Pain, Agitation/Sedation, Delirium, Immobility, Sleep Disruption, and Neuromuscular Blockade

Vecuronium: Intermediate-acting aminosteroid; often used as a continuous infusion

Pharmacokinetics: Hepatically metabolized (30%–50%); cleared renally (20%–30%), with

fecal excretion. Has an active metabolite, around half the activity of parent compound.

Duration 30 minutes after bolus intubation dose.

ii.

Adverse effects: Vagolytic activity at higher doses, prolonged weakness

iii.

Can be reversed with sugammadex by forming a complex that decreases the amount of

vecuronium available to bind to nicotinic receptors in the neuromuscular junction.

Rocuronium: An intermediate-acting aminosteroid; considered a suitable alternative to

succinylcholine for rapid sequence intubation (dose: 0.6–1.2 mg/kg) because of its rapid onset of

action (60–90 seconds). Duration 30–40 minutes.

Pharmacokinetics: Primarily hepatically metabolized, minimal renal excretion. No active

metabolite. Prolonged effects have been observed in patients with hepatic or renal failure.

ii.

Adverse effects: Vagolytic activity at higher doses, bradycardia

iii.

Can be reversed with sugammadex by forming a complex that decreases the amount of

rocuronium available to bind to nicotinic receptors in the neuromuscular junction.

15% cisatracurium)

Pharmacokinetics: Undergoes Hofmann elimination to form the toxic metabolite laudanosine

at high levels. Laudanosine is a cerebral stimulant that may precipitate seizure activity,

clearance dependent on liver and kidney function. Duration of atracurium 20–40 minutes.

ii.

Adverse effects: Histamine release may cause cardiovascular adverse effects and bronchospasm;

laudanosine accumulation may cause seizure activity.

Cisatracurium: An intermediate-acting benzyl isoquinolinium. Differences compared with

atracurium: It is only one isomer, has a slower onset at normal bolus doses, no histamine release.

Pharmacokinetics: Undergoes Hofmann elimination, forms laudanosine but at much lower

levels than atracurium. Renal and hepatic dysfunction do not alter cisatracurium clearance.

Duration 30–60 minutes.

ii.

Adverse effects: Prolonged weakness with continued use

can enhance or prolong the paralytic action.

Drugs decreasing the activity of NMBAs:

Calcium: Antagonizes the effect of magnesium on neuromuscular blockade

Carbamazepine: Competitor of acetylcholine receptor

Phenytoin: Depressed postsynaptic response to acetylcholine

Theophylline: Unknown mechanism

Antimicrobials:

Aminoglycosides,

clindamycin,

tetracyclines,

vancomycin.

Decreases

prejunctional acetylcholine release with decreased postjunctional acetylcholine receptor sensitivity;

blocks acetylcholine receptor.

Cardiac medications: β-Blockers, calcium channel blockers, procainamide, quinidine, and

furosemide. Decreases prejunctional acetylcholine release.

Immunosuppressants: Steroids (decrease end plate sensitivity to acetylcholine), cyclosporine

(inhibits metabolism of certain NMBAs)