Types and Causes of Bradycardia
Bradycardia is broadly classified into two main types: sinus node dysfunction (SND) and atrioventricular (AV) block, with bradycardia defined as a heart rate <50 beats per minute when clinically significant. 1
Types of Bradycardia
Sinus Node Dysfunction (SND)
Sinus node dysfunction encompasses disorders of impulse formation and includes several distinct electrocardiographic manifestations 1, 2:
- Sinus bradycardia: Sinus rate <50 bpm with normal P-wave morphology 1, 3
- Ectopic atrial bradycardia: Atrial depolarization from a pacemaker other than the sinus node with rate <50 bpm 1
- Sinoatrial exit block: Blocked conduction between the sinus node and adjacent atrial tissue, manifesting as "group beating" of atrial depolarization and sinus pauses 1
- Sinus pause: Sinus node depolarizes >3 seconds after the last atrial depolarization 1
- Sinus node arrest: No evidence of sinus node activity for prolonged periods 1, 3
- Chronotropic incompetence: Failure to reach a target heart rate with exertion (typically defined as failure to reach 80% of expected heart rate reserve, calculated as [220 - age] minus resting heart rate) 1
Atrioventricular (AV) Block
AV block represents disorders of conduction and is subdivided by severity 1, 2:
- First-degree AV block: Prolonged PR interval (>200 ms); generally benign and requires no treatment 3
- Second-degree AV block, Mobitz Type I (Wenckebach): Progressive PR prolongation until a P wave fails to conduct; often vagally mediated and may be benign 1
- Second-degree AV block, Mobitz Type II: Intermittent non-conducted P waves without progressive PR prolongation; often requires pacemaker placement 3
- Third-degree (complete) AV block: Complete dissociation between atrial and ventricular activity; often requires pacemaker placement 3
- High-grade AV block: Two or more consecutive non-conducted P waves 1
Bundle Branch Block
Infranodal conduction disturbances include bundle branch blocks, which can contribute to bradycardia when combined with other conduction abnormalities 2, 4.
Causes of Bradycardia
Physiologic Causes
- Athletic conditioning: Well-conditioned athletes commonly have resting heart rates of 40-45 bpm due to dominant parasympathetic tone; this is normal and requires no treatment 3
- Sleep: Bradycardia during sleep is physiologic, particularly when accompanied by sinus node slowing 1, 3
- Young healthy individuals: Enhanced vagal tone can produce asymptomatic bradycardia 3
Pathologic Causes
Intrinsic Cardiac Disease:
- Degenerative fibrosis of the conduction system (most common cause in elderly) 1
- Ischemic heart disease and myocardial infarction (particularly inferior MI affecting the AV node) 1, 5
- Structural heart disease and cardiomyopathy 3
- Infiltrative diseases (amyloidosis, sarcoidosis, hemochromatosis) 5
- Inflammatory conditions (myocarditis, Lyme disease, endocarditis) 5
- Congenital heart disease 5
Metabolic and Systemic Causes:
- Hypothyroidism: Should be screened with thyroid function tests 3
- Electrolyte abnormalities: Particularly hyperkalemia and hypomagnesemia 3
- Hypoxemia: A common and reversible cause that should be assessed immediately 1
- Hypothermia 5
- Obstructive sleep apnea: Should be screened if bradycardia occurs during sleep or risk factors present 3
Medication-Induced:
- Beta-blockers 3
- Calcium channel blockers (particularly non-dihydropyridines: diltiazem, verapamil) 3
- Digoxin 3
- Antiarrhythmic drugs (amiodarone, sotalol, procainamide) 1, 3
- Ivabradine 3
- Opioids and sedatives 5
Neurologic and Reflex-Mediated:
- Vasovagal syncope: Sudden increase in parasympathetic tone causing sinus slowing or arrest, sometimes with AV block 1
- Carotid sinus hypersensitivity 4
- Increased intracranial pressure 5
- Situational syncope (coughing, micturition, defecation) 6
Sick Sinus Syndrome
A constellation of brady- and tachyarrhythmias representing advanced sinus node dysfunction, often requiring both pharmacologic therapy for tachycardia and pacemaker therapy for bradycardia 4, 7.
Critical Clinical Distinction
The key determinant for treatment is not the absolute heart rate number, but rather the correlation between bradycardia and symptoms. 3, 8 Asymptomatic sinus bradycardia, even with rates as low as 37-40 bpm, requires no treatment and has a benign prognosis 3. Conversely, symptomatic bradycardia—defined as documented bradyarrhythmia directly causing syncope, presyncope, dizziness, heart failure symptoms, or confusional states from cerebral hypoperfusion—requires intervention 1, 8.
Common Pitfalls
- Treating asymptomatic bradycardia based solely on heart rate: There is no established minimum heart rate below which treatment is indicated in the absence of symptoms 3
- Failing to identify reversible causes: Always review medications, check thyroid function, assess electrolytes, and evaluate for hypoxemia before considering permanent pacing 3, 5
- Misattributing symptoms to bradycardia: Symptoms may represent underlying cardiac dysfunction rather than bradycardia itself; correlation through ambulatory monitoring is essential when symptoms are intermittent 3