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Skeletal muscle relaxants

Last updated: June 9, 2021

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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.

Overview of NMJ blockers
Depolarizing NMJ blockers (depolarizing muscle relaxants)
Time until onset of effect Duration of action Elimination Characteristics

Succinylcholine [1]

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


  • 2–4 min
  • 15–25 min
  • 90%: enzymatic hydrolysis
  • < 10%: hepatic clearance

Rocuronium [2][3]

  • 1–3 min
  • 60–90 min
  • 70% hepatic
  • 30% renal
  • Used for rapid-sequence induction of anesthesia when succinylcholine is contraindicated (second fastest acting muscle relaxant)
  • Does not cause histamine release (see “Side effects” below)
  • Specifically antagonized by sugammadex [4]
  • 2–3 min
  • 45–60 min
  • 60%: enzymatic hydrolysis
  • 30%: Hoffmann elimination
  • Ideal for patients with renal and hepatic insufficiency
  • Causes histamine release
Cisatracurium [5]
  • 3–5 min
  • 35–60 min
  • Ideal for patients with renal and hepatic insufficiency
  • Does not cause histamine release
Vecuronium [6]
  • 2–3 min
  • 60–90 min
  • 70% hepatic
  • 30% renal
Long-acting Pancuronium
  • 3–5 min
  • 90–120 min
  • 70% renal
  • 30% hepatic
  • Used if skeletal muscle paralysis > 1 hour is required
  • Cardiovascular side effects are common
  • ∼ 5 min
  • 60–120 min
  • ∼ 75% renal
  • ∼ 25% hepatic
  • Respiratory side effects are common

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.

Depolarizing NMJ blocker (succinylcholine)

Nondepolarizing NMJ blockers


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


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