What electrolyte abnormality indicates digoxin toxicity?

Digoxin toxicity is closely associated with hyperkalemia, which is an elevated level of potassium in the blood. Digoxin, a cardiac glycoside, exerts its effects by inhibiting the sodium-potassium ATPase pump, leading to an increase in intracellular sodium and subsequently, an increase in intracellular calcium, thereby improving cardiac contractility.

However, the inhibition of the sodium-potassium ATPase can also lead to disturbances in potassium balance. When digoxin toxicity occurs, the ability of the kidney to excrete potassium is impaired, resulting in hyperkalemia. Elevated potassium levels are a critical indicator of digoxin toxicity and can help guide clinical management. These hyperkalemic changes can also be seen on an ECG, characterized by peaked T waves and potentially other abnormal rhythms.

In contrast, other electrolyte abnormalities listed do not directly indicate digoxin toxicity. For example, hypokalemia (low potassium) can actually increase the risk of digoxin toxicity rather than indicate it. Therefore, identifying hyperkalemia is essential in the context of treating patients suspected of digoxin toxicity.