What medications cause AV block?

October 11, 2025 •

3 min read

According to several studies, a significant number of patients presenting with second- or third-degree atrioventricular (AV) block are receiving medications known to impair cardiac conduction. This highlights the critical importance of identifying and understanding what medications cause AV block, especially for individuals with underlying heart conditions.

Quick Summary

Certain medications, including beta-blockers, specific calcium channel blockers, digoxin, and antiarrhythmics, can slow electrical conduction through the heart's AV node, potentially leading to AV block.

Key Points

Primary culprits: Beta-blockers, specific calcium channel blockers (verapamil, diltiazem), digoxin, and antiarrhythmic drugs are the most common medications causing AV block.
Mechanism: These drugs slow the conduction of electrical impulses through the heart's atrioventricular (AV) node, leading to a delay or block in signal transmission to the ventricles.
Drug interactions: Combining AV nodal blocking agents, such as a beta-blocker with a non-dihydropyridine calcium channel blocker, significantly increases the risk of severe heart block.
Resolution: Discontinuing the offending medication is the first step in treating drug-induced AV block, and this can reverse the condition in many cases.
Underlying disease: Even after drug withdrawal, some patients experience persistent or recurrent AV block, suggesting the medication may have unmasked an underlying, pre-existing conduction system disease.
Pacemaker needed: Nearly half of patients with drug-induced AV block may ultimately require a permanent pacemaker, depending on the severity and persistence of the condition.
Symptoms to watch for: Common symptoms of AV block include dizziness, lightheadedness, fatigue, shortness of breath, and fainting.

Understanding Atrioventricular (AV) Block

Atrioventricular (AV) block is a condition where the electrical signal between the atria and ventricles is disrupted, affecting the heart's ability to pump effectively. This electrical pathway involves the SA node, AV node, and His-Purkinje system. Disruptions at the AV node lead to different degrees of heart block, identifiable on an ECG.

First-degree AV block: A delay in conduction shown as a prolonged PR interval on an ECG, often without symptoms.
Second-degree AV block: Intermittent failure of signals reaching the ventricles, causing dropped beats. It has two types, Mobitz I and Mobitz II.
Third-degree (Complete) AV block: A complete block of signals from atria to ventricles, requiring the ventricles to generate their own slow rhythm. This is a medical emergency.

Key Medication Classes Implicated

Several medications can cause or worsen AV block, particularly in those with existing heart conditions.

Beta-Blockers

Beta-blockers, such as metoprolol and carvedilol, are frequent causes of drug-induced AV block. They slow heart rate and AV node conduction by inhibiting the sympathetic nervous system. Patients with pre-existing conduction issues, the elderly, or those on multiple AV nodal blockers are at higher risk. While stopping the drug can help, underlying heart problems may persist.

Calcium Channel Blockers (Non-dihydropyridine)

Verapamil and diltiazem, non-dihydropyridine calcium channel blockers, significantly inhibit the AV node. They work by blocking calcium influx, essential for AV nodal conduction. Verapamil is more potent than diltiazem. Combining these with beta-blockers is very risky and can cause severe bradycardia and heart block.

Cardiac Glycosides

Digoxin is a well-known cardiac glycoside that can induce AV block, especially at toxic levels. It increases vagal tone, which directly slows AV nodal conduction. Risk factors for toxicity and AV block include kidney problems, electrolyte imbalances (low potassium), and use with other AV nodal blockers.

Antiarrhythmic Agents

Certain antiarrhythmic drugs can cause AV block by altering the heart's electrical activity. Class I drugs like flecainide and procainamide block sodium channels and can worsen conduction issues. Class III drugs such as amiodarone and sotalol, which block potassium channels, can also cause bradycardia and AV block. Sotalol also has beta-blocking effects, increasing its risk.

Comparison of AV Block-Causing Medications


Medication Class	Primary Mechanism	Common Examples	Interaction Risk with Beta-Blockers
Beta-Blockers	Antagonize sympathetic tone, slowing AV conduction.	Metoprolol, Carvedilol, Atenolol	High (Additive effect, significantly increases risk).
Non-Dihydropyridine CCBs	Inhibit calcium influx at the AV node.	Verapamil, Diltiazem	High (Additive effect, can cause severe bradycardia).
Cardiac Glycosides	Increase vagal tone, directly depressing AV nodal conduction.	Digoxin	High (Synergistic effect, dose adjustment needed).
Class I Antiarrhythmics	Sodium channel blockade, worsening conduction.	Flecainide, Propafenone	Moderate (Caution required with pre-existing conduction disease).
Class III Antiarrhythmics	Potassium channel blockade.	Amiodarone, Sotalol	Moderate (Amiodarone slows AV conduction; Sotalol has beta-blocking effects).

Risk Factors and Clinical Considerations

Patients taking these medications are at higher risk of AV block if they have underlying heart conditions, are elderly, or have electrolyte imbalances. Combining multiple AV nodal blocking agents is particularly risky. Careful medication review and monitoring are essential, especially when starting new drugs. For example, combining a beta-blocker with a non-dihydropyridine calcium channel blocker can lead to profound bradycardia.

Management of Drug-Induced AV Block

Managing drug-induced AV block starts with identifying and stopping the problematic medication. While this often resolves the block, many patients may have underlying issues that remain. For severe or symptomatic cases, immediate steps like atropine, isoproterenol, or temporary pacing may be needed. Specific antidotes might be used in overdose. Patients with persistent block or high recurrence risk may require a permanent pacemaker.

For more detailed information on managing arrhythmias, you can refer to the American Heart Association's scientific statements on drug-induced arrhythmias.

Conclusion

Medication-induced AV block is a serious side effect of drugs like beta-blockers, non-dihydropyridine calcium channel blockers, digoxin, and antiarrhythmics. The risk is increased with pre-existing heart conditions and using multiple such agents. Prompt identification and discontinuation of the offending drug are vital. While the condition can resolve, underlying conduction issues may necessitate a permanent pacemaker in some cases. Being aware of these risks is crucial for safe medication use.

Frequently Asked Questions

Common medications known to cause AV block include beta-blockers (e.g., metoprolol), non-dihydropyridine calcium channel blockers (e.g., verapamil, diltiazem), digoxin, and certain antiarrhythmic drugs (e.g., amiodarone, flecainide).

Many medications cause AV block by depressing the electrical conduction at the AV node. For example, beta-blockers reduce sympathetic tone, while non-dihydropyridine calcium channel blockers inhibit calcium influx, both of which slow signal transmission.

No, it is not always reversible. While withdrawing the medication can often resolve the block, studies indicate that a significant number of patients have underlying heart issues that persist even after the drug is stopped.

Risk factors include advanced age, pre-existing conduction system disease, electrolyte abnormalities (like hypokalemia), renal dysfunction, and the concomitant use of multiple AV nodal blocking medications.

The combination of a beta-blocker with a non-dihydropyridine calcium channel blocker is particularly dangerous. This combination can produce additive effects that lead to severe bradycardia, heart block, and potential cardiovascular collapse.

If drug-induced AV block is suspected, a medical professional should be consulted immediately. The first step is typically the withdrawal of the offending medication. Temporary pacing or other interventions may be necessary for symptomatic patients.

Yes, a permanent pacemaker may be required. If the AV block persists after the medication is discontinued, or if the patient has a high risk of recurrence due to underlying disease, a pacemaker may be implanted.