Pathophysiology
Clinical meaning
Neuromuscular blocking agents (NMBAs) act at the nicotinic acetylcholine receptors of the motor end plate at the neuromuscular junction. Depolarizing agents (succinylcholine) mimic acetylcholine and bind to nicotinic receptors causing initial depolarization and fasciculations, followed by sustained depolarization that renders the end plate refractory to further stimulation (Phase I block); prolonged exposure causes desensitization (Phase II block). Non-depolarizing agents (rocuronium, vecuronium, cisatracurium) competitively antagonize acetylcholine at the nicotinic receptor without causing depolarization, preventing sodium channel opening and muscle contraction. Paralysis follows a predictable pattern: small rapid muscles (eyes, fingers) → limb muscles → trunk → intercostals → diaphragm, with recovery occurring in reverse order.