Abstract
This chapter discusses the pharmacology and toxicology of halogenated anesthetics. Trichloroethylene is relatively soluble in blood, and induction of anesthesia is slow, as is recovery. In clinical practice, the slow induction time if offset partially by the high anesthetic potency of the drug. The minimum alveolar concentration (MAC) necessary to maintain the first plane of surgical anesthesia is 0.17%. Trichloroethylene was the first of the inhalation anesthetics demonstrated to be biotransformed. Halothane is relatively insoluble in blood, and induction of anesthesia is relatively rapid. The minimum alveolar concentration necessary to maintain the first plane of surgical anesthesia is 0.7%. Halothane is extremely soluble in fat, allowing the body to absorb large amounts of the anesthetic. Many halogenated hydrocarbons are known to be hepatotoxic, and at least in certain individuals, halothane is no exception. The usual clinical picture of halothane hepatitis presents with fever, leukocytosis, and with eosinophilia, followed by jaundice within 5– 21 days after anesthesia. Liver dysfunction is confirmed by finding high alkaline phosphatase, serum glutamic oxaloacetic transaminase (SGOT), and serum glutamic pyruvic transaminase (SGPT) levels.
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