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

References
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