Pulmonary edema is a potentially fatal complication of β-sympathomimetic therapy for premature labor. Isolated case reports have supported either primary pulmonary capillary membrane injury or left ventricular failure as the cause of pulmonary edema. By simultaneously monitoring cardiac function and extravascular lung water in six control and six ritodrine hydrochloride-treated pregnant baboons, we attempted to define this pathophysiology. The pulmonary capillary wedge pressure increased in treated animals, reaching significance at 16 hours of ritodrine treatment (p < 0.0001) concurrent with the maximum increase in cardiac index (p = 0.02). Treated animals also retained 61% of intravenously administered fluids compared with 23% in untreated control animals (p < 0.002). There were, however, no significant differences between groups in extravascular lung water, central venous pressure, or pulmonary artery pressure. Chest radiographs and arterial blood gas analysis were also comparable between ritodrine-treated and control animals. Fluid retention and elevated hydrostatic pressure are postulated as the etiology of β-sympathomimetic-induced pulmonary edema. There was no evidence to support a primary pulmonary capillary membrane injury by ritodrine.