Bradycardia

Definition

Figure: Sinus bradycardia (Lead III) - Guyton and Hall Textbook of Medical Physiology

Types

Causes

Physiological (non-pathological)

• Athletes: Well-trained hearts pump a large stroke volume per beat, triggering baroreceptor-mediated vagal feedback. Exercise training also downregulates the "funny current" (I_f) channels of the SA node, reducing intrinsic pacemaker activity.
• High resting vagal tone in young adults
• Sleep

Pathological

• Vagal stimulation: Carotid sinus syndrome (hypersensitive baroreceptors - even mild neck pressure can trigger extreme bradycardia and syncope), vasovagal syncope, hemoperitoneum
• Cardiac: Acute inferior wall MI (SA node involvement), sick sinus syndrome, cardiomyopathy, fibrotic degeneration (most common in elderly)
• Systemic: Hypothermia, hypoxia, severe sepsis
• Neurological: High cervical spinal cord injury (disrupts sympathetic outflow, leaving vagal tone unopposed)
• Drugs: Beta-blockers, calcium channel blockers, dexmedetomidine, digoxin
• Connective tissue diseases (associated with sick sinus syndrome)

Clinical Presentation

• Often asymptomatic - many patients with sinus bradycardia (especially athletes) need no treatment
• Symptomatic bradycardia: fatigue, dizziness, pre-syncope, syncope, dyspnea, chest pain
• Hemodynamic compromise: hypotension, altered consciousness - this is the key trigger for intervention
• When the rate drops below 40 bpm, a junctional escape rhythm may emerge
• Carotid sinus syndrome: bradycardia so profound it can stop the heart for 5-10 seconds, causing loss of consciousness

AV Blocks (a major cause of bradycardia)

Management

General Principle

Acute Pharmacological Treatment

• Atropine 1 mg IV every 3-5 minutes, up to 3 mg total - first-line for symptomatic sinus bradycardia
  • Not effective in junctional/ventricular bradycardia (acts on the AV node)
  • Not effective in post-cardiac transplant patients (denervated heart)
  • Not effective for dexmedetomidine-induced bradycardia (alpha-2 agonist mechanism bypasses muscarinic blockade)
• Dopamine or epinephrine infusion - second line
• Isoproterenol 2-10 mcg/min - preferred in post-heart transplant patients (works via beta-1 receptor, not vagal pathways)

Special Situations

• Cervical spinal cord injury: Atropine + vasopressors (treat neurogenic shock simultaneously)
• Dexmedetomidine-induced: Vasopressors until drug clears; pacing if hypotension is refractory
• Inferior wall MI: Atropine is appropriate
• Junctional/ventricular bradycardia: Temporary pacing if cardiac output falls

Electrical / Device Treatment

• Emergency cutaneous (transcutaneous) pacing - rarely needed for sinus bradycardia; useful for refractory cases
• Permanent pacemaker - for sick sinus syndrome with symptomatic bradycardia; also allows safe use of AV nodal blocking drugs for the tachycardic component of brady-tachy syndrome

Summary Points

• Rate < 60 bpm (some sources < 50 bpm for true sinus bradycardia)
• Physiological in athletes due to increased stroke volume and downregulated SA node I_f channels
• Pathological causes range from vagal stimulation and drug effects to MI, hypothermia, and intrinsic SA node disease
• Treat if symptomatic or hemodynamically unstable - atropine is the first-line drug
• Know the exceptions - transplanted hearts, dexmedetomidine, and junctional/ventricular rhythms do NOT respond to atropine
• Permanent pacing is the definitive treatment for sick sinus syndrome and recurrent high-degree AV block