Abstract
The circulation is designed for oxygen and carbon dioxide transport by the blood. Red cells collect oxygen in the lungs and carry it to the capillaries of the heart, brain and other tissues where it is metabolised. Physiological studies show that oxygen supply may be blood flow limited, but the role of blood rheology is ill-defined. This report outlines a simple cardiovascular model in which available hemodynamic and rheological data are embodied. Steady state transport optimisation data are calculated for the poorly compensated circulation assuming various ratios between capillary and systemic blood hematocrit. Limitations are defined and capillary perfusion velocity calculated for cardiac output-modulated flow through a typical bed at constant perfusion pressure. Oxygen tension profiles are predicted using the Krogh cylinder model. Tissue PO2 becomes a function of the systemic hematocrit and the capillary-systemic hematocrit ratio, being almost constant for hematocrits from 10–40% with a potentially lethal fall-off above about 50%.
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