Left Ventricular Afterload and Aortic Input Impedance: Implications of Pulsatile Blood Flow

T HE function of the heart is to pump a sufficient amount of blood through the arterial system to tissues to meet their metabolic requirements. When metabolic needs of tissues change (e.g., during exercise), the heart must adjust its output (i.e., change its function) to meet these needs. Cardiac output is adjusted through changes in one or more of four principal factors that determine myocardial function. These are preload (ventricular end-diastolic fiber length or volume), myocardial contractility (change in force of contraction without a change in initial fiber length), afterload (external factors opposing fiber shortening and ventricular ejection), and heart rate. In pump failure, alterations occur in these determinants of myocardial function that result in an inappropriate reduction in cardiac output. Improving ventricular emptying to enhance depressed cardiac output and relieving pulmonary congestion are fundamental objectives of heart failure therapy. Conventional treatment of pump failure has focused primarily on increasing cardiac output by changing ventricular volume (Frank-Starling mechanism) or by administering direct-acting positive inotropic agents. These methods of increasing cardiac output may increase myocardial oxygen demands, which is potentially detrimental in ischemic heart disease. Recently, a different approach has been taken to augment the depressed cardiac output. Isolated papillary muscle studies demonstrated the importance of “afterload” change on myocardial contraction.lm3 These studies showed that the lower the load placed on the muscle, the greater the velocity and extent of shortening during contraction (i.e., load is inversely related to shortening). In these isotonically contracting papillary muscle experiments, afterload is a weight that the muscle lifts during shortening. In this type of experiment, afterload is linearly related to the developed force. In extrapolating papillary muscle studies to the intact ventricle, an attempt has been made to utilize the same terminology; however, this practice poses a difficult problem. From isolated papillary muscle studies it would seem reasonable to use instantaneous ventricular wall force or stress as a measure of afterload during ejection. This calculation, obtained from measurements of ventricular pressure and geometry, changes constantly during ejection.4’5 Some investigators believe that this approach may not provide an adequate estimate of afterload since the ventricle pumps a pulsatile blood flow into a viscoelastic arterial system. Therefore, a consideration of pulsatile pressure-flow relations (aortic input impedance) as a measure of ventricular afterload has been proposed.6*7 The concept that aortic input impedance can represent the external load of the left ventricle is not new, The idea was proposed by Pate1 et al.* in 1963 in the first detailed study of input impedance of the ascending aorta and pulmonary artery of the dog. One argument in favor of using aortic input impedance as left ventricular afterload is that the physical properties of the arterial system are constant during ejection and do not depend on cardiac function, which is not the case for wall stress or intraventricular pressure. In this article we will review myocardial function and afterload in isolated papillary muscle experiments and discuss the concept of load in the intact ventricle, with emphasis on aortic input impedance.