Differentiating Causes of Bradycardia
The most effective approach to differentiate causes of bradycardia is to first identify the mechanism (sinus node dysfunction vs. AV block), then determine if it is physiologic or pathologic, and finally assess for reversible causes such as medications, hypoxemia, or electrolyte abnormalities. 1
Initial Assessment
Clinical Presentation
- Symptoms suggestive of clinically significant bradycardia:
- Syncope or presyncope
- Dizziness or lightheadedness
- Fatigue
- Dyspnea
- Chest pain
- Altered mental status
- Morgagni-Adams-Stokes seizures
- Heart failure symptoms 1
Immediate Evaluation
- Assess vital signs and hemodynamic stability
- Obtain 12-lead ECG to identify the specific bradyarrhythmia 2
- Check oxygen saturation (hypoxemia is a common cause of bradycardia) 2
- Establish IV access for potential emergency interventions 2
Diagnostic Algorithm for Bradycardia
Step 1: Determine the Mechanism
Based on ECG findings, differentiate between:
Sinus Node Dysfunction (SND)
- Sinus bradycardia (regular rhythm with normal P waves)
- Sinus arrest or pause
- Sinoatrial exit block
- Chronotropic incompetence
Atrioventricular (AV) Block
Step 2: Assess for Physiologic vs. Pathologic Causes
Physiologic Bradycardia:
- Athletic conditioning/high vagal tone
- Sleep
- Young healthy individuals
Pathologic Causes:
Cardiac Causes:
- Degenerative fibrosis of conduction system (age-related)
- Ischemic heart disease/myocardial infarction
- Infiltrative diseases (amyloidosis, sarcoidosis)
- Inflammatory conditions (myocarditis, endocarditis)
- Congenital heart disease
- Surgical trauma 1
Non-Cardiac Causes:
- Medications: Beta-blockers, non-dihydropyridine calcium channel blockers, digoxin, antiarrhythmics 1
- Autonomic influences: Vasovagal response, carotid sinus hypersensitivity
- Metabolic disorders: Hypothyroidism, hypothermia, electrolyte abnormalities (hyperkalemia)
- Increased intracranial pressure
- Infectious: Endocarditis, Lyme disease, Chagas disease
- Sleep apnea 2, 1
Step 3: Specific Diagnostic Features
For Sinus Node Dysfunction:
- Look for inappropriate sinus bradycardia for the clinical situation
- Check for sinus pauses >3 seconds
- Evaluate for tachy-brady syndrome (alternating bradycardia and tachycardia)
- Consider chronotropic incompetence during exercise 1
For AV Block:
- First-degree AV block: Usually benign, often medication-related
- Mobitz type I: Often transient and asymptomatic, typically at AV node level
- Mobitz type II: Usually below AV node in His-Purkinje system, often symptomatic with potential to progress to complete block
- Third-degree AV block: Complete dissociation between atria and ventricles, can occur at AV node, bundle of His, or bundle branches 2
Special Considerations
Medication Review
- Critical to review all medications including over-the-counter and nutraceuticals
- Common culprits: beta-blockers, calcium channel blockers, digoxin, amiodarone, clonidine 2, 1
Diagnostic Pitfalls
- Pseudobradycardias: Slow peripheral pulse due to frequent non-conducted atrial premature beats or ventricular bigeminy 3
- Concealed conduction: Paroxysmal supraventricular tachyarrhythmias causing concealment into the AV junction and sinus node suppression 3
Advanced Diagnostic Testing
For unclear cases or when correlation between symptoms and bradycardia is uncertain:
- Ambulatory ECG monitoring (24-hour Holter, event recorder)
- Exercise testing for chronotropic incompetence
- Electrophysiologic studies for suspected conduction system disease 2, 1
Management Considerations
Management should be guided by:
- Presence and severity of symptoms
- Underlying cause
- Reversibility of the condition
- Risk of progression to asystole 1
For acute symptomatic bradycardia:
- Atropine 0.5 mg IV every 3-5 minutes (maximum 3 mg)
- Avoid doses <0.5 mg which may paradoxically worsen bradycardia 2, 1
Permanent pacemaker implantation is indicated for symptomatic bradycardia without reversible causes, particularly with high-grade AV block 1