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Atrioventricular Block

  • Author: Chirag M Sandesara, MD; Chief Editor: Jeffrey N Rottman, MD  more...
 
Updated: Dec 18, 2014
 

Practice Essentials

Signs and symptoms

Signs and symptoms of atrioventricular (AV) block include the following:

  • First-degree AV block: Generally not associated with any symptoms; it is usually an incidental finding on electrocardiography
  • Second-degree AV block: Usually is asymptomatic, but in some patients, sensed irregularities of the heartbeat, presyncope, or syncope may occur; may manifest on physical examination as bradycardia (especially Mobitz II) and/or irregularity of heart rate (especially Mobitz I [Wenckebach])
  • Third-degree AV block: Frequently associated with symptoms such as fatigue, dizziness, light-headedness, presyncope, and syncope; associated with profound bradycardia unless the site of the block is located in the proximal portion of the atrioventricular node (AVN)

In third-degree AV block, exacerbation of ischemic heart disease or congestive heart failure caused by AV block–related bradycardia and reduced cardiac output may lead to specific, clinically recognizable symptoms, such as the following:

  • Chest pain
  • Dyspnea
  • Confusion
  • Pulmonary edema

See Clinical Presentation for more specific information.

Diagnosis

Laboratory studies

Although laboratory studies are not usually indicated in patients with AV block, the following may be helpful in certain cases:

  • Electrolyte and drug levels (eg, digitalis): In patients with second- or third-degree AV block, when suspicion of increased potassium level or drug toxicity exists
  • Cardiac enzyme levels: In patients with second- or third-degree AV block that might be a manifestation of acute myocardial infarction
  • Infection, myxedema, or connective tissue disease studies: If clinical evaluation suggests systemic illness

Electrocardiography

Routine electrocardiographic (ECG) recording and cardiac monitoring with careful evaluation of the relationship between P waves and QRS complexes are the standard tests leading to proper diagnosis of AV blocks. Identifying episodes of transient AV block with sudden pauses and/or low heart rate causing syncopal episodes may require any of the following:

  • 24-hour Holter monitoring
  • Multiple ECG recordings
  • Event (loop) ECG recordings
  • Monitoring with implantable loop recorders (Reveal, Medtronic, Inc; Confirm, St Jude Medical, Inc) in selected cases

Additional modalities

Other means of evaluating patients for AV block can include the following:

  • Electrophysiologic testing: Indicated in a patient with suspected AV block as the cause of syncope
  • Echocardiography: May be useful in diagnosing underlying comorbid conditions, such as aortic valve stenosis with calcification, wall motion abnormalities in acute ischemia, cardiomyopathy, and congenital heart disease (eg, congenitally corrected transposition of the great vessels)
  • Exercise: May be used to evaluate 2:1 heart block and to differentiate a Mobitz I second-degree AV block from a Mobitz II second-degree AV block

See Clinical Presentation and Workup for more specific information on the diagnosis of atrioventricular block.

Management

Pacemaker implantation

Implantation of a permanent pacemaker is the therapy of choice in advanced AV block. Recommendations for the implantation of pacemakers and arrhythmia devices, as devised by the American College of Cardiology (ACC), the American Heart Association (AHA), and the Heart Rhythm Society (HRS), include the following[1, 2] :

  • First-degree AV block and Mobitz I second-degree AV block: Do not generally require treatment unless they cause symptoms and are not due to a reversible cause
  • Mobitz II second-degree AV block and third-degree AV block: Usually require temporary and/or permanent cardiac pacing
  • Third-degree AV block: Patients with persistent bundle branch block and transient third-degree AV block may benefit from permanent pacing therapy, especially after anterior myocardial infarction; nonrandomized studies strongly suggest that permanent pacing improves survival in patients with third-degree AV block, especially if syncope has occurred

Pharmacologic therapy

Considerations regarding the administration of anticholinergic agents include the following:

  • Long-term medical therapy is not indicated in AV block
  • Atropine administration or isoproterenol infusion may improve AV conduction in emergencies in which bradycardia is caused by a proximal AV block
  • Atropine administration or isoproterenol infusion may worsen conduction if the block is in the His-Purkinje system

See Treatment and Medication for more specific information on the treatment of atrioventricular block.

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Background

Atrioventricular (AV) block occurs when atrial depolarizations fail to reach the ventricles or when atrial depolarization is conducted with a delay. Three degrees of AV block are recognized.

First-degree AV block consists of prolongation of the PR interval on the electrocardiogram (ECG) (>200 msec in adults and >160 msec in young children). The upper limit of the reference range for the PR interval is age-dependent in children. All atrial impulses reach the ventricles in first-degree AV block; however, conduction is delayed within the AV node (see the image below).

First-degree atrioventricular block. PR interval i First-degree atrioventricular block. PR interval is constant and is 280 msec.

Second-degree AV block is characterized by atrial impulses (generally occurring at a regular rate) that fail to conduct to the ventricles in 1 of the following 4 ways.

The first form of second-degree AV block is Mobitz I second-degree AV block (Wenckebach block), which consists of progressive prolongation of the PR interval with the subsequent occurrence of a single nonconducted P wave that results in a pause. The pause is shorter than the sum of any 2 consecutive conducted beats (R-R interval).

An episode of Mobitz I AV block usually consists of 3-5 beats, with a ratio of nonconducted to conducted beats of 4:3, 3:2, and so forth (see the image below). The block is generally in the AV node but can occasionally occur in the His-Purkinje system and is termed intrahisian or infrahisian Wenckebach (depending if the block occurs within or below the His-Purkinje system).

