Causes of Bradycardia
Bradycardia is broadly classified into two main categories: sinus node dysfunction (SND) and atrioventricular (AV) block, with causes ranging from reversible/treatable conditions to intrinsic conduction system disease. 1
Primary Mechanisms
The fundamental causes fall into these categories:
1. Sinus Node Dysfunction (SND)
- Intrinsic disease: Age-related fibrosis of the sinus node and surrounding atrial tissue 1
- Manifestations include:
- Sinus bradycardia (<50 bpm)
- Sinus pauses (>3 seconds)
- Sinoatrial exit block
- Tachy-brady syndrome (alternating tachycardia with bradycardia)
- Chronotropic incompetence (inability to increase heart rate with activity) 2
2. Atrioventricular Block
- Can be fixed or intermittent
- Includes first-degree, second-degree (Mobitz I and II), and third-degree AV block
- Vagally-mediated AV block (often nocturnal, benign) 1, 2
Reversible/Treatable Causes (Critical to Identify First)
Always evaluate and treat reversible causes before considering permanent pacing. 1, 2
Medications (Most Common Reversible Cause)
- Beta blockers
- Non-dihydropyridine calcium channel blockers (diltiazem, verapamil)
- Digoxin
- Antiarrhythmic drugs (sodium and potassium channel blockers)
- Lithium, methyldopa, risperidone, cisplatin, interferon 1, 2
Metabolic/Endocrine
- Hypothyroidism (responds well to T4 replacement) 2
- Hyperkalemia
- Hypokalemia
- Hypoglycemia
- Severe systemic acidosis 1, 3
Cardiac Ischemia/Structural
- Acute myocardial infarction (especially inferior MI)
- Cardiac surgery (valve replacement, CABG, maze procedure)
- Heart transplant (acute/chronic rejection) 1
Neurologic
- Elevated intracranial pressure (Cushing reflex: hypertension + bradycardia + apnea) 4
- Space-occupying lesions (subdural hematoma, tumors, hydrocephalus)
- Trigemino-cardiac reflex during neurosurgical procedures 4
Environmental/Physiologic
- Hypothermia (therapeutic post-cardiac arrest or environmental) 1, 5
- Hypoxemia, hypercarbia, acidosis 1
- Obstructive sleep apnea 2
- Hypovolemic shock 1
Infectious
- Lyme disease, legionella, psittacosis, typhoid fever, malaria, Dengue fever, viral hemorrhagic fevers, Guillain-Barré 1
Toxins
- Toluene, organophosphates, tetrodotoxin, cocaine 1
Other
- Athletic training (physiologic, not pathologic)
- Hypervagotonia
- Atrial fibrillation (can cause tachy-brady syndrome) 1
Key Clinical Distinctions
Physiologic vs. Pathologic
Physiologic bradycardia occurs in:
Pathologic bradycardia requires correlation with symptoms (syncope, presyncope, lightheadedness, dyspnea, fatigue, heart failure, confusion from cerebral hypoperfusion) 1, 2
Critical Pitfall
Nocturnal bradycardia or pauses are often physiologic due to increased parasympathetic tone during sleep and do not require pacing unless symptomatic. Vagally-mediated AV block during sleep shows concomitant sinus slowing (P-P prolongation), distinguishing it from intrinsic conduction disease. 1, 2
High-Risk "Cannot-Miss" Causes
When evaluating acute bradycardia, prioritize ruling out:
- Hyperkalemia
- Myocardial ischemia/infarction
- Toxins/drug overdose
- Hypoxia
- Increased intracranial pressure
- Thyroid dysfunction 3
These require immediate targeted intervention to prevent progression to bradycardic arrest.
Diagnostic Approach
The diagnosis requires correlation between documented bradyarrhythmia and symptoms. 1, 2 A 12-lead ECG during symptomatic episodes is essential. Ambulatory monitoring may be needed for intermittent bradycardia. Electrophysiology studies are rarely indicated and should not be performed in asymptomatic patients unless other indications exist. 1, 2