Anesthesia and analgesia
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Desflurane causes dose-dependent decreases in cerebrovascular resistance and cerebral metabolic rate of oxygen consumption (CMRO2), suggesting that desflurane is a cerebral arteriolar dilator with global flow-metabolism coupling similar to halothane and isoflurane. Desflurane is also similar to isoflurane in that cerebrovascular responsivity to carbon dioxide appears to be maintained. In the dog, arterial hypotension to 40 mm Hg induced with 2.4 MAC desflurane resulted in global decreases in cerebral blood flow of 60% and CMRO2 of 20%. ⋯ The electroencephalographic effects of desflurane are similar to those of isoflurane in humans, and burst suppression is easily achieved. There are no data available concerning possible interactions between desflurane and the outcome of a cerebral ischemic event. Similar to other potent volatile agents, desflurane can cause cerebral vasodilation and may result in intracranial pressure changes in vulnerable patients, but if adequate hyperventilation and depth of anesthesia are maintained, it is probably safe to use desflurane in a manner similar to isoflurane in patients with decreased intracranial compliance.
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Anesthesia and analgesia · Oct 1992
ReviewAn overview of induction and emergence characteristics of desflurane in pediatric, adult, and geriatric patients.
A major advantage of desflurane over currently available agents is that the blood-gas partition coefficient of desflurane is 0.42, lower than all available volatile anesthetics, and slightly lower than nitrous oxide. This property predicts rapid induction of and recovery from general anesthesia with desflurane. This review will summarize and compare results of studies that have examined various clinical characteristics of induction and emergence with desflurane in a variety of patient populations. ⋯ Several studies have compared emergence from anesthesia with desflurane with that from isoflurane-based anesthetics, and have demonstrated that initial emergence from a given depth of anesthesia, e.g., time to eye opening or response to verbal commands, is about twice as fast with desflurane. Similar results have been obtained in pediatric patients where emergence from desflurane is faster than that seen from halothane. Emergence from desflurane anesthesia appears similar in time-course to that from propofol-based anesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)
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The low solubility of desflurane contributes to rapid emergence after outpatient anesthesia. Compared with isoflurane, recovery times to eye opening, response to verbal commands, and orientation to person, place, and time have been significantly shorter. Even when compared with the rapid, short-acting intravenous anesthetic propofol for induction and maintenance of outpatient anesthesia, desflurane displayed more favorable early recovery characteristics. ⋯ As desflurane is pungent and possesses respiratory irritant properties, propofol will likely remain the induction agent of choice in the outpatient setting. In conclusion, desflurane appears to have few adverse effects on recovery after ambulatory surgery, but nausea and emesis were lower with propofol. Desflurane's relative ease of administration versus propofol may be an important determinant of its future role in outpatient anesthesia.
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Anesthesia and analgesia · Oct 1992
ReviewCharacteristics and implications of desflurane metabolism and toxicity.
The metabolism of desflurane has been assessed both in animals and humans by measuring the appearance of fluoride metabolites (fluoride ion, nonvolatile organic fluoride, trifluoroacetic acid) in blood and urine. Desflurane administered to rats (either pretreated or not pretreated with phenobarbital or ethanol) for 3.2 MAC-hours and to swine for 5.5 MAC-hours produced fluoride ion levels in blood that were almost indistinguishable from values measured in control animals. In contrast, a significant 17% increase in plasma fluoride ion concentration in swine was detected 4 h after exposure to desflurane. ⋯ Peak serum concentrations averaging 0.38 +/- 0.17 microM trifluoroacetic acid (mean +/- SD) and peak urinary excretion rates averaging 0.169 +/- 0.107 mumol/h were detected in volunteers 24 h after desflurane exposure. Although these increases in trifluoroacetic acid after exposure to desflurane were statistically significant, they are approximately 10-fold less than levels seen after exposure to isoflurane. Desflurane strongly resists biodegradation, and only a small amount is metabolized in animals and humans.
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Anesthesia and analgesia · Oct 1992
ReviewDesflurane animal and human pharmacology: aspects of kinetics, safety, and MAC.
Substitution of fluorine for the single chlorine atom in isoflurane produces the new anesthetic, desflurane. This seemingly small change produces several pharmacologic changes. The potency of desflurane (MAC equals 6.0% in middle-aged patients) is one-fifth that of isoflurane (1.15%), with MAC for each agent decreased by aging, hypothermia, or the addition of depressants such as midazolam, fentanyl, or nitrous oxide. ⋯ Of great importance, the substitution of fluorine for chlorine markedly decreases blood (desflurane blood-gas partition coefficient 0.42) and tissue solubility (e.g., brain-blood partition coefficient 1.3) relative to isoflurane (values 1.4 and 1.6, respectively). As a result, desflurane alveolar concentrations may be adjusted more rapidly and precisely; desflurane enters and leaves the lungs and tissues more rapidly; and recovery is quicker both for the short (first 10-20 min) and long (0.5-1.5 h) term. This greater precision of control and more rapid recovery are consistent with trends for new drug development in anesthesiology.