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.
Common causes of this disease include:
❑ bacterial, fungal, or viral infection (infectious pericarditis)
❑ neoplasms (primary, or metastases from lungs, breasts, or other organs)
❑ high-dose radiation to the chest
❑ uremia
❑ hypersensitivity, systemic disease, or autoimmune disease, such as acute rheumatic fever (most common cause of pericarditis in children), systemic lupus erythematosus, acquired immuno-deficiency syndrome–related disorders, or 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, nydrazid, phenytoin, and 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.
Clinical features vary in the acute and chronic forms.
In acute pericarditis, a sharp and commonly sudden pain usually starts over the sternum and radiates to the neck, shoulders, back, and arms. However, unlike the pain of an 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 the effects of heart failure — such as dyspnea, orthopnea, and tachycardia — as well as ill-defined substernal chest pain and a feeling of fullness in the chest.
If the fluid accumulates rapidly, cardiac tamponade may occur, resulting in pallor, clammy skin, hypotension, paradoxical pulse (a decrease in systolic blood pressure equal to or greater than 10 mm Hg 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, hepatomegaly).
Because pericarditis often coexists with other conditions, diagnosis of acute pericarditis depends on typical clinical features and elimination of other possible causes. It may be detected with X-ray, echocardiogram, magnetic resonance imaging, computed tomography, and coronary angiography. These tests may show scarring, contracture of the pericardium, or enlargement of the heart.
CLINICAL TIP: A classic symptom, the pericardial friction rub, is a grating sound heard as the heart moves. It can usually be auscultated best during forced expiration, with the patient leaning forward or resting on his hands and knees in the bed.
Pericardial friction rub may have up to three components, corresponding to the timing of atrial systole, ventricular systole, and the rapid-filling phase of ventricular diastole, Occasionally, it’s 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 large pericardial effusions, the physical examination reveals increased cardiac dullness and diminished or absent apical impulse and distant heart sounds. Acute inflammation or effusions don’t occur in patients with chronic pericarditis — only those with restricted cardiac filling.
Laboratory results reflect inflammation and may identify its cause:
❑ normal or elevated white blood cell count, especially in infectious pericarditis
❑ 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 shows the following changes in acute pericarditis: elevation of ST segments in the standard limb leads and most precordial leads without the significant changes in QRS-complex morphology that occur with an MI, atrial ectopic rhythms such as atrial fibrillation, and diminished QRS complex in pericardial effusion.
Other pertinent laboratory studies include blood urea nitrogen level 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.
The goal of treatment is to relieve symptoms and manage underlying systemic disease.
With acute idiopathic pericarditis, post-MI pericarditis, and postthoracotomy pericarditis, treatment consists of bed rest while fever and pain persist and nonsteroidal anti-inflammatory drugs, such as aspirin and indomethacin, to relieve pain and reduce inflammation.
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 paradoxical pulse, jugular vein distention, dyspnea, and shock.
Recurrent pericarditis may necessitate a partial pericardectomy, which creates a “window” that allows fluid to drain into the pleural space. In constrictive pericarditis, a 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.
❑ Provide complete bed rest.
❑ Assess pain in relation to respiration and body position to distinguish pericardial pain from myocardial ischemic pain.
❑ Place the patient in an upright position to relieve dyspnea and chest pain. Provide analgesics and oxygen, and reassure the patient with acute pericarditis that his condition is temporary and treatable.
❑ Monitor the patient for signs of cardiac compression or cardiac tamponade, possible complications of pericardial effusion. Signs include decreased blood pressure, increased central venous pressure, and paradoxical pulse. Because cardiac tamponade requires immediate treatment, keep a pericardiocentesis set handy whenever pericardial effusion is suspected.
❑ Explain 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.
Review other book chapters online related to Jacobs syndrome:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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Title: Handbook of Diseases Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2003 ISBN: 1-58255-266-5 
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