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.

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

References

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  3. Fisch C, DeSanctis RW, Dodge HT. Guidelines for Clinical Intracardiac Electrophysiologic Studies. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures. Circulation. Dec 1989;80(6):1925-39. [Medline].

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  7. Lange HW, Ameisen O, Mack R, et al. Prevalence and clinical correlates of non-Wenckebach, narrow-complex second-degree atrioventricular block detected by ambulatory ECG. Am Heart J. Jan 1988;115(1 Pt 1):114-20. [Medline].

  8. Massie B, Scheinman MM, Peters R, et al. Clinical and electrophysiologic findings in patients with paroxysmal slowing of the sinus rate and apparent Mobitz type II atrioventricular block. Circulation. Aug 1978;58(2):305-14. [Medline].

  9. Puesch P, Grolleau R, Guimond C. Incidence of different types of A-V block and their localization by His bundle recordings. In: Wellens HJJ, Lie KI, Janse MJ, eds. The Conduction System of the Heart. Philadelphia, Pa: Stenfert Kroese; 1976:. 467-84.

  10. Rardon D, Miles W, Zipes D. Atrioventricular block and dissociation. In: Zipes D, Jalife J, eds. Cardiac Electrophysiology: From Cell to Bedside. 3rd ed. Philadelphia, Pa: WB Saunders; 2000:. 451-8.

  11. Royer A, van Veen TA, Le Bouter S. Mouse model of SCN5A-linked hereditary Lenègre''s disease: age-related conduction slowing and myocardial fibrosis. Circulation. Apr 12 2005;111(14):1738-46.

  12. Schwartzman D. Atrioventricular block and Atrioventricular dissociation. In: Zipes D, Jalife J, eds. Cardiac Electrophysiology: From Cell to Bedside. 4th. 2004;485-7.

  13. Tan HL, Bink-Boelkens MT, Bezzina CR. A sodium-channel mutation causes isolated cardiac conduction disease. Nature. Feb 22 2001;409(6823):1043-7.

  14. Zeltser D, Justo D, Halkin A. Drug-induced atrioventricular block: prognosis after discontinuation of the culprit drug. J Am Coll Cardiol. Jul 7 2004;44(1):105-8.

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Further Reading

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

Contributor Information and Disclosures

Author

Ali A Sovari, MD, Research Fellow, Department of Medicine, Division of Cardiology, University of California at Los Angeles
Ali A Sovari, MD is a member of the following medical societies: American College of Physicians, American Heart Association, and American Medical 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, Heart Rhythm Society, and Illinois State Medical Society
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, 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: Nothing to disclose.

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

Leonard Ganz, MD, Associate Professor of Medicine, Temple University School of Medicine; Cardiac Electrophysiologist, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Cent, West Penn Hospital
Disclosure: Nothing to disclose.

 
 
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