Etomidate (Amidate)
Anesthesia Implications
Classification: Hypnotic
Therapeutic Effects: Sedation, Anticonvulsant
Time to Peak: 15-45 seconds
Duration: 3-12 minutes
Contraindications
Addison’s Disease
Sepsis patients
Patients with a history of Porphyria
Primary Considerations
Cardiac/Hemodynamic stability and minimal respiratory depressive effects are the primary reasons for selecting this drug. Patients with high sympathetic tone may still exhibit a drop in blood pressure after administration.
Does NOT blunt the sympathetic response to laryngoscopy unless combined with a potent opioid
Reduces CMRO2, CBF, ICP, EEG activity. Maintains CPP
Produces convulsion-like EEG patterns without convulsions, making it useful in epileptic patients for mapping brain activity
Adrenocortical suppression 8-24 hours after a single dose. Smaller doses do not reduce the suppression. For this reason, this drug should never be given to patients with adrenal suppression/fatigue. Developments are underway to remove this side-effect.
~30% of patients receiving this drug will experience PONV. Prophylaxis should be given
High incidence of myoclonus
High levels of pain on injection when given without an analgesic
Can cause thrombophlebitis
Can precipitate porphyria
The only IV induction agent that does not release histamine (most induction agents release a very small amount).
Reduced dose with increased age – this is due to a reduced volume of distribution and slower clearance. Brain sensitivity does NOT increase with age. Sensitivity to propofol and volatile anesthetics increase with age – but this is not the case with etomidate.
Highly plasma-protein bound (75%)
Concomitant administration of Fentanyl is known to increase the half-life and potency of Etomidate
SSEP – markedly increases amplitude, slightly increases latency
IV push dose
Induction: 0.2-0.3 mg/kg
Method of Action
Enhances GABA-A receptor binding in the brain. Positive modulation of glycine receptors.
Metabolism
Ester hydrolysis via plasma esterases and hepatic enzymes. Heavily relies on hepatic blood flow (perfusion limited). No active metabolites
Elimination
Elimination Half-life: 3-5 hours
Additional Notes
Suppresses adrenocortical function by inhibiting 11β-hyroxylase and 17α-hydroxylase
Flood. Stoelting’s Pharmacology and Physiology in Anesthetic Practice. 5th Edition. 2015. p. 168-169
Miller. Miller’s Anesthesia. 2015. p. 822, 850, 2418
Hemmings. Pharmacology and Physiology for Anesthesia. 1st Edition. 2012. p. 87, 90, 95, 142-143, 146
Barash. Clinical anesthesia. 7th edition. 2013. p. 478, 481-484, 489
Nagelhout. Nurse anesthesia. 6th edition. 2018. p. 1144
Butterworth. Morgan & Mikhail’s Clinical Anesthesiology. 2013. p. 181