Etomidate depresses the reticular activating system and mimics the inhibitory effects of GABA. Specifi-cally, etomidate—particularly the R(+) isomer— appears to bind to a subunit of the GABAA receptor, increasing the receptor’s affinity for GABA. Unlike barbiturates, etomidate may have disinhibitory effects on the parts of the nervous system that control extrapyramidal motor activity. This disinhi-bition offers a potential explanation for the 30–60% incidence of myoclonus with etomidate induction ofanesthesia.
Etomidate contains a carboxylated imidazole and is structurally unrelated to other anesthetic agents (see Figure 9–4). The imidazole ring provides water solubility in acidic solutions and lipid solubility at physiological pH. Therefore etomidate is dissolved in propylene glycol for injection. This solution often causes pain on injection that can be lessened by a prior intravenous injection of lidocaine.
Etomidate is available only for intravenous admin-istration and is used primarily for induction of gen-eral anesthesia (see Table 9–3). It is sometimes used for brief production of deep (unconscious) sedation such as prior to placement of retrobulbar blocks.
Although it is highly protein bound, etomidate is characterized by a very rapid onset of action due to its great lipid solubility and large nonionized fraction at physiological pH. Redistribution is responsible for decreasing the plasma concentration to awakening levels. Etomidate plasma kinetics are well explained by a two-compartment model.
Hepatic microsomal enzymes and plasma esterases rapidly hydrolyze etomidate to an inactive metabolite.
The end products of etomidate hydrolysis are pri-marily excreted in the urine.
Etomidate has minimal effects on the cardiovascu-lar system. A mild reduction in peripheral vascular resistance is responsible for a slight decline in arterial blood pressure. Myocardial contractility and cardiac output are usually unchanged. Etomidate does not release histamine. However, etomidate by itself, even in large doses, produces relatively light anesthesia for laryngoscopy, and marked increases in heart rate and blood pressure may be recorded when etomidate provides the only anesthetic depth for intubation.
Ventilation is affected less with etomidate than with barbiturates or benzodiazepines. Even induction doses usually do not result in apnea unless opioids have also been administered.
Etomidate decreases cerebral metabolic rate, cere-bral blood flow, and intracranial pressure. Because of minimal cardiovascular effects, CPP is well main-tained. Although changes on EEG resemble those associated with barbiturates, etomidate increases the amplitude of somatosensory evoked potentials. Postoperative nausea and vomiting are more com-mon following etomidate than following propofol or barbiturate induction. Etomidate lacks analgesic properties.
Induction doses of etomidate transiently inhibit enzymes involved in cortisol and aldosterone synthesis. It was used in the past for sedation in the intensive care unit (ICU) before reports of its consistent ability to produce adrenocortical suppression in that circumstance appeared. Long-term infusion and adrenocortical suppression were associated with an increased mortality rate in critically ill (particularly septic) patients.
Fentanyl increases the plasma level and prolongs the elimination half-life of etomidate. Opioids decrease the myoclonus characteristic of an etomi-date induction.
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