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  • Title: Implications of calculated intravascular volume changes upon atherosclerotic cardiovascular disease.
    Author: Blankfield RP.
    Journal: Clin Hemorheol Microcirc; 2008; 38(2):75-81. PubMed ID: 18198408.
    Abstract:
    There is evidence that changes in intravascular volume influence long-term cardiovascular events, and that this effect is independent of blood pressure. Using the Poiseuille-Hagen equation for laminar flow through a cylinder, assuming that blood pressure remains unchanged despite any change in intra-arterial volume, and assuming that blood in the large arteries has a constant viscosity, then it can be shown that the rate of arterial blood flow changes according to the equation Q2=Q1[1+(DeltaV/V TI)]2, where Q1 represents the original rate of flow, Q2 represents the new rate of flow, DeltaV represents the change in intra-arterial volume, and V(TI) represents the total intra-arterial volume. Furthermore, if one is willing to extrapolate from a single artery to the entire circulatory system, such that Q1 represents the initial cardiac output, Q2 represents the new cardiac output, DeltaV represents the change in intravascular volume, and V(TI) represents the total intravascular volume, then it can be demonstrated that even small changes in intravascular volume have hemodynamic consequences. Specifically, an intra-arterial volume change of 2.7 cc will alter cardiac output by approximately 1% in the average human, with hemodynamic consequences comparable to a 1 mm change in the mean arterial pressure. The calculations in this paper suffer from a number of weaknesses, and there are justifiable reasons to consider the assumptions and extrapolations employed in this paper to be invalid or overly simplistic. Despite these limitations, the primary rationale for believing the assumptions and extrapolations to have merit is that the conclusions that result are consistent with, and help explain, a considerable amount of current research literature. Based upon these calculations, even small changes in intravascular volume would be expected to change the pressure on endothelial cells at arterial branch points and bifurcations, thereby influencing the development of atherosclerosis.
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