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Epidemiology
Pericarditis and pericardial effusions have many etiologies, including inflammation, infection, immunologic disorders, malignancy, myxedema, uremia, pregnancy, aortic dissection, cardiac rupture, trauma, myocardial infarction, cirrhosis, and heart failure. The three most common etiologies are neoplasia, uremia, and idiopathic causes. Cardiac tamponade usually is caused by bleeding, followed by other sources of chronic effusions.
Pathophysiology
The pathophysiology of pericardial inflammation relates to the underlying causes of pericardial effusions and pericarditis. Effusions generally arise when pericardial fluid production exceeds reabsorption. With pericardial tamponade, there is a rapid increase in intrapericardial pressure and diminished diastolic compliance, ultimately resulting in equalization of right and left atrial, right and left ventricular, pulmonary artery wedge, and intrapericardial pressures. Pericarditis arises from inflammation of the pericardial sac. In constrictive pericarditis, there is a limitation in cardiac filling that is reflected in a “square root” sign seen in ventricular pressure tracings during cardiac catheterization.
Clinical features
The symptoms of pericardial effusions include dyspnea, fever, and chest pain, although many effusions are asymptomatic. The signs include a pericardial friction rub, global electrocardiogram (ECG) changes, and pulsus paradoxus. Cardiac tamponade presents as hypotension and decreased cardiac output; Beck’s triad includes muffled heart sounds, elevated venous pressure, and decreased systemic arterial pressure. Significant constrictive pericarditis manifests with symptoms of right-sided heart failure, including jugular venous distention, worsening peripheral edema, and pleural effusions.
Diagnostics
Echocardiography is the gold standard for the diagnosis of pericardial effusions. Cardiac tamponade is a clinical diagnosis but can be confirmed or substantiated with echocardiography. Computed tomography is useful in identifying the thickened pericardial sac in patients with pericarditis, although magnetic resonance imaging is more sensitive and specific in diagnosing constrictive pericarditis. Right and left cardiac catheterization is the gold standard for diagnosing constrictive pericarditis.
Treatment
Pericardial effusions are treated most readily with drainage, pericardiocentesis, or a pericardial window. Adjunctive medical therapy can be successful, depending on the etiology of the effusion. Depending on the etiology, tamponade can be treated with pericardiocentesis, a pericardial window, or surgical (re)exploration. Medical treatment of constrictive pericarditis is predicated on treating the underlying cause; however, the mainstay of therapy is pericardiectomy.
Outcomes and prognosis
The outcomes and prognoses for pericardial effusions and tamponade depend on the etiology. Early mortality for pericardiectomy ranges from 5 to 10 percent, with 5-year survival ranging from 65 to 90 percent. Predictors of poor outcome are prior radiation, renal insufficiency, poor ventricular function, pulmonary hypertension, New York Heart Association functional class IV, hyponatremia, ascites, and hyperbilirubinemia.
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Historical Highlights
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Galen was the first to describe pericardial disease in animals (circa 160 AD) and subsequently described in two patients the surgical drainage of purulent pericardial effusions.1 This predated Lower’s 1669 description of pericarditis in humans.2 There are apocryphal references of penetrating heart wounds being treated, usually by the removal of the offending object, without much information about how subsequent drainage of the ...