Skeletal muscle relaxants

Last updated: September 1, 2023

Summarytoggle arrow icon

Skeletal muscle relaxants are drugs that block the neuromuscular junction (NMJ) by binding to acetylcholine (ACh) receptors located on it. This process leads to paralysis of all skeletal muscles, starting with the small muscles of the face and paralyzing the diaphragm last. Succinylcholine, the only depolarizing NMJ-blocking drug, binds to ACh receptors and causes a prolonged depolarization of the motor end plate, resulting in flaccid paralysis. Nondepolarizing NMJ-blocking drugs bind to the ACh receptors and prevent depolarization of the motor end plate (depolarization block). These drugs are subdivided into short-acting, intermediate-acting, and long-acting agents. Based on the duration of action, NMJ-blocking drugs are useful adjuncts to anesthetic agents and are, therefore, used for laryngeal intubation, artificial ventilation, or intraoperative skeletal muscle relaxation. All NMJ-blocking drugs cause respiratory arrest (apnea) by paralyzing the diaphragm and intercostal muscles, requiring patients to be artificially ventilated. Succinylcholine is a known trigger of malignant hyperthermia and can also cause hyperkalemia, postoperative muscle pain, and cardiac arrhythmias. Nondepolarizing drugs that cause histamine release (atracurium) or have sympathomimetic properties (pancuronium) can cause bronchospasms and tachycardia. Patients who have received NMJ-blocking drugs must be monitored either clinically (e.g., ability to lift head/legs or open eyes) or with a peripheral nerve stimulator to assess the degree of skeletal muscle paralysis. Antagonists to nondepolarizing drugs (neostigmine, pyridostigmine, sugammadex) are used to reverse the NMJ block. Inadequate reversal can cause respiratory complications. Succinylcholine does not have a specific antagonist.

Overviewtoggle arrow icon

Overview of NMJ blockers
Depolarizing NMJ blockers (depolarizing muscle relaxants)
Mechanism of action Onset Duration Elimination Indications Adverse effects Additional considerations

Succinylcholine [1]

  • ∼ 60 second
  • 5–10 min
Nondepolarizing NMJ blockers (nondepolarizing muscle relaxants)


  • 2–4 min
  • 15–25 min

Rocuronium [3][4]

  • 1–3 min
  • 60–90 min
  • 70% hepatic
  • 30% renal
  • Rapid-sequence induction of anesthesia when succinylcholine is contraindicated
  • Second-fastest acting muscle relaxant
Vecuronium [6]
  • 2–3 min
  • Ongoing paralysis
  • 2–3 min
  • 45–60 min
  • 70%: enzymatic hydrolysis
  • 30%: Hofmann elimination (a process in which a compound spontaneously degrades in the plasma and tissue)
  • Ideal for patients with renal and hepatic insufficiency
Cisatracurium [7]
  • 3–5 min
  • 35–60 min
Long-acting Pancuronium
  • 3–5 min
  • 90–120 min
  • 70% renal
  • 30% hepatic
  • Respiratory depression or apnea
  • Sympathomimetic properties
  • Dose adjustments required in renal/hepatic insufficiency
  • ∼ 5 min
  • 60–120 min
  • ∼ 75% renal
  • ∼ 25% hepatic
  • Not used in clinical practice
  • Naturally occuring alkaloid

Pharmacodynamicstoggle arrow icon

Depolarizing and nondepolarizing muscle relaxants only target Nm nicotinic receptors at the NMJ; they do not target autonomic Nn receptors.

Depolarizing muscle relaxants

Nondepolarizing muscle relaxants

Paralysis affects the small muscles of the face first, progresses to the extremities and trunk, and affects the intercostal muscles and diaphragm last.

Adverse effectstoggle arrow icon

Depolarizing NMJ blocker (succinylcholine)

Nondepolarizing NMJ blockers


We list the most important adverse effects. The selection is not exhaustive.

Indicationstoggle arrow icon


Monitoringtoggle arrow icon

  • Patients who have been given NMJ blockers should be monitored.
  • Clinical assessment: ability of the patient to spontaneously open the eyes, lift the head/legs, or the presence of spontaneous ventilation help determine the degree of paralysis
  • Neuromuscular monitoring: objectively determines degree of muscle paralysis with the help of a peripheral nerve stimulator
    • Method: train-of-four response
    • Interpretation
      • 0 twitches indicates profound NMJ block
      • 1–2 twitches indicate a partial block.
      • 1 twitch per electric stimulus indicates no NMJ block.
    • Inadequate reversal (postoperative residual neuromuscular weakness) can lead to upper airway obstruction (pharyngeal muscle weakness) and inadequate ventilation

Referencestoggle arrow icon

  1. Succinylcholine Chloride. Updated: January 1, 2018. Accessed: March 7, 2018.
  2. $MIVACRON (mivacurium chloride) injection, solution.
  3. Rocuronium Bromide. Updated: February 18, 2017. Accessed: February 18, 2017.
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  5. Singh D, Sivashanmugam T, Kumar H, Nag K, Parthasarathy S, Shetti A. Sugammadex: A revolutionary drug in neuromuscular pharmacology. Anesth Essays Res. 2013; 7 (3): p.302.doi: 10.4103/0259-1162.123211 . | Open in Read by QxMD
  6. Kunjappan VE, Brown EM, Alexander GD. Rapid sequence induction using vecuronium. Anesth Analg. 1986; 65 (5): p.503-6.
  7. Nimbex (cisatracurium besylate injection) drug. . Accessed: February 18, 2021.
  8. Neuromuscular Blockers. Updated: February 18, 2017. Accessed: February 18, 2017.
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  16. Huggins RM, Kennedy WK, Melroy MJ, Tollerton DG. Cardiac arrest from succinylcholine-induced hyperkalemia. Am J Health Syst Pharm. 2003; 60 (7): p.694-697.
  17. Meakin GH. Neuromuscular blocking drugs in infants and children. Contin Educ Anaesth Crit Care Pain. 2007; 7 (5): p.143-147.doi: 10.1093/bjaceaccp/mkm032 . | Open in Read by QxMD
  18. Moss J. Muscle relaxants and histamine release. Acta Anaesthesiol Scand Suppl. 1995; 106: p.7-12.
  19. $Pharmacology of Muscle Relaxants and their Antagonists.
  20. Tietze KJ. Use of Neuromuscular Blocking Medications in Critically Ill Patients. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. Last updated: October 25, 2016. Accessed: February 18, 2017.

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