The Effects of Halothane on the Interactions Between Myocardial Contractility, Aortic Impedance, and Left Ventricular Performance I: Theoretical Considerations and Results

Abstract

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. Halothane has justifiably achieved wide popularity of both. In searching for a predominant cardiovasin clinical use, and yet, despite the wide range of cular action of halothane in animals, Price and Price both clinical and experimental studies of its actions, (1966) concluded that there was no single or predothere is still uncertainty about its effects on the minant cause for the circulatory depression produced cardiovascular system. While most observers are by halothane. Further studies have conclusively agreed that halothane causes a dose-dependent arte-demonstrated that in concentrations which are assorial hypotension in most species, not all are agreed ciated with surgical anaesthesia, halothane decreases as to whether in man this is predominantly the the myocardial contractile force in both man result of reduced cardiac output (Severinghaus and

Effect of Cardioselective β‐Blockers on the Heart Rate and Arterial Pressure Responses to Laryngoscopy

“…In contrast, PRYS-ROBERTS et al (1973), who studied hypertensive patients under halothane/nitrous oxide anaesthesia, found that variations in arterial pressure were attenuated both by i.v. and by oral practolol.…”

“…The discrepancy in results may possibly be explained by halothane, which reduces myocardial contractility (PRYS-ROBERTS et al 1972) and depresses baroreflexes (VATNER & BRAUNWALD 1975). Thus, the P-blocker may have potentiated the effect of halothane.…”

“…Conflicting results have been obtained. Thus, PRYS-ROBERTS et al (1973) found a good effect of practolol and SIEDLECKI (1975) found none. MANNERS & WALTERS (1979) found that patients, in whom oral P-blockers are withdrawn 2-8 days before surgery, have higher arterial pressures after intubation than those whose therapy is continued.…”

Cardiovascular actions of an experimental antitumor agent, homoharringtonine, in anesthetized dogs

“…Several investigators have suggested that the ratio peak dPldtiI. P. is a better index of cardiac contractility since this ratio is independent of either changes in preload or afterload and varies only with changes in inotropism [Prys-Roberts et al, 1972;Jandhyala et al, 19771. This index of contractility was also not altered by homoharringtonine.…”

Halothane‐Relaxant Anaesthesia in Elderly Patients

“…Halothane is the most thoroughly investigated agent and there are abundant reports of a dose-dependent depression of myocardial contractility, with increases in right and left ventricular filling pressures, both in animals (2) and in man (3, 4,5). The fall in cardiac output during halothane anaesthesia has been attributed to the impairment of cardiac function (6). Although the oxygen uptake is reduced, cardiac output is often reported to decrease to an even greater extent (7,8,9), leading to an increase in oxygen extraction.…”