In MH, skeletal muscle acutely and unexpectedly increases its oxygen consumption and lactate production, resulting in greater heat production, respiratory and metabolic acidosis, muscle ridigity, sympathetic stimulation, and increased cellular permeability. The best-accepted theory is that MH is due to an inability to control calcium concentrations within the muscle fiber, and may involve a generalized alteration in cellular or subcellular membrane permeability. Episodes are predictably initiated in susceptible people and swine by potent volative anethetic agents or succinylcholine. In addition, in swine, MH is consistently triggered by excitement, apprehension, exercise, or environmental stress such as heat or hypoxia. Several genetic factors probably control the human and porcine inheritance of MH. Sympathetic involvement in MH, while controversial, is probably a response to stress that affects blood flow, heat loss, and myocardial function, rather than a direct sympathetic activation of susceptible muscle. Diagnosis is based upon extraordinary temperature and acid-base and muscle aberrations. Specific treatment is the action of dantrolene upon muscle calcium movements; sympatomatic treatment is by reversal of acid-base and temperature changes. Evaluation of affected families is guided by measurements of circulating creatine phosphokinase and by analysis of drug-induced contractures in muscle biopsy specimens. Anesthesia for susceptible patients includes thiopental, opiates, droperidol, pancuronium, nitrous oxide, and preoperative oral doses of dantrolene.