Effect of heart rate on the canine end-systolic pressure-volume relationship

Although the rate dependence of isolated muscle contractility is well known, the ventricular end-systolic pressure-volume relationship (ESPVR) has been reported to be insensitive to heart rate. To resolve this contradiction, we used an isolated, ejecting canine heart preparation perfused at a constant coronary arterial pressure. Heart rate was changed from 60 to 200 beats/min in steps of 20 beats/min. At least 10 pressure-volume loops under different filling pressures were obtained at each heart rate in each of six hearts. Over a heart rate range from 60 to 120 beats/min, the slope of the ESPVR (E(es)) increased significantly from 3.5 ± 0.4 (SE) to 5.3 ± 0.6 mm Hg/ml. In the range between 120 and 180 beats/min there was little change in E(es) (5.3 ± 0.6 to 5.4 ± 0.6 mm Hg/ml), but at 200 beats/min E(es) increased slightly to 5.7 ± 0.5 mm Hg/ml. The volume axis intercept (V₀) of the ESPVR changed little over the range of heart rate from 60 to 160 beats/min (10.2 ± 2 ml to 9.4 ± 1.3 ml) but increased to 15.2 ± 1.2 ml at a rate of 200 beats/min. The change in ESPVR with increase in heart rate from 60 to 120 beats/min (i.e., increase in E(es) without change in V(₀) is the same as those seen with a positive intropic intervention with calcium or cathecholamines, whereas the V₀ changes over the range from 160 to 200 beats/min is similar to those seen with regional ischemia. The insensitivity of ESPVR in the midrange may be the result of a balance of positive and negative influences on ventricular contraction or a restricted range for the increase in inotropic state with higher rate.