Effects of preload, afterload and inotropy on dynamics of ischemic segmental wall motion

This study sought to explore the separate and combined effects of changes in preload, afterload and contractility on the dynamics of systolic bulging.

The extent of ischemic systolic bulging has been shown to be mechanically disadvantageous to left ventricular pump performance. The factors that determine ischemic segmental wall motion have not been systematically studied.

Fourteen beagles were instrumented with sonomicrometers, micromanometer pressure gauges and a balloon in the inferior vena cava. Regional function was evaluated before and after 90 s of proximal left circumflex coronary artery occlusion. Occlusions were repeated after increasing systolic pressure by 5 to 10 (afterload I) and 15 to 20 mm Hg (afterload II) with graded aortic occlusion during inotropic stimulation with dobutamine (2.5 and 5 micrograms/kg body weight per min intravenously), with simultaneous 5 micrograms/kg per min dobutamine infusion and afterload II and during 2.5% halothane (negative inotrope) concentration. A 20-min recovery period was allowed between each stage of the experiment so that regional function returned to its preocclusion level. Ischemic wall motion was characterized by percent systolic bulging and its peak positive systolic lengthening rate (+dL/dt).

Because bulging is markedly influenced by regional preload, systolic bulging was characterized over a wide range of end-diastolic lengths of the ischemic segment during caval balloon occlusion. During each intervention, a decrease in regional preload increased the extent of percent systolic bulging. This preload dependency was more pronounced with dobutamine infusions. An increase in afterload was not associated with increased percent systolic bulging at any given preload. At a predetermined preload, bulging was not appreciably altered when an increase in left ventricular systolic pressure was not associated with a change in peak positive first derivative of left ventricular pressure (+dP/dt) but was significantly worse when peak +dP/dt increased. Dobutamine caused a dose-dependent increase in percent systolic bulging and peak +dL/dt that was positively correlated with peak +dP/dt.

By using different loading and inotropic interventions and analyzing the regional wall motion behavior over a range of regional preloads, we can conclude that preload and rate of pressure (tension) development are the principal determinants of systolic bulging. Increases in left ventricular pressure alone had a minimal effect on systolic bulging.