BradycardiaEdit

Bradycardia refers to a slower-than-normal heart rate. In adults, a resting heart rate below 60 beats per minute is commonly used as a threshold, though this alone does not establish a medical problem. Many healthy individuals, including well-trained athletes and people at rest during sleep, may have bradycardia without symptoms or adverse outcomes. True bradycardia is a clinical finding when a slow heart rate is associated with symptoms such as dizziness, lightheadedness, fatigue, fainting, or signs of poor organ perfusion. The condition can arise from disturbances in the heart’s electrical system, from medications or metabolic conditions, or from systemic illnesses. Understanding its causes and appropriate evaluation is essential to distinguish physiologic adaptation from reversible or progressive pathology.

Bradycardia can reflect dysfunction in the heart’s electrical conduction network, most commonly involving the sinoatrial node and the atrioventricular conduction pathway. It may also arise from external influences such as medications that slow heart rate or from systemic diseases that affect the heart's pace-making ability. Management depends on the underlying cause, the presence of symptoms, and the potential for adverse outcomes.

Classification and causes

• Physiologic (benign) bradycardia

  • Athletic bradycardia or athlete’s heart: intense physical training can lower resting heart rate due to autonomic balance and structural heart adaptations. See athlete's heart for related concepts.
  • Sleep-related bradycardia: vagal tone during sleep can temporarily reduce heart rate.

• Pathologic bradycardia

  • Sinus bradycardia: slowed impulse generation at the sinoatrial node, the natural pacemaker of the heart. See sinoatrial node.
  • Atrioventricular block (heart block): delayed or blocked conduction between the atria and ventricles. This includes:
  • First-degree AV block
  • Second-degree AV block (Mobitz type I/Wenckebach)
  • Second-degree AV block (Mobitz type II)
  • Third-degree (complete) AV block See atrioventricular block.
  • Sick sinus syndrome: a combination of sinus node dysfunction and intermittent pauses that cause bradycardia and symptoms. See sick sinus syndrome.
  • Junctional bradycardia and tachy-brady syndromes: slower rhythms originating near the AV node, sometimes with accompanying episodes of faster rhythms.
  • Conduction system disease with chronic degeneration or fibrosis.

• Drug- and toxin-induced bradycardia

  • Beta-blockers, non-dihydropyridine calcium channel blockers (e.g., verapamil, diltiazem), certain antiarrhythmics, and digoxin can slow the heart rate.
  • Other drugs or toxins that influence autonomic tone or conduction may contribute.

• Metabolic and systemic causes

  • Hypothyroidism
  • Electrolyte disturbances (e.g., hyperkalemia, severe hypokalemia)
  • Ischemic heart disease or infarction affecting the conduction system
  • Infiltrative diseases or myocarditis

• congenital bradycardia

  • Some people are born with conduction system abnormalities that cause slow heart rates from birth.

Clinical presentation

• Symptoms

  • Dizziness, lightheadedness, near-fainting or syncope
  • Fatigue, exercise intolerance
  • Shortness of breath or chest discomfort in some circumstances
  • Signs of reduced cardiac output, such as confusion in older adults

• Signs and findings

  • A slow pulse on physical examination, sometimes with hypotension
  • Evidence of underlying disease on history or ancillary testing (e.g., hypothyroidism, electrolyte imbalance)
  • Abnormalities on an electrocardiogram or ambulatory monitoring

Diagnosis

• Electrocardiography

  • A resting ECG can identify sinus bradycardia, AV block, or other conduction abnormalities. See electrocardiogram.

• Ambulatory monitoring

  • Holter monitoring or extended event monitors capture intermittent bradycardia and correlate symptoms with rhythm disturbances. See Holter monitor and ambulatory electrocardiography.

• Exercise testing

  • Sometimes used to assess chronotropic response (the heart rate increase with exercise) and to differentiate physiologic from pathologic bradycardia. See exercise stress test.

• Laboratory evaluation

  • Assess thyroid function, electrolytes, and other conditions that can contribute to bradycardia. See hypothyroidism and electrolyte imbalance.

• Imaging and specialized studies

  • Echocardiography may evaluate structural heart disease that could influence conduction. See echocardiography.
  • Electrophysiology studies may be considered in selected cases to map conduction and guide management. See electrophysiology study.

Management

• When observation is appropriate

  • Physiologic bradycardia without symptoms and with preserved hemodynamics may just require observation and reassurance. The underlying physiologic context, such as athletic conditioning or sleep, informs the approach.

• Treat reversible or causative conditions

  • Modify or discontinue medications that contribute to bradycardia where clinically feasible.
  • Correct metabolic or electrolyte disturbances.
  • Treat underlying thyroid disease or ischemia if present.

• Indications for pacing and device therapy

  • Persistent, symptomatic bradycardia due to sinus node dysfunction or high-degree AV block despite reversible causes typically warrants device therapy.
  • Pacemakers are the primary long-term treatment for sustained symptomatic bradycardia or advanced AV block. See pacemaker.
  • In certain cases, temporary pacing may be required in acute settings, with definitive therapy planned after stabilization.

• Considerations for specific populations

  • Athletes with true bradycardia may have a different approach if asymptomatic and well-tolerated; decisions are individualized. See athlete's heart.
  • Elderly patients may have more complex conduction disease and higher competing risks, affecting the risk-benefit assessment for pacing.

Prognosis

• Outcomes depend on the cause and the heart’s response to treatment. Physiologic bradycardia associated with athletic training or sleep generally carries an excellent prognosis. Pathologic bradycardia with high-grade AV block or symptomatic sinus node dysfunction can carry significant risks if not appropriately managed, but modern pacing therapies have substantially improved outcomes for many patients. See prognosis.

Controversies and debates (medical context)

• Thresholds for intervention

  • Debates exist about when asymptomatic bradycardia should be treated with a pacemaker, particularly in older adults or those with complex comorbidity. Clinicians weigh risks of device therapy against potential benefits on quality of life and survival.

• Athletic bradycardia vs pathology

  • Distinguishing physiologic adaptation from disease in athletes can be nuanced. Comprehensive assessment considers exercise tolerance, rhythm stability, and structural heart findings. See athlete's heart.

• Guideline variations

  • Different professional societies publish guidelines that may differ in thresholds for testing, monitoring, and device implantation. Clinicians balance guideline recommendations with individual patient factors. See ACC/AHA guidelines and European Society of Cardiology guidelines.

• Medication management and polypharmacy

  • In older patients, multiple drugs can contribute to bradycardia. Debates center on when to deprescribe versus when to continue essential therapies, especially in the setting of comorbid conditions.

See also

• sinoatrial node
• atrioventricular block
• bradyarrhythmia
• pacemaker
• tachycardia
• athlete's heart
• hypothyroidism
• electrocardiogram
• Holter monitor