A trauma patient arrives in haemorrhagic shock (HR 130, BP 70/40 mmHg). Ketamine is chosen for induction. In this patient's adrenergically depleted state, what direct myocardial effect of ketamine would be most likely to manifest?
- A Positive inotropy through direct catecholamine release
- B Vasodilation via GABA-A receptor activation
- C Coronary vasospasm via thromboxane A2 release
- D Myocardial depression due to direct negative inotropic effect ✓
Explanation
Ketamine's usual clinical cardiovascular stimulation results from indirect sympathomimetic effects (inhibition of catecholamine reuptake at sympathetic nerve terminals). In states of severe haemorrhagic shock where endogenous catecholamine stores are depleted, ketamine's direct myocardial depressant effect (calcium channel antagonism, NMDA receptor-mediated) is unmasked, potentially causing cardiovascular collapse. This is why ketamine should be used cautiously in profoundly shocked patients. Ketamine does not act on GABA-A receptors; that is the mechanism of propofol/benzodiazepines.
Reference: Morgan & Mikhail's Clinical Anesthesiology, 6th ed.
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