Bradycardia: Evaluation and Management
Initial Assessment: Symptoms Drive All Management Decisions
The single most critical determination is whether bradycardia is causing symptoms—asymptomatic bradycardia requires no treatment regardless of heart rate, even if as low as 37-40 bpm. 1
Symptoms Requiring Immediate Intervention (Class I)
- Altered mental status (confusion, decreased responsiveness) 2, 3
- Ischemic chest pain or angina 2, 3
- Hypotension (systolic BP <90 mmHg) or shock with end-organ hypoperfusion 2, 3
- Acute heart failure (pulmonary edema, dyspnea) 2, 3
- Syncope or presyncope, particularly with trauma risk 2, 3
Less Urgent but Clinically Relevant Symptoms
- Exertional dyspnea and exercise intolerance 2
- Chronic fatigue (though less specific) 1, 2
- Lightheadedness or dizziness 1
Common Pitfall: Do not treat based solely on heart rate numbers. A rate of 46 bpm in an asymptomatic 70-year-old or 37 bpm in an asymptomatic athlete requires no intervention. 2, 4
Immediate Management Algorithm for Symptomatic Bradycardia
Step 1: Stabilize and Document (Class I)
- Assess hemodynamic stability immediately—look for signs of poor perfusion 3, 5
- Obtain 12-lead ECG to document rhythm, rate, PR interval, QRS duration, and conduction abnormalities 2, 3
- Establish IV access and maintain airway/oxygenation 3
- Identify the bradycardia type: sinus bradycardia, sinus node dysfunction (SND), AV block (first-degree, Mobitz I, Mobitz II, third-degree), or bradycardic atrial fibrillation 1, 2
Step 2: Identify and Treat Reversible Causes FIRST (Class I)
Before any pharmacologic or device therapy, systematically evaluate for reversible etiologies—this is the highest priority. 1
| Reversible Cause | Evaluation | Treatment |
|---|---|---|
| Medications | Review beta-blockers, non-dihydropyridine calcium channel blockers (diltiazem, verapamil), digoxin, amiodarone, sotalol, ivabradine | Discontinue or reduce dose [1] |
| Hypothyroidism | Check TSH and free T4 | Thyroxine replacement [1,5] |
| Electrolyte abnormalities | Serum potassium, magnesium | Correct hyper-/hypokalemia, hypomagnesemia [1,5] |
| Acute myocardial infarction (especially inferior MI) | Cardiac biomarkers, ECG changes | Treat ischemia; bradycardia often resolves [1,6] |
| Drug toxicity | History of overdose (beta-blockers, calcium channel blockers, digoxin) | Specific antidotes (see below) [1] |
| Obstructive sleep apnea | History of nocturnal bradycardia | Sleep study if suspected [1,2] |
| Elevated intracranial pressure | Neurologic exam, imaging | Neurosurgical consultation [1,2] |
| Hypothermia | Core temperature | Rewarming [1] |
| Infections (Lyme disease, viral myocarditis) | Clinical context, serology | Antimicrobial therapy [1] |
If symptoms resolve after treating reversible causes, no further intervention is needed. 2
Acute Pharmacologic Management (When Reversible Causes Persist or Are Absent)
First-Line: Atropine (Class I for symptomatic bradycardia; Class IIa for SND)
- Dose: 0.5–1 mg IV bolus, repeat every 3–5 minutes to a maximum total dose of 3 mg 1, 3
- Mechanism: Most effective for sinus bradycardia and AV nodal blocks (Mobitz I); less effective for infranodal blocks (Mobitz II, third-degree with wide QRS) 2, 3
- Critical Warning (Class III: Harm): Never give atropine to heart transplant recipients—it may cause paradoxical high-grade AV block due to denervated hearts 1, 2
- Avoid doses <0.5 mg, which may paradoxically worsen bradycardia 2, 3
Second-Line: Catecholamine Infusions (Class IIb)
Use when atropine fails and patient has low risk for coronary ischemia. 1
| Agent | Dose | Notes |
|---|---|---|
| Dopamine | 5–20 µg/kg/min IV, titrate by 5 µg/kg/min every 2 min | Preferred for combined chronotropic and inotropic support [2] |
| Epinephrine | 2–10 µg/min IV or 0.1–0.5 µg/kg/min IV | Titrate to heart rate response [1,2] |
| Isoproterenol | 20–60 µg IV bolus or 1–20 µg/min infusion | Pure beta-agonist; avoid in ischemia [1,2] |
Avoid catecholamines in patients at high risk for coronary ischemia (Class I). 2
Special Situations: Specific Antidotes (Class I)
| Overdose | Treatment |
|---|---|
| Calcium channel blocker toxicity | 10% calcium chloride 1–2 g IV every 10–20 min OR 10% calcium gluconate 3–6 g IV every 10–20 min [2] |
| Beta-blocker or calcium channel blocker overdose | Glucagon 3–10 mg IV bolus, then 3–5 mg/h infusion [2] |
| Inferior MI with high-grade AV block | Aminophylline 250 mg IV bolus [1,2] |
| Spinal cord injury (refractory to atropine) | Theophylline or aminophylline (adenosine receptor blockade) [1] |
| Heart transplant recipients | Theophylline 100–200 mg IV (max 250 mg) OR catecholamine infusions [1,2] |
Temporary Pacing: Bridge Therapy Only
