A patient on digoxin who is also receiving parenteral nutrition develops signs of digoxin toxicity. Which electrolyte abnormality should be assessed?

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Multiple Choice

A patient on digoxin who is also receiving parenteral nutrition develops signs of digoxin toxicity. Which electrolyte abnormality should be assessed?

Explanation:
Potassium status is the key factor that changes how digoxin behaves in the heart. Digoxin inhibits the Na+/K+ ATPase pump, which increases intracellular calcium and strengthens cardiac contraction. When extracellular potassium is low, the pump has more room to be inhibited, so digoxin binding is effectively enhanced, raising the risk of digoxin toxicity and related arrhythmias. In patients receiving parenteral nutrition, potassium imbalances are common, so monitoring and correcting hypokalemia helps prevent toxicity. Hyperkalemia can occur as a consequence of toxicity, but it’s not the predisposing factor you’re aiming to assess. Magnesium and phosphate disturbances are less directly tied to digoxin’s mechanism than potassium is.

Potassium status is the key factor that changes how digoxin behaves in the heart. Digoxin inhibits the Na+/K+ ATPase pump, which increases intracellular calcium and strengthens cardiac contraction. When extracellular potassium is low, the pump has more room to be inhibited, so digoxin binding is effectively enhanced, raising the risk of digoxin toxicity and related arrhythmias. In patients receiving parenteral nutrition, potassium imbalances are common, so monitoring and correcting hypokalemia helps prevent toxicity. Hyperkalemia can occur as a consequence of toxicity, but it’s not the predisposing factor you’re aiming to assess. Magnesium and phosphate disturbances are less directly tied to digoxin’s mechanism than potassium is.

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