Succinylcholine — Pharmacology Summary
Mechanism, duration, and three categories of serious adverse effect
- Nicotinic receptor agonist — persistent depolarization
- Fasciculations then flaccid paralysis
- Onset: 60 seconds (fastest of all agents)
- Duration: 5–10 minutes (normal enzyme)
- Metabolized by plasma cholinesterase (pseudocholinesterase)
- Not reversed by anticholinesterases
- Use: rapid sequence intubation
- Extrajunctional receptor upregulation → massive potassium efflux
- Risk conditions: burns, crush injury, denervation, prolonged immobilization
- Risk onset: after first 24–48 hours post-injury
- Can cause ventricular fibrillation and cardiac arrest
- Pseudocholinesterase deficiency: prolonged apnea, no reversal
- Triggers: succinylcholine + volatile anesthetics
- Defect: ryanodine receptor → uncontrolled calcium release
- Signs: rising CO₂, rigidity, hyperthermia, acidosis
- Treatment: dantrolene immediately; discontinue triggers
- History of susceptibility: absolute contraindication
Critical Principle
Succinylcholine phase I block has no reversal agent. Anticholinesterase drugs (neostigmine) would worsen and prolong the block. Management of prolonged block — whether from pseudocholinesterase deficiency or any other cause — is mechanical ventilation until succinylcholine is cleared.