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Bradicardia


Bradycardia is a cardiac condition characterized by a slower than normal heart rate. While it may occur in healthy individuals, it can also indicate underlying medical problems that require attention. Understanding its definition, types, and classification is essential for proper diagnosis and management.

Introduction

Bradycardia refers to a heart rate that is slower than the normal resting rate, typically defined as fewer than 60 beats per minute in adults. It can be asymptomatic in some individuals, particularly athletes, but in others, it may lead to serious clinical manifestations. Early recognition is crucial to prevent complications associated with reduced cardiac output.

Definition

Bradycardia is defined as a heart rate of less than 60 beats per minute in adults. The condition can be classified based on its origin within the heart’s conduction system, physiological adaptation, or underlying pathology. While some cases are benign and do not require treatment, others may result in inadequate perfusion to vital organs and necessitate medical intervention.

Classification

Bradycardia can be classified based on physiological conditions, pathological causes, or the location of conduction abnormalities within the heart. Accurate classification helps guide appropriate management strategies.

Physiological Bradycardia

This type of bradycardia occurs as a normal adaptation in certain individuals. It is commonly seen in athletes and during sleep. Physiological bradycardia is usually asymptomatic and does not require treatment.

Pathological Bradycardia

Pathological bradycardia results from underlying medical conditions that disrupt normal cardiac conduction. It can lead to symptoms such as fatigue, dizziness, or syncope, and may require medical intervention.

Types Based on Location of Conduction Abnormality

  • Sinus Bradycardia: Slowing of the sinus node activity, which is the natural pacemaker of the heart.
  • Atrioventricular (AV) Block: Impaired conduction between the atria and ventricles.
    • First-degree AV block: Prolonged PR interval without missed beats.
    • Second-degree AV block: Some atrial impulses fail to conduct to the ventricles.
      • Mobitz type I (Wenckebach): Progressive PR prolongation followed by a dropped beat.
      • Mobitz type II: Intermittent non-conducted beats without PR prolongation.
    • Third-degree (Complete) AV block: Complete dissociation between atrial and ventricular activity.
  • Junctional Bradycardia: Pacemaker activity arises from the AV junction due to sinus node dysfunction.
  • Ventricular Bradycardia / Idioventricular Rhythm: Slow rhythm originating from the ventricles, often seen in severe cardiac disease.

Etiology / Causes

The causes of bradycardia can be physiological or pathological. Identifying the underlying cause is essential for determining the appropriate treatment approach.

Physiological Causes

  • High-level athletic training resulting in enhanced vagal tone.
  • Sleep, particularly during non-REM stages.
  • Vagal stimulation from activities such as coughing, vomiting, or carotid massage.

Pathological Causes

  • Cardiac Causes:
    • Ischemic heart disease
    • Myocarditis
    • Cardiomyopathy
    • Conduction system fibrosis
  • Metabolic and Endocrine Causes:
    • Hypothyroidism
    • Electrolyte imbalances such as hyperkalemia
  • Medication-Induced:
    • Beta-blockers
    • Calcium channel blockers
    • Antiarrhythmic drugs
  • Autonomic dysfunction affecting heart rate regulation
  • Other causes:
    • Hypothermia
    • Sleep apnea
    • Infections affecting the cardiac conduction system

Pathophysiology

Bradycardia occurs due to disturbances in the heart’s electrical conduction system or abnormal autonomic regulation. These disruptions reduce the rate at which impulses are generated or transmitted, leading to a slower heart rate.

Conduction System Abnormalities

Disorders affecting the sinoatrial (SA) node, atrioventricular (AV) node, or His-Purkinje system can impair impulse generation or conduction. Sinus node dysfunction may cause inappropriate slowing of the heart rate, while AV blocks can prevent atrial impulses from reaching the ventricles effectively.

Autonomic Nervous System Influence

The autonomic nervous system plays a key role in regulating heart rate. Increased vagal tone or decreased sympathetic activity can result in physiological bradycardia. Pathological conditions affecting autonomic balance may similarly lead to abnormally slow heart rates.

Clinical Presentation

The symptoms and signs of bradycardia depend on the severity and underlying cause. Some individuals may remain asymptomatic, while others experience manifestations related to reduced cardiac output.

Symptoms

  • Fatigue and general weakness
  • Dizziness or lightheadedness
  • Syncope or fainting episodes
  • Shortness of breath, particularly on exertion
  • Palpitations or awareness of slow heartbeat
  • Chest pain in cases associated with ischemia

Signs

  • Bradycardic pulse rate, typically less than 60 beats per minute
  • Hypotension in symptomatic cases
  • Signs of heart failure such as peripheral edema or pulmonary congestion in severe bradycardia
  • Jugular venous distension if AV block leads to atrioventricular dyssynchrony

Diagnostic Evaluation

Diagnosing bradycardia requires a combination of clinical assessment and investigative tests. Determining the underlying cause is critical to guide appropriate treatment and management.

