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ESSENTIALS OF DIAGNOSIS

Pericardial effusion

  • Clinical impact determined by the speed of accumulation.

  • May or may not cause pain.

Tamponade

  • Tachycardia with an elevated JVP and either hypotension or a paradoxical pulse.

  • Low voltage or electrical alternans on ECG.

  • Echocardiography is diagnostic.

Pericardial effusion can develop during any of the acute pericarditis processes. Because the pericardium covers the ascending aorta and arch, aortic dissection and/or rupture can lead to tamponade as well. The speed of accumulation determines the physiologic importance of the effusion. Because of pericardial stretch, effusions larger than 1000 mL that develop slowly may produce no hemodynamic effects. Conversely, smaller effusions that appear rapidly can cause tamponade due to the curvilinear relationship between the volume of fluid and the intrapericardial pressure. Tamponade is characterized by elevated intrapericardial pressure (greater than 15 mm Hg), which restricts venous return and ventricular filling. As a result, the stroke volume and arterial pulse pressure fall, and the heart rate and venous pressure rise. Shock and death may result.

CLINICAL FINDINGS

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. Cardiac tamponade can be a life-threatening syndrome evidenced by tachycardia, hypotension, pulsus paradoxicus, raised JVP, muffled heart sounds, and decreased ECG voltage or electrical alternans. Other symptoms may result from the primary disease. The prognosis is a function of the cause. Large idiopathic chronic effusions (over 3 months) have a 30–35% risk of progression to cardiac tamponade.

A pericardial friction rub may be present even with large effusions (see AUDIO 10–23). In cardiac tamponade, tachycardia, tachypnea, a narrow pulse pressure, and a relatively preserved systolic pressure are characteristic. Pulsus paradoxus is defined as a decline of greater than 10 mm Hg in systolic pressure during inspiration. Since the RV and LV share the same pericardium, when there is significant pericardial effusion, as the RV enlarges with inspiratory filling, septal motion toward the LV chamber reduces LV filling and results in an accentuated drop in the stroke volume and systemic BP with inspiration (the paradoxical pulse). Central venous pressure is elevated and, since the intrapericardial, and thus intracardiac, pressures are high even at the initiation of diastole, there is no evident y descent in the RA, RV, or LV hemodynamic tracings because the pericardial pressure prevents early ventricular filling. This differs from constriction where most of the initial filling of the RV and LV occurs during early diastole (rapid y descent), and it is only in mid to late diastole that the ventricles can no longer fill. In tamponade, ventricular filling is inhibited throughout diastole. Edema or ascites are rarely present in tamponade; these signs favor a more chronic process.

B. Laboratory Findings

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