Abstract

A normal artery can serve as a conduit for many times the resting flow without significant loss of energy or production of murmurs. In such vessels, the rate of flow is determined primarily by the peripheral vascular conductance (rate of flow/drop in pressure) rather than by the characteristics of the artery. In a system of vessels connected in series, the rate of flow is limited by the segment of lowest conductance. Thus, when the conductance of the peripheral vascular bed is low, a partially stenotic lesion has no effect on the rate of flow. When an arteriovenous fistula or an increase in metabolic activity markedly increases the delivery through an arterial narrowing, the stenotic segment becomes the limiting factor, and a systolic bruit indicates that the stream is no longer laminar. Thus, a murmur is the announcement that the caliber of a vessel or valve is inadequate to provide for laminar flow. With further increases in peripheral vascular conductance and rate of flow, the murmur increases in intensity, pitch, and duration. Cross flow is minimal in an anastomosis between two parallel arteries which deliver blood to separate vascular beds of equal conductance. If a stenosis is present in one of the arterial roots, blood will shunt from the normal vessel to the vascular bed of the narrowed vessel. If the stenosis is severe, the deviation of blood will be marked and the tissues normally supplied by the normal vessel will become ischemic (steal syndrome). The interaction (hydrodynamic drag) of the stream with the vessel wall determines vascular caliber. Laminar streams interact normally with the wall. The separation of the stream lines from the wall at the downstream lip of a stenotic orifice produces a locus at which stream-wall interaction is minimal, with the result that the narrowing becomes progressively marked. In the poststenotic segment, turbulence increases the interaction of stream and wall, and stimulates a localized enlargement (poststenotic dilatation).

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