Etomidate (Amidate)

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

Addison's Disease Sepsis patients Patients with a history of Porphyria

Induction: 0.2-0.3 mg/kg

Enhances GABA-A receptor binding in the brain. Positive modulation of glycine receptors.

Ester hydrolysis via plasma esterases and hepatic enzymes. Heavily relies on hepatic blood flow (perfusion limited). No active metabolites

Elimination Half-life: 3-5 hours

Suppresses adrenocortical function by inhibiting 11β-hyroxylase and 17α-hydroxylase