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The use of etomidate is most appropriate in patients with cardiovascular disease, reactive airway disease, intracranial hypertension, or any combination of disorders indicating the need for an induction agent with limited or beneficial physiologic side effects. The hemodynamic stability of etomidate is unique among the rapid-onset induction agents.
Etomidate has been primarily used in sick patients. In multiple studies, etomidate has been used for induction in patients with a compromised cardiovascular system who are undergoing coronary artery bypass surgery or valve surgery, in patients requiring induction of general anesthesia for percutaneous transluminal coronary angioplasty, and in other similar situations.[631] [634] [654] In cardiovascular surgery, particularly surgery for aortic aneurysms, etomidate is an excellent induction anesthetic. When etomidate is used in combination with fentanyl, titrating etomidate up to 0.6 mg/kg maintains blood pressure and heart rate in a narrow range; coronary perfusion pressure is preserved in these patients with probable coronary artery disease while the response to intubation is blunted and unnecessary stress on the aneurysm is avoided. For cardiothoracic procedures, especially cardiac and lung transplantation, the required rapid-sequence induction and hemodynamic stability make etomidate the drug of choice for induction. For patients with concomitant coronary artery disease and reactive airway disease, etomidate induction does not release histamine, and a relatively large dose (0.6 mg/kg) may be titrated to provide a deep level of anesthesia for intubation without compromising hemodynamics and coronary perfusion pressure. For cardioversion, the rapid onset, quick recovery, and maintenance of blood pressure in these sometimes hemodynamically tenuous patients, combined with continued spontaneous respiration, make etomidate an acceptable choice,[275] although in one report, myoclonus interfered with electrocardiographic evaluation. [655] Even though definitive proof of etomidate's neuroprotective effect in humans is lacking, the combination of animal data and anecdotal reports of successful use of etomidate for neurosurgical procedures such as clipping of giant aneurysms makes etomidate a reasonable choice during neurosurgical induction. [597] [609] [611] [656] In addition, because of its ability to reduce increased ICP, etomidate should be considered when maintenance of cerebral or coronary perfusion pressure is important. Trauma patients with questionable volume status may be well served by induction with etomidate. Although the indirect sympathomimetic effect seen with ketamine induction is absent, there is no direct myocardial depression and no confusion in the differential diagnosis of postoperative delirium. This is especially important in patients whose trauma may be related to drug or alcohol use (or both).
During an infusion, hemodynamic status is well maintained along with adequate spontaneous ventilation.[420] [657] The incidence of pain on injection, myoclonus, and thrombophlebitis tends to be less with an infusion technique.[24] [596] [657] A concentrated form of etomidate used for continuous infusion in Europe is not available in the United States.
Short-term sedation with etomidate is useful in hemodynamically unstable patients, such as those requiring cardioversion,[275] those with acute myocardial infarction or unstable angina who require sedation for a minor operative procedure,[634] or those who require intubation in the emergency room or the ICU. In addition, etomidate has been used to produce short-term sedation for placement of a retrobulbar block and for electroconvulsive therapy, during which maintenance of spontaneous respirations and quick recovery are important features. When used during electroconvulsive therapy, etomidate can produce longer seizures than possible with other hypnotics.[658]
Prolonged sedation for patients in the ICU, though initially popular after the release of etomidate, is now contraindicated because of inhibition of corticosteroid and mineralocorticoid production and a subsequent increase in morbidity.[577] [579] [636]
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