Transcutaneous Pacing (Class IIb)
- Indication: Severe symptoms or hemodynamic compromise unresponsive to atropine and catecholamines 1
- Role: Bridge to transvenous or permanent pacing; not superior to drug therapy 2
- Limitations: Painful, less reliable capture 1, 2
Transvenous Pacing (Class IIa)
- Indication: Persistent hemodynamic instability refractory to medical therapy 1
- Complications: 14–40% complication rate (venous thrombosis 18–85% with femoral approach, pulmonary emboli 50–60%, arrhythmias, loss of capture, perforation) 1, 7
- Infection risk: Increases risk of permanent pacemaker infection if temporary wire precedes implantation 1
Class III (Harm): Do not perform temporary pacing in patients with minimal or infrequent symptoms without hemodynamic compromise. 1
Diagnostic Monitoring for Intermittent Symptoms
When symptoms are intermittent, correlation between documented bradycardia and symptoms is the gold standard before permanent pacing. 1, 2, 3
| Symptom Frequency | Monitoring Strategy | Class |
|---|---|---|
| Daily or near-daily | 24–72 hour Holter monitor | Class I [1,2,3] |
| Weekly | 7–30 day event recorder | Class I [1,2,3] |
| Monthly or less frequent | Implantable loop recorder (diagnostic yield 43–50% at 2 years, ~80% at 4 years) | Class IIa [2] |
The initial 12-lead ECG provides a definitive diagnosis in only ~5% of syncope patients, but abnormal findings predict adverse outcomes. 3
Indications for Permanent Pacemaker
Class I (Strong Recommendation)
- Symptomatic bradycardia persisting after reversible causes have been excluded or adequately treated 1, 2
- High-grade AV block (Mobitz II or third-degree) with symptoms 1, 2
- Symptomatic bradycardia resulting from guideline-directed medical therapy (e.g., beta-blockers for heart failure) when no alternative treatment exists and continued therapy is clinically necessary 2
Class IIa (Reasonable)
- Tachy-brady syndrome with symptoms attributable to bradycardia 2
- Symptomatic chronotropic incompetence (inability to increase heart rate with exertion) 2
Class III (Not Indicated)
- Asymptomatic sinus node dysfunction 2
- Asymptomatic bradycardia in athletes or during sleep (physiologic) 2, 4
- Symptoms clearly present without accompanying bradycardia 2
Pacing Mode: Atrial-based pacing (dual-chamber or single-chamber atrial) is preferred over single-chamber ventricular pacing for sinus node dysfunction with intact AV conduction. 2
Special Populations
Elderly Patients (≥70 years)
- Age alone is not a contraindication to pacing if symptoms are present and reversible causes have been excluded 2
- Decision-making should incorporate functional status, life expectancy, and quality-of-life priorities through shared decision-making 2
Athletes and Young Healthy Individuals
- Resting heart rates of 40–50 bpm (awake) and 30 bpm (sleep) are physiologic 2
- Occasional sinus pauses or Mobitz I AV block during sleep are normal findings 2
- Key discriminant: Does episodic bradycardia correlate with symptoms of cerebral hypoperfusion? 2
Heart Transplant Recipients
- Atropine is absolutely contraindicated (Class III: Harm) 1, 2
- Use catecholamine infusions or theophylline/aminophylline instead 1, 2
Role of Electrophysiology Study (EPS)
- Class III (Not Indicated): Do not perform EPS in asymptomatic patients 2
- Class IIb (May Be Considered): When symptoms are present and noninvasive testing is nondiagnostic, EPS may help localize the anatomic site of conduction block 2
- Higher yield in: Patients with structural heart disease, abnormal baseline ECG (bundle branch block, prior MI) 2
Common Pitfalls to Avoid
- Treating asymptomatic bradycardia based solely on heart rate numbers (Class III) 2, 4
- Implanting a permanent pacemaker before fully evaluating and correcting reversible causes (Class III) 2
- Administering atropine doses <0.5 mg, which may worsen bradycardia 2, 3
- Giving atropine to heart transplant patients (Class III: Harm) 1, 2
- Failing to document symptom-rhythm correlation prior to permanent pacing 2, 3
- Unnecessary hospital admission or continuous monitoring for truly asymptomatic individuals (Class III) 2
- Delaying permanent pacemaker on weekends when indicated—weekend admissions increase temporary transvenous pacing complications and prolong length of stay 7
Prognosis
- Asymptomatic sinus bradycardia has a benign prognosis and does not affect survival 1, 2
- Symptomatic sinus node dysfunction is associated with high risk of cardiovascular events (syncope, atrial fibrillation, heart failure) 1, 2
- Chronotropic incompetence is associated with increased risk of cardiovascular death and overall mortality 1, 2
- 30-day mortality in patients presenting with compromising bradycardia is approximately 5% 8