Second-Degree Atrioventricular Block

Introduction
Background

Second-degree atrioventricular (AV) block is characterized by disturbance, delay, or interruption of impulse conduction through the AV node. This excludes block due to premature atrial beats. The AV block can be permanent or transient, depending on the anatomical or functional impairment in the conduction system. Typically, it is classified 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. Type I is characterized by a progressive lengthening of the conduction time until an impulse is not conducted; type II is characterized by occasional or repetitive sudden block of conduction of an impulse without prior measurable lengthening of the conduction time. 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 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 high-grade AV block. In high-grade AV block, some beats are conducted in contrast to third-degree AV block.

Pathophysiology

Type I atrioventricular (AV) block most often results from conduction disturbances in the AV node; however, in rare cases, it may be due to infranodal 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 in well-trained athletes, cardiac glycoside (ie, digoxin) excess, or neurally mediated syncope 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 infranodal block carries a worse prognosis compared with AV nodal block. The location of a type II block is most often infranodal. 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. Atrioventricular (AV) nodal blocks, which are the vast majority of type I blocks, carry a favorable prognosis, whereas infranodal blocks, whether type I or type II, may progress to complete block with a worse prognosis. However, type I block may be significantly symptomatic.
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 (infranodal).
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 of second-degree atrioventricular block 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.
Enhanced vagal tone due to pain, carotid sinus massage, or hypersensitive carotid sinus syndrome can result in slowing of the sinus rate and/or the development of AV block. Therefore, vagally mediated AV block can be associated with electrocardiographic evidence of sinus slowing. High vagal tone can occur in young subjects or athletes at rest. Mobitz type I has been described in 2-10% of long distance runners.1
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, sodium channel blockers, such as procainamide, cause more distal block in the His-Purkinje system. Persistent second-degree AV block following adenosine infusion for nuclear stress testing has been reported.2 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. At toxic levels, other pharmacologic agents such as tricyclic antidepressants and lithium may be associated with AV block. Presynaptic alpha agonists (eg, clonidine) may also be associated with, or exacerbate, AVblock.
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: AV conduction abnormalities can be the first sign of sarcoidosis.3
Infiltrative malignancies, such as Hodgkin lymphoma and other lymphomas, and multiple myeloma4
Metabolic and endocrine disorders
Hyperkalemia
Hypermagnesemia
Addison disease
Hyperthyroidism
Myxedema
Thyrotoxic periodic paralysis5
Collagen vascular diseases
Ankylosing spondylitis
Dermatomyositis
Rheumatoid arthritis
Scleroderma
Lupus erythematosus
Reiter syndrome
Mixed connective tissue disease6
Other conditions associated with AV block:
Cardiac tumors
Trauma (including catheter-related, especially in the setting of preexisting left bundle branch block)
Myocardial bridging7
Ethanol septal reduction – Also called transcoronary ablation of septal hypertrophy for the treatment of obstructive hypertrophic cardiomyopathy
Transcatheter closure of atrial and ventricular septal defects8,9
Corrective congenital heart surgery, especially those near the septum
Progressive (age-related) idiopathic fibrosis of the cardiac skeleton
Valvular heart disease complications, especially aortic stenosis and aortic valve replacement surgery
Obstructive sleep apnea (OSA) is associated with a variety of cardiac arrhythmias including AV block.10
Muscular dystrophies: The conduction defects in patients with muscular dystrophy are progressive; therefore, these patients should undergo careful workup and follow-up, even if they present with a benign conduction defect such as first-degree atrioventricular block.11
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.

http://emedicine.medscape.com/article/161919-overview