Vecuronium (Norcuron) is a nondepolarizing, aminosteroid neuromuscular junction blocker that, like rocuronium, works at the level of neuromuscular end plate’s nicotinic acetylcholine receptors (AChR) as a competitive antagonist. Because it competes with acetylcholine for a similar binding site, vecuronium’s effects can be overcome to increasing the amount of “normal” substrate to displace it. This is the rationale for using drugs like neostigmine or edrophonium for paralytic reversal since both of these prevent the degradation of acetylcholine (thereby increasing its concentration to outcompete vecuronium).
As an anesthesiologist, I sometimes use vecuronium for the maintenance of an anesthetic when neuromuscular relaxation is indicated. In comparison to rocuronium, vecuronium is roughly 5-10 times more potent and must be reconstituted in bacteriostatic water as the medication comes as a powder. Rocuronium’s onset in equipotent doses is faster because a larger dose is required. This translates to more molecules being available to bind the postsynaptic nicotinic receptor to produce relaxation. Remember, ROcuronium = Rapid Onset-curonium. Both medications are also reversible with the cyclodextrin sugammadex.
As an intensivist, the idea of neuromuscular relaxation in the ICU is a double-edged sword. When used in the short term at the right time, it seems that paralysis helps facilitate oxygenation, less pulmonary inflammation (perhaps less alveolar distention required?), and may even improve mortality when used early in acute respiratory distress syndrome (ARDS). However, critical illness polyneuromyopathy (CIPM) is a debilitating condition that, when coupled with the deconditioning associated with prolonged ICU stays, can translate to difficulty in weaning from mechanical ventilation, extended rehabilitation, etc.
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