Physiologic abnormalities were evaluated by sequential hemodynamic and oxygen transport measurements in 33 patients with acute pancreatitis. The hypotensive crisis, which was defined as the lowest mean arterial pressure (MAP), was used as the common temporal reference point to align the data in a coherent fashion. The data of the 48-hour periods before and after the hypotensive crisis then were evaluated. The patients were divided into normotensive and hypotensive groups and the latter were divided into survivors and nonsurvivors to evaluate the severity of the disorder and to identify the patterns representative of survival and death. The physiologic abnormalities of the hypotensive patients include decreased systemic vascular resistance index (SVRI) and compromised cardiac function. The latter was demonstrated during the hypotensive episode by significantly reduced left ventricular stroke work index (LSWI), despite increases in heart rate (HR), central venous pressure (CVP), pulmonary capillary wedge pressure (WP), and cardiac index (CI). The normotensive group had increased oxygen consumption (Vo2), oxygen delivery (Do2), pulmonary shunt (Qsp/Qt), LSWI, normal SVRI, and high CI. The hypotensive nonsurvivors had lower MAP, LSWI, SVRI, Do, and hematocrit as well as higher pulmonary vascular resistance index (PVRI) and Qsp/Qt than did the survivors. These findings do not support myocardial depression as the primary cardiovascular abnormality in acute pancreatitis, but rather suggest the decreased vascular tone from flow maldistribution in the peripheral microcirculation limits tissue oxygenation in the face of increased metabolic requirements of the hypercatabolic state.