History and Physical Examination

A detailed patient history should assess symptoms such as syncope, dizziness, fatigue, or palpitations. Examination includes measuring pulse rate, blood pressure, and signs of heart failure or other systemic conditions.

Electrocardiography (ECG)

  • Resting ECG: Identifies the type and location of conduction abnormality, such as sinus bradycardia or AV block.
  • Holter Monitoring: Continuous 24–48 hour ECG monitoring to detect intermittent bradycardia episodes.
  • Event Recorder: Used for infrequent symptomatic episodes to capture transient conduction abnormalities.

Laboratory Tests

  • Electrolyte levels to detect abnormalities such as hyperkalemia or hypokalemia
  • Thyroid function tests to identify hypothyroidism
  • Cardiac enzymes if ischemic heart disease is suspected

Imaging Studies

  • Echocardiography to assess structural heart disease and ventricular function
  • Cardiac MRI if myocarditis or cardiomyopathy is suspected

Management

The management of bradycardia depends on the severity of symptoms, underlying cause, and risk of complications. Treatment ranges from observation in asymptomatic cases to medical therapy or pacemaker implantation in severe cases.

General Measures

Asymptomatic physiological bradycardia often requires no treatment. Patients should be monitored regularly to ensure stability of heart rate and absence of progression to symptomatic bradycardia.

Medical Therapy

  • Adjustment or discontinuation of medications that may cause bradycardia, such as beta-blockers or calcium channel blockers
  • Treatment of underlying conditions, including hypothyroidism or electrolyte imbalances

Pacemaker Therapy

  • Indications: Symptomatic bradycardia, high-grade AV block, or sinus node dysfunction unresponsive to medical therapy
  • Types of Pacemakers: Single-chamber, dual-chamber, or biventricular pacemakers based on conduction abnormality
  • Complications: Infection, lead displacement, or device malfunction

Emergency Management

  • Bradycardic arrest requires immediate advanced cardiac life support
  • Pharmacological interventions such as intravenous atropine for acute symptomatic bradycardia
  • Temporary pacing in hemodynamically unstable patients

Prognosis

The prognosis of bradycardia depends on its underlying cause, severity, and response to treatment. Many cases of physiological bradycardia have an excellent prognosis, whereas pathological bradycardia may carry risks of complications if untreated.

Factors Influencing Prognosis

  • Severity of bradycardia and heart rate reduction
  • Presence of symptoms such as syncope or heart failure
  • Underlying cardiac or systemic diseases
  • Effectiveness of treatment, including pacemaker implantation when indicated

Long-Term Outcomes

Patients with physiological bradycardia usually remain asymptomatic with no long-term consequences. In contrast, patients with pathological bradycardia may require ongoing monitoring and interventions. Timely management significantly improves quality of life and reduces the risk of adverse events such as sudden cardiac arrest.

Prevention

Preventing bradycardia involves identifying and managing risk factors, avoiding causative medications when possible, and monitoring at-risk individuals closely.

Primary Prevention

  • Avoid unnecessary use of medications that may slow heart rate
  • Maintain adequate electrolyte balance and thyroid function
  • Regular cardiovascular check-ups for individuals with predisposing conditions

Secondary Prevention

  • Close monitoring of patients with known bradycardia or conduction abnormalities
  • Timely adjustment of medications that may exacerbate bradycardia
  • Pacemaker follow-up to ensure optimal function and prevent complications

References

  1. Marriott HJ, Henry WL. Clinical Electrocardiography: A Textbook. 8th ed. Philadelphia: Elsevier; 2018.
  2. Zipes DP, Jalife J. Cardiac Electrophysiology: From Cell to Bedside. 7th ed. Philadelphia: Elsevier; 2018.
  3. Fuster V, Walsh RA, Harrington RA. Hurst’s The Heart. 15th ed. New York: McGraw-Hill; 2022.
  4. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. Circulation. 2018;138:e272–e391.
  5. Brignole M, et al. 2018 ESC Guidelines for the Diagnosis and Management of Syncope. European Heart Journal. 2018;39:1883–1948.
  6. Goldberger ZD, et al. Evaluation and Management of Bradycardia. N Engl J Med. 2019;380:1433–1442.
  7. Kusumoto FM, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay. J Am Coll Cardiol. 2019;74:e51–e156.
  8. Fitzgerald PJ. Pathophysiology of Bradycardia and Conduction Disorders. Progress in Cardiovascular Diseases. 2020;63:43–52.
  9. Goldberger AL, et al. Clinical Approach to Bradycardia. Lancet. 2021;398:1223–1234.
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