The effects of positive end-expiratory pressure (PEEP) at 5, 10, 15, and 20 cm H2O on the distribution of ventilation-perfusion (VA/Q) ratios was determined in four normal dogs and in ten with oleic acid-induced acute hemorrhagic pulmonary edema. Tidal volume and frequency were held constant at all times with mechanical ventilation during intravenous pentobarbital and gallamine anesthesia. Normal dogs had little or no shunt, and no areas of low (less than 0.1) or high VA/Q (greater than 10.0) at zero end-expiratory pressure (intermittent positive-pressure breathing). In these animals increasing PEEP caused progressive depression of cardiac output, associated with an increase in ventilation to both high VA/Q and unperfused regions. PEEP greater than or equal to 10 cm H2O resulted in a reduction in Pao2 and an increase in PaCO2. In dogs with pulmonary edema, PEEP's of 5 and 10 cm H2O resulted in dramatic reductions in shunt, virtual obliteration of low VA/Q regions, and market improvement in Pao2. However, at 15 and 20 cm H2O PEEP's high VA/Q and dead space ventilation with CO2 retention again developed in all but the most severely affected (shunt greater than 40%) dogs.