Neuromuscular blocking agents (NMBAs) interfere with the binding of acetylcholine to the motor endplate, which blocks the transmission of nerve impulses at the myoneural junction and results in temporary paralysis of the skeletal muscle.¹ The NMBAs are categorized according to their mechanism of action as depolarizing NMBAs and non-depolarizing NMBAs. The depolarizing NMBAs bind to cholinergic receptors on the motor endplate, resulting in initial depolarization of the endplate membrane and then neuromuscular transmission blockade. The non-depolarizing NMBAs bind to acetylcholine receptors and either prevent conformational changes in the receptors or obstruct the ion channels preventing generation of the endplate potential.¹

The introduction of NMBAs, which induce temporary paralysis, transformed the practice of anesthesia and NMBAs have become an important component of general anesthesia.^1,2 However, it is essential to have successful recovery from neuromuscular blockade when it is no longer required, to avoid residual paralysis and its detrimental consequences.² Recovery from neuromuscular blockade may be spontaneous or may require the use of pharmacologic reversal agents.² The timing and dosing of these reversal agents are determined by the extent of spontaneous recovery.²

Neuromuscular blockade can be assessed by different ways such as assessment based on clinical signs and assessments based on train of four (TOF). Clinical signs include spontaneous ventilation, eye opening and five-second head lift.^3,4 TOF involves stimulation of the peripheral nerves. Using a peripheral nerve stimulator, four shocks of 2 Hz each are applied to the ulnar or facial nerves and visual observation of the muscular response is used to determine the degree of neuromuscular blockade.⁴ This enables assessment of the extent of neuromuscular transmission when NMBAs are administered to block musculoskeletal activity. Patients treated with NMBAs have progressive reduction in the magnitude of response to the TOF stimuli and TOF stimulation and monitoring may be used to assist in the titration of the NMBA dose.¹ Appropriate titration may prevent unnecessary prolonged paralysis.

In the intensive care unit (ICU), NMBAs may be used to facilitate short procedures under general anesthesia, to facilitate mechanical ventilation, to manage patients with increased intracranial pressure, massive hemoptysis, tetanus, or neuroleptic malignant syndrome.^1,5

There appears to be controversy regarding the use of neuromuscular monitoring. One review¹ has reported on three trials comparing neuromuscular monitoring using the peripheral nerve stimulator (TOF monitoring) versus clinical assessment and reported conflicting results, with benefit being demonstrated with TOF in one trial and not in two trials.

The purpose of this report is to review the clinical efficacy and the evidence-based guidelines regarding neuromuscular monitoring for guiding treatment and therapy for patients in the intensive care unit receiving continuous paralytic or neuromuscular blocking agents.