Etomidate is chosen over propofol for induction in a haemodynamically unstable trauma patient. Which mechanism accounts for its superior cardiovascular stability?
- A Etomidate stimulates baroreceptors, reflexly increasing blood pressure
- B Etomidate produces vasoconstriction by alpha-1 receptor agonism
- C Etomidate selectively enhances inhibitory GABA-A currents without significantly reducing sympathetic tone, systemic vascular resistance, or myocardial contractility ✓
- D Etomidate does not cross the blood-brain barrier at induction doses
Correct answer: C. Etomidate selectively enhances inhibitory GABA-A currents without significantly reducing sympathetic tone, systemic vascular resistance, or myocardial contractility
Explanation
Etomidate potentiates GABA-A receptor function, producing anaesthesia with minimal cardiovascular effects. It does not inhibit sympathetic ganglia, does not reduce cardiac output, and has minimal effect on SVR, making it the induction agent of choice in compromised cardiovascular states. The key trade-off is adrenocortical suppression (inhibition of 11-β-hydroxylase), which even with a single dose causes blunted cortisol response to surgical stress for up to 24 hours — a concern in septic patients.
Reference: Morgan & Mikhail's Clinical Anesthesiology, 6th ed.
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