Cardiology

Background 

Sinus bradycardia is a type of bradyarrhythmia in which the heart rate is <60 beats per minute, originating from the sinoatrial (SA) node with a normal P wave preceding each QRS complex and a regular rhythm. It represents a slower-than-normal sinus rhythm and may be physiologic (as in athletes or during sleep) or pathologic due to intrinsic sinus node dysfunction or extrinsic factors like medications or hypothyroidism. 

II) Classification/Types

By Etiology: 

• Physiologic: Seen in well-trained athletes, during sleep, or increased vagal tone 

• Pathologic: Due to intrinsic sinus node dysfunction (sick sinus syndrome), medications, metabolic abnormalities 

By Clinical Impact: 

• Asymptomatic sinus bradycardia: No clinical manifestations 

• Symptomatic sinus bradycardia: Fatigue, dizziness, syncope, heart failure symptoms 

Pathophysiology 

Sinus bradycardia results from reduced automaticity of the SA node. This may be due to increased parasympathetic activity, decreased sympathetic tone, structural damage to the sinus node (e.g., fibrosis), or suppression by medications or metabolic disorders. Inadequate heart rate may impair cardiac output, particularly during exertion, leading to symptoms of cerebral hypoperfusion or heart failure. 

Epidemiology 

• Common in athletes and healthy individuals during sleep 

• More prevalent with aging due to degenerative changes in the SA node 

• Frequently observed in hospitalized patients receiving AV nodal blocking agents 

• Sinus node dysfunction accounts for ~50% of pacemaker placements in the U.S. 

Etiology 

I) Causes

• Increased vagal tone (athletes, Valsalva, vomiting) 

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

• Hypothyroidism 

• Hypothermia 

• Hypoxia or increased intracranial pressure 

• Electrolyte disturbances: hyperkalemia, hypokalemia 

• Sinus node fibrosis or ischemia (especially post-MI) 

• Obstructive sleep apnea 

• Post-cardiac surgery or catheter ablation 

II) Risk Factors

• Elderly age 

• History of cardiac ischemia or fibrosis 

• Use of AV nodal blocking medications 

• Hypothyroidism or other metabolic derangements 

• Obstructive sleep apnea 

• Autonomic dysfunction (e.g., in diabetes or Parkinson’s) 

Clinical Presentation 

I) History (Symptoms)

• Often asymptomatic in healthy individuals 

• Fatigue or exercise intolerance 

• Dizziness, lightheadedness 

• Syncope or near-syncope 

• Palpitations (if associated with escape beats or tachy-brady syndrome) 

• Confusion or worsening of heart failure in patients with impaired LV function 

II) Physical Exam (Signs)

• Slow but regular heart rate (<60 bpm) 

• Cool extremities or hypotension (in severe cases) 

• No specific murmurs or abnormal heart sounds unless associated conditions exist 

• Signs of hypoperfusion or altered mentation in advanced presentations 

Differential Diagnosis (DDx) 

• Normal physiologic bradycardia (e.g., in athletes) 

• AV nodal block (first-degree or higher) 

• Junctional escape rhythm 

• Sick sinus syndrome (may include tachy-brady episodes) 

• Hypothyroidism 

• Vasovagal syncope 

• Increased intracranial pressure 

Diagnostic Tests 

Initial Work-Up 

• ECG: Shows normal P waves preceding each QRS, regular rhythm, rate <60 bpm 

• Holter monitor/Event recorder: For intermittent symptoms 

• Electrolytes, TSH, glucose: Rule out reversible causes 

• Drug review: Identify bradycardia-inducing medications 

• Echocardiography: To assess underlying cardiac structure 

• Sleep study: If obstructive sleep apnea is suspected 

Treatment 

I) Acute Management

• Asymptomatic: No intervention needed 

• Symptomatic: 

• Atropine 0.5 mg IV every 3–5 minutes (up to 3 mg) 

• Temporary pacing if unresponsive to atropine 

• Dopamine or epinephrine infusion as a bridge to pacing 

II) Chronic Management

• Discontinue or reduce dose of AV nodal blocking agents 

• Correct underlying metabolic or endocrine abnormalities (e.g., hypothyroidism) 

• Permanent pacemaker indicated for: 

• Symptomatic sinus bradycardia not attributable to reversible causes 

• Chronotropic incompetence limiting activity 

• Tachy-brady syndrome with pauses 

Medications 

Device Therapy 

• Permanent Pacemaker (PPM): Mainstay for symptomatic sinus node dysfunction 

• Temporary pacing: Used acutely if severe bradycardia causes hemodynamic compromise 

• No role for ICD unless concomitant ventricular arrhythmia risk 

Patient Education, Screening, Vaccines 

Education 

• Monitor for symptoms like dizziness or syncope 

• Avoid or modify use of medications that slow heart rate 

• Understand pacemaker function and follow-up protocol if implanted 

Screening/Prevention 

• Routine ECG in patients on AV nodal blockers or with suggestive symptoms 

• Regular medication review in elderly or bradycardia-prone individuals 

• Screening for sleep apnea in high-risk populations 

Vaccinations 

• Standard immunizations recommended 

• No specific vaccine for sinus bradycardia 

Consults/Referrals 

• Cardiology: For persistent symptomatic cases or consideration of pacing 

• Electrophysiology: For complex sinus node dysfunction or tachy-brady syndrome 

• Endocrinology: If related to hypothyroidism or adrenal insufficiency 

• Sleep specialist: For evaluation and management of sleep apnea 

Follow-Up 

Short-Term 

• Monitor for recurrence of symptoms 

• Reassess after correction of reversible factors 

• Repeat ECG and labs as indicated 

Long-Term 

• Regular follow-up for those with pacemakers 

• Repeat Holter monitoring for evolving symptoms 

• Monitor progression to sick sinus syndrome or tachy-brady syndrome 

Prognosis 

• Excellent in physiologic or reversible causes 

• Sinus node dysfunction may progress over time and require pacemaker 

• Prognosis depends on underlying disease and timely treatment 

• Risk of syncope or falls in elderly if left untreated