Pharm 101: Suxamethonium

Class

Paralytic agent

Pharmacodynamics
  • Depolarising neuromuscular blocker that causes rapid neuromuscular blockade at motor endplate nicotinic receptors
  • Two phases of action: Phase 1 (depolarising) and Phase 2 (desensitising)
  • Phase 1:
    • Binding of drug to nicotinic receptors causes depolarisation of motor endplate
    • Fasciculations (transient contractions of muscle motor units) occur due to spread of impulse to adjacent membranes
    • Depolarised membranes remain depolarised and unresponsive to subsequent impulses, causing flaccid paralysis
  • Phase 2:
    • With prolonged exposure, initial end plate depolarisation decreases and membranes become repolarised
    • Membrane is desensitised and cannot easily be depolarised again
Pharmacokinetics
  • Rapid onset
  • Short duration of action 5-10 minutes
  • Rapid hydrolysis by:
    • Pseudocholinesterase in plasma (main pathway)
    • Butyrylcholinesterase in liver
  • Because plasma cholinesterase has an enormous capacity to hydrolyse suxamethonium, only a small percentage of the original intravenous dose ever reaches the neuromuscular junction
Clinical uses
  • Rapid Sequence Induction (RSI)
    • Dose 0.75-1.50 mg/kg
  • Clinical effects
    • Transient muscle fasciculations occur over chest and abdomen within 30 seconds following administration
    • As paralysis develops rapidly (< 90 seconds), the arm, neck and leg muscles are initially relaxed followed by respiratory muscles
    • Duration of blockade ~5-10 minutes
Adverse effects
  • Cardiac arrhythmias:
    • Stimulates nicotinic receptors at both sympathetic and parasympathetic ganglia and muscarinic receptors in the heart (e.g. sinus node)
    • Negative inotropic and chronotropic responses
  • Hyperkalaemia:
    • Fasciculations following administration of suxamethonium cause release of potassium from muscles
    • Patients with burns, nerve damage or neuromuscular disease, closed head injury and other trauma may develop proliferation of extrajunctional acetylcholine receptors
    • If proliferation is great enough, hyperkalaemia causing cardiac arrest may ensue
  • Raised intraocular pressure
  • Raised intragastric pressure
    • Increases of 5-40 cm H2O in heavily muscled patients due to fasciculations
  • Post-operative myalgia
    • Common in patients who receive large doses
    • Incidence 1-20%
  • Prolongation of neuromuscular blockade in patients with plasma cholinesterase deficiency
Further Reading
Pharm 101 700

Pharmacology 101

Top 200 drugs

MBBS (UWA) CCPU (RCE, Biliary, DVT, E-FAST, AAA) Emergency Medicine Advanced Trainee in Melbourne, Australia. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation. Editor-in-chief of the LITFL ECG Library. Twitter: @rob_buttner

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