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 ( r 2 = 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 Address for reprint requests and other correspondence: C. M. Quick, Michael E. DeBakey Institute, M. S. 4466, Texas A&M Univ., College Station, TX 77843-4466 (e-mail: cquick{at}tamu.edu )