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The Bradyarrhythmias: Disorders of the Atrioventricular Node

Chapter 252 | Part 6: Disorders of the Cardiovascular System

KEY CLINICAL POINTS

  • AV block is classified electrocardiographically into first-degree (prolonged PR interval), second-degree (intermittent conduction failure), and third-degree (complete heart block).
  • Pacemaker implantation is indicated for symptomatic bradycardia, documented AV block with risk of asystole, and certain structural heart diseases.
  • Mobitz I (Wenckebach) block is typically hemodynamically stable and may not require pacing, while Mobitz II block often requires permanent pacing.
  • AV block can result from fibrosis, ischemia, medications (e.g., beta-blockers, digoxin), or iatrogenic causes (e.g., cardiac surgery, catheter ablation).
  • Leadless pacemakers are viable for selected patients with single-chamber ventricular pacing needs and vascular access limitations.

1. DEFINITION & OVERVIEW

Bradyarrhythmias involving the AV node include conduction delays or blocks between atria and ventricles. The AV node acts as a physiological 'gatekeeper' with slow conduction to delay ventricular activation. AV block can be intrinsic (fibrosis, ischemia) or extrinsic (autonomic, pharmacologic).

Table 252-1 Electrocardiographic Classification of Atrioventricular (AV) Block

Type ECG Features Clinical Implications
First-Degree AV Block PR interval >200 ms, all P waves conducted Usually benign, may indicate underlying conduction disease
Second-Degree AV Block (Mobitz I) Progressive PR prolongation with dropped QRS Hemodynamically stable, often transient
Second-Degree AV Block (Mobitz II) Fixed PR interval with intermittent nonconducted P waves Higher risk of progression to complete block
Third-Degree AV Block Complete dissociation of atrial and ventricular activity Requires permanent pacing

1.1 AV Node Physiology

The AV node is specialized for slow conduction via gap junctions and extracellular matrix. It has a resting membrane potential of ~–60 mV and exhibits spontaneous phase 4 depolarization. Conduction is modulated by sympathetic/parasympathetic innervation.

1.2 Conduction System Anatomy

The AV node transitions into the His bundle, which splits into left and right bundle branches. Purkinje fibers ensure rapid ventricular activation. Fibrosis/sclerosis of these structures is a common cause of acquired AV block.

2. EPIDEMIOLOGY

AV block is more common in elderly patients due to senile degeneration (Lev’s disease) and fibrosis. Incidence of complete heart block (CHB) in the U.S. is ~1/5000/year. Iatrogenic causes (e.g., cardiac surgery, ablation) account for ~10% of cases.

2.1 Risk Factors

Age >65 years, ischemic heart disease, hypertension, diabetes, myocardial infarction (especially inferior MI), and infiltrative diseases (e.g., sarcoidosis, amyloidosis).

2.2 Demographics

More prevalent in males; associated with structural heart disease, neuromuscular disorders (e.g., myotonic dystrophy), and autoimmune conditions (e.g., lupus).

3. ETIOLOGY & PATHOPHYSIOLOGY

AV block arises from intrinsic (fibrosis, ischemia, infiltrative diseases) or extrinsic (autonomic, pharmacologic) causes. Fibrosis/sclerosis accounts for ~50% of acquired cases, while ischemia is common in acute MI.

Table 252-2 Causes of AV Block

Cause Mechanism
Fibrosis/Sclerosis Idiopathic or secondary to ischemia, aging, infiltrative diseases
Ischemia Myocardial infarction, coronary spasm
Medications Beta-blockers, calcium channel blockers, digoxin
Infectious Lyme disease, viral myocarditis, Chagas’ disease
Iatrogenic Cardiac surgery, catheter ablation, TAVR

3.1 Intrinsic Causes

Senile degeneration, Lev’s disease (proximal bundle branch fibrosis), Lenègre’s disease (distal bundle branch sclerosis), and infiltrative diseases (amyloid, sarcoidosis).

3.2 Extrinsic Causes

Increased vagal tone (sleep, vasovagal syncope), medications (beta-blockers, calcium channel blockers, digoxin), and iatrogenic factors (surgery, ablation).

