Etomidate is preferred as an induction agent in a haemodynamically unstable patient. Which receptor mechanism best explains its cardiovascular stability?
- A It directly stimulates myocardial contractility via calcium channel facilitation
- B It blocks cardiac muscarinic receptors, increasing heart rate and cardiac output
- C It produces minimal decrease in systemic vascular resistance by lacking histamine release and having minimal effect on the adrenergic system ✓
- D It produces vasoconstriction via alpha-1 adrenoreceptor agonism
Explanation
Etomidate is uniquely cardiovascularly stable among induction agents because it produces minimal changes in heart rate, stroke volume, cardiac output, and systemic vascular resistance. It does not cause histamine release (unlike morphine or atracurium) and has negligible effect on the sympathetic nervous system. Its GABA-A agonism is highly selective for CNS hypnotic effects. The principal drawback is reversible adrenocortical suppression (inhibition of 11-beta hydroxylase), particularly with infusion, making it unsuitable for ICU sedation. Etomidate does not directly affect calcium channels or stimulate contractility.
Reference: Morgan & Mikhail's Clinical Anesthesiology, 6th ed.
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