The effects of halothane on the interactions between myocardial contractility, aortic impedance, and left ventricular performance. I. Theoretical considerations and results.

The effects of halothane (1.0-1.5%) on myocardial contractility, systemic vascular resistance (representing the majority of impedance to oscillatory flow), and left ventricular performance, and the interactions of these functions have been studied in openchested dogs, artificially ventilated and maintained in a state of basal narcosis with chloralose and urethane. Halothane reversibly depressed myocardial contractility as estimated by three indices: maximum left ventricular (dP/dt)/IP, maximum left ventricular (dP/dt)/PCIP, and maximum aortic acceleration, but produced no significant changes of left ventricular end-diastolic pressure or of systemic vascular resistance. Stroke volume fell in proportion to the depression of myocardial contractility at constant heart rates maintained by atrial pacing, though the reduction of stroke volume was greatest when systemic vascular resistance increased slightly. The concept is proposed that, irrespective of minor changes in the peripheral venous bed during halothane anaesthesia, depression of myocardial contractility impairs ventricular emptying rather than ventricular filling. This concept is based on the observation that since peak aortic flow and acceleration are decreased during halothane anaesthesia, the force acting on blood and the momentum imparted to it during the early phase of ventricular ejection are reduced. Experimental evidence supported this hypothesis: thus, when the contractility of the myocardium was depressed by halothane anaesthesia, independent changes of systemic vascular resistance significantly modified the stroke output of the heart. It is concluded that the major cause of arterial hypotension during halothane anaesthesia is a fall in cardiac output, and that the predominant mechanism causing this fall is the depression of myocardial contractility.