Why does hypokalemia worsen digoxin toxicity

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Smith TW, et al. Digitalis glycosides: mechanisms and manifestations of toxicity. Prog Cardiovasc Dis. Your email address will not be published. NYU Langone Health. In the true spirit of Emergency Medicine our content is available to anyone, anywhere, anytime. Have feedback? Suggestions on how we can improve the site? Note: this service is provided by a third party, we do not collect your information in any way.

Digoxin Toxicity Background Digoxin is the most common formulation of digitalis, a cardiac glycoside used in the management of systolic heart failure and atrial arrhythmias.

The use of medicinal plants containing cardiac glycosides dates back to the ancient Egyptians. Modern digitalis is derived from the foxglove plant and has been used for the last years Although the use of digoxin has declined over the past 2 decades, digoxin toxicity exposure rates have risen, possibly because of increased use in the elderly.

Digoxin toxicity can present acutely or chronically. Acute presentations can occur with accidental or intentional ingestions. Chronic presentations are seen with renal failure, supratherapeutic dosing, or drug-drug interactions, especially inhibitors of p-glycoprotein e. Pharmacology Digoxin undergoes hepatic metabolism independent of CYP system and is renally excreted. Half-life is 1. Digoxin has a narrow therapeutic window, typically 0. We are the EMCrit Project , a team of independent medical bloggers and podcasters joined together by our common love of cutting-edge care, iconoclastic ramblings, and FOAM.

Clinical Manifestations The toxic manifestations can be extrapolated from the mechanism of action. If you determine that this is a chronic exposure, there are other very important considerations: What is the level? Though the therapeutic range reported by most laboratories document concentrations between 0. When was the last dose ingested? Digoxin levels measured within 6 hours pre-distribution from the last dose are falsely elevated and leave you shaking your head and confused as to what they mean.

What, if any, concurrent metabolic abnormalities are occurring? What does the patient look like? What are their vital signs? What does the ECG show? What other medications are they on? How much digoxin-Fab should be given? To Bind or Not to Bind? Emergency hospitalizations for adverse drug events in older Americans.

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Drug Metab Rev. Chan B, Buckley N. Digoxin-specific antibody fragments in the treatment of digoxin toxicity. Clin Toxicol Phila. Ledwitch K, Roberts A. AAPS J. Marcus F. Pharmacokinetic interactions between digoxin and other drugs.

J Am Coll Cardiol. Inactivation of digoxin by Eubacterium lentum, an anaerobe of the human gut flora. Trans Assoc Am Physicians. Drug-drug interactions among elderly patients hospitalized for drug toxicity. Risk of digoxin intoxication in heart failure patients exposed to digoxin-diuretic interactions: a population-based study. Hyperkalemia in acute digitalis poisoning: prognostic significance and therapeutic implications.

Clin Toxicol. Kelly R, Smith T. Recognition and management of digitalis toxicity. Am J Cardiol. Hack JB. Nelson L. Toxicologic myocardial sensitization. J Toxicol Clin Toxicol. Clinical outcomes from early use of digoxin-specific antibodies versus observation in chronic digoxin poisoning ATOM December Author Recent Posts.

Financial Disclosures Unless otherwise noted at the top of the post, the speaker s and related parties have no relevant financial disclosures.

We may delete without a full, true name. Your Job i. Digoxin toxicity can induce literally every arrhythmia except for rapidly conducted atrial arrhythmias atrial fibrillation and atrial flutter. The classic arrhythmias seen during digoxin toxicity include atrial tachycardia with a conduction, bidirectional ventricular tachycardia and atrial fibrillation with a slow ventricular response.

This is depicted below, followed by full lead ECG examples of digoxin toxicity, atrial tachycardia with block and bidirecitonal ventricular tachycardia.

Enlarge Cardiac arrest and death can occur from ventricular fibrillation, ventricular tachycardia and severe bradyarrhythmias. Neurological symptoms including altered mental status can occur, even without hypoperfusion of the brain. Ocular manifestations include xanthopsia , or seeing yellow. Most experts believe that the famous artist Vincent van Gogh was using foxglove, the flower from which digoxin is derived, which could explain the yellow paintings toward the end of his life.

The mechanism by which this decreases AV conduction is not clear but is perhaps due to increased vagal tone. Intracellular calcium within the cardiac myocytes is increased by digoxin, resulting in increased inotropy, or contractility. Digoxin toxicity causes hyperkalemia, or high potassium. Blocking this mechanism results in higher serum potassium levels.