Which electrolyte abnormality increases the risk for digoxin toxicity?

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Multiple Choice

Which electrolyte abnormality increases the risk for digoxin toxicity?

Explanation:
Digoxin toxicity risk rises when potassium is low because digoxin binds to the Na+/K+ ATPase pump at the same site as potassium. In hypokalemia, there are fewer circulating K+ ions competing for that binding site, so digoxin binds more readily and inhibits the pump more strongly. This inhibition increases intracellular Na+, which reduces the activity of the Na+/Ca2+ exchanger, leading to higher intracellular calcium. The extra calcium boosts cardiac contractility but also makes the heart more prone to arrhythmias and conduction abnormalities typical of digoxin toxicity, even at therapeutic drug levels. Other electrolytes can influence cardiac function in their own ways, but low potassium is the key factor that heightens digoxin’s effects and toxicity risk.

Digoxin toxicity risk rises when potassium is low because digoxin binds to the Na+/K+ ATPase pump at the same site as potassium. In hypokalemia, there are fewer circulating K+ ions competing for that binding site, so digoxin binds more readily and inhibits the pump more strongly. This inhibition increases intracellular Na+, which reduces the activity of the Na+/Ca2+ exchanger, leading to higher intracellular calcium. The extra calcium boosts cardiac contractility but also makes the heart more prone to arrhythmias and conduction abnormalities typical of digoxin toxicity, even at therapeutic drug levels. Other electrolytes can influence cardiac function in their own ways, but low potassium is the key factor that heightens digoxin’s effects and toxicity risk.

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