Contractile State of the Heart Characterized by Force‐Velocity Relations in Variably Afterloaded and Isovolumic Beats

Relations between tension and the velocity of shortening in the intact left ventricle of the dog were examined in a manner analogous to that employed in isolated muscle, i.e., by serial, reproducible variations in the afterload alone, from a constant end diastolic volume. Sudden increases or decreases in the aortic pressure during diastole were produced, and ejection rate was measured with an electromagnetic flowmeter; LV wall tension and the shortening velocities of the myocardial fibers and the contractile elements were then calculated. By analyzing isovolume points early in ejection, effects resulting from two other determinants of shortening velocity, duration of active state and instantaneous muscle length, were minimized. Shifts in the basic force-velocity relation with alterations in Vmax, obtained by extrapolation, and maximum tension were clearly demonstrated. Norepinephrine and paired electrical stimulation caused a shift in this relation to the right, with increases in velocity at any tension, and acute heart failure produced a shift to the left, with decreases in velocity at any tension. Similar shifts were also apparent in curves relating tension to velocity, calculated during single isovolumic contractions. It was suggested that determination of these relations expands traditional definitions of ventricular performance, and that estimation of changes in maximum velocity as well as maximum strength relative to muscle length provides direct information concerning alterations in the contractile state of the intact heart.