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Arterial hypotension and the development of postanesthetic myopathy in halothane-anesthetized horses.

The effect of halothane-induced hypotension on the development of postanesthetic myopathy was studied, using 6 healthy adult horses. Horses were anesthetized with halothane in oxygen for 3.5 hours on each of 2 occasions. Intermittent positive-pressure ventilation was used to maintain PaCO2 of 45 to 55 mm of Hg throughout both anesthetic exposures. By regulating the inspired halothane concentration, a mean arterial blood pressure of 85 to 95 mm of Hg (normotension) was maintained throughout the 1st anesthetic exposure, and a mean arterial blood pressure of 55 to 65 mm of Hg (hypotension) was maintained during the 2nd anesthetic exposure. All horses recovered uneventfully from normotensive anesthesia, but all had some muscle dysfunction after prolonged hypotensive anesthesia. Because of apparent animal discomfort and lameness involving more than 1 limb, 3 horses were euthanatized soon after they recovered from hypotensive anesthesia. The 3 other horses showed a degree of lameness. In addition, 1 horse had raised, swollen plaques over the hip, rib, and facial areas which were in contact with the surgical table, and another had evidence of facial nerve paralysis. One hour after the 6 horses stood after hypotensive anesthesia was completed, values obtained for aspartate transaminase and creatinine were significantly (P less than 0.05) greater than those obtained after normotensive anesthesia was completed. Aspartate transaminase, total bilirubin, and creatinine values were significantly (P less than 0.05) increased when compared with those obtained before horses were anesthetized. A large increase was measured in creatine kinase. Twenty-four hours after hypotensive anesthesia was completed, creatine kinase and lactate dehydrogenase in the 3 surviving horses were significantly (P less than 0.05) greater than those values after normotensive anesthesia was completed.