Tissue perfusion during normovolemic hemodilution investigated by a hydraulic model of the cardiovascular system.
Normovolemic hemodilution on a whole body basis is studied by means of a steady flow, hydraulic analogue simulation of the cardiovascular system, based on the Casson's model and current hemodynamic and rheological data. The vasculature is divided into serially connected compartments whose hydraulic resistance is characterized by the average diameter, length, number of vessels, and the corresponding rheological properties of blood formulated by Dintenfass (1971) and Lipowsky et al. (1980). This model computes the pressure distributions in all compartments, where the calculated venous pressure modulates the cardiac function according to the Starling mechanism for cardiac performance. The alterations of flow induced by the action of the heart are added to the effects due to changes in peripheral vascular resistance as a result of hematocrit variation. This model shows that when the response of heart to the changes of venous pressure is impaired, the maximum oxygen carrying capacity occurs at 40% hematocrit (H) where it is 1% higher than normal hematocrit (H = 44%). The normal cardiac response to the changes of venous pressure, causes the maximum oxygen carrying capacity to occur at 32% H where it is 12% greater than that at normal hematocrit. Mean arteriolar pressure and capillary pressure increase while venular pressure is slightly reduced during normovolemic hemodilution.
D001794:Blood Pressure; D002302:Cardiac Output; D002306:Cardiac Volume; D002319:Cardiovascular System; D003327:Coronary Disease / Q000097:blood / Q000503:physiopathology; D006400:Hematocrit; D006438:Hemodilution; D008955:Models, Cardiovascular; D010100:Oxygen / Q000097:blood*; D010477:Perfusion; D014018:Tissue Distribution; D014690:Venous Pressure
D010100:Oxygen