resulting in earlier cardiovascular collapse because of cardiac injury or early respiratory decompensation because of lung injury.
All of the currently used inhalational anesthetics including halothane, enflurane, isoflurane, desflurane, and sevoflurane may exhibit depressant effects on the cardiovascular system when they are administered at doses of between 1.0 and 2.0 the minimum alveolar concentrations. The cardiac depressant effects of halothane, enflurane, isoflurane, desflurane, and sevoflurane have been demonstrated in isolated heart preparations and in the unanesthetized chronically instrumented dog (Pagel et al., 1991a,b). These studies have indicated that these anesthetics have negative inotropic effects and impair ventricular diastolic function (Pagel et al., 1991c). Among the intravenous anesthetics, barbiturates, the benzodiazepines, etomidate, and propofol, all produce dose-dependent cardiovascular effects (Merin, 1996). Greater controversy exists with regard to ketamine, which may produce transient stimulating effects on the heart and peripheral circulation, but these effects are eliminated in animal models when the sympathetic nervous system is blocked or inhibited (Pagel et al., 1992). The minimal depressant effects of newer narcotics such as fentanyl and its derivatives have been confirmed by studies with animals and humans, but such efforts are found only at higher narcotic levels if ventilation is maintained since respiratory depression is a common finding at higher doses (Merin, 1996).
Among the physiologic responses to acute hemorrhage that occur while receiving potent inhalational anesthetics and many intravenous anesthetics are depression of (1) both high-pressure and cardiac low-pressure reflexes, (2) the chemoreceptor reflex, and (3) sympathetic nervous system responses. Studies with human volunteers have demonstrated inhibition of carotid sinus and aortic sinus reflexes by halothane (Duke et al., 1977), enflurane (Morton et al., 1980), and isoflurane (Kotrly et al., 1984). Other studies with humans have demonstrated that halothane has an inhibitory effect on cardiopulmonary reflex regulation of limb and vascular resistance (Kotrly et al., 1985). The potent anesthetics halothane and isoflurane have been shown (Seagard et al., 1983, 1985) to inhibit the carotid sinus reflex at multiple sites including the central nervous system, sympathetic pre- and postganglionic sites, and neuroeffector junctions in the heart and in the arteries and venules. Direct inhibitory effects of halothane on sympathetic ganglia have also been demonstrated (Bosnjak et al., 1988).
Inhibition of chemoreflex regulation of the cardiovascular system by potent volatile anesthetics has been demonstrated in animal models during halothane (Stekiel et al., 1992) and isoflurane (Stekiel et al., 1995) anesthesia. These effects were demonstrated for arterial resistance vessels as well as venous capacitance vessels.
In summary, direct depressant effects of potent volatile anesthetic agents and many intravenous anesthetics on the heart and peripheral blood vessels as a