eMedicine Specialties > Cardiology > Arrhythmias

Second-Degree Atrioventricular Block

Author: Ali A Sovari, MD, Research Fellow, Department of Medicine, Division of Cardiology, University of California at Los Angeles
Coauthor(s): Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago; Ryan L Cooley, MD, Consulting Staff, Heart Care Associates LLC, Wisconsin Electrophysiology Group; Assistant Professor, Department of Medicine, University of Wisconsin Medical School at Milwaukee
Contributor Information and Disclosures

Updated: Jun 29, 2006

Introduction

Background

Second-degree atrioventricular (AV) block is characterized by block of some, but not all, atrial beats. This excludes block due to premature atrial beats. Typically, it is divided into Mobitz type I block or Wenckebach block, Mobitz type II block, 2:1 block, and high-grade AV block. The diagnosis of type I and II second-degree AV block is based on electrocardiographic patterns, not on the anatomic site of the block. Precise localization of the site of the block within the specialized conduction system is critical to the appropriate treatment of individuals with second-degree AV block.

By itself, a 2:1 AV block cannot be classified as type I or II mechanism because only 1 PR interval is available for analysis before the block. Both a 2:1 AV block and a block involving 2 or more consecutive sinus P waves are sometimes referred to as advanced second-degree AV block.

Pathophysiology

Type I AV block most often results from conduction disturbances in the AV node; however, in rare cases, it may be due to intra- or infra-His bundle block. Type I block is rarely secondary to AV nodal structural abnormalities when the QRS complex is narrow in width and no underlying cardiac disease is present. In this setting, type I block can be vagally mediated and may be observed in conditions associated with relative activation of the parasympathetic nervous system, such as (1) well-trained athletes, (2) cardiac glycoside (ie, digoxin) excess, or (3) neurally mediated syncopal syndromes.

A vagally mediated AV block occurs in the AV node when vagal discharge is enhanced and often is associated with electrocardiographic evidence of sinus slowing. A vagally mediated AV block improves with exercise and may occur more commonly during sleep when parasympathetic tone dominates. If an increase in sympathetic tone (eg, exercise) initiates or exacerbates a type I block, infranodal block should be considered.

Cardioactive drugs are another important cause of AV block. They may exert negative (ie, dromotropic) effects on the AV node directly, indirectly via the autonomic nervous system, or both. Digoxin, beta-blockers, calcium channel blockers, and certain antiarrhythmic drugs have been implicated in second-degree AV block.

Various inflammatory, infiltrative, metabolic, endocrine, and collagen vascular disorders have been associated with AV nodal block.

Less commonly, type I block can occur with a block localized to the His bundle or distal to the His bundle. In this situation, the QRS complex may be wide, and the baseline PR interval is usually shorter with smaller PR increments preceding the block. Type I block with intra- or infra-His bundle block carries a worse prognosis compared with AV nodal block.

Type II block most often occurs in the His-Purkinje system. As such, this poses higher risk to the patient.

Frequency

United States

Nearly 3% of patients with underlying structural heart disease develop some form of second-degree AV block.

Mortality/Morbidity

The level of the block determines the prognosis. AV nodal blocks, which are the vast majority of type I blocks, carry a good prognosis while intra- or infra-His bundle blocks, whether type I or type II, may progress to complete block with a worse prognosis.

• Type I block (in the AV node) is often nonprogressive and benign from a mortality standpoint. The risk of progression to complete heart block is significant when the level of block is in the specialized His-Purkinje conduction system.
• Type II AV block often progresses to third-degree block and, as such, carries a more worrisome prognosis. Type II block may produce Stokes-Adams syncopal attacks.
• Vagally mediated AV block is typically benign from a mortality standpoint but may lead to dizziness and syncope.

Sex

• The male-to-female ratio is 1:1.

Clinical

History

Symptoms related to type I block vary substantially, ranging from asymptomatic in well-trained athletes and those without structural heart disease, to recurrent syncope, presyncope, and bradycardia in patients with heart disease. AV block may provoke heart failure and angina.

Causes

Second-degree AV block may occur in the presence or absence of structural heart disease.

• Vagally mediated AV block occurs in the AV node when vagal activation is enhanced. It can be associated with electrocardiographic evidence of sinus slowing.
• Cardioactive drugs are another important cause of AV block. They may exert negative effects on the AV node directly, indirectly via the autonomic nervous system, or both. Digoxin, beta-blockers, calcium channel blockers, and certain antiarrhythmic drugs have been implicated in second-degree AV block. Several antiarrhythmic medications may cause second-degree AV block, and among them, Na channel blockers, such as procainamide, cause more distal block in the His-Purkinje system. The AV block may not resolve in many of the patients who take cardioactive medications. This suggests an underlying conduction disturbance in addition to the medications as the etiology of the AV block.
• Various inflammatory, infiltrative, metabolic, endocrine, and collagen vascular disorders that have been associated with AV nodal block are as follows:
  • Inflammatory diseases
    • Endocarditis
    • Myocarditis
    • Lyme disease
    • Acute rheumatic fever
  • Infiltrative diseases
    • Amyloidosis
    • Hemochromatosis
    • Sarcoidosis
  • Metabolic and endocrine disorders
    • Hyperkalemia
    • Hypermagnesemia
    • Addison disease
  • Collagen vascular diseases
    • Ankylosing spondylitis
    • Dermatomyositis
    • Rheumatoid arthritis
    • Scleroderma
    • Lupus erythematosus
    • Reiter syndrome
• Some of the more common causes of infranodal AV block (type II) include the following:
  • Progressive (age-related) idiopathic fibrosis of the cardiac skeleton
  • Valvular heart disease complications, especially aortic stenosis and aortic valve replacement surgery
  • Infiltrative and inflammatory conditions listed above
  • Muscular dystrophies
  • Corrective congenital heart surgery, especially those in close proximity to the septum
• Acute myocardial infarction (MI) may cause second-degree AV block.
• In some patients, AV block may be an autosomal dominant trait and a familial disease. Several mutations in the SCN5A gene have been linked to familial AV block. Different mutations in the same gene have been reported in other dysrhythmias such as long QT syndrome and Brugada syndrome.

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