eMedicine Specialties > Cardiology > Arrhythmias

Second-Degree Atrioventricular Block

Author: Ali A Sovari, MD, Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois at Chicago
Coauthor(s): Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago; Raluca B Arimie, MD, Assistant Professor of Internal Medicine, Department of Medicine, Division of Cardiology, University of California at Los Angeles; Consulting Staff, Santa Monica Cardiology; 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: Sep 2, 2009

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:
  • 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.

More on Second-Degree Atrioventricular Block

Overview: Second-Degree Atrioventricular Block
Differential Diagnoses & Workup: Second-Degree Atrioventricular Block
Treatment & Medication: Second-Degree Atrioventricular Block
Follow-up: Second-Degree Atrioventricular Block
Multimedia: Second-Degree Atrioventricular Block
References
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References

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Further Reading

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Keywords

second-degree atrioventricular block, heart block, 2nd degree heart block, second-degree AV block, 2nd degree AV block, AV block, Mobitz AV block, Mobitz heart block, Mobitz type I, Mobitz type II, Wenckebach phenomenon, Wenckebach heart block, high-grade AV block, complete heart block, third-degree AV block, Stokes-Adams syncopal attack, heart failure, angina, acute myocardial infarction, sinus slowing, cardioactive drugs, endocarditis, myocarditis, Lyme disease, acute rheumatic fever, amyloidosis, hemochromatosis, sarcoidosis, hyperkalemia, hypermagnesemia, Addison disease, ankylosing spondylitis, dermatomyositis, rheumatoid arthritis, scleroderma, lupus erythematosus, Reiter syndrome, progressive idiopathic fibrosis of the cardiac skeleton, aortic stenosis, aortic valve replacement surgery, muscular dystrophies, corrective congenital heart surgery

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Contributor Information and Disclosures

Author

Ali A Sovari, MD, Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois at Chicago
Ali A Sovari, MD is a member of the following medical societies: American College of Physicians and American Heart Association
Disclosure: Nothing to disclose.

Coauthor(s)

Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Abraham G Kocheril, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, Cardiac Electrophysiology Society, Central Society for Clinical Research, Heart Failure Society of America, and Illinois State Medical Society
Disclosure: Nothing to disclose.

Raluca B Arimie, MD, Assistant Professor of Internal Medicine, Department of Medicine, Division of Cardiology, University of California at Los Angeles; Consulting Staff, Santa Monica Cardiology
Disclosure: Nothing to disclose.

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
Ryan L Cooley, MD is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Robert E Fowles, MD, Clinical Professor of Medicine, University of Utah College of Medicine; Consulting Staff, Intermountain Medical Center and LDS Hospital; Director and Consulting Staff, Department of Cardiology, Salt Lake Clinic
Robert E Fowles, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine
Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences
Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Reliant Grant/research funds Other; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD, Professor of Medicine and Pharmacology, Director, Clinical Cardiac Electrophysiology Fellowship Program, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center
Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)
Disclosure: Nothing to disclose.

 
 
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