Brands, Medical Use, Clinical Data
- Neuromuscular Depolarizing Agents
- Skeletal Muscle Relaxants
Brands / Synonyms
Anectine; Quelicin; Quelicin Preservative Free; Succinylcholine Chloride; Sucostrin
Used in surgical procedures where a rapid onset and brief duration of muscle relaxation is needed (includes intubation, endoscopies, and ECT)
Succinylcholine is indicated as an adjunct to general anesthesia, to facilitate tracheal intubation, and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Succinylcholine is a depolarizing skeletal muscle relaxant. As does acetylcholine, it combines with the cholinergic receptors of the motor end plate to produce depolarization. This depolarization may be observed as fasciculations. Subsequent neuromuscular transmission is inhibited so long as adequate concentration of succinylcholine remains at the receptor site. Succinylcholine has no direct action on the uterus or other smooth muscle structures.
Mechanism of Action
The mechanism of action of Succinylcholine involves what appears to be a "persistent" depolarization of the neuromuscular junction. This depolarization is caused by Succinylcholine mimicking the effect of acetylcholine but without being rapidly hydrolysed by acetylcholinesterase. This depolarization leads to desensitization.
Biotrnasformation / Drug Metabolism
Succinylcholine is contraindicated in persons with personal or familial history of malignant
hyperthermia, skeletal muscle myopathies, and known hypersensitivity to the drug. It is also contraindicated in
patients after the acute phase of injury following major burns, multiple trauma, extensive denervation of skeletal
muscle, or upper motor neuron injury, because succinylcholine administered to such individuals may result in severe
hyperkalemia which may result in cardiac arrest. The risk of hyperkalemia in these patients increases over time and
usually peaks at 7 to 10 days after the injury. The risk is dependent on the extent and location of the injury. The
precise time of onset and the duration of the risk period are not known.
Drugs which may enhance the neuromuscular blocking action of succinylcholine include: promazine,
oxytocin, aprotinin, certain non-penicillin antibiotics, quinidine, b-adrenergic blockers,
procainamide, lidocaine, trimethaphan, lithium carbonate, magnesium salts, quinine, chloroquine, diethylether,
isoflurane, desflurane, metoclopramide, and terbutaline. The neuromuscular blocking effect of succinylcholine may be
enhanced by drugs that reduce plasma cholinesterase activity (e.g., chronically administered oral contraceptives,
glucocorticoids, or certain monoamine oxidase inhibitors) or by drugs that irreversibly inhibit plasma
If other neuromuscular blocking agents are to be used during the same procedure, the possibility of a
synergistic or antagonistic effect should be considered.