What is the effect of beta blockers on first-degree atrioventricular (AV) block?

From the Guidelines

Beta blockers should be used with caution in patients with first-degree AV block, but they are not absolutely contraindicated, as stated in the 2011 ACCF/AHA guidelines 1. First-degree AV block is characterized by prolonged PR interval (>200 ms) on ECG, indicating delayed conduction through the AV node. Beta blockers like metoprolol, atenolol, and carvedilol can further slow AV nodal conduction, potentially worsening the block. If beta blockers are clinically necessary (for conditions like hypertension, heart failure, or post-MI), start with a low dose (e.g., metoprolol 12.5-25 mg twice daily) and titrate slowly while monitoring the ECG for PR interval prolongation. Regular ECG monitoring is essential, especially after dose increases. If the PR interval exceeds 300 ms or if the patient develops symptoms like dizziness, syncope, or progresses to higher-degree AV block, the beta blocker should be reduced or discontinued. Alternative medications like calcium channel blockers (amlodipine) or ACE inhibitors may be considered for conditions like hypertension if the risk of worsening AV block is significant. The caution with beta blockers stems from their mechanism of blocking beta-adrenergic receptors, which decreases sympathetic stimulation of the heart and can further slow conduction through an already compromised AV node. Some key points to consider when using beta blockers in patients with first-degree AV block include:

• Starting with a low dose and titrating slowly
• Monitoring the ECG for PR interval prolongation
• Being cautious in patients with marked first-degree AV block (PR interval > 0.24 s) or other conduction abnormalities
• Considering alternative medications if the risk of worsening AV block is significant, as recommended in the 2007 ACC/AHA guidelines 1. It's also important to note that beta blockers are strongly recommended before discharge in patients with compensated heart failure or left ventricular systolic dysfunction for secondary prevention, as stated in the 2011 ACCF/AHA guidelines 1.

From the FDA Drug Label

The effect of verapamil on AV conduction and the SA node may cause asymptomatic first-degree AV block and transient bradycardia, sometimes accompanied by nodal escape rhythms. Beta-blockers: Concomitant therapy with beta-adrenergic blockers and verapamil may result in additive negative effects on heart rate, atrioventricular conduction and/or cardiac contractility.

The use of beta blockers in patients with first degree AV block who are taking verapamil may result in additive negative effects on heart rate, atrioventricular conduction, and/or cardiac contractility.

• Key considerations include:
  • Asymptomatic first-degree AV block may occur due to verapamil's effect on AV conduction and the SA node.
  • Concomitant therapy with beta-adrenergic blockers and verapamil requires caution and close monitoring due to the potential for excessive bradycardia and AV block.
  • The combination of sustained-release verapamil and beta-adrenergic blocking agents has not been studied, but reports of excessive bradycardia and AV block have occurred when used together for hypertension treatment.
  • Risks of combined therapy may outweigh potential benefits for hypertensive patients, and the combination should be used with caution. 2 2

From the Research

First Degree AV Block and Beta Blockers

• First-degree atrioventricular (AV) block is a delay within the AV conduction system, defined as a prolongation of the PR interval beyond the upper limit of what is considered normal (generally 0.20 s) 3.
• Beta blockers have a negative dromotropic effect on the AV node, prolonging the AH interval and AV nodal refractory periods, and may lengthen the PR interval 4.
• The prolonged PR interval rarely results in more than first degree AV block in patients receiving maintenance therapy with beta blockers 4.
• In patients with first-degree AV block, beta blockers can affect AV nodal function, but the increase in PR interval caused by these drugs is usually minimal and asymptomatic 4.

Clinical Manifestations and Indications for Pacing

• Marked first-degree AV block (PR ≥ 0.30 s) can produce a clinical condition similar to that of the pacemaker syndrome, and clinical evaluation often requires a treadmill stress test 5.
• Uncontrolled studies have shown that many symptomatic patients with normal left ventricular (LV) function improve with conventional dual chamber pacing (Class IIa indication) 5.
• Patients with suboptimally programmed pacemakers may develop functional atrial undersensing, and a relatively short postventricular atrial refractory period (PVARP) can often be used at rest with little risk of endless loop tachycardia 5.

Interaction between First Degree AV Block and Beta Blockers

• The effect of beta blockers on AV nodal conduction is substrate-dependent, and the shorter the baseline Rrmin (and higher heart rate), the more potent is the effect due to action of beta blockers 6.
• Beta blockers can increase latent conduction, manifesting in a significant rise of Rrmax, range of RR intervals, and in increased latent conduction (Rrmax/Rrmin) 6.
• The combination of beta blockers and slow channel blockers (such as verapamil and diltiazem) can affect AV nodal function, but the optimal treatment strategy is not well established 6, 4.