STEPTRACKERPHARMACOLOGY + ANESTHESIOLOGY | NEUROLOGY | HIGH-YIELD REVIEW
Anesthetics & Neuromuscular Blockers
General anesthetics switch off consciousness, local anesthetics block nerve conduction, and neuromuscular blockers paralyze — each with rules about potency, speed and reversal.
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Inhaled anesthetics: potency ∝ lipid solubility (↓
MAC = more potent); speed ∝
low blood solubility (low blood/gas coefficient: N₂O, desflurane fast). Adverse: ↓ BP, respiratory depression, ↑ cerebral flow;
malignant hyperthermia (RYR1; with succinylcholine) →
dantrolene; halothane hepatitis; N₂O → B12 inactivation.
IV:
propofol (GABA-A; hypotension, propofol infusion syndrome),
ketamine (NMDA; ↑ BP, dissociation, bronchodilation),
etomidate (hemodynamically stable; adrenal suppression), midazolam, barbiturates, opioids.
Local anesthetics block Na⁺ channels from inside (non-ionized form crosses);
esters (procaine, tetracaine, benzocaine — PABA allergy) vs
amides (lidocaine, bupivacaine, ropivacaine). Infection (acidic) ↓ effect; epinephrine prolongs. Toxicity: CNS → seizures, cardiovascular (bupivacaine) →
lipid emulsion; benzocaine → methemoglobinemia.
NM blockers:
succinylcholine (depolarizing;
hyperkalemia — avoid in burns, crush, denervation; MH; reversal none, phase II block) vs
nondepolarizing (rocuronium, vecuronium, cisatracurium — Hofmann elimination) reversed by
neostigmine + glycopyrrolate or
sugammadex.