ALTERATIONS IN CANINE LEFT VENTRICULAR-ARTERIAL COUPLING AND MECHANICAL EFFICIENCY PRODUCED BY PROPOFOL

Background: Propofol reduces blood pressure by decreasing left ventric ular (LV) afterload and myocardial contractility, This investigation t ested the hypothesis that propofol preserves LV-arterial coupling and mechanical efficiency because of these simultaneous hemodynamic action s. Methods: Experiments were conducted in open-chest dogs (n = 8) inst rumented for measurement of aortic and LV pressure, dP/dt(max), and LV volume. Myocardial contractility was assessed with the slope (E-es) o f the LV end systolic pressure-volume relationship. Effective arterial elastance (E-a; the ratio of end systolic arterial pressure to stroke volume), stroke work (SW), and pressure-volume area (PVA) were determ ined from the LV pressure-volume relationships. Dogs were studied 30 m in after instrumentation and after 15-min intravenous infusions of pro pofol at 5, 10, 20, and 40 mg.kg(-1).h(-1). Results: Propofol caused d ose-dependent decreases in E-es (4.7 +/- 0.9 during control to 2.7 +/- 0.5 mmHg/ml during the high dosage) and dP/dt(max), indicating a dire ct negative inotropic effect. E-a increased at the 10 mg.kg(-1).h(-1) dose of propofol but decreased at higher dosages. Propofol decreased t he ratio of E-es to E-a (0.88 +/- 0.13 during control to 0.56 +/- 0.10 during the high dosage), consistent with impairment of LV-arterial co upling, Propofol also reduced the ratio SW to PVA (0.54 +/- 0.03 durin g control to 0.45 +/- 0.03 during the 20 mg.kg(-1).h(-1)), suggesting a decline in LV mechanical efficiency. SW and PVA recovered toward bas eline values at the 40 mg.kg(-1).h(-1) dose. Conclusions: Although pro pofol depresses mechanical matching of the LV to the arterial system a nd reduces LV efficiency, these alterations plateau at higher dosages of propofol because reductions in afterload begin to offset further de clines in myocardial contractile function.