Rocuronium is an aminosteroid nondepolarizing neuromuscular junction blocker (NMJB) I routinely use to facilitate tracheal intubation. The name rocuronium comes from the fact that it’s a rapid onset -curonium (referring to its steroid structure). With a “rapid sequence” dose (usually 1.2 mg/kg), it has an onset almost as fast as succinylcholine without the risks of malignant hyperthermia or significant hyperkalemia in the context of various denervation injuries.
Like all nondepolarizing NMJBs, rocuronium works at the level of neuromuscular end plate’s nicotinic acetylcholine receptors as a competitive antagonist. As such, its effects can be overcome by increasing the amount of “normal” substrate (acetylcholine). This is the rationale behind using drugs like neostigmine or edrophonium which prevent the degradation of acetylcholine.
In 2015, the FDA approved cyclodextrin drug sugammadex, as selective relaxant binding agent, to reverse the effects of rocuronium and vecuronium. This alternative means of reversing paralysis is, in my opinion, much cleaner than the more traditional combination of neostigmine with glycopyrrolate; however, in larger patients with more profound residual paralysis, sugammadex is arguably more expensive.
As always, drop me a comment below with questions! 🙂