Bradyarrhythmias are a group of cardiac rhythm disorders characterized by an abnormally slow heart rate, typically defined as fewer than 60 beats per minute (bpm) in adults. While bradycardia can occur as a normal physiological phenomenon—such as in athletes or during sleep—it may also signify underlying pathology, particularly when associated with symptoms like dizziness, syncope, fatigue, or heart failure. One of the most clinically significant causes of bradyarrhythmias is heart block, a disorder of electrical conduction within the heart.
Heart blocks are classified into first-degree, second-degree (Mobitz I and II), and third-degree (complete) AV block, each with distinct electrophysiological mechanisms, ECG characteristics, and clinical implications. This comprehensive post will explore bradyarrhythmias, their causes, and the pathophysiology, diagnosis, and management of various heart blocks.
1. Understanding Bradyarrhythmias
1.1 Definition
Bradyarrhythmias refer to heart rhythms that are abnormally slow, usually less than 60 bpm. They may arise due to:
- Sinus node dysfunction (SND): Impairment of the sinoatrial (SA) node, the heart’s natural pacemaker.
- Atrioventricular (AV) conduction disturbances: Abnormal conduction from the atria to the ventricles, as seen in heart blocks.
- Medication effects: Beta-blockers, calcium channel blockers, digoxin, and antiarrhythmic drugs.
- Autonomic dysfunction: Enhanced vagal tone, particularly in athletes or during sleep.
- Systemic disorders: Hypothyroidism, electrolyte imbalances (especially hyperkalemia), myocardial ischemia, or infarction.
1.2 Clinical Presentation
Symptoms of bradyarrhythmias are primarily due to decreased cardiac output:
- Fatigue and lethargy
- Dizziness or presyncope
- Syncope (fainting)
- Shortness of breath
- Exercise intolerance
- Chest discomfort in severe cases
In asymptomatic patients, bradycardia may be incidental, especially in trained athletes or healthy elderly individuals.
1.3 Pathophysiology
Normal cardiac rhythm originates in the SA node, travels through the atria, AV node, His-Purkinje system, and finally to the ventricles. Bradyarrhythmias occur due to:
- Reduced SA node automaticity: Slower generation of impulses.
- Impaired conduction through AV node or His-Purkinje system: Leads to delayed or blocked impulses reaching the ventricles.
2. Heart Blocks: Overview
Heart block refers to delayed or interrupted conduction of electrical impulses from the atria to the ventricles. It is categorized into:
- First-degree AV block
- Second-degree AV block
- Mobitz type I (Wenckebach)
- Mobitz type II
- Third-degree (complete) AV block
The site of block can be at the AV node, bundle of His, or bundle branches, which has implications for prognosis and management.
3. First-Degree AV Block
3.1 Definition
First-degree AV block is characterized by prolonged conduction from the atria to the ventricles without missed beats. On ECG:
- PR interval > 200 ms (0.20 seconds)
- Each atrial impulse eventually conducts to the ventricles
- Regular atrial and ventricular rates
3.2 Pathophysiology
The block occurs at the AV node, often due to:
- Increased vagal tone
- Ischemia or infarction
- Fibrosis or degeneration of the conduction system
- Medications (beta-blockers, calcium channel blockers, digoxin)
3.3 Clinical Significance
- Often asymptomatic
- Rarely progresses to higher-degree AV block
- Usually does not require treatment unless associated with symptoms or other conduction disorders
3.4 Management
- Identify and treat underlying cause
- Adjust medications if drug-induced
- Monitor for progression
4. Second-Degree AV Block
Second-degree AV block involves intermittent failure of atrial impulses to conduct to the ventricles. There are two main types:
4.1 Mobitz Type I (Wenckebach)
4.1.1 Definition
- Progressive prolongation of the PR interval until a beat is dropped (non-conducted P wave)
- Usually narrow QRS if block is in the AV node
4.1.2 ECG Features
- Gradually increasing PR interval
- Dropped QRS complex after progressive prolongation
- Grouped beating pattern
4.1.3 Pathophysiology
- Block occurs at the AV node
- Often benign and may be seen in healthy individuals, particularly during sleep or in athletes
- Can result from ischemia, medications, or heightened vagal tone
4.1.4 Clinical Significance
- Usually asymptomatic
- Rarely causes syncope
- Typically does not require pacing
4.1.5 Management
- Treat underlying cause
- Discontinue offending drugs
- Monitor symptoms
4.2 Mobitz Type II
4.2.1 Definition
- Intermittent failure of atrial impulses to conduct to ventricles without prior PR prolongation
- Usually associated with widened QRS if block is below AV node (His-Purkinje system)
4.2.2 ECG Features
