Physiological and pathophysiological implications of ventricular/vascular coupling.
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 other. 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, findings 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.
D001011:Aorta / Q000502:physiology; D001158:Arteries / Q000502:physiology; D001698:Biomedical Engineering; D001775:Blood Circulation / Q000187:drug effects; D003326:Coronary Circulation; D006321:Heart / Q000502:physiology; D006352:Heart Ventricles / Q000187:drug effects; D006801:Humans; D008954:Models, Biological; D005996:Nitroglycerin / Q000494:pharmacology; D014655:Vascular Resistance; D016276:Ventricular Function
D005996:Nitroglycerin