Workup for Bradycardia
Begin with a 12-lead ECG to document the rhythm, rate, and conduction abnormalities, followed by a comprehensive history focusing on symptom-bradycardia correlation, medication review, and assessment for reversible causes. 1
Initial Assessment and Documentation
Obtain a 12-lead ECG immediately to document the cardiac rhythm, heart rate, conduction patterns, and screen for structural heart disease or systemic illness. 1 This is the cornerstone of bradycardia evaluation, though it provides definitive rhythm-symptom correlation in only approximately 5% of patients presenting with syncope. 1
Critical History Elements
Focus your history on these specific components:
- Symptom characteristics: Document frequency, timing, duration, severity, circumstances, triggers (urination, defecation, cough, prolonged standing, shaving, tight collars, head turning), and alleviating factors. 1, 2
- Cardinal symptoms requiring immediate attention: Syncope or presyncope (particularly with trauma), fatigue, dyspnea on exertion, chest pain/angina, altered mental status, hypotension, or signs of heart failure. 2, 3
- Medication review: Systematically review ALL medications including over-the-counter and nutraceuticals, specifically beta-blockers, calcium channel blockers, digoxin, antiarrhythmic drugs, and ivabradine. 1, 2, 4
- Relationship to activities: Assess correlation with meals, medical interventions, emotional distress, physical exertion, and positional changes. 1
Physical Examination Priorities
Examine for signs of bradycardia-induced compromise AND underlying structural heart disease:
- Hemodynamic assessment: Blood pressure (systolic <90 mmHg), cool extremities, delayed capillary refill, altered mental status. 3, 4
- Heart failure signs: Pulmonary edema, jugular venous distension. 3
- Evidence of structural heart disease: Murmurs, gallops, peripheral edema. 1
Cardiac Rhythm Monitoring Strategy
Select monitoring duration based on symptom frequency to establish symptom-bradycardia correlation. 1, 2 The specific monitor type should be chosen based on how often symptoms occur:
- Daily or near-daily symptoms: 24-72 hour Holter monitor. 1, 2
- Weekly symptoms: 30-day external event monitor or patient-activated transtelephonic monitor. 1, 2
- Monthly or infrequent symptoms: Implantable loop recorder (records continuously for weeks to months, patient or auto-triggered). 1, 2
- Smartphone-based systems: Consider for patients with access to technology and intermittent symptoms. 1
Laboratory and Additional Testing
Order targeted laboratory tests based on clinical suspicion, not routinely:
- Thyroid function tests: Screen for hypothyroidism as a reversible cause. 2, 4
- Electrolytes: Particularly potassium and magnesium, as hyperkalemia and hypokalemia can contribute to bradycardia. 2, 4
- Lyme titer: If travel history or clinical presentation suggests Lyme disease. 2
- Troponin: If acute myocardial ischemia or infarction suspected (especially inferior MI). 4
Exercise Electrocardiographic Testing
Exercise testing is reasonable in two specific scenarios:
- Suspected chronotropic incompetence: To confirm diagnosis and provide prognostic information. 1, 2
- Exercise-related symptoms or 2:1 AV block of unknown level: To provoke bradycardia or conduction abnormalities during exertion. 1, 2
Exercise testing rarely uncovers occult conduction disorders but can identify exercise-induced blocks that may be precipitated by myocardial ischemia or coronary vasospasm. 1
Echocardiography
Obtain echocardiography if structural heart disease is suspected based on ECG findings (bundle branch blocks, fascicular blocks) or physical examination abnormalities. 2 This is particularly important in patients with left bundle branch block who may have heart failure attributable to cardiac dyssynchrony. 1
Identifying Reversible Causes
Systematically evaluate for these reversible etiologies before considering permanent pacing:
- Medications: Beta-blockers, calcium channel blockers, digoxin, antiarrhythmic drugs, ivabradine. 2, 3, 4
- Metabolic: Hypothyroidism (responds to thyroxine replacement), electrolyte abnormalities. 2, 3, 4
- Cardiac: Acute myocardial ischemia/infarction (especially inferior MI), increased intracranial pressure. 4
- Other: Hypothermia, infections, obstructive sleep apnea (particularly if bradycardia occurs during sleep). 2, 4
Critical Pitfalls to Avoid
Do not rely solely on the initial ECG for diagnosis—it provides rhythm-symptom correlation in only ~5% of syncope cases, though an abnormal ECG predicts adverse outcomes and underlying structural heart disease. 1
Never treat based solely on heart rate number—asymptomatic sinus bradycardia, even as low as 37-40 bpm, requires no treatment or monitoring. 2, 3 Correlation between symptoms and documented bradycardia is the key determinant for therapy. 3
Do not delay treatment to obtain a 12-lead ECG in unstable patients—if the patient has signs of poor perfusion (altered mental status, ischemic chest pain, acute heart failure, hypotension, shock), initiate treatment immediately. 4
Avoid atropine in heart transplant patients without evidence of autonomic reinnervation, as it can cause paradoxical effects. 4
When to Consider Electrophysiology Study
An electrophysiology study may be considered when diagnosis remains uncertain after noninvasive evaluation, but should NOT be performed in asymptomatic patients. 3 This is reserved for complex cases where the mechanism of bradycardia or conduction disorder cannot be determined through standard workup.
Genetic Testing Considerations
Consider genetic testing in patients with family history of inherited conduction disease or first-degree relatives of patients with identified conduction disorder-causative mutations. 2 This is particularly relevant in younger patients with unexplained conduction abnormalities.