Malignant hyperthermia (MH) is a potentially lifethreatening hypermetabolic condition triggered by inhaled halogenated anesthetic agents (eg, halothane, isoflurane, enflurane, desflurane, sevoflurane) or succinylcholine in otherwise normal but genetically susceptible individuals. This disorder was initially de scribed in 1960 by Denborough et al, 2-6 who published the first formal case of MH in an Australian family. MH is inherited as an autosomal dominant disease characterized by uncontrollable skeletal muscle hypermetabolism, rhabdomyolysis, increased oxygen consumption and CO 2 production, tachycardia, hypercapnia, hyperthermia, elevated creatinine kinase, and other features after exposure to a trigger agent. Most MH-susceptible individuals are asymptomatic until they are truly exposed to such an agent. Some genes can counter mutations related to susceptibility to MH; the most widely studied and frequently found of these is the gene for the ryanodine receptor RyR1, located in chromosome 19, which accounts for approximately 50% of the susceptible persons. MH occurs in all ethnic groups, and preva lence varies according to region and age. 2,8 Its exact incidence is unknown but is estimated to be 1:15,000 in children and adolescents and 1:50,000 in adults. The decreased incidence with age may have 2 explanations: a reduced expression of the disease and the death of susceptible individuals before they become adults. 3