Cardiology

Background 

Bradyarrhythmia refers to a group of rhythm disturbances characterized by a slow heart rate, typically <60 beats per minute (bpm), due to impaired impulse generation from the sinoatrial (SA) node or impaired conduction through the atrioventricular (AV) node or His-Purkinje system. While some bradycardias are physiologic (e.g., in athletes), pathologic bradyarrhythmias may result in dizziness, syncope, or sudden cardiac arrest. 

II) Classification/Types

By Anatomic Origin: 

• Sinus node dysfunction (SND): Includes sinus bradycardia, sinus arrest, sinoatrial exit block 

• AV block: 

• First-degree AV block: PR interval >200 ms 

• Second-degree AV block: 

• Mobitz I (Wenckebach): Progressive PR prolongation with dropped beat 

• Mobitz II: Fixed PR with intermittent non-conducted P waves 

• Third-degree (complete) AV block: No AV conduction; atria and ventricles beat independently 

By Chronicity: 

• Transient bradyarrhythmia: Reversible (e.g., drug-induced, metabolic) 

• Persistent bradyarrhythmia: Structural or degenerative 

Pathophysiology 

Bradyarrhythmias result from impaired automaticity or conduction. Sinus node dysfunction leads to decreased impulse initiation. AV block results from impaired impulse conduction from atria to ventricles due to fibrosis, ischemia, or medications. Severe bradycardia compromises cardiac output and cerebral perfusion, increasing the risk of syncope and sudden death. 

Epidemiology 

• More common in elderly due to age-related conduction system fibrosis 

• Sinus node dysfunction is a major indication for pacemaker implantation 

• AV block associated with ischemic heart disease, especially inferior MI 

• Increased incidence in patients on beta-blockers, calcium channel blockers, and digoxin 

Etiology 

I) Causes

• Fibrosis of conduction system (Lenègre’s or Lev’s disease) 

• Ischemic heart disease (especially inferior MI) 

• Medications: beta-blockers, non-dihydropyridine calcium channel blockers, digoxin, amiodarone 

• Electrolyte disturbances: hyperkalemia, hypokalemia 

• Hypothyroidism 

• Increased vagal tone (athletes, sleep, vomiting) 

• Infections (e.g., Lyme disease, myocarditis) 

• Post-cardiac surgery or TAVR 

II) Risk Factors

• Advanced age 

• Ischemic or structural heart disease 

• History of syncope or dizziness 

• Sleep apnea 

• Medications affecting AV node 

• Infiltrative or inflammatory cardiac diseases 

Clinical Presentation 

I) History (Symptoms)

• May be asymptomatic 

• Fatigue, lightheadedness 

• Dizziness, near-syncope or syncope 

• Exertional intolerance 

• Palpitations (from escape rhythms) 

• Confusion or heart failure (if CO is compromised) 

II) Physical Exam (Signs)

• Bradycardia (<60 bpm) 

• Irregular pulse in second-degree AV block 

• Cannon A waves in JVP (third-degree AV block) 

• Variable intensity of S1 

• Signs of heart failure in advanced cases 

Differential Diagnosis (DDx) 

• Vasovagal syncope 

• Orthostatic hypotension 

• Sick sinus syndrome vs. physiologic sinus bradycardia 

• AV block (Mobitz I vs. II vs. complete) 

• Junctional escape rhythms 

• Atrial fibrillation with slow ventricular response 

Diagnostic Tests 

Initial Work-Up 

• ECG: Determine type and severity of bradyarrhythmia 

• Holter monitor/Event recorder: For intermittent symptoms 

• Electrolytes, TSH: Rule out metabolic or endocrine causes 

• Drug review: Look for AV nodal blockers 

• Echocardiography: Assess for structural heart disease 

• Stress testing: Evaluate chronotropic competence if needed 

• Electrophysiology Study (EPS): Rarely needed unless diagnosis unclear 

Treatment 

I) Acute Management

• Symptomatic bradycardia (e.g., hypotension, syncope): 

• Atropine 0.5 mg IV every 3–5 min (max 3 mg) 

• Temporary pacing (transcutaneous or transvenous) if atropine fails 

• Dopamine or epinephrine infusion as bridge to pacing 

II) Chronic Management

• Address reversible causes: Stop AV nodal blockers, correct electrolytes 

• Pacemaker placement for: 

• Symptomatic sinus node dysfunction 

• Mobitz II or third-degree AV block 

• Asymptomatic complete AV block with high-risk features (e.g., wide QRS) 

Medications 

Device Therapy 

• Permanent Pacemaker (PPM): Mainstay for chronic symptomatic bradyarrhythmia 

• Temporary pacing: For acute, reversible bradycardia 

• ICD (if indicated): If patient also meets criteria for ventricular arrhythmia prophylaxis 

Patient Education, Screening, Vaccines 

Education 

• Avoid AV nodal blocking agents unless indicated 

• Recognize signs of bradycardia (dizziness, fatigue) 

• Importance of pacemaker follow-up 

• Symptom diary if episodes are intermittent 

Screening/Prevention 

• Routine ECGs in high-risk or elderly patients 

• Medication review in patients with AV nodal dysfunction 

• Periodic Holter if symptoms suggest intermittent block 

Vaccinations 

• Standard age-appropriate vaccinations 

• No bradyarrhythmia-specific vaccines 

Consults/Referrals 

• Cardiology: For all symptomatic or advanced AV block 

• Electrophysiology: For pacemaker planning or complex rhythm evaluation 

• Endocrinology: For thyroid-related bradycardia 

• Infectious disease: For Lyme or myocarditis 

Follow-Up 

Short-Term 

• ECG after any med adjustment 

• Monitor resolution of reversible causes 

• Evaluate response to pacing 

Long-Term 

• Pacemaker interrogation every 3–6 months 

• Annual echocardiography if structural heart disease present 

• Monitor for progression to more advanced conduction block 

Prognosis 

• Excellent with pacemaker therapy for symptomatic bradyarrhythmias 

• Prognosis depends on underlying etiology 

• High recurrence risk if untreated or if secondary to progressive conduction disease 

• Mortality related to comorbid cardiac disease, not bradycardia itself