachycardia), ill-defined substernal chest pain, and a feeling of fullness in the chest. (See Patterns of cardiac pain.)
Alert If the fluid accumulates rapidly, cardiac tamponade may occur, resulting in pallor, clammy skin, hypotension, pulsus paradoxus (a decrease in systolic blood pressure of 15 mm Hg or more during slow inspiration), jugular vein distention and, eventually, cardiovascular collapse and death.
Chronic constrictive pericarditis causes a gradual increase in systemic venous pressure and produces symptoms similar to those of chronic right-sided heart failure (fluid retention, ascites, and hepatomegaly).
Diagnosis
Because pericarditis commonly coexists with other conditions, diagnosis of acute pericarditis depends on typical clinical features and elimination of other possible causes. The pericardial friction rub, a classic symptom, is a grating sound heard as the heart moves. It can usually be auscultated best during forced expiration, while the patient leans forward or is on his hands and knees in bed. It may have up to three components, corresponding to the timing of atrial systole, ventricular systole, and the rapid-filling phase of ventricular diastole. Occasionally, this friction rub is heard only briefly or not at all. Nevertheless, its presence, together with other characteristic features, is diagnostic of acute pericarditis. In addition, if acute pericarditis has caused very large pericardial effusions, physical examination reveals increased cardiac dullness and diminished or absent apical impulse and distant heart sounds.
Chest X-ray, echocardiogram, chest magnetic resonance imaging (MRI), heart MRI, heart computed tomography scan, and radionuclide scanning can detect fluid that has accumulated in the pericardial sac. They may also show enlargement of the heart and signs of inflammation or scarring, depending on the cause of pericarditis.
In patients with chronic pericarditis, acute inflammation or effusions don’t occur — only restricted cardiac filling.
Laboratory results reflect inflammation and may identify its cause:
❑ normal or elevated white blood cell count, especially in infectious pericarditis
❑ elevated erythrocyte sedimentation rate
❑ slightly elevated cardiac enzyme levels with associated myocarditis
❑ culture of pericardial fluid obtained by open surgical drainage or cardiocentesis (sometimes identifies a causative organism in bacterial or fungal pericarditis)
❑ electrocardiography showing the following changes in acute pericarditis: elevation of ST segments in the standard limb leads and most precordial leads without significant changes in QRS morphology that occur with MI, atrial ectopic rhythms such as atrial fibrillation and, in pericardial effusion, diminished QRS voltage.
Other pertinent laboratory data include blood urea nitrogen levels to check for uremia, antistreptolysin-O titers to detect rheumatic fever, and a purified protein derivative skin test to check for tuberculosis. In pericardial effusion, echocardiography is diagnostic when it shows an echo-free space between the ventricular wall and the pericardium.
Treatment
The goal of treatment is to relieve symptoms and manage the underlying systemic disease. In acute idiopathic pericarditis and postthoracotomy pericarditis, treatment consists of bed rest as long as fever and pain persist, and nonsteroidal drugs, such as aspirin and indomethacin, to relieve pain and reduce inflammation. Post-MI patients should avoid nonsteroidal anti-inflammatory drugs and steroids because they may interfere with myocardial scar formation. If these drugs fail to relieve symptoms, corticosteroids may be used. Although corticosteroids produce rapid and effective relief, they must be used cautiously because episodes may recur when therapy is discontinued.
Infectious pericarditis that results from disease of the left pleural space, mediastinal abscesses, or septicemia requires antibiotics (possibly by direct pericardial injection), surgical drainage, or both. Cardiac tamponade may require pericardiocentesis. Signs of tamponade include pulsus paradoxus, jugular vein distention, dyspnea, and shock.
Recurrent pericarditis may necessitate partial pericardectomy, which creates a “window’’ that allows fluid to drain into the pleural space. In constrictive pericarditis, total pericardectomy to permit adequate filling and contraction of the heart may be necessary. Treatment must also include management of rheumatic fever, uremia, tuberculosis, and other underlying disorders.
Special considerations
A patient with pericarditis needs complete bed rest. In addition, health care includes:
❑ assessing pain in relation to respiration and body position to distinguish pericardial pain from myocardial ischemic pain.
❑ placing the patient in an upright position to relieve dyspnea and chest pain; providing analgesics and oxygen; and reassuring the patient with acute pericarditis that his condition is temporary and treatable.
❑ monitoring for signs of cardiac compression or cardiac tamponade, possible complications of pericardial effusion. Signs include decreased blood pressure, increased central venous pressure, and pulsus paradoxus. Because cardiac tamponade requires immediate treatment, keep a pericardiocentesis set handy whenever pericardial effusion is suspected.
❑ explaining tests and treatments to the patient. If surgery is necessary, he should learn deep-breathing and coughing exercises beforehand. Postoperative care is similar to that given after cardiothoracic surgery.
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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