The pharmacology of isoflurane.

The physical and pharmacological properties of the structural isomers isoflurane and enflurane differ from each other and from those of other potent inhaled anaesthetics. The minimum alveolar concentration (MAC) for isoflurane (1.15%) is one-and-one-half times that for halothane (0.75%) and two-thirds that for enflurane (1.7%). The blood/gas partition coefficient (1.4) for isoflurane is lower than the coefficients for all other potent inhaled agents. Despite this lower blood solubility, induction of anaesthesia is slightly faster with halothane because of isoflurane's mild pungency. Enflurane depresses ventilation more than isoflurane, which in turn is slightly more depressant than halothane. All these agents dilate constricted bronchi, and thus are useful in the anaesthetic management of patients who have asthma or chronic obstructive pulmonary disease. Isoflurane has the largest circulatory margin of safety of all potent halogenated agents; it produces the least myocardial depression at a given multiple of MAC. Isoflurane may increase heart rate, particularly in younger patients, and occasionally is associated with tachycardia. It decreases total peripheral resistance, thereby decreasing systemic arterial pressure. Although results from one study suggest that isoflurane may produce a "steal" or coronary blood flow in patients with coronary artery disease, results from other studies suggest that, even in the presence of coronary artery disease, coronary blood flow to all parts of the heart remains as adequate with isoflurane as with other anaesthetics. Greater concentrations of isoflurane (1.6 MAC) increase cerebral blood flow less than does halothane. Isoflurane does not produce convulsive activity, but can produce profound muscle relaxation. It enhances the action of tubocurarine or pancuronium, and (to a lesser extent) vecuronium or atracurium. The enhancement is comparable to that produced by enflurane. Less enhancement is produced by halothane or nitrous oxide-narcotic. Only 0.17% of isoflurane taken up in man appears as urinary metabolites. This resistance to biodegradation may explain the minimal or absent hepatotoxicity and nephrotoxicity of isoflurane.