Hemodynamic consequences of hemodilution
The hemodynamic alterations following hemodilution for extracorporeal circulation are almost entirely the result of changes in blood viscosity. Although these changes unequivocally improve quality of perfusion, they also pose special problems after perfusion. For present purposes hemodilution describes acute normovolemic anemia at a hematocrit not less than 20%.
The well known relationship between mean arterial blood pressure, systemic vascular resistance and cardiac output (MAP = SVR × CO) assumes blood viscosity to remain constant. The true relationship is expressed as MAP = viscosity × vascular resistance × cardiac output. Among the major determinants of blood viscosity are hematocrit and temperature. Unfortunately, simple quantitative relationships cannot be drawn between these since blood viscosity is highly dependent on blood flow velocity (shear rate) which rises with vessel size. The smaller the vessel, the slower the blood velocity and the higher the viscosity. A reasonable approximation of the direct relationship between viscosity and hematocrit is that they change proportionately. A 50% decrease in hematocrit is associated with approximately 50% decrease in viscosity.On the other hand, viscosity is inversely related to tempertature and the proportionality is not so uniform. As an approximation, a 10-C decrease in temperature increases blood viscosity by 20% to 25%.
Among the clinical implications of these physical phenomena, one particularly applies to induced hypothermia. To maintain viscosity constant during induced hypothermia to 20 C, hematocrit would have to be reduced from 45% to approximately 25%. Failure to hemodilute leads to increased resistance to flow by increased viscosity with an approximate . . .