The contractile behavior of the heart and its functional coupling to the circulation

Abstract

The integrated function of the heart and lungs provides for the transfer of O 2 from the atmosphere, for its delivery to the metabolizing tissues, and for the removal of CO 2. When cardiac output is compromised as in heart failure, a series of reflexive and neurohumoral adjustments follow with activation of the adrenergic and renin-angiotensin systems. The resultant vasoconstriction constrains the performance of the failing heart. Accordingly, vasodilators have been used to attenuate this vasoconstriction and to improve cardiac performance in patients with cardiac failure. An understanding of the physiologic consequences of vasodilation, as well as the selection of the most appropriate vasodilator for these patients, requires an understanding of the contractile behavior of the normal and failing heart and of the factors that regulate their performance. Because the myocardium is composed largely of cardiac muscle, muscle force, length, and shortening are used to describe its contractile behavior. Myocardial contractile behavior is a function of: (A) instantaneous shortening load, or the ejection force (afterload), which the muscular wall has to support during its contraction; (b) shortening length; and (c) myocardial contractile state. The failing myocardium characteristically has both a depressed contractile state and an abnormal shortening load. In order to describe the functional coupling of the heart to its arterial and venous circulations, the concept of a mechanical pump having elastic and resistive properties is used. These mechanical properties of the pump determine its ability to generate pressure and flow. Unlike the normal heart, the failing pump with its decreased elastance (i.e., increased volume at normal chamber pressure) is more sensitive to vascular loading, and hence its more favorable response to vasodilators. Finally, the performance of the heart is determined by the coordination and integration of the right and left hearts that result from their anatomical arrangement and the mobile interventricular septum, the pericardium, and the pleural pressure surrounding the heart and lungs. Vasodilators improve the pump function of the failing heart by reducing ventricular interaction and by augmenting chamber distensibility. The consequences of pharmacologic vasodilation in heart failure, then, can best be appreciated by understanding the intrinsic properties of cardiac muscle, the functional coupling of the heart to the arterial and venous circulations, the interplay between ventricles, and the interaction of the heart with its pericardium and with pleural pressure.