Effect of Afterload on Force-Velocity Relations and Contractile Element Work in the Intact Dog Heart
The effects of heightened afterload on force-velocity relations and on contractile element work of single systoles were examined in the intact dog heart. The force-velocity curve described during the course of a normal systole represents a composite of curves, each with its own projected isometric force determined by instantaneous changes in fiber length. During the first systole following an afterload intervention, reciprocal changes in force and velocity were observed together with an extension of the projected isometric-force.
The effect of afterload on contractile element work was determined by: (1) the direction and magnitude of the afterload, and (2) the afterload of the control beat itself. When the control beat was lightly loaded, an increase in afterload increased contractile element work by two additive mechanisms: (1) an increase in mean isometric force, and (2) a shift of force-velocity relations to positions of greater power and work production. In normally loaded control beats, an increase in afterload resulted in a decrease in contractile element work, despite the fact that mean isometric force was increased. In this instance, force-velocity relations were shifted to positions where less power and work could be achieved. Thus, the normal systole appears to function at the apex of the contractile element work-load curve (near 60% of the isometric load).
Evidence is presented which suggests that the apparent maximum active state of the entire left ventricle is generally achieved within 30 to 50 msec after the onset of pressure rise, and that its decay is accompanied by abrupt divergence of the force-velocity relations from the inverse curve of that beat. A sudden increase in afterload does not appear to influence the duration of the maximum active state, although the duration of positive contractile element work is shortened and that of negative contractile element work prolonged.
- Accepted December 13, 1965.
- © 1966 American Heart Association, Inc.