EFFECTS OF ALTERED HEMATOCRIT ON PULMONARY-ARTERY PRESSURE-FLOW CHARACTERISTICS IN CANINE PULMONARY-EMBOLISM

We used the relationship between mean pulmonary artery pressure (PAP) and cardiac output (CO) to investigate pulmonary hemodynamic effects of altered hematocrit in an intact canine model of embolic pulmonary hypertension. The slope of the PAP-CO relationship defines the incremental vascular resistance OR) and the extrapolated pressure intercept (P1) represents the effective vascular outflow pressure. Injection of autologous clot did not affect ventricular filling pressures, but decreased CO (from 3.1 to 1.9 l/min-1, P < .01) and markedly increased PAP, from 15 to 35 mm Hg (P < .01). In this setting isovolemic exchange transfusion decreased Hct from 42% to 21 % (P < .01) and markedly improved pulmonary hemodynamics. Since P1 was unaffected, this improvement was entirely explained by a decrease in the incremental vascular resistance. Hemodilution decreased IR by 25% from 4.4 to 3.3 mm Hg/l-1 /min (P < .05). We conclude that in this canine model of embolic pulmonary hypertension a decrease in viscosity significantly alters pulmonary hemodynamics by decreasing the slope of the pressure-flow relationship. These findings do not address the clinical implications of hemodilution on systemic oxygen delivery. © 1990.