The Paradoxical Link: Can Digoxin Cause Tachycardia?

October 11, 2025 •

4 min read

The incidence of adverse reactions to digoxin has been reported to be between 5% and 20%, with cardiac toxicity accounting for about half of these events [1.7.3]. While often used to slow the heart, a key question remains for patients and clinicians: can digoxin cause tachycardia? The answer is a resounding yes, primarily in the context of toxicity.

Quick Summary

Digoxin is a medication used for heart failure and atrial fibrillation to slow heart rate. Paradoxically, at toxic levels, it can lead to various dangerous heart rhythm disturbances, including several forms of tachycardia.

Key Points

Paradoxical Effect: While therapeutically used to slow heart rate, digoxin can cause life-threatening tachycardia at toxic levels [1.4.1].
Mechanism of Toxicity: Toxic levels of digoxin cause an overload of intracellular calcium, leading to increased cardiac cell excitability and abnormal heart rhythms [1.4.2].
Characteristic Arrhythmias: Digoxin toxicity can induce specific, dangerous tachycardias like atrial tachycardia with AV block and bidirectional ventricular tachycardia [1.2.1].
Narrow Therapeutic Window: The margin between a therapeutic and a toxic dose of digoxin is very small, increasing the risk of adverse events [1.5.5].
Key Risk Factors: Renal impairment, electrolyte imbalances (especially low potassium), and interactions with other common drugs significantly increase toxicity risk [1.5.1, 1.5.3].
Antidote Availability: Life-threatening digoxin-induced arrhythmias are treated with an effective antidote called digoxin immune Fab [1.4.1].
Primary Use: Digoxin is primarily prescribed for heart failure and to control the heart rate in atrial fibrillation [1.8.1, 1.8.2].

Understanding Digoxin and Its Primary Function

Digoxin, a cardiac glycoside derived from the foxglove plant, has been used for over 200 years to treat heart conditions [1.3.6]. Its FDA-approved indications are for managing heart failure with reduced ejection fraction and for controlling the heart rate in atrial fibrillation [1.8.4]. It works through two main mechanisms. First, it has a positive inotropic effect, meaning it increases the force of the heart's contraction by inhibiting an enzyme called Na+/K+ ATPase in heart muscle cells [1.3.1]. This leads to an increase in intracellular calcium, which enhances contractility and helps the heart pump more efficiently [1.3.1, 1.3.4]. Second, it has a parasympathomimetic (or vagomimetic) effect, which slows down electrical conduction through the atrioventricular (AV) node, thereby reducing the heart rate [1.3.1, 1.3.5]. This second action is why it is prescribed to control a rapid ventricular rate in conditions like atrial fibrillation [1.2.2].

The Paradoxical Effect: When Digoxin Causes Tachycardia

While digoxin's therapeutic purpose is often to slow the heart, it carries a significant risk of causing the opposite effect—tachycardia (a heart rate over 100 beats per minute)—when drug levels become toxic [1.4.1, 1.4.3]. This phenomenon is a hallmark of digoxin toxicity. At toxic concentrations, the same mechanism that helps the heart contract more forcefully becomes overstimulated. The excessive buildup of intracellular calcium increases cell excitability and can trigger abnormal electrical impulses known as afterdepolarizations [1.2.3, 1.4.2]. These spontaneous electrical signals can lead to a wide array of heart rhythm disturbances (arrhythmias). In fact, digoxin toxicity can cause almost every type of arrhythmia except for rapidly conducted atrial arrhythmias [1.2.1]. The development of tachyarrhythmias is a leading cause of death for those with digoxin toxicity [1.2.3].

Types of Tachycardia Associated with Digoxin Toxicity

Digoxin toxicity can manifest as several specific types of tachycardia, which are serious and require immediate medical attention. These arrhythmias result from a combination of increased automaticity (the heart's ability to generate its own electrical impulses) and impaired conduction through the AV node [1.2.4].

Atrial Tachycardia with AV block: This is considered a classic arrhythmia of digoxin toxicity [1.2.1]. It involves a rapid heart rate originating in the atria, combined with a blockage of some of those signals at the AV node, which is also an effect of the drug.
Bidirectional Ventricular Tachycardia (VT): This is a rare and dangerous ventricular dysrhythmia that is considered pathognomonic, or highly characteristic, of severe digoxin toxicity [1.2.3, 1.2.6]. It's identified on an ECG by a QRS axis that shifts 180° with each alternating beat [1.2.6].
Nonparoxysmal Junctional Tachycardia: In this arrhythmia, the heart's rhythm originates from the AV junction at an accelerated rate, typically between 70 and 130 beats per minute [1.8.3].
Ventricular Tachycardia and Ventricular Fibrillation: Digoxin toxicity can escalate to life-threatening ventricular tachycardia and even ventricular fibrillation, a chaotic rhythm that can lead to cardiac arrest [1.2.1].

