Medications That Cause AV Block
Beta-blockers, calcium channel blockers (particularly verapamil and diltiazem), digoxin, and certain antiarrhythmic medications are the most common medications that cause AV block by slowing conduction through the AV node. 1, 2, 3
Common Medication Classes That Cause AV Block
1. Beta-Blockers
- Mechanism: Antagonize sympathetic tone in nodal tissue, resulting in slowing of AV conduction
- Examples:
- Metoprolol
- Atenolol
- Propranolol
- Nadolol
- Carvedilol
- Risk factors: Pre-existing conduction disease, elderly patients, concomitant use with other AV nodal blocking agents 1, 4
2. Non-Dihydropyridine Calcium Channel Blockers
- Mechanism: Inhibit calcium influx across cell membranes in the AV node, prolonging refractory period
- Examples:
- Verapamil: Potent AV nodal blocker with significant risk of AV block
- Diltiazem: Similar but slightly less potent than verapamil
- Risk factors: Pre-existing AV conduction disease, concomitant use with beta-blockers 1, 2
3. Cardiac Glycosides
- Mechanism: Increase vagal tone and directly depress AV nodal conduction
- Example: Digoxin
- Risk factors: Renal dysfunction, electrolyte abnormalities (especially hypokalemia), concomitant use with other AV nodal blocking agents 1, 5
4. Class I Antiarrhythmic Agents
- Mechanism: Sodium channel blockade affecting cardiac conduction
- Examples:
- Flecainide
- Propafenone
- Disopyramide
- Procainamide
- Risk factors: Pre-existing conduction disease, structural heart disease 1
5. Class III Antiarrhythmic Agents
- Mechanism: Potassium channel blockade prolonging repolarization
- Examples:
- Amiodarone
- Sotalol (also has beta-blocking properties)
- Risk factors: Pre-existing QT prolongation, electrolyte abnormalities 1
High-Risk Drug Combinations
Beta-blocker + Non-dihydropyridine calcium channel blocker
Digoxin + Beta-blocker or calcium channel blocker
Multiple AV nodal blocking agents
- Risk increases with each additional agent
- Particular caution with triple therapy (beta-blocker + calcium channel blocker + digoxin) 1
Clinical Considerations
Persistence vs. Reversibility: While AV block is commonly associated with medications, studies show that only about 15-41% of cases are truly caused by drugs and completely resolve after drug discontinuation 7, 5
Recurrence Risk: Even when AV block resolves after drug discontinuation, approximately 27-56% of patients experience recurrence of AV block despite discontinuation of the culprit drug 7, 5
Medication-Specific Differences:
- Carvedilol-induced AV block typically resolves after discontinuation and rarely recurs
- Metoprolol-induced AV block more commonly persists or recurs despite drug discontinuation
- Digoxin-induced AV block usually improves after withdrawal of the drug 5
Pacemaker Requirement: Approximately half of patients with drug-induced AV block ultimately require permanent pacemaker implantation 5
Monitoring and Prevention
High-Risk Patients:
- Elderly patients
- Pre-existing conduction disease
- Renal or hepatic dysfunction
- Multiple AV nodal blocking agents
- Electrolyte abnormalities
ECG Monitoring:
- Baseline ECG before starting AV nodal blocking agents
- Follow-up ECG after dose increases or addition of other AV nodal blocking agents
- Monitor for PR interval prolongation as early warning sign
Pharmacological Testing:
- In patients with bundle branch block, pharmacological stress testing with class IA antiarrhythmic agents (ajmaline, procainamide, disopyramide) can identify those at high risk for developing AV block 1
Remember that drug-induced AV block is a serious condition that can lead to significant morbidity and mortality if not properly recognized and managed. Prompt identification of the culprit medication and appropriate management are essential.