Enflurane (Ethrane) depresses myocardial contractility and lowers systemic vascular resistance. In contrast to halothane, it does not block sympathetic reflexes, and therefore, its administration results in tachycardia. However, the increased heart rate is not sufficient to oppose enflurane's other cardiovascular actions, so cardiac output and blood pressure fall. In addition, enflurane sensitizes the myocardium to catecholamine-induced arrhythmias, although to a lesser extent than with halothane. Enflurane depresses respiration through mechanisms similar to halothane's and requires that the patient's ventilation be assisted.

Neuromuscular transmission is depressed by enflurane, resulting in some skeletal muscle paralysis.Although muscle relaxation is inadequate for many surgical procedures, the anesthetic enhances the action of neuromuscu-lar blocking agents, thereby lowering the dose of the paralytic agent needed and minimizing side effects.

Deep anesthesia with enflurane is associated with the appearance of seizurelike electroencephalographic (EEG) changes. Occasionally frank tonic-clonic seizures are observed. Consequently, other inhalational agents are usually given to patients with preexisting seizure disorders.

Another concern associated with the use of enflu-rane is its biotransformation, which leads to increased plasma fluoride. Following lengthy procedures in healthy patients, fluoride may reach levels that result in a mild reduction in renal concentrating ability. Thus, en-flurane should be used cautiously in patients with clinically significant renal disease.

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