Mechanism of action
The drug acts as an NM-cholinergic receptor agonist of the motor end-plate. Interacting with them, it causes membrane depolarization, which clinically manifests as fasciculations (muscle twitches). Unlike acetylcholine, suxamethonium is resistant to synaptic acetylcholinesterase, so it remains in the synapse for a long time, maintaining depolarization and rendering the membrane refractory to new impulses.
Pharmacological effects
The main effect is rapid and short-term skeletal muscle relaxation. The drug exhibits muscarinic (M-cholinomimetic) activity, which can lead to bradycardia and hypersalivation. An increase in intraocular pressure due to tonic contraction of extraocular muscles is also noted.
Indications and prescribing features
It is used for tracheal intubation and prolonged muscle relaxation during surgical procedures. For continuous maintenance, the drug is administered fractionally (every 5–7 minutes), after preliminary dilution in 15–20 ml of 0.9% NaCl solution. It is important to remember: anticholinesterase agents are not antagonists of suxamethonium, but on the contrary, enhance its effect by inhibiting plasma pseudocholinesterase.
Side effects and contraindications
Severe complications include malignant hyperthermia (the risk increases when combined with inhalation anesthetics), rhabdomyolysis, and myoglobinemia. In case of plasma pseudocholinesterase deficiency, the duration of the drug's effect is prolonged from 5–7 minutes to several hours, causing prolonged apnea. Contraindicated in glaucoma, liver disease, anemia, pregnancy, and infancy.
Briefly: answers to topical questions
What side effects does suxamethonium cause?
Suxamethonium causes systemic autonomic, specific muscular, and severe organ side effects.
- M-cholinomimetic action — manifests as bradycardia and increased salivary gland secretion.
- Ophthalmological effects — increased intraocular pressure due to tonic contraction of extraocular muscles.
- Severe muscular complications — rhabdomyolysis (destruction of muscle tissue) and myoglobinemia.
- Organ toxicity — hepatotoxicity (formation of toxic metabolites) and nephrotoxicity.
- Malignant hyperthermia — a life-threatening condition with a sharp temperature spike up to 41–43 °C and skeletal muscle spasm.
- Prolonged neuromuscular blockade — prolonged apnea in plasma pseudocholinesterase deficiency.
What are the contraindications for using suxamethonium?
Contraindications for suxamethonium use:
- Glaucoma — due to the risk of increased intraocular pressure.
- Liver dysfunction — the liver is the site of synthesis of pseudocholinesterase, which degrades the drug.
- Anemia.
- Pregnancy.
- Infancy.
Suxamethonium is a "double acetylcholine": it "hit" the receptor twice, caused "fasciculations," and "froze" on the membrane.
Class and exam questions
Why are anticholinesterase agents not used as an antidote in suxamethonium overdose?
They inhibit plasma cholinesterase, which degrades suxamethonium, thereby only prolonging its action.
What is the "dual block" phenomenon?
This is a state during repeated administration of suxamethonium when a depolarizing block is replaced by a nondepolarizing (antidepolarizing) block due to receptor desensitization.
Why is suxamethonium contraindicated in glaucoma?
The drug causes tonic contraction of extraocular muscles, which mechanically impairs aqueous humor outflow and increases intraocular pressure.
What else to study on this topic
- Genetic pseudocholinesterase deficiency: diagnosis and management.
- Comparative profile of depolarizing and nondepolarizing neuromuscular blockers.
- Pathogenesis of malignant hyperthermia and the role of dantrolene.
- Metabolic characteristics of esters and amides in the body.
- Clinical significance of fasciculations upon suxamethonium administration.
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