- Constant PR interval for conducted beats
- Sudden dropped QRS complex
- Can have 2:1, 3:1 conduction ratios
4.2.3 Pathophysiology
- Block occurs below the AV node, often in the His-Purkinje system
- Associated with structural heart disease
- More likely to progress to complete heart block
4.2.4 Clinical Significance
- May cause syncope or near-syncope
- High risk of sudden cardiac arrest
- Requires urgent evaluation
4.2.5 Management
- Permanent pacemaker is often indicated
- Address reversible causes (ischemia, drugs, electrolyte imbalance)
5. Third-Degree AV Block (Complete Heart Block)
5.1 Definition
Third-degree AV block is defined as complete dissociation between atrial and ventricular activity:
- No atrial impulses conduct to the ventricles
- Atria and ventricles beat independently
- Ventricular rate depends on escape rhythm (junctional: 40–60 bpm, ventricular: 20–40 bpm)
5.2 ECG Features
- P waves not related to QRS complexes
- Wide QRS if ventricular escape rhythm originates in ventricles
- Regular atrial rhythm; usually regular ventricular rhythm, slower than atria
5.3 Pathophysiology
- Block may occur at AV node, His bundle, or distal conduction system
- Causes include:
- Degenerative conduction disease (Lenegre’s disease)
- Myocardial infarction (especially inferior or anterior)
- Cardiomyopathy
- Medications (beta-blockers, calcium channel blockers, digoxin)
- Inflammatory or infiltrative diseases
5.4 Clinical Significance
- Severe bradycardia and decreased cardiac output
- Syncope, presyncope, hypotension
- Risk of sudden cardiac death if ventricular escape is unreliable
5.5 Management
- Immediate temporary pacing if symptomatic
- Correct reversible causes
- Permanent pacemaker implantation is standard
6. Causes of Bradyarrhythmias and Heart Blocks
6.1 Intrinsic Causes
- Degeneration of conduction system
- Ischemic heart disease
- Myocarditis
- Cardiomyopathies
- Congenital AV block
6.2 Extrinsic Causes
- Medications (beta-blockers, digoxin, calcium channel blockers)
- Electrolyte imbalances (hyperkalemia)
- Hypothyroidism
- Increased vagal tone
- Hypothermia
7. Diagnostic Approach
7.1 Electrocardiography (ECG)
- First-degree: PR interval > 200 ms
- Mobitz I: Progressive PR prolongation with dropped beat
- Mobitz II: Sudden dropped beat without PR change
- Third-degree: AV dissociation; P waves unrelated to QRS
7.2 Holter Monitoring
- Detect intermittent or asymptomatic bradyarrhythmias
- Useful in syncope evaluation
7.3 Electrophysiological Studies
- Assess conduction system dysfunction
- Evaluate site of block and need for pacemaker
7.4 Laboratory Tests
- Electrolytes, thyroid function, drug levels
- Cardiac biomarkers if ischemia suspected
8. Clinical Management
8.1 General Principles
- Treat underlying reversible causes
- Monitor hemodynamics
- Symptomatic bradycardia often requires intervention
8.2 Pharmacologic Support
- Atropine: Used in acute symptomatic bradycardia (especially AV node-mediated)
- Isoproterenol or dopamine: In certain cases awaiting pacing
8.3 Pacing
- Temporary transcutaneous or transvenous pacing: For acute symptomatic patients
- Permanent pacemaker:
- Indicated for symptomatic bradycardia, Mobitz II, and third-degree AV block
- Mode depends on site of block and patient factors (single- vs dual-chamber pacing)
8.4 Lifestyle and Monitoring
- Avoid bradycardia-inducing drugs if unnecessary
- Regular follow-up for pacemaker function
- Exercise and activity adjustments based on symptoms
9. Prognosis
- First-degree and Mobitz I: Usually benign
- Mobitz II and third-degree: Higher risk of sudden cardiac events; require pacing
- Prognosis depends on underlying heart disease, presence of symptoms, and timely intervention
10. Special Considerations
10.1 Bradyarrhythmias in Athletes
- Sinus bradycardia common due to high vagal tone
- Often asymptomatic and does not require treatment
10.2 Post-Myocardial Infarction
- Inferior MI: Often causes transient AV block (usually benign)
- Anterior MI: Associated with Mobitz II or complete AV block; poor prognosis
10.3 Drug-Induced Bradyarrhythmias
- Beta-blockers, digoxin, and non-dihydropyridine calcium channel blockers are common culprits
- Dose adjustment or discontinuation often resolves bradycardia
11. Key ECG Patterns Summary
| Type | ECG Feature | Site of Block | Clinical Significance |
|---|---|---|---|
| First-degree | PR interval > 200 ms | AV node | Usually benign |
| Mobitz I (Wenckebach) | Progressive PR prolongation, dropped QRS | AV node | Usually benign |
| Mobitz II | Constant PR, sudden dropped QRS | His-Purkinje system | High risk, needs pacing |
| Third-degree | AV dissociation, unrelated P and QRS | AV node or below | Symptomatic, pacing required |
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