ANZCA Primary cheat sheet

Minimum alveolar concentration (MAC) is the end-tidal concentration at which 50% of subjects do not move in response to a standard surgical stimulus; MAC-awake is roughly one-third of MAC.

MAC is reduced by ~25-30% per decade of age after 40, by hypothermia, pregnancy, opioids, and IV anaesthetics; it is increased by hyperthermia and chronic ethanol use.

Oxygen delivery: DO2 = cardiac output × arterial oxygen content (CaO2), where CaO2 = (1.34 × Hb × SaO2) + (0.003 × PaO2).

Critical oxygen delivery occurs near 300-330 mL/min in adults; below this, oxygen consumption becomes supply-dependent and anaerobic metabolism ensues.

Frank-Starling relationship: stroke volume rises with preload until the plateau of the ventricular function curve; contractility shifts the whole curve upward and leftward.

Neuromuscular block: depolarising (suxamethonium) causes fasciculations and phase I block; non-depolarising agents are competitive antagonists at the postjunctional nicotinic receptor.

Train-of-four: a ratio >0.9 at the adductor pollicis indicates adequate recovery of neuromuscular function; fade indicates non-depolarising block.

Rapid sequence induction uses a pre-calculated induction dose of a fast-onset agent plus neuromuscular blockade without interposed ventilation, with cricoid force applied where indicated.

Local anaesthetic systemic toxicity: early CNS excitation (perioral tingling, tinnitus) precedes seizures and later cardiac toxicity; lipid emulsion is the specific rescue therapy.

Nociception involves transduction, transmission, modulation, and perception; primary afferents are A-delta (fast, sharp) and C fibres (slow, burning).

Gate control theory: large-diameter Aβ afferent input inhibits dorsal horn transmission of small-fibre nociceptive input via inhibitory interneurons.

Opioid receptors are mu, kappa, and delta (G-protein coupled); mu activation causes analgesia, respiratory depression, miosis, and constipation.

Equianalgesic conversion: oral morphine 30 mg ≈ oral oxycodone 20 mg ≈ oral hydromorphone 6 mg; always reduce the calculated dose for incomplete cross-tolerance (typically 25-50%).

Neuropathic pain is described with terms such as burning, shooting, and electric-shock quality, and responds to gabapentinoids, tricyclics, and SNRIs rather than simple analgesics.

NSAIDs inhibit cyclo-oxygenase, reducing prostaglandin synthesis; they carry risks of gastric ulceration, renal impairment, and platelet dysfunction.

Multimodal analgesia combines agents acting at different sites (paracetamol, NSAID, opioid, regional block) to reduce total opioid requirement and adverse effects.

Central sensitisation (wind-up) is activity-dependent increase in dorsal horn neuronal excitability mediated by NMDA receptor activation; ketamine is an NMDA antagonist.

Revised cardiac risk index (RCRI) predictors: ischaemic heart disease, heart failure, cerebrovascular disease, insulin-treated diabetes, renal impairment (creatinine >177 µmol/L), and high-risk surgery.

Perioperative beta-blockade should generally be continued in patients already taking it; abrupt withdrawal risks rebound tachycardia and ischaemia.

Postoperative nausea and vomiting risk factors (Apfel): female sex, non-smoker, history of PONV or motion sickness, and postoperative opioid use - each adds roughly 20%.

Enhanced recovery principles: preoperative optimisation and carbohydrate loading, opioid-sparing multimodal analgesia, early mobilisation, and early enteral feeding.

Perioperative hyperglycaemia is associated with increased infection and mortality; target blood glucose approximately 6-10 mmol/L in the perioperative period.

Venous thromboembolism prophylaxis should be risk-stratified by procedure and patient factors; mechanical methods plus pharmacological agents where bleeding risk permits.

Perioperative anaphylaxis: common culprits include neuromuscular blocking agents, antibiotics, chlorhexidine, and latex; tryptase sampling supports later diagnosis.

Preoperative fasting for clear fluids is typically 2 hours and for light meals 6 hours, reflecting gastric emptying rather than a fixed midnight cut-off.

Henderson-Hasselbalch: pH = 6.1 + log([HCO3-]/(0.03 × PaCO2)); a rise in PaCO2 of 10 mmHg lowers pH by about 0.08 acutely.

Oxygen-haemoglobin dissociation curve shifts right (reduced affinity) with increased temperature, CO2, 2,3-DPG, and acidosis (Bohr effect); fetal Hb shifts left.

Nernst equation: E = (RT/zF) × ln([ion]out/[ion]in); the resting membrane potential sits near the potassium equilibrium potential.

Starling equation: fluid flux = Kf[(Pc - Pi) - σ(πc - πi)]; increased capillary hydrostatic pressure or reduced oncotic pressure promotes oedema.

Functional residual capacity is the volume remaining after passive expiration (ERV + RV) and is reduced by supine position, obesity, pregnancy, and anaesthesia.

Graham's law: the rate of diffusion of a gas is inversely proportional to the square root of its molecular weight; this underlies nitrous oxide's rapid alveolar uptake.

Clearance = rate of elimination / plasma concentration; half-life = 0.693 × volume of distribution / clearance.

Renal handling: inulin clearance measures GFR; para-aminohippurate clearance approximates effective renal plasma flow.

Acid-base: the anion gap = Na+ - (Cl- + HCO3-), normally 8-12 mmol/L; a raised gap suggests accumulation of unmeasured anions such as lactate or ketones.