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Clinical use of neuromuscular blocking agents in critically ill patients

Edward A Bittner, MD, PhD, MSEd, FCCM
Section Editor
Polly E Parsons, MD
Deputy Editors
Geraldine Finlay, MD
Marianna Crowley, MD


Neuromuscular blocking agents (NMBAs) paralyze skeletal muscles by blocking the transmission of nerve impulses at the myoneural junction. NMBAs may be useful in the intensive care unit (ICU) for several indications.

The clinical use, administration, and potential adverse effects of NMBAs in critically ill patients will be discussed here. The pharmacology of NMBAs and use in patients undergoing anesthesia, and intubation in the emergency department, are discussed separately. (See "Clinical use of neuromuscular blocking agents in anesthesia" and "Neuromuscular blocking agents (NMBAs) for rapid sequence intubation in adults outside of the operating room".)


Neuromuscular blocking agents (NMBAs) (table 1) block the binding of acetylcholine (ACh) to the motor endplate. They are divided into depolarizing or nondepolarizing agents based upon their mechanism of action [1-4].

Depolarizing NMBAs bind to cholinergic receptors on the motor endplate, causing initial depolarization on the endplate membrane followed by blockade of neuromuscular transmission. Succinylcholine is the only depolarizing agent available in the United States and is utilized almost exclusively to facilitate intubation or treat laryngospasm [3,5].

Nondepolarizing NMBAs competitively inhibit the ACh receptor on the motor endplate. Drug binding to the ACh receptor either prevents the conformational change in the receptor or physically obstructs the ion channels so that an endplate potential is not generated [6,7]. Nondepolarizing NMBAs are divided into aminosteroid compounds (eg, pancuronium, vecuronium, rocuronium) and benzylisoquinolinium compounds (eg, atracurium, cisatracurium, mivacurium).

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Literature review current through: Nov 2017. | This topic last updated: Oct 25, 2017.
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