Module 6.2 - Digoxin and Cardioactive Steroid Toxicology - Podcast

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This comprehensive review offers a deep dive into digoxin toxicology, a crucial topic given this cardioactive steroid’s narrow therapeutic index. We begin by examining the pharmacology of digoxin, which reversibly inhibits the Na+K+-ATPase pump. This leads to increased intracellular sodium, reversing the sodium-calcium exchanger (NCX) and increasing intracellular calcium, ultimately causing positive inotropy (enhanced contractility) and negative chronotropy (slower heart rate).
Patient safety hinges on identifying predisposing factors for toxicity, including advanced age, underlying cardiac disease, renal insufficiency (as digoxin is primarily renally excreted), and key electrolyte disturbances such as hypokalemia, hypomagnesemia, and hypercalcemia.
A major focus is distinguishing between acute and chronic toxicity:
Acute poisoning often results from a single large dose, where hyperkalemia is a strong predictor of poor outcomes and indicates the need for anti-digoxin Fab fragments.
Chronic toxicity is more common, developing gradually, especially in patients with renal failure. It frequently presents with non-specific gastrointestinal, neurological, or visual symptoms (like xanthopsia—seeing yellow halos), and is often associated with hypokalemia.
The mainstay of managing severe toxicity is the prompt administration of Digoxin-specific Fab fragments (DSFab), the primary antidote, indicated for life-threatening arrhythmias, hyperkalemia , or hemodynamic instability. We detail calculation methods for DSFab dosing, based on either ingested amount or serum concentration, while noting that empirical dosing is often necessary due to clinical uncertainties.
A vital clinical pearl for supportive care is the critical avoidance of calcium salts when managing hyperkalemia in this setting. Giving calcium can exacerbate toxicity by further increasing myocardial intracellular calcium overload, potentially leading to dangerous arrhythmias. Close monitoring and correction of electrolyte disturbances (especially hypokalemia) are essential before and after Fab fragment treatment. Sharpen your knowledge to ensure effective management of this complex cardioactive steroid!