The hemodynamics of cardiac tamponade and constrictive pericarditis.

Abstract This review of the hemodynamic alterations that accompany cardiac tamponade and constrictive pericarditis describes studies carried out in man and in experimental animals. Both constrictive pericarditis and cardiac tamponade increase pulmonary and systemic venous pressure and decrease cardiac output and stroke volume. In cardiac tamponade, the superior and inferior vena caval pressure record shows a single nadir, the x descent; this pressure event is accompanied by an increase in velocity of blood flow and, by inference, in quantity of blood flow. The y descent is absent from the vena caval and right atrial pressure curves, and no early diastolic dip appears in the right ventricular pressure tracing. During inspiration, blood flow velocity and, by inference, forward flow increase in the superior and inferior venae cavae and in the pulmonary artery. Pulsus paradoxus is almost invariably present. The major factors causing pulsus paradoxus are related to inspiratory augmentation of systemic venous return. The ensuing expansion of right-sided heart volume increases intrapericardial pressure, but does not increase systemic arterial pressure and flow until the subsequent expiration. In constrictive pericarditis a peak of blood flow velocity accompanies the x descent of superior vena caval pressure. A second flow velocity peak accompanies the y descent. Respiration fails to alter superior vena caval pressure or blood flow velocity, but during inspiration the velocity of pulmonary arterial blood flow increases. Pulsus paradoxus occurs much less often than in cardiac tamponade, and its mechanism is not well understood. Atrial fibrillation is common, and myocardial contractility is impaired.