## Mechanism of Calcium Gluconate in Acute Hyperkalemia **Key Point:** Calcium gluconate does NOT lower serum potassium — it **stabilizes the cardiac cell membrane** and is a temporizing measure for life-threatening dysrhythmias. ### Cellular Mechanism **High-Yield:** Hyperkalemia depolarizes the resting membrane potential, narrowing the difference between resting potential and threshold potential. This increases cardiac excitability and risk of dysrhythmia. Calcium gluconate **raises the threshold potential** (makes it less negative), thereby **widening the safety margin** between resting and threshold potentials. This stabilizes the myocardium and prevents dysrhythmias, even though serum K+ remains elevated. ### Pharmacodynamics | Property | Detail | |---|---| | **Onset** | 1–3 minutes (fastest of all hyperkalemia treatments) | | **Duration** | 30–60 minutes | | **Effect on K+** | None — does not lower serum K+ | | **Indication** | Symptomatic hyperkalemia with ECG changes (peaked T, widened QRS, dysrhythmia) | | **Route** | IV only (10 mL of 10% solution over 2–5 minutes) | **Clinical Pearl:** Calcium gluconate is **cardioprotective**, not **potassium-lowering**. It buys time while other agents (insulin + glucose, β-agonists, diuretics, dialysis) work to reduce serum K+. **Mnemonic: "CALCIUM RAISES THE THRESHOLD"** — Think of it as raising a barrier: the higher the threshold, the harder it is for the depolarized cell to fire an ectopic beat. ### Why Other Options Are Wrong 1. **Shifting K+ intracellularly** is the mechanism of insulin, β-agonists, and sodium bicarbonate — not calcium. 2. **GI binding** is the mechanism of cation-exchange resins (sodium polystyrene sulfonate, patiromer). 3. **Urinary excretion** is achieved by loop diuretics + volume expansion, not calcium. [cite:KD Tripathi 8e Ch 26]
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