Clinical pharmacology of general anesthetics

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Abstract
The past decade has seen great interest in the clinical pharmacology of general anesthetics. Recently introduced drugs, such as halothane or methoxyflurane, have already been studied in more detail than ether or nitrous oxide had been during the first century of their clinical use. This review discusses some aspects of the actions of anesthetics of immediate clinical significance to the practicing anesthesiologist. Uptake and distribution of anesthetics in the body follows certain well‐defined laws and is a continuously changing process. Volatility and the blood to gas partition ratio are the main factors influencing the onset of inhalation anesthetics, while a high blood to tissue ratio will aid recovery. Lack of ionization and high lipoid solubility explain the rapid onset of the useful intravenous agents. With these drugs the clinical “depth” of anesthesia is often unrelated to the blood level, their action being markedly influenced by dosage and premedication. Most general anesthetics are direct myocardial depressants and cause a variable degree of peripheral vasodilation, but those which increase blood catecholamine levels cause less hypotension. Hypercarbia is a major cause of cardiac arrhythmias during anesthesia, particularly with cyclopropane and halothane. Contrary to some opinions, liver dysfunction is probably no more common after halothane than after other agents, although there may be a particular danger associated with its repeated administration. Many factors other than the general anesthetic itself increase the incidence of postoperative vomiting; opiate premedication is the main factor which is under the direct control of the anesthesiologist.