Toxicokineticsĭigoxin's therapeutic half-life is between 30 to 40 hours, but this may change in overdose. The role of potassium is less clear in chronic toxicity, although it has been linked to higher mortality despite traditional teaching that hypokalemia worsens the dysfunction at the Na-K transporter. Hyperkalemia can be a marker of severe toxicity in acute poisoning. The former leads to increased automaticity and inotropy the latter leads to decreased dromotropy.

Increased intracellular calcium from the poisoning of the Na-K transporter and AV nodal blockade from increased vagal tone are the primary causes of digoxin toxicity. In general, ventricular dysrhythmias are more common in the elderly, whereas supraventricular dysrhythmias are more common in children. Plant ingestions account for 80% of pediatric exposure the remaining 20% of pediatric ingestions arise from medications. Additionally, 1% of adverse drug effects in patients greater than age 40 are due to digoxin toxicity the incidence rises to greater than 3% in patients over age 85. EpidemiologyĪpproximately 1% of patients with heart failure treated with digoxin develop toxicity. This can be used to control atrial tachydysrhythmias.

Digoxin also increases vagal tone by decreasing dromotropy at the AV node. At toxic levels, automaticity can be increased as well. Higher intracellular calcium increases inotropy, which can be of symptomatic benefit in CHF. The subsequent increase in intracellular sodium leads to increased intracellular calcium by decreasing calcium expulsion through the sodium-calcium cation exchanger. Etiologyĭigoxin exhibits its therapeutic and toxic effects by poisoning the sodium-potassium ATPase. Similar toxicity can occur after exposure to cardioactive steroids in plants such as oleander, red squill, or dogbane or from animals such as Bufo toads. Digoxin toxicity can present acutely, by an intentional or accidental overdose (i.e., therapeutic misadventure), or chronically, such as when patients on digoxin develop an acute kidney injury. Digoxin may improve the quality of life in CHF patients, but it does not confer a mortality benefit, and its narrow therapeutic index limits its utility.

Explain interprofessional team strategies for enhancing care coordination and communication to advance the detection and management of digoxin toxicity and improve outcomes.ĭerived from the foxglove plant (Digitalis spp.), digoxin is a cardiac glycoside that historically was used for 'dropsy' (edema) and is currently used as an inotrope to improve systolic dysfunction in patients with congestive heart failure (CHF) and as an atrioventricular nodal blocking agent for managing atrial tachydysrhythmias.

Summarize the management of digoxin toxicity.

Describe the pathophysiology of digoxin toxicity.

Identify the etiology of digoxin toxicity.

This activity reviews the clinical presentation, evaluation, and management of digoxin toxicity and highlights the role of the interprofessional team in caring for affected patients. Digoxin toxicity can present acutely after an overdose or chronically, as is often seen in patients on digoxin that develop acute kidney injury. It has inotropic effects and is utilized in the management of systolic dysfunction in patients with congestive heart failure (CHF) and as an atrioventricular nodal blocking agent for managing atrial tachydysrhythmias. Digoxin is a cardiac glycoside derived from the foxglove plant (digitalis species).

Digoxin antidote