Comparison of Digoxin's Effects: Therapeutic vs. Toxic


Feature	Therapeutic Effect	Toxic Effect
Heart Rate	Decreases rate (negative chronotropy) [1.3.4]	Can cause both bradycardia (slow heart rate) and various tachycardias [1.4.3].
Heart Rhythm	Controls ventricular response in atrial fibrillation [1.2.2].	Can induce almost any arrhythmia, including atrial tachycardia with block and ventricular tachycardia [1.2.1].
Contractility	Increases force of contraction (positive inotropy) [1.3.1].	Excessive intracellular calcium leads to dangerous afterdepolarizations and arrhythmias [1.4.2].
ECG Changes	PR prolongation, scooped ST segments ("reverse checkmark") [1.4.2].	Can show high-degree AV block, ventricular arrhythmias, and bidirectional VT [1.2.1, 1.4.1].
Symptoms	Improved symptoms of heart failure (e.g., reduced swelling) [1.8.1].	Nausea, vomiting, visual disturbances (yellow halos), confusion, fatigue, and life-threatening cardiac events [1.4.1, 1.4.3].

Risk Factors, Diagnosis, and Management

Digoxin has a narrow therapeutic index, meaning the difference between a therapeutic dose and a toxic dose is very small [1.5.5]. The risk of toxicity is increased by several factors, including:

Impaired Renal Function: Digoxin is primarily cleared by the kidneys, so poor kidney function can cause the drug to build up to toxic levels [1.5.1, 1.5.3].
Electrolyte Imbalances: Low potassium (hypokalemia), low magnesium (hypomagnesemia), and high calcium (hypercalcemia) all increase the heart's sensitivity to digoxin and the risk of arrhythmias [1.5.3, 1.5.6]. Hypokalemia is a particularly significant risk factor [1.2.6].
Drug Interactions: Many common medications can increase digoxin levels. These include certain antibiotics (macrolides), antiarrhythmics (amiodarone, verapamil), and diuretics that cause potassium loss [1.5.1, 1.2.5].
Advanced Age and Low Body Weight: Older adults often have reduced renal function and less muscle mass, which acts as a reservoir for digoxin, increasing plasma levels [1.2.2, 1.5.1].

Diagnosis of digoxin toxicity is based on clinical signs, symptoms, ECG findings, and serum digoxin levels, though levels don't always correlate perfectly with toxicity [1.4.2].

Management of digoxin-induced tachycardia involves immediately stopping the drug, correcting electrolyte imbalances, and providing supportive care [1.6.3]. For severe, life-threatening arrhythmias like ventricular tachycardia, the primary treatment is an antidote called digoxin immune Fab (brand names include Digibind and DigiFab) [1.4.1, 1.6.2]. This antidote consists of antibody fragments that bind to digoxin in the blood, neutralizing it and allowing it to be excreted by the kidneys [1.5.3]. Other antiarrhythmic drugs like lidocaine or phenytoin may also be used to manage ventricular arrhythmias while awaiting the effects of the antidote [1.4.1, 1.5.5].

Conclusion

So, can digoxin cause tachycardia? Yes, it absolutely can. While therapeutically used to slow the heart rate in conditions like atrial fibrillation and to strengthen contractions in heart failure, it possesses a dangerous paradoxical effect at toxic levels. Digoxin toxicity disrupts the heart's electrical stability, leading to a host of potentially fatal tachyarrhythmias. Due to its narrow therapeutic window and the serious risks involved, patients on digoxin require careful monitoring of their kidney function, electrolyte levels, and for any signs of toxicity. Understanding this dual nature of digoxin is crucial for its safe and effective use in clinical practice.

For more detailed information on digoxin from a regulatory agency, you can visit the FDA's drug information page.

Frequently Asked Questions

At toxic levels, digoxin causes an excessive buildup of calcium inside heart cells. This increases the cells' electrical excitability and can trigger rapid, abnormal heart rhythms like tachycardia [1.2.3, 1.4.2].

No, tachycardia is not a side effect at normal, therapeutic doses. In fact, digoxin is often used to slow the heart rate. Tachycardia is a sign of digoxin toxicity, which occurs when there is too much of the drug in the body [1.4.5, 1.3.4].

Bidirectional ventricular tachycardia is a rare but highly characteristic (pathognomonic) arrhythmia for severe digoxin toxicity. Atrial tachycardia with AV block is also considered a classic sign [1.2.3, 1.2.1].

If you are on digoxin and experience a sudden onset of rapid heartbeat, palpitations, or other symptoms like nausea, vision changes, or confusion, you should seek immediate medical attention as these could be signs of digoxin toxicity [1.4.3].

The first step is to stop the medication. For life-threatening tachycardia caused by digoxin, the primary treatment is an antidote called digoxin immune Fab, which neutralizes the drug in the bloodstream. Other antiarrhythmic medications and supportive care may also be used [1.6.2, 1.4.1].

The risk is increased by factors that lead to digoxin toxicity, such as poor kidney function, electrolyte imbalances like low potassium or magnesium, dehydration, and interactions with other medications like amiodarone or certain diuretics [1.5.1, 1.5.6].

Yes, this is the paradox of digoxin. Its therapeutic effect is to slow the heart rate (bradycardia) by acting on the AV node. However, in toxicity, it can cause both severe bradycardia (from excessive AV block) and various forms of life-threatening tachycardia (from increased automaticity) [1.4.3, 1.2.1].