Which metabolic imbalance may potentiate cardiac toxicity secondary to hyperkalemia?

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Multiple Choice

Which metabolic imbalance may potentiate cardiac toxicity secondary to hyperkalemia?

Explanation:
Calcium helps stabilize cardiac cell membranes and modulates the action potential, especially the plateau phase. When potassium is high, the resting membrane potential becomes less negative, sodium channels stay inactivated longer, and conduction slows—setting the stage for dangerous arrhythmias. If calcium is low, the membrane becomes more unstable and more excitable, so the combination with hyperkalemia markedly amplifies the risk of conduction abnormalities and life‑threatening arrhythmias. Hypercalcemia would tend to stabilize membranes and counteract hyperkalemia’s toxicity, not potentiate it, and while metabolic acidosis with hyperkalemia worsens toxicity, the direct potentiating factor here is hypocalcemia.

Calcium helps stabilize cardiac cell membranes and modulates the action potential, especially the plateau phase. When potassium is high, the resting membrane potential becomes less negative, sodium channels stay inactivated longer, and conduction slows—setting the stage for dangerous arrhythmias. If calcium is low, the membrane becomes more unstable and more excitable, so the combination with hyperkalemia markedly amplifies the risk of conduction abnormalities and life‑threatening arrhythmias. Hypercalcemia would tend to stabilize membranes and counteract hyperkalemia’s toxicity, not potentiate it, and while metabolic acidosis with hyperkalemia worsens toxicity, the direct potentiating factor here is hypocalcemia.

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