Basic Sciences (Anatomy, Physiology, Pathophysiology, Pharmacology)
Core physiology and pharmacology
Build the exam around a handful of organizing ideas. Pharmacokinetics: volume of distribution, clearance, context-sensitive half-time, and the effect-site equilibration constant (ke0) explain why propofol and alfentanil wake quickly after long infusions while thiopental and fentanyl do not. Pharmacodynamics: MAC is the median concentration preventing movement to a noxious stimulus; it is additive across agents, lower in the elderly, pregnant, hypothermic, or opioid-loaded patient, and higher in children. Receptors: GABA-A (propofol, benzodiazepines, volatiles), NMDA (ketamine, nitrous oxide), and alpha-2 (dexmedetomidine).
Physiology: closing capacity rises with age relative to FRC, producing airway closure and shunt; hypoxic pulmonary vasoconstriction limits that shunt; LaPlace and Frank-Starling govern ventricular loading; the oxyhemoglobin curve shifts with pH, temperature, 2,3-DPG, and fetal hemoglobin.
Local anesthetics: the unionized fraction crosses the membrane, but the ionized form blocks from within. pKa relative to tissue pH sets onset (inflamed, acidic tissue slows it), lipophilicity drives potency, and protein binding drives duration.
Trap: questions swap potency for onset, or ignore a second inhaled agent when asking about depth.
Worked example: isoflurane MAC 1.15%, nitrous oxide MAC 104%. Giving 0.6% isoflurane plus 70% N2O yields 0.52 + 0.67 = about 1.19 MAC. Contributions are strictly additive, and the nitrous oxide share is not negligible.