| Structure/Class |
- Suxemethonium’s chemical structure is essentially two ACh molecules bound together.
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| Pharmacodynamics |
- Suxemethonium binds to the nicotinic receptor and activates it, causing depolarization of the motor end plate and spreading of the action potential.
- However, it is not metabolized by true acetylcholinesterase at the NM junction, and therefore, repolarization cannot occur.
- Since muscular contraction requires repetitive firing, a flaccid paralysis then occurs. The initial flaccid paralysis is known as phase I (depolarizing) block, and is further augmented by acetylcholinesterase inhibitors.
- Prolonged exposure to suxemethonium causes a repolarization of the membrane, but it is not easily depolarized again. The membrane is said to be desensitized (phase II). The channel behaves as if it were blocked by non-depolarising agents and this phase may be reversed with acetylcholinesterase inhibitors.
- Overall suxemethonium causes a paralysis in ~30s, affecting the arm, neck and leg muscles first before respiratory muscles.
- CVS effects of suxemethonium
- Suxemethonium stimulates nicotinic receptors at the sympathetic and parasympathetic ganglia, as well as muscarinic receptors in the heart. This leads to negative inotropy and negative chronotropy. Administration of an anti-cholinergic medication concurrently may reduce the response.
- A second dose of Sux within 5 minutes may also cause bradycardia.
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| Absorption/administration |
- IV only
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| Distribution |
- Very polar – small Vd.
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| Metabolism |
- Sux is broken down by plasma cholinesterase and bytyrylcholinesterase (pseudocholinesterase)
- No/very little metabolism occurs at the NMJ.
- The offset of action is due to Sux diffusing away from the NMJ.
- Onset time is 30-45s (slower in low cardiac output states) and offset time is 8-10 minutes.
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| Excretion |
- Action terminated by diffusion
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| Indications |
- RSI, due to rapid onset
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| Contraindications |
- Hyperkalemia
- Also CI in other conditions that may release K+, e.g. burns, nerve damage, neuromuscular disease, closed head injury.
- Pseudocholinesterase deficiency
- Open anterior chamber/globe rupture
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| Special precautions |
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| Interactions |
- Halothane gas – cardiac arrhythmias
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| Adverse events |
- Hyperkalemia
- Raised intra-ocular pressure (note that Sux is not an absolute CI unless the anterior chamber is open due to globe rupture)
- Increased intra-gastric pressure (higher risk of aspiration)
- Myalgia post-op
- Malignant hyperthermia
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| Dosing/administration |
- 1mg/kg in adults
- 1-2mg/kg in paediatric population
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| Toxicology |
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| Withdrawal syndrome |
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| Special notes |
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