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Digoxin Toxicity
What is it?
Digoxin is a cardiac glycoside used in CHF refractory to other meds, atrial flutter/atrial fibrillation.
Cause of digoxin toxicity?
– Ingestion by children
– Intentional suicidality
– Dosing error in the elderly (not accounting for renal impairment)
– Drug drug interactions leading to changes in digoxin clearance.
Digoxin has a narrow therapeutic index making it easy for patients to be symptomatic when above the normal range.
How does digoxin work?
– It inhibits the Na+K+ ATPase. Because the amount of intracellular Na+ will determine how much calcium will be extruded from the cell, there is an increase in the amount of intracellular calcium during repolarization. Inhibition of the Na+K+ ATPase causes atria and ventricles to exhibit increased automaticity and excitability result in extrasysoles and tachydysrhthmias. Conduction velocity is reduced on both myocardial and nodal tissue result in an increase in PR interval and AV nodal block accompanied by a decrease in the QT interval.
Cardiac Effects of digoxin:
Dig toxicity may cause any dysrhthmias. However, PVCs are the most. Other rhythms that may be found include:
– SA block
– High degree AV block
– Ventricular ectopic activity
– Ventricular fibrillation
– Sinus bradycardia
Bidirectional ventricular tachycardia is particularly characteristic of severe digoxin toxicity.
Extracardiac effects of digoxin toxicity:
Visual aberration is often the earliest indication of digoxin toxicity. Yellow green distortion is the most common. Nausea, vomiting and drowsiness are also very common extracardiac manifestations.
Hyperkalemia in the initial stage of digoxin intoxication has important prognostic implications, in that serum potassium concentration has a better prognostic correlation than either initial EKG changes or the serum digoxin concentration. This is because hyperkalemia causes further depolarization of myocardial tissue, particularly the AV node, leading to an exacerbation of digoxin induced conduction delays.
Hypokalemia exacerbates the effect of dig toxicity by exacerbating the sodium pump inhibition due to cardiac glycosides.
Management of Digoxin Toxicity:
Activated charcoal: Like many toxin in its acute stage of ingestion, activated charcoal may be used to prevent further GI absorption. The effectiveness of activated charcoal is dependent on the time elapsed since ingestion.
Treat electrolyte abnormalities: especially hyperkalemia and hypokalemia which can worsen dig toxicity. Treat concomitant hypomagnesemia.
Digibind(FAB): antibody for digoxin. FAB-digoxin complex accumulates in the blood and is excreted in the kidneys. Each digibind vial contains 38mg.
To calculate the number of vials needed in an adult:
Dose in #vials= serum digoxin concentration (in ng/ml) x (weight in kg)
100
References: Nelson Lewis, Lewin, Neal Goldfrank’s Toxicologic Emergencies. 9th ed. Pgs 793-797
Schreiber, Donald. “Emergent Management of Digitalis Toxicity”. www. Emedicine.com. updated August 23, 2011.
Jay Khadpe MD
- Editor in Chief of "The Original Kings of County"
- Assistant Professor of Emergency Medicine
- Assistant Residency Director
- SUNY Downstate / Kings County Hospital
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