Abstract
Previous work has demonstrated that approximately one-third of patients with pneumonia have a hypodynamic circulatory response. This response is characterized by an abnormally wide arteriovenous oxygen difference, a low cardiac output, increased peripheral resistance, and an increased hematocrit. This state was found to abate in convalescence. In an attempt to elucidate the pathogenesis of this hypodynamic state, nine additional patients were studied hemodynamically during the acute phase of pneumonia before and during acute expansion of blood volume by low molecular weight dextran (seven patients) or normal saline (two patients). Five patients were restudied before and during acute blood volume expansion in convalescence. Three patients with pneumonia had a normal arteriovenous oxygen difference (< 5.5 vol%), and six patients were hypodynamic in that their arteriovenous oxygen differences were greater than 5.5 vol%. With expansion of blood volume in the acute phase of pneumonia, all patients showed an increase in cardiac output, a decrease in arteriovenous oxygen difference, and a decrease in peripheral vascular resistance; however, the percentage change in the hypodynamic patients was not as great as occurred in the patients with normal hemodynamics nor as great as occurred when restudied in convalescence. Likewise, all patients had a normal or near normal hemodynamic profile in convalescence. In addition, ventricular function in the acute phase of pneumonia was depressed. The findings suggest that the hypodynamic state associated with acute pneumonia is due to depressed myocardial contractility to which relative hypovolemia may contribute.