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Anaes TopicsNeuromuscular blockade & reversal

Anaes · Neuromuscular blockade & reversal

Atracurium, cisatracurium and mivacurium

Also known as Benzylisoquinoline non-depolarising neuromuscular blockers · Organ-independent muscle relaxants · Hofmann-elimination relaxants

Atracurium, cisatracurium and mivacurium are the benzylisoquinoline non-depolarising neuromuscular blockers, competitive antagonists at the postsynaptic nicotinic (muscle-type) acetylcholine receptor that displace acetylcholine without activating the receptor, producing flaccid paralysis without depolarisation or fasciculation (Radkowski, 2026). Atracurium and cisatracurium are defined by ORGAN-INDEPENDENT elimination — Hofmann elimination (a non-enzymatic, pH- and temperature-dependent spontaneous degradation) plus ester hydrolysis by non-specific plasma esterases — so they are preferred in hepatic and renal failure and for prolonged intensive-care infusion, with the laudanosine metabolite (which crosses the blood-brain barrier and causes cerebral excitation and seizures at high concentrations) as the principal concern (Radkowski, 2025; 2026). Both atracurium and mivacurium release histamine on rapid bolus, but cisatracurium — a stereoisomer (the 1R-cis, 1R-prime-cis isomer) with NEGLIGIBLE histamine release and greater potency (so a lower dose and less laudanosine) — has largely replaced atracurium for cardiac surgery and intensive care (Roy, 2025; He, 2026). Mivacurium is the shortest-acting non-depolariser and is metabolised by plasma butyrylcholinesterase (the same enzyme as suxamethonium), so it is markedly prolonged in butyrylcholinesterase deficiency (Kempff-Andersen, 2026; Snak de Souza, 2026). The class is reversed by neostigmine and NOT by sugammadex (which encapsulates only the aminosteroids rocuronium and vecuronium), and anaphylaxis is a class risk (Zofia Lisiecka, 2026).

high8 referencesUpdated 26 July 202610 min readVerification in progress

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Red flags

  • Atracurium (and mivacurium) release HISTAMINE on rapid bolus — flushing, hypotension, tachycardia and bronchospasm; inject slowly and avoid in severe cardiovascular instability or asthma; use cisatracurium where histamine matters.
  • Laudanosine, the Hofmann-elimination metabolite of atracurium (and cisatracurium), crosses the blood-brain barrier and causes cerebral EXCITATION and seizures at high concentrations — it accumulates in renal failure, the elderly and prolonged high-dose infusion; use cisatracurium (lower dose, less laudanosine) and avoid prolonged high-dose atracurium infusions.
  • Mivacurium is metabolised by plasma butyrylcholinesterase (like suxamethonium) — it is PROLONGED in butyrylcholinesterase deficiency (genetic or acquired) and there is no pharmacological reversal; manage by sedation and ventilation.
  • The benzylisoquinolines are NOT reversed by sugammadex (it encapsulates only the aminosteroids rocuronium and vecuronium) — reverse with neostigmine, and for mivacurium await butyrylcholinesterase hydrolysis.
  • Hofmann elimination is slowed by hypothermia and acidosis — atracurium and cisatracurium duration is prolonged in the cold, acidotic patient despite being organ-independent.
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ANZCAFRCAABAEDAICFCAIFCA_SA

Red flags

  • Atracurium (and mivacurium) release HISTAMINE on rapid bolus — flushing, hypotension, tachycardia and bronchospasm; inject slowly and avoid in severe cardiovascular instability or asthma; use cisatracurium where histamine matters.
  • Laudanosine, the Hofmann-elimination metabolite of atracurium (and cisatracurium), crosses the blood-brain barrier and causes cerebral EXCITATION and seizures at high concentrations — it accumulates in renal failure, the elderly and prolonged high-dose infusion; use cisatracurium (lower dose, less laudanosine) and avoid prolonged high-dose atracurium infusions.
  • Mivacurium is metabolised by plasma butyrylcholinesterase (like suxamethonium) — it is PROLONGED in butyrylcholinesterase deficiency (genetic or acquired) and there is no pharmacological reversal; manage by sedation and ventilation.
  • The benzylisoquinolines are NOT reversed by sugammadex (it encapsulates only the aminosteroids rocuronium and vecuronium) — reverse with neostigmine, and for mivacurium await butyrylcholinesterase hydrolysis.
  • Hofmann elimination is slowed by hypothermia and acidosis — atracurium and cisatracurium duration is prolonged in the cold, acidotic patient despite being organ-independent.
The one-line answer

Atracurium, cisatracurium and mivacurium are the benzylisoquinoline non-depolarising neuromuscular blockers — competitive antagonists at the postsynaptic nicotinic receptor that produce flaccid paralysis without depolarisation. Atracurium and cisatracurium are defined by organ-independent elimination (Hofmann elimination plus ester hydrolysis), so they are the relaxants of choice in hepatic and renal failure and for prolonged ICU infusion. Cisatracurium spares you the histamine release of atracurium and mivacurium. None of the three is reversed by sugammadex — reverse with neostigmine, and for mivacurium await butyrylcholinesterase hydrolysis.[1]

Meet the patient

A 68-year-old man with end-stage liver and kidney disease from the medical ward needs emergency laparotomy for a perforated viscus. He is cardiovascularly fragile, and any relaxant that depends on hepatic or renal clearance will accumulate and prolong his paralysis unpredictably. The benzylisoquinolines exist for exactly this patient — their elimination does not need the liver or the kidney.[1]

Hold the four ideas that hold the whole family together: all three are competitive nicotinic antagonists (flaccid, non-depolarising); atracurium and cisatracurium clear independently of the organs that clear the aminosteroids; the family carries a shared liability — histamine release and the laudanosine metabolite — that cisatracurium was built to avoid; and sugammadex does not touch any of them.[1]

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References8ShowHide
  1. [1]Radkowski P, et al. Neuromuscular Blocking Agents in Anesthesia: A Narrative Review of Contemporary Challenges and Reversal Approaches J Clin Med, 2026.PMID 42123245
  2. [2]Radkowski P, et al. Use of Neuromuscular Blocking Agents in Elderly Patients: A Narrative Review in Geriatric Medicine Int J Gen Med, 2025.PMID 41399428
  3. [3]Roy VC, et al. The Use of Cisatracurium in Cardiac Surgery Turk J Anaesthesiol Reanim, 2025.PMID 40677119
  4. [4]Kempff-Andersen S, et al. Butyrylcholinesterase activity and prolonged duration of action of mivacurium in elderly patients (≥80 years): A secondary analysis of a clinical trial Eur J Anaesthesiol, 2026.PMID 42298973
  5. [5]Rybka H, et al. In silico assessment of neuromuscular blocking agents and fluoroquinolones as ligands of the Mas-related G protein-coupled receptor X2 Pharmacol Rep, 2026.PMID 41385156
  6. [6]He ZY, et al. Comparison of propofol-remifentanil target-controlled infusion with lidocaine versus neuromuscular blockade for laryngoscopy Minerva Anestesiol, 2026.PMID 42267885
  7. [7]Snak de Souza CD, et al. Genotype-phenotype relationships in butyrylcholinesterase deficiency: a systematic review Br J Anaesth, 2026.PMID 42120224
  8. [8]Zofia Lisiecka M, et al. Allergic reactions to anaesthetics in surgery: current challenges and perspectives Drug Metab Pers Ther, 2026.PMID 42229044

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