Positive end-expiratory pressure is thought to improve oxygenation in patients with adult respiratory distress syndrome (ARDS) by recruiting alveoli to augment a decreased functional residual capacity. At high levels, typically >10 cm H2O, positive end-expiratory pressure may have deleterious hemodynamic effects. Positive end-expiratory pressure may decrease cardiac output, and therefore oxygen delivery, by reducing right and left ventricular preload, decreasing ventricular compliance, and increasing right ventricular afterload (1). Positive end-expiratory pressure can increase right ventricular afterload by increasing the pulmonary vascular resistance (2–5). As lung volume increases, the alveoli become more distended, compress the alveolar capillary bed, and increase the pulmonary vascular resistance. A decrease in Pao2with an increase of positive end-expiratory pressure has been described in the setting of unilateral lung disease, where positive end-expiratory pressure overdistends the more compliant lung and redirects blood flow to the diseased lung (6, 7).