Hemodynamic and O2 transport effects of ketamine anesthesia were evaluated in 22 critically ill patients. After placement of radial and pulmonary artery catheters, simultaneous measurement were made of cardiac output, intravascular pressures, arterial and mixed venous gases, saturations, pH, and Hct; cardiorespiratory values then were calculated for a preinduction control period and sequentially at frequent intervals over a 15-min observation period. In general, there was an early progressive increase in HR, cardiac index (CI), arterial and venous pressures, stroke work, and O2 delivery (DO2); O2 consumption (VO2) and O2 extraction (O2 Ext) decreased. In general, ketamine produced an inotropic cardiac response, but these responses were not uniform; a relatively small percentage had reduced pressures, flow, and reduced myocardial performance that were related to hypovolemia and associated medical conditions.