4. CLINICAL FEATURES

Symptoms include syncope, fatigue, dizziness, and presyncope. Signs may include narrow or wide QRS escape rhythms, AV dissociation, and evidence of underlying heart disease (e.g., valvular abnormalities).

4.1 Symptomatic Presentation

Syncope (most common), chest discomfort, exertional dyspnea, and fatigue. Asystole may occur in severe cases.

4.2 Physical Exam Findings

Evidence of structural heart disease (e.g., valvular abnormalities), signs of heart failure, and abnormal QRS morphology (wide vs. narrow complex).

5. DIFFERENTIAL DIAGNOSIS

Differential includes sinus node disease, bundle branch block, intraventricular conduction delay, and drug-induced effects. Distinguishing Mobitz I vs. II block is critical for management.

5.1 Key Differentiators

Mobitz I: Progressive PR prolongation with dropped beats; Mobitz II: Fixed PR interval with intermittent nonconducted P waves. Third-degree block shows complete AV dissociation.

6. INVESTIGATIONS & DIAGNOSIS

ECG is the primary diagnostic tool. Advanced imaging (MRI, CT, PET) is used for infiltrative diseases. Electrophysiologic studies help localize block and assess conduction reserve.

Table 252-3 Diagnostic Algorithm for AV Block

Step Test Indication
1 ECG Initial assessment of conduction delay/block
2 Echocardiography Evaluate structural heart disease
3 Advanced Imaging (MRI/CT/PET) Infiltrative diseases, congenital anomalies
4 Electrophysiologic Study Localize block and assess conduction reserve

6.1 Diagnostic Algorithms

Figure 252-3: Initial evaluation algorithm includes ECG, echocardiography, and advanced imaging. Electrophysiologic studies are indicated for syncope or suspected high-grade block.

6.2 Key Tests

ECG (PR interval, QRS morphology), echocardiography (structural assessment), and His bundle electrogram (to localize block).

7. MANAGEMENT & TREATMENT

Management depends on block severity and symptoms. Temporary pacing is used for acute cases; permanent pacing is indicated for symptomatic or irreversible block.

Table 252-4 Indications for Pacing

Block Type Indications Pacing Mode
Mobitz I Symptomatic or high-risk patients DDD (preferred)
Mobitz II All cases DDD or VVI
Third-Degree All cases DDD or VVI
First-Degree Symptomatic or with bundle branch block DDD

7.1 Acute Management

Atropine for high vagal tone, correction of electrolyte abnormalities, and discontinuation of AV-conducting drugs. Transcutaneous pacing for unstable patients.

7.2 Permanent Pacing

Indicated for Mobitz II, third-degree block, or symptomatic first-degree block. Dual-chamber (DDD) or single-chamber (VVI) pacing based on patient needs.

7.3 Leadless Pacemakers

Suitable for selected patients with vascular access limitations. May preserve AV synchrony via atrial sensing and ventricular pacing.

8. PROGNOSIS & COMPLICATIONS

Prognosis varies: Mobitz I is usually benign, while Mobitz II and third-degree block carry higher mortality. Complications include pacemaker syndrome, lead dislodgment, and infection.

8.1 Complications of Pacemaker Implantation

Infection, lead failure, and inappropriate programming. 'Twiddler’s syndrome' may occur with lead dislodgment.

8.2 Long-Term Outcomes

Patients with asymptomatic AV block may have a favorable prognosis, but those with underlying heart disease (e.g., ischemia, infiltrative disease) face higher risks.

9. SPECIAL CONSIDERATIONS

Pregnancy requires careful monitoring due to increased vagal tone. Pediatric patients may present with congenital AV block (e.g., maternal lupus). Elderly patients are at higher risk for fibrosis and drug-induced block.

9.1 Neuromuscular Diseases

Myotonic dystrophy, Kearns-Sayre syndrome, and other dystrophies increase risk of AV block and require permanent pacing.

10. KEY POINTS & CLINICAL PEARLS

  1. AV block is classified by ECG and conduction level (node vs. infranodal). 2. Mobitz I is typically benign; Mobitz II and third-degree block require pacing. 3. Leadless pacemakers are viable for selected patients. 4. Distinguish between intrinsic and extrinsic causes to guide management. 5. Permanent pacing is indicated for symptomatic or irreversible block.