Vecuronium: An Advanced Review of a Neuromuscular Blocking Agent

Vecuronium is a widely utilised aminosteroid-derived neuromuscular blocking agent (NMBA) classified as a non-depolarising muscle relaxant. By competitively antagonising nicotinic acetylcholine receptors at the neuromuscular junction, it induces reversible skeletal muscle paralysis, making it indispensable in anaesthetic and critical care settings. The agent's pharmacological profile ensures its role in facilitating endotracheal intubation, optimising mechanical ventilation, and enabling precise skeletal muscle relaxation during surgical interventions.

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Clinical Applications of Vecuronium

The principal indications for Vecuronium include:

Facilitation of endotracheal intubation, especially in anaesthesia and emergency airway management.
Adjunctive use in general anaesthesia, ensuring optimal muscular relaxation during surgical procedures.
Mechanical ventilation in intensive care units (ICUs) to minimise oxygen consumption and improve ventilatory synchrony.
Electroconvulsive therapy (ECT) adjunct, mitigating excessive muscular contractions and associated injury.

Dosage and Administration

The dosing regimen of Vecuronium is contingent upon patient-specific factors such as age, weight, renal and hepatic function, and comorbid conditions.

Intubation Dose: 0.08–0.1 mg/kg IV bolus.
Maintenance Dose: 0.01–0.02 mg/kg IV at intervals of 20–45 minutes.
Continuous Infusion: Initiated at 1–2 mcg/kg/min, titrated to neuromuscular blockade depth.
Paediatric Considerations: While similar dosing is employed, neonates exhibit prolonged drug effects due to immature hepatic metabolism.

Dose Modifications in Renal and Hepatic Dysfunction

Renal Insufficiency

Given that Vecuronium is primarily hepatically metabolised with minor renal excretion, patients with renal impairment may experience prolonged neuromuscular blockade.

Mild to moderate renal dysfunction: Standard dosing with enhanced neuromuscular monitoring.
End-stage renal disease (ESRD): Consider dose reduction or alternative NMBA due to unpredictable clearance.

Hepatic Dysfunction

As Vecuronium undergoes extensive hepatic metabolism, its clearance is significantly impaired in hepatic insufficiency, leading to prolonged paralysis.

Moderate to severe hepatic impairment: Require reduced dosing and meticulous neuromuscular monitoring.

Pharmacological Effects and Adverse Reactions

Therapeutic Effects

Profound skeletal muscle relaxation to facilitate controlled ventilation and surgical procedures.
Predictable duration of action allowing precise titration.

Adverse Reactions

Extended paralysis in predisposed individuals.
Hypotension and tachycardia, occasionally secondary to histamine release.
Residual neuromuscular blockade, necessitating appropriate reversal strategies.

Concomitant Drug Use

Vecuronium is frequently co-administered with various pharmacologic agents:

Opioids (e.g., fentanyl, remifentanil): Enhancing analgesic coverage.
Intravenous anaesthetics (e.g., propofol, thiopental): Inducing unconsciousness.
Neuromuscular reversal agents (e.g., sugammadex, neostigmine): Ensuring timely recovery from blockade.

Formulation and Availability

Vecuronium is available as a lyophilised powder in 10 mg vials, requiring reconstitution with sterile water or saline prior to intravenous administration.

Pharmacokinetics and Pharmacodynamics

Onset of Action: 2–3 minutes post IV administration.
Duration: 25–40 minutes (dose-dependent).
Metabolism: Primarily hepatic biotransformation.
Elimination: Predominantly biliary excretion, with minor renal contribution.
Half-life: 51–80 minutes, prolonged in hepatic impairment.

Drug Interactions

Vecuronium demonstrates significant pharmacodynamic interactions:

Enhanced neuromuscular blockade with aminoglycosides (e.g., gentamicin) and magnesium sulphate.
Reduced efficacy with chronic anticonvulsant therapy (e.g., phenytoin, carbamazepine).
Prolonged blockade with volatile anaesthetics (e.g., sevoflurane, desflurane).

Comparative Analysis of Non-Depolarising Neuromuscular Blockers

Drug	Onset	Duration	Metabolism	Reversal
Vecuronium	2–3 min	25–40 min	Hepatic	Neostigmine/Sugammadex
Rocuronium	1 min	30–50 min	Hepatic	Sugammadex
Pancuronium	3–5 min	60–90 min	Renal & hepatic	Neostigmine
Atracurium	2–3 min	20–35 min	Hofmann elimination	Neostigmine

Safety Considerations and Special Precautions

Myasthenia gravis patients exhibit exaggerated sensitivity to Vecuronium.
Elderly and critically ill patients require reduced dosing due to prolonged clearance.
Neuromuscular monitoring is essential to prevent residual blockade.

Toxicity, Overdose, and Management

Clinical Manifestations

Prolonged neuromuscular blockade leading to respiratory paralysis.
Haemodynamic instability in severe cases.

Intervention Strategies

Mechanical ventilation to sustain respiration.
Pharmacological reversal via neostigmine with atropine or sugammadex.
Haemodialysis is ineffective due to high protein binding.

Recent Advances and 2025 Guidelines

Sugammadex remains the gold-standard reversal agent, providing rapid and complete recovery from Vecuronium-induced blockade.
New ASA recommendations advocate lower dosing in renal-compromised patients to mitigate prolonged paralysis.
Comparative trials suggest rocuronium as a superior choice for rapid sequence intubation owing to its expedited onset.

Key Takeaways

Vecuronium lacks intrinsic sedative or analgesic properties, necessitating adjunctive anaesthetics.
Preferred in prolonged procedures over short-acting alternatives like suxamethonium.
Neuromuscular monitoring is indispensable to avert inadvertent overdosing.

References

Miller’s Anaesthesia, 2025 Edition.
British Journal of Anaesthesia, 2025 Guidelines.
ASA Neuromuscular Blocking Agents Guidelines, 2025.
European Society of Anaesthesiology 2025 Review.
Pharmacology and Physiology in Anaesthetic Practice, 5th Edition.

Pages

Vecuronium