Critical Arterial Stenosis Revisited
archie, j. p.
Show abstract
IntroductionStenosis of an organ/tissue primary artery can produce ischemia or only reduce blood flow reserve. Despite incomplete hemodynamic understanding of critical arterial stenosis, degree of diameter stenosis continues to be an index for patient management. This study aims to use the law of conservation of energy to quantitate the arterial pressure gradient produced by stenosis, determine organ/tissue perfusion pressure, blood flow and reserve as a function of degree of diameter stenosis and determine ischemic critical diameter stenosis. MethodsThe three-component model is parallel stenotic artery and collateral arteries supplying an organ/tissue. The three hemodynamic variables are blood pressure, blood flow and frictional percent diameter stenosis. Two new non-dimensional variables, K and C, are introduced to simplify understanding. K is the magnitude of arterial diameter stenosis produced energy dissipation. C is the magnitude of potential collateral blood flow. Conservation of energy analysis of arterial stenosis gives the pressure gradient produced and stenosis vascular resistance. Organs/tissues intrinsically autoregulate blood flow when perfusion pressure is greater than threshold value. Model energy analysis defines collateral vascular resistance and gives perfusion pressure, blood flow and reserve as a function of diameter stenosis. Results are illustrated in both pressure-stenosis domain and blood flow-stenosis domain. Renal and internal carotid artery (ICA) stenosis numerical results are in cm/gram/sec (CGS) units. ResultsThe magnitude of arterial stenosis energy dissipation is proportional to K, a fourth power function of stenosis diameter with a steep slope between 65% and 80%, (K = 67 to 625). Organs/tissues without collaterals, C = 0, have specific critical arterial stenosis values within this range. For a renal artery with average diameter and blood flow critical stenosis is 74% (K = 233). Organ tissues with collateral blood flow potential equal to their normal resting blood flow have C = 1.0. Those with poor collaterals, C < 1, have critical stenosis from 65% to 99% depending on collateral magnitude, 0 < C < 1. In this group critical ischemic ICA stenosis begins at 70% and up to 99%, (K = 132 to {infty}). Organ/tissues with good collateral circulation, C > 1, do not have ischemic critical stenosis, including the ICA. However, in these patients stenosis progression reduces blood flow reserve. ConclusionArterial stenosis may or may not produce an ischemic critical value for specific organ/tissue supplied depending on the magnitude of collateral circulation.
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