| Class | Depolarising NMJ blocker |
|---|---|
| Chemistry |
Bis-choline esther |
| Routes of administration |
IV or IM only |
| Absorption |
Poor absorption; minimal oral bioavailability |
| Solubility |
pKa=at least 13.0; good water solubility; basically insoluble in lipid |
| Distribution |
VOD=0.14L/kg, 20% protein-bound |
| Metabolism |
Metabolised by butyrylcholinesterase. |
| Elimination |
Minimal renal or hepattic clearance |
| Time course of action |
Half-life 1-2 minutes (duration of action 5-6 minutes) |
| Target receptor |
Nicotinic acetylcholine receptors at the neuromuscular junction |
| Mechanism of action |
Depolarising neuromuscular junction blocker (non-competitive partial agonist of the nicotinic receptor). By binding to and activating the nicotinic acetylcholine receptor, suxamethonium depolarises the motor endplate of the neuromuscular junction, resulting in an action potential. After the membrane is depolarised, suxamethonium maintains it in a partially depolarised state, preventing the perijunctional voltage-gated sodium channels from returning to the active state. This prevents the generation of any further action potentials, blocking the junction. |
| Clinical effects |
Depolarising neuromuscular junction blockade; also a series of adverse effects: |
| Literature reference |
Lee (2009) |
| CICM details of understanding | Level 1 |
| Mentioned around Deranged Physiology | |
| Related SAQs |
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