Abstract
The purpose of this paper is to consider “ideal” ventricular/vascular coupling, and how this may be manifest in the time domain and in the frequency domain. The paper will also consider how such “ideal” coupling is achieved, and how it might be disturbed. The arterial system plays a crucial role in ventricular/vascular coupling since it separates the smallest vessels where flow is almost perfectly continuous from the ventricle, whose output is intermittent. Ventricular/vascular coupling can be assessed from measurements of pressure and flow in the ascending aorta (AA) (for left ventricle/systemic circulation), and in the main, pulmonary artery (MPA) (for right ventricle/pulmonary circulation). Ideal coupling is manifest as low pressure fluctuation in AA and MPA. Low pressure fluctuation results in pressure during systole being only slightly greater than pressure throughout the whole cardiac cycle, and pressure during diastole being only slightly less. This is desirable because pressure during systole determines ventricular output (when inotropic state and ventricular filling are constant), and ventricular metabolic requirement, while pressure during diastole in AA is a major determinant of coronary blood flow. In the frequency domain, “ideal” coupling is manifest as a correspondence between minimal values of impedance modulus in AA and MPA with maximal values of flow harmonics in AA and MPA, respectively. Factors responsible for “ideal” coupling have been identified as high distensibility of proximal arteries (with decreasing distensibility in peripheral arteries), wave reflection at arterial terminations, and a “match” between heart rate on the one hand and arterial length and wave velocity on the orther. This favourable “match” results in the heart operating for both systemic and pulmonary circulations close to a node of pressure and antinode of flow; this match is improved under conditions which simulate flight and fight. While ventricular/vascular coupling appears to be close to ideal in most large mammals, it appears to be less than ideal in adult humans and some small mammals including guinea pigs, rats, and mice. The cause for mismatch in small mammals is unclear. In humans however, finding are attributable to progressive arterial degeneration which is known to commence in childhood and is apparent in the elderly as dilated tortuous arteries, high pulse pressure, and high likelihood of developing ventricular failure.
Similar content being viewed by others
References
Avolio, A.P., M.F. O'Rourke, K. Mang, P.T. Bason, and B. Gow. A comparative study of pulsatile arterial hemodynamics in rabbits and guinea pigs.Am. J. Physiol. 230:868–875, 1976.
C.G. Caro, and D.A. McDonald. The relation of pulsatile pressure and flow in the pulmonary vascular bed.J. Physiol. 157:426–453, 1961.
Feldman, R.L., C.J. Pepine, and C.R. Conti. Magnitude of dilation of large and small coronary arteries by nitroglycerin.Circulation 64:324–333, 1981.
Fitchett, D.H. The effects of nitroglycerin on forearm arterial compliance.J. Clin. Invest. Med. 5(Suppl. 1):31, 1982.
Gregg, D.E., E.M. Khouri, and C.R. Rayford. Systemic and coronary energetics in the resting dog.Cir. Res. 16:102–113, 1965.
Hales, S.Statical essays, 3rd Edition. London: Wilson and Nichol, 1769, pp. 22–23.
Harvey, W.De motu cordis et sanguinis in animalibus. Frankfurt: Willus Fitzer, 1628. p. 12.
Kannel, W.B., W.P. Castelli, P.M. McNamara, P.A. McKee, and M. Feinleib. Role of blood pressure in the development of congestive heart failure. The Framingham study.N. Engl. J. Med. 287:781–787, 1972.
McDonald, D.A.Blood Flow in Arteries. London: Arnold, 1974, p. 176.
Nichols, W.W., C.R. Conti, W.W. Walker, and W.R. Milnor. Input impedance of the systemic circulation in man.Circ. Res. 40:451–458, 1977.
O'Rourke M.F. Steady and pulsatile losses in the systemic circulation under normal conditions and in simulated arterial disease.Cardiovasc. Res. 1:313–326, 1967.
O'Rourke, M.F. Impact pressure, lateral pressure and impedance in the proximal aorta and pulmonary artery.J. Appl. Physiol. 25:533–541, 1968.
O'Rourke, M.F.Arterial Function in Health and Disease. Churchill: Edinburgh, 1982, pp. 153–169.
O'Rourke, M.F. Vascular impedance in studies of arterial and cardiac function.Physiol. Rev. 62:570–623, 1982.
O'Rourke, M.F., and M.G. Taylor. Vascular impedance of the femoral bed.Circ. Res. 18:126–139, 1966.
O'Rourke, M.F., and M.G. Taylor. Input impedance of the systemic circulation.Circ. Res. 20:365–380, 1967.
Sarnoff, S.J., E. Braunwald, G.H. Welch, W.N. Stainsby, and R. Macruz. Hemodynamic determinants of oxygen consumption of the heart with special reference to the tension-time index.Am. J. Physiol. 192:148–156, 1958.
Simon, A.C., J.A. Levenson, B.Y. Levy, J.E. Bouthier, P.P. Peronneau, and M.E. Safar. Effects of nitroglycerin on peripheral large arteries in hypertension.Br. J. Clin. Pharmacol. 14:241–246, 1982.
Taylor, M.G. An approach to an analysis of the arterial pulse wave: I. Oscillations in an attenuating line.Phys. Med. Biol. 1:258–269, 1957.
Taylor, M.G. An approach to an analysis of the arterial pulse wave: II. Fluid oscillations in an elastic pipe.Phys. Med. Biol. 1:321–329, 1957.
Taylor, M.G. An experimental determination of the propagation of fluid oscillations in a tube with a visco-elastic wall, together with the characteristics required in an electrical analogue.Phys. Med. Biol. 4:63–82, 1959.
Taylor, M.G. Wave travel in arteries and the design of the cardiovascular system. InPulsatile Blood Flow edited by E. Attinger. Philadelphia: McGraw, 1965, pp. 343–372.
Taylor, M.G. Wave travel in a non-uniform transmission line, in relation to pulses in arteries.Phys. Med. Biol. 10:539–550, 1965.
Taylor, M.G. The input impedance of an assembly of branching elastic tubes.Biophys. J. 6:29–51, 1966.
Taylor, M.G. The elastic properties of arteries in relation to the physiological functions of the arterial system.Gastroenterology 52:358–363, 1967.
Wikman-Coffelt, J., W.W. Parmley, and D.T. Mason. The cardiac hypertrophy process: Analysis of factors determining pathological vs. physiological development.Circ. Res. 45:697–707, 1979.
Womersley, J.R. Oscillatory flow in arteries; the reflection of the pulse wave at junctions and rigid inserts in the arterial system.Phys. Med. Biol. 2:313–323, 1958.
Yaginuma, T., J. Morgan, P. Roy, D. Baron, M. Feneley, J. Branson, A. Avolio, and M. O'Rourke Mechanism of nitroglycerin action in human adults without heart failure: A new hypothesis.Aust. NZ J. Med. 13:418, 1983.
Young, T. Hydraulic investigations subservient to an intended Croonian lecture on the motion of the blood.Philos. Trans. R. Soc. London 98:164–186, 1808.
Yin, F., P. Guzman, K. Brin, W. Maughan, J. Brinkler, T. Trail, J. Weiss, and M. Weisfeldt. Effect of nitroprusside on hydraulic vascular loads on the right and left ventricle of patients with heart failure.Circulation 67:1330–1339 1983.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
O'Rourke, M.F., Yaginuma, T. & Avolio, A.P. Physiological and pathophysiological implications of ventricular/vascular coupling. Ann Biomed Eng 12, 119–134 (1984). https://doi.org/10.1007/BF02584226
Issue Date:
DOI: https://doi.org/10.1007/BF02584226