Pericardiocentesis

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18 Pericardiocentesis

Cardiac tamponade is a life-threatening disorder that can result from any condition that causes a pericardial effusion. Although the most frequent cause is malignancy, tamponade may also occur from pericarditis (e.g., viral, uremic, inflammatory, or idiopathic), aortic dissection (with disruption of the aortic annulus), or ventricular rupture from myocardial infarction. In the cardiac catheterization laboratory, tamponade can result as a complication of a variety of invasive procedures and lead to rapid demise of the patient due to the swift accumulation of fluid in a poorly compliant pericardial space. Prompt recognition of the salient hemodynamic features and immediate pericardiocentesis are essential to the successful treatment of cardiac tamponade. The rate of pericardial fluid accumulation relative to the stiffness of the pericardium determines how quickly the clinical syndrome of tamponade will occur. Figure 18-1 shows a normal pericardial membrane and the mechanisms of pericardial tamponade.

Diagnosis of Tamponade

The hemodynamic effects of a pericardial effusion may be acute or gradual, depending on the amount and rate of fluid accumulation. Normally, the pericardial space contains 15 to 50mL of fluid with an intrapericardial pressure that approximates intrapleural pressure (−5 to +5cm H2O). Fluid accumulation and pericardial restraint lead to rises in intrapericardial pressure. Tamponade occurs when intrapericardial pressure exceeds intracardiac pressure, leading to impaired ventricular filling, increases in pulmonary venous and jugular venous pressures, and reduction in forward stroke volume. During interventional procedures, tamponade may be signaled by hypotension. Tachycardia, which usually occurs, may not be present in patients receiving beta blockers. A high index of suspicion of tamponade should accompany any procedure in which a distal guidewire position appears unusual or in which oversized stents are used. All procedures with rotational atherectomy have a higher incidence of perforation and subsequent tamponade.

Hemodynamics

The invasive hemodynamic hallmarks of cardiac tamponade include pulsus paradoxus on the arterial tracing (Fig. 18-3) and prominent x descents and blunted y descents in the atrial pressure tracings (Fig. 18-4). Preservation of the x descent occurs because of the decrease in intracardiac volume during systolic ejection, which leads to a temporary reduction in intrapericardial and right atrial pressures (See Kern (2011) The Cardiac Catheterization Handbook 5th ed., Chapter 3 Hemodynamics). Elevated intrapericardial pressure impairs ventricular filling during the remainder of the cardiac cycle, resulting in blunting of the y descent. In patients with cardiac tamponade, the driving pressure to fill the left ventricle falls during inspiration. Consequently, there is a reduction in left ventricular filling and stroke volume, which manifests as a decrease in aortic pulse pressure during inspiration in a manner analogous to the bedside finding of pulsus paradoxus (see Fig. 18-3).

On relief of pericardial pressure and removal of the effusion, right atrial pressure and pericardial pressure fall usually to normal values if no residual pericardial disease is present (Fig. 18-5). However, in some cases, although pericardiocentesis empties the pericardial space and pericardial pressure falls to near zero, right atrial pressure may be unaffected, signifying the syndrome of effusive-constrictive pericardial disease (Fig. 18-6).

Cardiac tamponade should be suspected in any patient in the cardiac catheterization laboratory with unexplained hypotension, elevated venous pressure, and a compatible history. Unusual manifestations also can occur. Tamponade may occur without elevated jugular venous pressure because of low intracardiac filling pressures (i.e., low-pressure tamponade), such as in dehydrated patients with malignant effusions. Localized tamponade can result from loculated pericardial effusions, such as those that may be present adjacent to the atria in the postoperative setting. Of note, pericardiocentesis should not be performed in patients with tamponade and aortic dissection. In such patients, relief of the tamponade will lead to an abrupt increase in systolic blood pressure that may exacerbate the aortic dissection. Careful imaging with transthoracic or transesophageal echocardiography is required to determine the presence of these manifestations of tamponade.

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