I take atenolol 25 mg every other day and have a resting heart rate of 47–50 bpm; is this bradycardia due to the beta‑blocker and should I discontinue it?

Management of Atenolol-Induced Bradycardia

You should discontinue atenolol immediately, as a resting heart rate of 47-50 bpm on this medication represents symptomatic bradycardia that is a contraindication to continued beta-blocker therapy.

Understanding Your Bradycardia

Your heart rate of 47-50 bpm is almost certainly caused by the atenolol, even at the low dose of 25 mg every other day. Beta-blockers like atenolol are well-known to cause bradycardia as their primary mechanism of action is to slow the heart rate 1, 2. The European Society of Cardiology identifies symptomatic bradycardia (heart rate <50-60 bpm) as an absolute contraindication to continued beta-blocker therapy 1.

• Bradycardia is the most common adverse effect of atenolol, occurring in approximately 3% of patients in clinical trials, though this likely underestimates the true incidence 2.
• Even low doses taken intermittently can cause significant bradycardia, particularly in elderly patients or those with underlying conduction system disease 1.
• The fact that you're taking it every other day rather than daily doesn't eliminate the risk—atenolol has a half-life of 6-7 hours but its cardiac effects can persist for 24 hours or longer 3.

Immediate Action Required

Stop taking atenolol now. The European Society of Cardiology recommends immediate discontinuation when symptomatic bradycardia develops 1. Your heart rate should improve within 2-5 days after stopping the medication, as atenolol is eliminated by the kidneys with a half-life of approximately 6-9 hours 2.

• Do not attempt to "taper" this low dose—at 25 mg every other day, you're already at a minimal dose and can safely stop abruptly 2.
• Monitor for symptoms of hypoperfusion including dizziness, lightheadedness, fatigue, or confusion 1.
• If you develop severe symptoms (syncope, chest pain, severe dizziness), seek emergency care immediately 1.

When to Seek Emergency Care

Go to the emergency department immediately if you experience:

• Heart rate dropping below 40 bpm 1
• Syncope or near-syncope (fainting or feeling like you're about to faint) 1
• Chest pain or pressure 1
• Severe dizziness or altered mental status 1
• Signs of shock (cold extremities, confusion, very low blood pressure) 4

Emergency treatment may include intravenous atropine 0.5-1 mg or temporary pacing if your bradycardia is severe and causing hemodynamic compromise 1, 5.

Why This Happened

Several factors may have contributed to your bradycardia:

• Age-related changes: If you're elderly, you're at higher risk for beta-blocker-induced bradycardia due to decreased baroreceptor response and increased drug sensitivity 6.
• Drug interactions: If you're taking other medications that slow heart rate (calcium channel blockers like diltiazem or verapamil, digoxin, amiodarone), the combination dramatically increases bradycardia risk 1, 4, 7.
• Underlying conduction disease: You may have undiagnosed sinus node dysfunction that becomes apparent only when challenged with a beta-blocker 1.
• Renal impairment: Atenolol is eliminated by the kidneys, and even mild renal dysfunction can lead to drug accumulation 2.

What Your Doctor Should Check

After stopping atenolol, your physician should:

• Obtain a 12-lead ECG to rule out underlying conduction abnormalities (AV block, sick sinus syndrome) 1.
• Check renal function (creatinine, estimated GFR) since atenolol accumulates in kidney disease 2.
• Review all medications for other agents that cause bradycardia 1, 4.
• Assess for hypothyroidism, which can cause bradycardia and is often overlooked 6.
• Determine if you actually need a beta-blocker for your underlying condition—many patients are prescribed these medications without clear indication 1.

Alternative Management Strategies

If you were taking atenolol for a legitimate indication (hypertension, angina, atrial fibrillation), discuss these alternatives with your physician:

For Hypertension:

• ACE inhibitors or ARBs (lisinopril, losartan) do not cause bradycardia and are first-line for most patients 8.
• Calcium channel blockers (amlodipine) are effective and do not affect heart rate, though non-dihydropyridines like diltiazem should be avoided as they also cause bradycardia 1, 8.

For Atrial Fibrillation Rate Control:

• Diltiazem or verapamil can be used, but these also cause bradycardia—just less than beta-blockers in some patients 1.
• Digoxin may be considered, though it's less effective and also causes bradycardia 1.

For Angina:

• Long-acting nitrates (isosorbide mononitrate) or calcium channel blockers (amlodipine) are alternatives 8.

Common Pitfalls to Avoid

• Do not restart atenolol after your heart rate normalizes—you've demonstrated intolerance to the medication 5.
• Do not switch to another beta-blocker (metoprolol, carvedilol) without careful consideration, as all beta-blockers cause bradycardia; if a beta-blocker is absolutely necessary, you'll need very close monitoring and likely a lower dose 1, 6.
• Do not ignore persistent bradycardia after stopping atenolol—if your heart rate remains <50 bpm after 5-7 days off the medication, you may have underlying sinus node disease requiring pacemaker evaluation 1.
• Avoid the misconception that "some beta-blocker is better than none" in your case—the European Society of Cardiology is clear that symptomatic bradycardia is an absolute contraindication 1.

Expected Recovery Timeline

• Days 1-2: Heart rate should begin to increase as atenolol is eliminated 2.
• Days 3-5: Heart rate should normalize to your baseline (typically 60-80 bpm) 2.
• Week 1: Any symptoms of bradycardia (fatigue, dizziness) should resolve 2.
• If bradycardia persists beyond 7 days, you need cardiology evaluation for possible underlying conduction disease 1.

Special Consideration: Athletic Individuals

If you're a trained athlete, resting heart rates of 40-50 bpm can be physiological and do not require intervention 1. However, since you're on atenolol, this is almost certainly drug-induced rather than athletic conditioning. The European Society of Cardiology notes that bradycardia of 40-50 bpm at rest or 30 bpm during sleep is accepted as physiological in trained athletes and does not require pacing 1—but this doesn't apply to medication-induced bradycardia.