Cardiovascular effects of the inhalation agents
Timothy S.J. Shine, MD and Neil G. Feinglass, MD, FCCP, FASE
There is no one perfect anesthetic agent, though inhalation agents come closest to providing the components of a complete anesthetic (i.e., analgesia, amnesia, hypnosis, and muscle relaxation) as a single agent. All of the inhalation agents depress the cardiovascular system in a dose-dependent fashion (Figure 66-1) through one or more mechanisms, the overall effect of which is a decrease in mean arterial pressure.
Systemic vascular resistance
The decrease in blood pressure that occurs with the use of halothane is due to a reduction in myocardial contractility, heart rate, and systemic vascular resistance (SVR). Isoflurane, sevoflurane, and desflurane decrease blood pressure primarily by decreasing SVR. Isoflurane and desflurane are potent vasodilators (Figure 66-2), with halothane causing a more modest reduction in SVR at equipotent doses. Isoflurane causes up to a 50% reduction in SVR at 1.9 minimum alveolar concentration.
) with those of isoflurane (O) and halothane (Δ) on systemic vascular resistance (SVR) in healthy young men. MAC, Minimum alveolar concentration. (From Weiskopf RB, Cahalan MK, Eger EI II, et al. Cardiovascular actions of desflurane in normocarbic volunteers. Anesth Analg. 1991;73:143-156.)Heart rate
Isoflurane, sevoflurane, and desflurane may increase heart rate (Figure 66-3). Halothane may cause no change or a decrease in heart rate because it impairs baroreceptor function. Isoflurane is less depressant to the baroreflex, and, with a decrease in SVR, a compensatory increase occurs in heart rate even though isoflurane also depresses sympathetic nervous system activity; however, halothane has less effect on the parasympathetic system than on the sympathetic nervous system. Isoflurane anesthesia appears, clinically, to have less effect on cardiac chronicity in patients younger than 40 years of age, as compared with older patients.
