How do I evaluate and manage a patient with bradycardia potentially due to beta‑blocker therapy?

Approach to Bradycardia Potentially Due to Beta-Blocker Therapy

First, determine whether the bradycardia is symptomatic—asymptomatic bradycardia, even with rates as low as 37–40 bpm, requires no treatment, monitoring, or intervention regardless of beta-blocker use. 1

Initial Assessment: Symptom Evaluation

Immediately assess for symptoms indicating hemodynamic compromise or cerebral hypoperfusion:

• Syncope or presyncope – the most debilitating symptoms requiring urgent intervention 2
• Altered mental status (confusion, decreased responsiveness) 2
• Ischemic chest pain or angina 2
• Signs of acute heart failure (dyspnea, pulmonary edema, jugular venous distension) 2
• Hypotension (systolic BP <90 mmHg, cool extremities, delayed capillary refill) 2
• Cardiogenic shock with end-organ hypoperfusion 2

If the patient has none of these symptoms, no treatment is indicated—discharge without specific intervention. 2

Diagnostic Workup

• Obtain a 12-lead ECG to document rhythm, rate, PR interval, QRS duration, and conduction abnormalities 2
• Review the complete medication list systematically, focusing on beta-blockers (metoprolol, atenolol, carvedilol, bisoprolol, etc.), non-dihydropyridine calcium-channel blockers, digoxin, amiodarone, sotalol, and ivabradine 1, 2
• Check thyroid function (TSH, free T4) to exclude hypothyroidism 2
• Measure serum electrolytes (potassium, magnesium) as hyperkalemia synergistically worsens beta-blocker-induced bradycardia, particularly in renal failure 3
• Assess renal function (creatinine, eGFR) because renal impairment causes accumulation of renally-cleared beta-blockers (atenolol, sotalol) and potentiates bradycardia 3

Management Algorithm for Symptomatic Beta-Blocker-Induced Bradycardia

Step 1: Immediate Stabilization (if hemodynamically unstable)

• Atropine 0.5–1 mg IV bolus is first-line therapy; repeat every 3–5 minutes up to a total of 3 mg 1, 2
• Critical caveat: Doses <0.5 mg may paradoxically worsen bradycardia 1, 2
• Absolute contraindication: Never give atropine to heart-transplant recipients (risk of paradoxical high-grade AV block) 1

Step 2: Beta-Blocker Overdose-Specific Therapy (if atropine fails)

For confirmed or suspected beta-blocker overdose with persistent symptomatic bradycardia, the 2018 ACC/AHA/HRS guideline recommends:

• Glucagon 3–10 mg IV bolus over 3–5 minutes, followed by continuous infusion of 3–5 mg/hour (Class IIa recommendation) 1, 4

  • Glucagon bypasses blocked beta-receptors by directly activating adenyl cyclase 4
  • Secure airway before administration due to high risk of vomiting 4
  • Anticipate need for >100 mg glucagon in first 24 hours 4

• High-dose insulin euglycemia therapy is equally reasonable (Class IIa) and may be superior in refractory shock 1, 4:

  • Bolus: 1 U/kg regular insulin IV + 0.5 g/kg dextrose IV simultaneously 4
  • Infusion: 0.5–1 U/kg/hour insulin (titrate up to 10 U/kg/hour) + 0.5 g/kg/hour dextrose 4
  • Glucose target: 100–250 mg/dL; check glucose every 15 minutes during titration 4
  • Monitor potassium closely; insulin drives potassium intracellularly—maintain potassium 2.5–2.8 mEq/L and avoid aggressive repletion to prevent asystole 4

Step 3: Vasopressor Support (if hypotension persists)

• Norepinephrine for vasoplegic shock or epinephrine for additional inotropic support (Class I) 4
• Dopamine 5–20 µg/kg/min is an alternative but less preferred than epinephrine/norepinephrine 1
• Isoproterenol 1–20 µg/min may be used but is strictly second-line and must be avoided if coronary ischemia is suspected because it increases myocardial oxygen demand while decreasing coronary perfusion 1, 5

Step 4: Temporary Pacing (bridge therapy)

• Transcutaneous pacing is reasonable for severe symptoms unresponsive to atropine and catecholamines, serving as a bridge to transvenous or permanent pacing 2
• Transvenous pacing is indicated for persistent hemodynamic instability refractory to medical therapy 2

Step 5: Extracorporeal Membrane Oxygenation (ECMO)

• Consider ECMO for cardiogenic shock unresponsive to maximal pharmacologic therapy (insulin, glucagon, vasopressors, calcium) (Class IIa) 4

Management of Therapeutic Beta-Blocker Use (Non-Overdose)

If bradycardia is due to therapeutic beta-blocker dosing rather than overdose:

• Discontinue or reduce the beta-blocker dose if the medication is non-essential (Class I) 1, 2
• If the beta-blocker is essential for guideline-directed therapy (e.g., heart failure, post-MI), permanent pacemaker implantation may be necessary to continue therapy (Class I) 2
• Do not abruptly discontinue beta-blockers in patients with coronary artery disease—taper over 1–2 weeks to avoid rebound angina, myocardial infarction, or ventricular arrhythmias 6

Indications for Permanent Pacemaker

• Symptomatic bradycardia persisting after beta-blocker discontinuation or dose reduction (Class I) 2
• Symptomatic bradycardia resulting from essential guideline-directed beta-blocker therapy with no alternative treatment (Class I) 2
• High-grade AV block (Mobitz II or third-degree) with symptoms (Class I) 2

Special Considerations: Synergistic Bradycardia

Beta-blocker-induced bradycardia is potentiated by:

• Renal failure causing drug accumulation (especially atenolol, sotalol) 3
• Hyperkalemia synergistically worsening AV nodal conduction 3
• Concomitant use of other AV nodal blockers (calcium-channel blockers, digoxin, amiodarone) 2

This creates a vicious cycle: worsening renal failure → beta-blocker accumulation + hyperkalemia → bradycardia/hypotension → poor renal perfusion → further renal failure 3

Management requires addressing all three components: correct hyperkalemia, support renal perfusion with vasopressors, and consider hemodialysis for water-soluble beta-blockers (atenolol, sotalol) 4

Common Pitfalls to Avoid

• Do not treat asymptomatic bradycardia based solely on heart rate numbers 2
• Do not give atropine doses <0.5 mg (may worsen bradycardia) 1, 2
• Do not use lipid emulsion therapy for beta-blocker poisoning (Class III, no benefit) 4
• Do not delay escalation to high-dose insulin if glucagon fails 4
• Do not aggressively replace potassium during high-dose insulin therapy—maintain low-normal levels to prevent fatal arrhythmias 4
• Do not implant a permanent pacemaker before fully evaluating and correcting reversible causes 2