A 40-year-old man in haemorrhagic shock following a road traffic accident requires urgent intubation. Compared with the same patient when normovolaemic, his requirement for thiopentone will be markedly reduced. What is the pharmacokinetic explanation?
- A Reduced cardiac output slows redistribution from vessel-rich tissues, so a greater fraction of each bolus reaches the brain ✓
- B Increased plasma protein binding leaves more free drug available to the brain
- C Hypoxia upregulates GABA-A receptors, increasing sensitivity to barbiturates
- D Reduced hepatic blood flow impairs clearance within the first minutes of injection
Explanation
Termination of thiopentone effect depends on redistribution from brain to lean muscle and fat, a process perfusion dependent. In shock, low cardiac output preferentially maintains flow to the vessel-rich group, including brain, and delays delivery to muscle. The same bolus therefore produces higher brain concentrations for longer, so the dose must be reduced substantially. Hepatic clearance is irrelevant to awakening after a single bolus because redistribution, not metabolism, terminates the effect.
Reference: Morgan and Mikhail's Clinical Anesthesiology, 7th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.