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This Article Full Text Full Text (PDF) All Versions of this Article: 293/2/H1164    most recent 00133.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Mohiuddin, M. W. Articles by Quick, C. M. Search for Related Content PubMed PubMed Citation Articles by Mohiuddin, M. W. Articles by Quick, C. M.

Increase in pulse wavelength causes the systemic arterial tree to degenerate into a classical windkessel

Michael E. DeBakey Institute, Texas A&M University, College Station, Texas

Submitted 1 February 2007 ; accepted in final form 30 April 2007

Two competing schools of thought ascribe vascular disease states such as isolated systolic hypertension to fundamentally different arterial system properties. The "windkessel school" describes the arterial system as a compliant chamber that distends and stores blood and relates pulse pressure to total peripheral resistance (R_tot) and total arterial compliance (C_tot). Inherent in this description is the assumption that arterial pulse wavelengths are infinite. The "transmission school," assuming a finite pulse wavelength, describes the arterial system as a network of vessels that transmits pulses and relates pulse pressure to the magnitude, timing, and sites of pulse-wave reflection. We hypothesized that the systemic arterial system, described by the transmission school, degenerates into a windkessel when pulse wavelengths increase sufficiently. Parameters affecting pulse wavelength (i.e., heart rate, arterial compliances, and radii) were systematically altered in a realistic, large-scale, human arterial system model, and the resulting pressures were compared with those assuming a classical (2-element) windkessel with the same R_tot and C_tot. Increasing pulse wavelength as little as 50% (by changing heart rate –33.3%, compliances –55.5%, or radii +50%) caused the distributed arterial system model to degenerate into a classical windkessel (r² = 0.99). Model results were validated with analysis of representative human aortic pressure and flow waveforms. Because reported changes in arterial properties with age can markedly increase pulse wavelength, results suggest that isolated systolic hypertension is a manifestation of an arterial system that has degenerated into a windkessel, and thus arterial pressure is a function only of aortic flow, R_tot, and C_tot.

mathematical modeling; hemodynamics; hypertension; input impedance