The mechanics of left ventricular contraction in acute experimental cardiac failure.

The effects of acute cardiac failure induced by pentobarbital or pronethalol on the basic mechanical properties of the intact left ventricle were examined in the dog, and the influence on auxotonic and isovolumic contractions of the increase in end-diastolic volume that usually accompanies cardiac failure was assessed. The right heart bypass preparation was employed, and isovolumic beats were induced by sudden balloon occlusion of the aortic root. The ventricular pressure-volume curve was determined directly, and the mechanical responses of the myocardial fibers and contractile elements were calculated.When end-diastolic pressure was held constant, failure reduced the extent of circumferential fiber shortening, and the tension-velocity relation calculated during isovolumic beats was always shifted, with reductions in both maximal velocity (average decrease 30%) and maximal developed tension (average 23%); in addition, during failure achievement of maximal contractile element velocity and maximal tension was delayed, whereas the total duration of contraction was always prolonged. Acetylstrophanthidin tended to reverse all of these changes. When end-diastolic volume was augmented during failure at a constant stroke volume, the extent of circumferential fiber shortening was reduced (3.82 cm to 2.02 cm), and during ejection the fiber and contractile element velocities were diminished at wall tensions comparable to control; maximal velocity and velocity at peak tension were also decreased. The tension-velocity relation during isovolumic beats was shifted by failure with consistent reductions in maximal shortening velocity, but changes in maximal tension were small. Maximal instantaneous power was always reduced by failure, and a striking alteration occurred in the relation between work expended in stretching the series elastic component and the external work; the former, "internal work," increased by an average of 90%, the latter diminished by 11%, and the total contractile element work remained essentially unchanged. These findings are discussed within the framework of a three dimensional model that included fiber length, wall tension, and contractile element velocity. The experimental techniques employed appear to permit a more complete definition of the abnormalities of the ventricular myocardium in experimental failure. They are potentially applicable in the closed-chest animal and allow quantitative determinations of the contractile properties of the left ventricle.