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Inhaled anesthetic agents.

Abstract

PURPOSE: The pharmacology, bioavailability and pharmacokinetics, indications, clinical efficacy, adverse effects and toxicities, and dosage and administration of the inhaled anesthetics are reviewed. SUMMARY: The inhaled anesthetics include desflurane, enflurane, halothane, isoflurane, and sevoflurane and are thought to enhance inhibitory postsynaptic channel activity and inhibit excitatory synaptic activity. The mechanism of action of inhaled anesthetics has not been completely defined. A number of factors can influence the pharmacokinetics of inhaled anesthetics, including solubility in blood, cardiac output, tissue equilibration, extent of tissue perfusion, metabolism, and age. All of the available inhaled anesthetics are effective for inducing or maintaining anesthesia or both. Most clinical trials of inhaled anesthetics have evaluated differences in induction and emergence from anesthesia by comparing (1) times to loss of reflex, extubation, and response to verbal commands; orientation to time and place; and ability to sit up without assistance, (2) need for post-surgical analgesia, and (3) time to discharge as measures of efficacy. Adverse effects and toxicities of the inhaled anesthetics include nephrotoxicity, hepatotoxicity, cardiac arrhythmias, neurotoxicity, postoperative nausea and vomiting, respiratory depression and irritation, malignant hyperthermia, and postanesthesia agitation. Safety issues surrounding these gases include occupational exposure and intraoperative fires within the delivery systems used with inhaled anesthetics. Drugs used for anesthesia during surgery can account for 5-13% of a hospital's drug budget. CONCLUSION: The inhaled anesthetics have been shown to be both safe and effective in inducing and maintaining anesthesia. These agents differ in potency, adverse-effect profile, and cost. Newer anesthetic gases, such as sevoflurane and desflurane, appear to have more favorable physico-chemical properties. These factors, as well as patient characteristics and duration and type of procedure, must be considered when selecting an inhaled anesthetic.

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BibTeXRIS

Joan Stachnik. 2006-04-01. Inhaled anesthetic agents.. https://doi.org/10.2146/ajhp050460

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Anesthetics, Inhalation↗

A randomized crossover comparison of the effects of propofol and sevoflurane on cerebral hemodynamics during carotid endarterectomy.

BACKGROUND: Intravenous and inhalational anesthetic agents have differing effects on cerebral hemodynamics: Sevoflurane causes some vasodilation, whereas propofol does not. The authors hypothesized that these differences affect internal carotid artery pressure (ICAP) and the apparent zero flow pressure (critical closing pressure) during carotid endarterectomy. Vasodilation is expected to increase blood flow, reduce ICAP, and reduce apparent zero flow pressure. METHODS: In a randomized crossover study, the gradient between systemic arterial pressure and ICAP during carotid clamping was measured while changing between sevoflurane and propofol in 32 patients. Middle cerebral artery blood velocity, recorded by transcranial Doppler, and ICAP waveforms were analyzed to determine the apparent zero flow pressure. RESULTS: ICAP increased when changing from sevoflurane to propofol, causing the mean gradient between arterial pressure and ICAP to decrease by 10 mmHg (95% confidence interval, 6-14 mmHg; P<0.0001). Changing from propofol to sevoflurane had the opposite effect: The pressure gradient increased by 5 mmHg (95% confidence interval, 2-7 mmHg; P=0.002). Ipsilateral middle cerebral artery blood velocity decreased when changing from sevoflurane to propofol. Cerebral steal was detected in one patient after changing from propofol to sevoflurane. The apparent zero flow pressure (mean+/-SD) was 22+/-10 mmHg with sevoflurane and 30+/-14 mmHg with propofol (P<0.01). There was incomplete drug crossover due to the limited duration of carotid clamping. CONCLUSIONS: Compared with sevoflurane, ipsilateral ICAP and apparent zero flow pressure are both higher with propofol. Vasodilatation associated with sevoflurane can cause cerebral steal.

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