Key result
Acute renal failure precipitates digoxin toxicity presenting as atrial fibrillation with slow ventricular response.
Why the study?
Digoxin has a narrow therapeutic index and can cause life-threatening toxicity and dysrhythmias, including AFib with slow ventricular response secondary to acute renal failure.
Case Report
Atrial fibrillation with slow ventricular response should be recognized as a clinical sign of digoxin toxicity, particularly in the setting of acute renal failure.
Answers are grounded in this paper and cite their sources.
AF with slow ventricular response may indicate digoxin toxicity from acute renal failure; case reports leave the association hypothesis-generating.
Digoxin is a cardiac glycoside that has been used for centuries for atrial fibrillation (AFib) and congestive heart failure (CHF). Digoxin has a narrow therapeutic index with a potential for toxicity that can be life-threatening1-5. Toxicity can result from accidental or intentional overdose, renal failure, and/or hypokalemia. Cardiac manifestations of digoxin toxicity cause dysrhythmias of different types2,6. Bidirectional ventricular tachycardia is a specific dysrhythmia in the setting of digitalis toxicity, but AFib with slow ventricular response (SVR) is another digoxin toxicity-related dysrhythmia7. Here, we report AFib with SVR as a sign of digoxin toxicity secondary to acute renal failure (ARF).
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Yewedalsew et al. (2024) conducted a case report in Atrial fibrillation with slow ventricular response secondary to digoxin toxicity and acute renal failure. Digoxin toxicity secondary to acute renal failure was evaluated. Digoxin toxicity secondary to acute renal failure is presented in the title as a cause of atrial fibrillation with slow ventricular response, though the text contains only journal author guidelines.
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