Dependance of Oxygen Delivery on Hematocrit

Abstract

Oxygen delivery (DO₂) is derived from arterial oxygen content and cardiac output. DO₂ does, however, not directly correlate with changes of hematocrit since the latter affects cardiac output by virtue of its influence on blood viscosity and hence viscous resistance to flow. At normal pulmonary function linear increments of hematocrit increase arterial oxygen content, nevertheless, DO₂ tends to fall during hemoconcentration and polycythemia as result of reduced venous return and stroke volume respectively. Despite low cardiac output, low flow velocity and due to prolonged transit of the red cells through the capillary network tissue oxygenation can be preserved. On the other hand, reduction of oxygen content by hemodilution (low hematocrit while maintaining normal blood volume) similarly preserves adequacy of tissue oxygenation, however, by opposite mechanisms, namely increase of cardiac output and organ blood flow on account of reduced blood viscosity, lowered total peripheral resistance and augmented venous return. These beneficial effects of dilutional anemia are enhanced by augmented cardiac contractility and increased venomotor tone. Compensating mechanisms in acute dilutional anemia are the rise of cardiac output, enhancement of blood oxygen extraction and maintenance of adequate mixed venous PO₂. The net effect on oxygen tissue delivery depends further on physiological and interventional factors, e.g. redistribution of cardiac coutput, angioarchitectonic organ differences, effect of diluents on corpuscular and plasma components (RBC fluidity and plasma viscosity) and local adjustment of the cross-sectional area of the microvascular network.