Bradycardia: Causes and Treatment
Causes of Bradycardia
Bradycardia (heart rate <50-60 bpm) results from either intrinsic cardiac dysfunction or extrinsic reversible causes, and identifying reversible causes is the critical first step before considering permanent interventions. 1
Medication-Induced Causes
- Beta-blockers, non-dihydropyridine calcium channel blockers (diltiazem, verapamil), and digoxin are the most common medication culprits and should be discontinued or dose-reduced when causing symptomatic bradycardia 2, 3, 1
- Antiarrhythmic drugs (particularly sotalol), lithium, methyldopa, risperidone, cisplatin, and interferon can all cause bradycardia 3
- Drugs transmitted transplacentally or through breast milk can cause bradycardia in neonates 1
Cardiac Causes
- Sinus node dysfunction characterized by abnormal impulse formation and conduction within the sinoatrial node 2
- Acute myocardial ischemia or infarction affecting sinus node function 2, 3
- AV blocks (first-, second-, and third-degree) caused by structural problems from AMI or other myocardial diseases 4
- Infiltrative diseases such as lymphoma or amyloidosis affecting the conduction system 2
- Myocarditis causing direct inflammation of the conduction system 1
Metabolic and Electrolyte Causes
- Hypothyroidism is a key reversible metabolic cause requiring thyroxine replacement 3, 1
- Electrolyte abnormalities: hyperkalemia, hypokalemia, severe hypoglycemia, and systemic acidosis 2, 3, 1
Neurologic and Vagal Causes
- Increased intracranial pressure from any cause triggers reflex bradycardia through vagal stimulation 1
- Increased vagal tone during feeding, sleep, defecation causes physiologic bradycardia in neonates 1
- Gastrointestinal distress and acute abdominal pain trigger vagal reflexes causing transient bradycardia 1
- Carotid sinus hypersensitivity 5
Environmental and Toxic Causes
- Hypothermia causes dose-dependent bradycardia and requires active rewarming 1
- Toxins including toluene, organophosphates, tetrodotoxin, and cocaine 3
- Hypoxemia is a common cause requiring immediate evaluation 4
Treatment Algorithm
Step 1: Initial Assessment and Stabilization
Assess if bradycardia is causing symptoms and hemodynamic compromise—heart rate typically <50 bpm if clinically significant. 4
- Identify signs of increased work of breathing (tachypnea, intercostal retractions, suprasternal retractions) and check oxyhemoglobin saturation 4
- Provide supplementary oxygen if hypoxemic or showing increased work of breathing 4
- Attach cardiac monitor, evaluate blood pressure, establish IV access 4
- Obtain 12-lead ECG to define rhythm (don't delay therapy) 4
Step 2: Identify and Treat Reversible Causes (CRITICAL FIRST STEP)
The most important clinical error is failing to identify reversible causes before considering permanent pacing. 1
- Discontinue offending medications (beta-blockers, calcium channel blockers, digoxin) 2, 3, 1
- Correct electrolyte abnormalities (hyperkalemia, hypokalemia, hypoglycemia) 2, 3, 1
- Treat hypothyroidism with thyroxine replacement 3, 1
- Rewarm if hypothermic 1
- Investigate for increased intracranial pressure, infections, and myocarditis 1
Step 3: Determine if Symptoms are Due to Bradycardia
Look for acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock directly attributable to bradycardia. 4
- Asymptomatic or minimally symptomatic patients do not require treatment unless the rhythm is likely to progress (e.g., Mobitz type II second-degree AV block in setting of AMI) 4
- Asymptomatic sinus bradycardia has not been associated with adverse outcomes and typically does not require treatment 2
Step 4: Acute Pharmacologic Treatment for Symptomatic Bradycardia
Atropine 0.5-1 mg IV is reasonable to increase sinus rate in patients with symptomatic bradycardia associated with hemodynamic compromise. 3, 6
- Atropine abolishes reflex vagal cardiac slowing or asystole and prevents bradycardia produced by choline esters or anticholinesterase agents 6
- Atropine's effects on heart rate are delayed by 7-8 minutes after IV administration 6
- Common pitfall: Atropine may cause transient initial bradycardia before characteristic tachycardia develops due to paralysis of vagal control 6
- Occasionally large doses may cause AV block and nodal rhythm 6
Step 5: Temporary Pacing
- Consider transcutaneous or transvenous pacing as a bridge to definitive treatment in unstable patients 4, 7
- Expert consultation should be obtained 4
Step 6: Permanent Pacemaker Implantation
Permanent pacemaker implantation is recommended for persistent symptomatic bradycardia despite addressing reversible causes. 2, 3
- Indicated when symptoms directly correlate with bradycardia and reversible causes have been excluded 3
- Physiological pacing (atrial or dual-chamber) is superior to VVI pacing for sick sinus syndrome 3
- Symptomatic patients with sick sinus syndrome and high second- or third-degree AV blocks require permanent pacemakers 7
- For patients with infrequent symptoms suspected to be caused by bradycardia, long-term monitoring with an implantable cardiac monitor is reasonable if initial non-invasive evaluation is non-diagnostic 2
Special Considerations and Pitfalls
High-Risk Populations
- Symptomatic patients with sinus node dysfunction have high risk of cardiovascular events including syncope, atrial fibrillation, and heart failure 2
- Chronotropic incompetence with age is associated with increased risk of cardiovascular death and overall mortality 2
- The elimination half-life of atropine is more than doubled in children under 2 years and elderly (>65 years) 6
Pregnancy and Lactation
- Severe or life-threatening muscarinic events are medical emergencies in pregnancy; life-sustaining therapy should not be withheld due to concerns about fetal effects 6
- Atropine crosses the placenta but is not found in amniotic fluid 6
- To minimize infant exposure, women may pump and discard milk for 24 hours after atropine use before resuming breastfeeding 6