Neuromuscular blocker
Succinylcholine
Also called sux
Indications
- Rapid sequence intubation in the emergency department and ICU, for the fastest onset and shortest action of any paralytic
- Tracheal intubation and brief relaxation for short procedures under general anesthesia
- Laryngospasm that persists despite positive-pressure ventilation
- Intramuscular use for an emergency airway when no vein is available
Dosing
| Where | Dose |
|---|---|
| Airway and RSI | Succinylcholine: 1–1.5 mg/kg; avoid in hyperkalemia, burns or crush over 24–72 h old, neuromuscular disease, malignant hyperthermia history |
On the quick cards
Mechanism of action
Succinylcholine is two acetylcholine molecules joined through their acetyl groups. It binds the acetylcholine sites on the two α1 subunits of the adult muscle nicotinic receptor (α1, α1, β1, δ, ε) and opens its cation channel, so the end plate depolarizes and the fibers fasciculate. Acetylcholinesterase in the cleft does not hydrolyze it, so the end plate stays depolarized, the surrounding voltage-gated sodium channels stay inactivated and no new action potential can start: the muscle goes flaccid (phase I block). Large or repeated doses desensitize the receptors, and the block takes on nondepolarizing features (phase II).
Pharmacology
- Neuromuscular: fasciculations, then flaccid paralysis spreading from the face and glottis to the intercostals and diaphragm; phase I block shows no fade on train-of-four and is deepened, not reversed, by neostigmine
- Cardiovascular: also stimulates muscarinic receptors and autonomic ganglia; bradycardia, junctional rhythm or asystole are likeliest with a second dose and in children, while ganglionic stimulation can raise heart rate and blood pressure
- Metabolic: potassium rises about 0.5–1 mEq/L; after burns, crush, denervation or immobility, immature (γ) and α7 receptors spread over the whole fiber, the drug and its metabolite choline hold them open, and the potassium leak can stop the heart
- Other: brief rises in intraocular, intragastric and intracranial pressure; myalgia; masseter spasm; triggers malignant hyperthermia in carriers of RYR1 or CACNA1S variants
- CNS: none; it does not cross the blood-brain barrier and gives no sedation, amnesia or analgesia
Pharmacokinetics
| Onset | Under 1 min IV (30–60 s); 2–3 min IM |
|---|---|
| Peak | Full block about 1 min after an IV dose, held for about 2 min |
| Duration | Recovery over the next 4–6 min, so under 10 min in all after an intubating dose |
| Half-life | About 47 s in plasma (Torda 1997); undetectable 2.5 min after 1–2 mg/kg |
| Distribution | Mostly extracellular fluid; permanently charged and poorly lipid soluble, so little crosses the blood-brain barrier or placenta |
| Metabolism | Plasma cholinesterase (butyrylcholinesterase, made in the liver) hydrolyzes most of a dose before it reaches the end plate: first to succinylmonocholine, a negligible blocker, then more slowly to succinic acid and choline |
| Elimination | The block ends as drug diffuses from the junction back into plasma; about 10% is excreted unchanged in urine |
| Cholinesterase variants | Homozygous atypical BCHE genes (about 1 in 2,500–5,000 people) prolong paralysis to several hours; heterozygotes only modestly. Dibucaine number 70–90 normal, 30–70 heterozygous, under 30 homozygous |
| Low enzyme activity | Pregnancy (about 24% lower), severe liver or kidney disease, cancer, burns, infection, myxedema; organophosphates, echothiophate, some chemotherapy, MAOIs, chronic steroids or oral contraceptives |
Chemistry
- Dicholine ester of succinic acid: two quaternary ammonium heads joined by a short diester chain
- Achiral; its two permanent positive charges make it very water soluble and almost insoluble in lipid at any pH
- 20 mg/mL at pH about 3.5 (multidose vials contain methylparaben; prefilled syringes are preservative-free); the ester hydrolyzes in alkaline solution, so never mix it with thiopental or anything above pH 8.5
- Refrigerate at 2–8 °C; vials and syringes keep up to 14 days at room temperature, so date them when they leave the refrigerator
Adverse effects and cautions
In the one-pagers
- Airway and RSIRSI drugs: Avoid succinylcholine with hyperkalemia, malignant hyperthermia risk, myopathy, or burns, crush, stroke or cord injury past the acute phase (risk peaks 7–10 days).
- Myasthenic Crisis and Guillain-Barré SyndromeNIV or intubation: GBS: no succinylcholine (denervation hyperkalemia, even in recovery)
- Toxidromes and AntidotesSerotonin toxicity, NMS and malignant hyperthermia: Trigger: Serotonergic drug started, raised or combined: Dopamine blocker, or stopping levodopa: Volatile anesthetic or succinylcholine
- BurnsInhalation injury, airway, CO and cyanide: Succinylcholine is acceptable in the first 24 hours (Datta 2022); after that, upregulated acetylcholine receptors risk severe hyperkalemia until the wounds heal.
- Mass Casualty Triage and Incident CommandCBRNE: decontamination, nerve agents and radiation: Nerve agents inhibit acetylcholinesterase. Vapor acts in seconds to minutes: miosis, rhinorrhea and chest tightness, then bronchorrhea, bronchospasm, fasciculations, seizures and apnea. Liquid on skin can take up to 18 hours to cause systemic effects (Merck 2026). In Tokyo, over 20% of St Luke's staff had symptoms of secondary exposure (Ohbu 1997
- Spinal Motion RestrictionBreathing after high cord injury: Intubate with manual in-line stabilization and the collar front open, by video laryngoscope or awake fiberoptic technique, with fluid, a vasopressor and atropine ready: up to 30% of patients with tetraplegia become hypotensive on induction. Avoid succinylcholine after the first 48 hours, when denervated muscle can release enough potassium to stop the heart (Consor
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Sources
- FDA label: Anectine (2023)
- Torda 1997 (half-life)
- Martyn 2006 (hyperkalemia)
- MedlinePlus Genetics: pseudocholinesterase deficiency (2025)
For education and exam preparation only. Follow your institution’s protocols. Typical adult values for study. Follow the order, the label and your institution's protocols.