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Succinylcholine

Dithylinum

For medical students2 min readUpdated 2026-10-10

Succinylcholine is a depolarizing neuromuscular blocker consisting of a double acetylcholine molecule. It acts on the peripheral nervous system to induce brief, rapid skeletal muscle relaxation.

Mechanism of ActionNM receptor agonist that causes prolonged depolarization of the postsynaptic membrane.
Formulations2% solution (5 and 10 mL), 0.1 g and 0.2 g vials.
Clinical UseRapid sequence intubation (1.5–2 mg/kg) and maintenance of neuromuscular blockade (0.5–1 mg/kg every 5–7 min).
MetabolismHydrolyzed by plasma cholinesterase (pseudocholinesterase); resistant to acetylcholinesterase.
Key RisksMalignant hyperthermia, rhabdomyolysis, increased intraocular pressure.

Mechanism of Action

The drug acts as an NM receptor agonist at the motor end plate. By binding to these receptors, it induces membrane depolarization, clinically manifested as fasciculations (muscle twitches). Unlike acetylcholine, succinylcholine is resistant to synaptic acetylcholinesterase, allowing it to persist in the synapse, prolong depolarization, and render the membrane refractory to subsequent impulses.

Pharmacological Effects

The primary effect is rapid and brief skeletal muscle relaxation. The drug also exhibits muscarinic agonist activity, which can lead to bradycardia and hypersalivation. Additionally, it increases intraocular pressure due to tonic contraction of the extraocular muscles.

Indications and Administration

It is used for endotracheal intubation and short-term muscle relaxation during surgical procedures. For prolonged maintenance, the drug is administered intermittently (every 5–7 minutes) after dilution in 15–20 mL of 0.9% NaCl. Important clinical pearl: anticholinesterase agents are not antagonists of succinylcholine; rather, they potentiate its effect by inhibiting plasma pseudocholinesterase.

Side Effects and Contraindications

Severe complications include malignant hyperthermia (risk increases when combined with volatile inhaled anesthetics), rhabdomyolysis, and myoglobinemia. In patients with pseudocholinesterase deficiency, the duration of action is prolonged from 5–7 minutes to several hours, causing prolonged apnea. It is contraindicated in glaucoma, severe liver disease, anemia, pregnancy, and infancy.

Mnemonic

Succinylcholine is a "double acetylcholine": it hits the receptor twice, causes "fasciculations," and "freezes" the membrane in a depolarized state.

Frequently asked questions

What side effects does succinylcholine cause?

Succinylcholine causes systemic autonomic, specific muscular, and severe organ-system side effects:

  • Muscarinic effects — manifested as bradycardia and increased salivary gland secretion.
  • Ophthalmologic effects — increased intraocular pressure due to tonic contraction of extraocular muscles.
  • Severe muscular complications — rhabdomyolysis (breakdown of muscle tissue) and myoglobinemia.
  • Organ toxicity — hepatotoxicity (via toxic metabolites) and nephrotoxicity.
  • Malignant hyperthermia — a life-threatening condition characterized by a sharp temperature spike to 41–43 °C and skeletal muscle rigidity.
  • Prolonged neuromuscular blockade — extended apnea in patients with plasma pseudocholinesterase deficiency.
What are the contraindications for succinylcholine?

Contraindications include:

  • Glaucoma — due to the risk of elevated intraocular pressure.
  • Liver dysfunction — the liver synthesizes pseudocholinesterase, which metabolizes the drug.
  • Anemia.
  • Pregnancy.
  • Infancy.
Why are anticholinesterase drugs not used as an antidote for succinylcholine overdose?

They inhibit plasma cholinesterase, which is responsible for breaking down succinylcholine, thereby only prolonging its duration of action.

What is the "dual block" (phase II block) phenomenon?

It is a condition seen with repeated administration of succinylcholine where the initial depolarizing block transitions into a non-depolarizing (desensitization) block due to prolonged receptor occupation.

Why is succinylcholine contraindicated in glaucoma?

The drug causes tonic contraction of the extraocular muscles, which mechanically obstructs the outflow of aqueous humor and raises intraocular pressure.

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