Concepts of the mechanisms of heart failure have changed considerably since the relation between diastolic filling of the left ventricle and its stroke volume began to dominate the thinking of cardiac physiologists. The Frank-Starling "curve" is still respected, and the effect of left ventricular end-diastolic pressure, volume, and myocardial fiber length on the cardiac output is well recognized. This is compatible with the implied therapeutic value of reducing venous return of the failing heart by salt restriction, diuretics, and phlebotomy.
But we appreciate that other factors also play a part in the mechanism of cardiac decompensation and its therapy. One such factor is the contractile state of the myocardium as reflected in the rate of left ventricular pressure development during contraction (dp/dt). This and other measures of myocardial contractility and its responses to inotropic drugs, such as digitalis and isoproterenol, have been investigated extensively during the past decade.