Halothane (Fluothane) depresses respiratory function, leading to decreased tidal volume and an increased rate of ventilation. Since the increased rate does not adequately compensate for the decrease in tidal volume, minute ventilation will be reduced; plasma PaCO2 rises, and hypoxic drive is depressed. With surgical anesthesia, spontaneous ventilation is inadequate, and the patient's ventilation must be controlled.

Halothane administration can result in a marked reduction in arterial blood pressure that is due primarily to direct myocardial depression, which reduces cardiac output. The fall in pressure is not opposed by reflex sympathetic activation, however, since halothane also blunts baroreceptor and carotid reflexes. Systemic vascular resistance is unchanged, although blood flow to various tissues is redistributed. Halothane also sensitizes the heart to the arrhythmogenic effect of cate-cholamines. Thus, maintenance of the patient's blood pressure with epinephrine must be done cautiously.

It is clinically significant that cerebral blood flow increases as a result of a direct relaxant action of halothane on cerebral vasculature. Intracranial pressure may rise to a level at which it can become dangerous in patients with intracranial pathology. Although the coronary arteries are dilated, coronary blood flow decreases because of the overall reduction in systemic blood pressure. Thus, the balance between myocardial perfusion and oxygen demand (which is reduced with halothane) should be taken into account for patients with cardiac disease.

Similar disturbances in intracranial pressure and coronary blood flow occur with most of the halogenated hydrocarbons. In addition, renal blood flow, filtration, and urine output decrease with the use of halothane. These changes also occur with other inhalational agents that reduce arterial blood pressure.

Halothane and all other halogenated hydrocarbons cause some relaxation of skeletal muscle. The relaxation is not adequate when muscle paralysis is a requirement of the operative procedure, but halothane's action will b a potentiate the effect of neuromuscular blocking drugs, reducing their dose requirement.

Although recovery from anesthesia does not rely on metabolic factors, halothane and many of the halo-genated hydrocarbons undergo some biotransformation. Halothane is oxidized in the liver to trifluoroacetic acid, Br", and Cl". In the absence of oxygen, reductive intermediates of halothane metabolism may form and damage liver tissue. These intermediates have been implicated in a controversial syndrome of halothane hep-atitis.This rare syndrome (1:35,000 anesthetics) is histo-logically indistinguishable from viral hepatitis. The likelihood of liver dysfunction increases with repeated administrations of halothane, and antibodies to hepato-cytes are obtained from patients who develop liver dysfunction following halothane. It has been suggested that liver necrosis may be a hypersensitivity reaction, perhaps initiated by the reactive intermediates formed during halothane metabolism. It seems prudent to limit the use of halothane in patients with liver dysfunction that resulted from a previous exposure to the anesthetic.

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