Pericardial effusion can develop during any of the processes discussed in the preceding paragraphs. The speed of accumulation determines the physiologic importance of the effusion. Because the pericardium stretches, large effusions (> 1000 mL) that develop slowly may produce no hemodynamic effects. Smaller effusions that appear rapidly can cause tamponade. Tamponade is characterized by elevated intrapericardial pressure (> 15 mm Hg), which restricts venous return and ventricular filling. As a result, the stroke volume and pulse pressure fall, and the heart rate and venous pressure rise. Shock and death may result.
A. Symptoms and Signs
Pericardial effusions may be associated with pain if they occur as part of an acute inflammatory process or may be painless, as is often the case with neoplastic or uremic effusion. Dyspnea and cough are common, especially with tamponade. Other symptoms may result from the primary disease.
A pericardial friction rub may be present even with large effusions. In Cardiac tamponade, tachycardia, tachypnea, a narrow pulse pressure, and a relatively preserved systolic pressure are characteristic. Pulsus paradoxus - a greater than 10 mm Hg decline in systolic pressure during inspiration due to further impairment of left ventricular filling - is the classic finding, but it may also occur with obstructive lung disease. Central venous pressure is elevated, and edema or ascites may be present; these signs favor a more chronic process.
B. Laboratory Findings
Laboratory tests tend to reflect the underlying processes.
C. Diagnostic Studies
Chest x-ray can suggest effusion by an enlarged cardiac silhouette with a globular configuration but may appear normal. The ECG often reveals nonspecific T wave changes and low QRS voltage. Electrical alternans is present uncommonly but is pathognomonic. Echocardiography is the primary method for demonstrating pericardial effusion. Tamponade presents a characteristic picture of inadequate ventricular filling (diastolic collapse of the right ventricle or right atrium). The echocardiogram readily discriminates pericardial effusion from congestive heart failure. MRI also demonstrates pericardial fluid and lesions. Diagnostic pericardiocentesis or biopsy is often indicated for microbiologic and cytologic studies; a pericardial biopsy may be performed relatively simply through a small subxiphoid incision.
Small effusions can be followed clinically and with the aid of echocardiograms. When tamponade is present, urgent pericardiocentesis is required. Removal of a small amount of fluid often produces immediate hemodynamic benefit, but complete drainage with a catheter is preferable. Continued drainage may be indicated.
Additional therapy is determined by the nature of the primary process. Recurrent effusion in neoplastic disease and uremia, in particular, may require partial pericardiectomy.
Burgess LJ et al: Role of biochemical tests in the diagnosis of large pericardial effusions. Chest 2002;121:495.
Karam N et al: Diagnosis and management of chronic pericardial effusions. Am J Med Sci 2001;322:79.
Soler-Soler J et al: Management of pericardial effusion. Heart 2001;86:235.
Tsang TS: Outcomes of primary and secondary treatment of pericardial effusion in patients with malignancy. Mayo Clin Proc 2000;75:248.
Tsang TS et al: Consecutive 1127 therapeutic echocardiographically guided pericardiocenteses: clinical profile, practice patterns, and outcomes spanning 21 years. Mayo Clin Proc 2002;77:429.
Wang ZJ et al: CT and MR imaging of pericardial disease. Radiographics 2003;23 Spec No:S167.
Revision date: July 6, 2011
Last revised: by Dave R. Roger, M.D.