Anaesthesia: Core Pharmacology and Physiology Reasoning
What you must understand
Anaesthesia questions reward a mechanistic chain, not a memorised list. For any drug, be able to move from receptor or channel → organ effect → measurable change → clinical consequence. Core anchors: volatile agents (MAC concept, blood:gas and oil:gas partition coefficients, second-gas effect, concentration effect), IV induction agents (propofol, ketamine, thiopentone, etomidate), neuromuscular blockers (depolarising vs non-depolarising, phase I vs phase II block, sugammadex encapsulation), and local anaesthetics (weak-base pKa logic, pH-dependent ion trapping, use-dependent block, cardiotoxicity ranking).
Traps that appear in questions
- Confusing potency (MAC, lower = more potent) with speed of onset (blood:gas solubility, lower = faster).
- Forgetting that a more soluble agent has a slower rise in alveolar concentration.
- Mixing up context-sensitive half-time (accumulation with infusion) with elimination half-life.
- Assuming a weak base works equally well in acidic tissue - it does not; less unionised drug crosses the membrane.
- Attributing hypotension solely to myocardial depression when vasodilation dominates.
Worked rule of thumb
For onset speed, invert solubility: lower blood:gas → faster equilibration → faster onset. Desflurane (blood:gas ≈0.42) beats sevoflurane (≈0.65) beats isoflurane (≈1.4). Apply the same logic to LA: pKa closest to pH 7.4 gives the greatest unionised fraction and fastest onset (e.g., lidocaine pKa 7.9 vs bupivacaine 8.1).