Basic Sciences Applied to Anesthesiology
What you must understand
Master the physiology that drives every intraoperative decision: oxygen delivery (DO2 = CO × CaO2), the oxyhemoglobin dissociation curve and its shifts (right shift: ↑CO2, ↑H+, ↑temperature, ↑2,3-DPG; left shift: fetal Hb, CO, alkalosis, hypothermia), lung volumes and closing capacity (closure increases with age and supine position, promoting atelectasis and shunt), and the Frank-Starling relationship. Learn receptor pharmacology as a system: GABA-A (propofol, benzodiazepines, volatile agents), NMDA (ketamine), mu-opioid (fentanyl family), and the ester vs amide metabolism of local anesthetics (pseudocholinesterase vs hepatic; amides are the ones implicated in LAST). Understand MAC as a potency measure and its modifiers (age, temperature, pregnancy, drugs).
Traps in questions
The classic trap is confusing potency with speed: MAC is potency, not onset. Another is the ionized vs total drug concept - only un-ionized, non-protein-bound drug crosses membranes, so hypoalbuminemia increases free fraction of highly bound drugs (e.g., phenytoin, midazolam). Questions often test that bupivacaine is more cardiotoxic than lidocaine and that ropivacaine/levobupivacaine are less so. Watch for pseudocholinesterase deficiency presenting as prolonged paralysis after succinylcholine, not after non-depolarizers.
Rule of thumb
For any "why is this drug/state different in the elderly/pregnant/neonate" question, reason from altered protein binding, altered cardiac output, and altered receptor sensitivity - never from a memorized number alone.
Worked example: A patient with cirrhosis has low albumin. Highly protein-bound anesthetics have more free drug, so the same dose produces a greater effect - reduce dose and titrate.