## Mechanism of Succinylcholine-Induced Hyperkalaemia **Key Point:** Depolarising agents cause sustained depolarisation of the muscle membrane, triggering massive potassium efflux from the intracellular compartment. Non-depolarising agents do not depolarise, so no K⁺ release occurs. ## Pathophysiology of K⁺ Release ```mermaid flowchart TD A[Succinylcholine binds nicotinic receptor]:::action --> B[Sustained depolarisation of muscle membrane]:::action B --> C[Uncontrolled muscle action potentials]:::action C --> D[Massive K⁺ efflux from sarcoplasm]:::outcome D --> E[Serum K⁺ rises 0.5-1.0 mEq/L]:::outcome E --> F{Risk factors present?}:::decision F -->|Burns, crush, denervation, malignancy| G[Exaggerated K⁺ rise 5-10 mEq/L]:::urgent F -->|Normal patient| H[Mild rise, usually tolerated]:::outcome ``` **High-Yield:** Normal patients experience a **0.5–1.0 mEq/L rise** in serum potassium. Susceptible patients (burns >20% BSA, crush injuries, spinal cord injury, denervation, malignancy) can develop **life-threatening hyperkalaemia** (K⁺ > 6 mEq/L) → cardiac arrhythmias → cardiac arrest. ## Comparison: Depolarising vs Non-depolarising | Feature | Depolarising (Succinylcholine) | Non-depolarising | | --- | --- | --- | | Membrane potential change | Sustained depolarisation | No depolarisation | | K⁺ release | Yes (0.5–1.0 mEq/L baseline) | No | | Hyperkalaemia risk | High (especially in susceptible patients) | Absent | | Fasciculations | Present | Absent | | Mechanism of paralysis | Depolarisation → desensitisation | Competitive blockade | **Clinical Pearl:** The fasciculations themselves are responsible for K⁺ release — uncontrolled muscle contractions pump K⁺ out of cells. Pre-treatment with a non-depolarising agent (defasciculation) prevents fasciculations and reduces K⁺ efflux by ~50%. **Mnemonic:** **SUCK** = **S**uccinylcholine **U**ncontrolled **C**ontractions cause **K**⁺ release.
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