Second-degree atrioventricular block, Mobitz type Second-degree atrioventricular block, Mobitz type I (Wenckebach). Note the prolongation of the PR interval preceding the dropped beat and the shortened PR interval following the dropped beat.

The second form is Mobitz II second-degree AV block, which is characterized by a constant PR interval followed by sudden failure of a P wave to be conducted to the ventricles, so that either an occasional dropped P wave or a regular conduction pattern of 2:1 (2 conducted and 1 blocked), 3:1 (3 conducted and 1 blocked), and so on is observed (see the image below).

Second-degree atrioventricular block, Mobitz type Second-degree atrioventricular block, Mobitz type II. A constant PR interval in conducted beats is present. Intraventricular conduction delay also is present.

The third form is high-grade AV block, which consists of multiple P waves in a row that should conduct, but do not. The conduction ratio can be 3:1 or higher, and the PR interval of conducted beats is constant. This is a distinct form of complete AV block, in that the P waves that conduct to the QRS complexes occur at fixed intervals. For complete AV block, no relationship exists between the P waves and QRS complexes.

The fourth form is 2:1 AV block. This could be either Mobitz I or Mobitz II, but distinguishing one variety from the other is nearly impossible.

Third-degree AV block is diagnosed when no supraventricular impulses are conducted to the ventricles. P waves on the rhythm strip reflect a sinus node rhythm independent from QRS wave complexes. The QRS complexes represent an escape rhythm, either junctional or ventricular. The escape rhythm originating from the junctional or high septal region is characterized by narrow QRS complexes at a rate of 40-50 beats/min, whereas escape rhythm from low ventricular sites is characterized by broad QRS complexes at a rate of 30-40 beats/min.

No relationship exists between the rhythm of P waves and the rhythm of QRS complexes in third-degree AV block. The frequency of P waves (atrial rate) is higher than the frequency of QRS complexes (ventricular rate) (see the image below).

Third-degree atrioventricular block (complete hear Third-degree atrioventricular block (complete heart block). The atrial rate is faster than the ventricular rate, and no association exists between the atrial and ventricular activity.

AV dissociation is a rhythm identified by atrial and ventricular activation occurring from different pacemakers. AV dissociation does not indicate the presence of AV block and is distinctly different. Ventricular activation may be from either junctional pacemakers or infranodal.

AV dissociation can occur in the presence of intact AV conduction, especially when rates of the pacemaker, either junctional or ventricular, exceed the atrial rate. Third-degree AV block can occur with AV dissociation. However, in AV dissociation without AV block, the ventricular rate can exceed the atrial rate and conduction can occasionally occur dependent on the timing between the P wave and the QRS complex.

AV block may also occur in patients with atrial fibrillation (see the Atrial Fibrillation Center). Regular R-R intervals are possible in the presence of AV block (generally at slow regular rates).

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Pathophysiology

The atrioventricular node (AVN) is part of the conduction system of the heart that allows electrical impulses to be transmitted from the sinus node via atrial tissue (intra-atrial fascicles) to the ventricles. This node consists of 3 parts—atrionodal (transitional zone), nodal (compact portion), and nodal-His (penetrating His bundle). The nodal portion causes the slowest conduction.

The AVN is supplied by the right coronary artery (90%) or by the circumflex artery (10%) and is innervated by both sympathetic and parasympathetic fibers. It receives impulses anteriorly via the intra-atrial fibers in the septum and posteriorly via the crista terminalis. Impulses arriving at the AVN are transmitted to the ventricle in a 1:1 ratio. As faster impulses arrive, the conduction to the ventricles slows; this is called decremental conduction.

The His-Purkinje system is composed of 2 bundles of Purkinje fibers (the left and right bundle) that conduct electrical impulses to allow rapid ventricular activation. The His-Purkinje system is yet another location where AV block may occur.

First-degree AV block and second-degree Mobitz I AV block usually involve a delay at the level of the AVN, whereas second-degree Mobitz II AV block generally involves blockage in the His bundle or lower regions of the conduction system. Third-degree AV block involves conduction disturbances in the AV node or the His-Purkinje system.

In most cases of complete AV block, an escape rhythm originates from the ventricles, with wide QRS complexes at a low regular rate of 30-40 beats/min. A higher anatomic location of the block results in a higher location of the escape rhythm pacemaker, a faster escape rhythm (40-60 beats/min in the region of His bundle), and a narrower QRS duration.

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Etiology

Delay or lack of conduction through the AV node has multiple causes.

First-degree AV block and Mobitz I (Wenckebach) second-degree AV block may occur in healthy, well-conditioned people as a physiologic manifestation of high vagal tone. Mobitz I AV block also may occur physiologically at high heart rates (especially with pacing) as a result of increased refractoriness of the AVN, which protects against conducting an accelerated arrhythmia to the ventricles.

AV block may be caused by acute myocardial ischemia or infarction. Inferior myocardial infarction may lead to third-degree block, usually at the AVN level; this may occur through other mechanisms via the Bezold-Jarisch reflex. Anterior myocardial infarction usually is associated with third-degree block resulting from ischemia or infarction of bundle branches.

Degenerative changes in the AVN or bundle branches (eg, fibrosis, calcification, or infiltration) are the most common cause of nonischemic AV block. Lenegre-Lev syndrome is an acquired complete heart block due to idiopathic fibrosis and calcification of the electrical conduction system of the heart. It is most commonly seen in the elderly and is often described as senile degeneration of the conduction system and may lead to third-degree AV block.

In 1999, degenerative changes in the AV conduction system were linked to mutations of the SCN5A sodium channel gene (mutations of the same gene may lead to congenital long QT syndrome type 3 and to Brugada syndrome).[3]

Infiltrative myocardial diseases resulting in AV block include sarcoidosis,[4] myxedema, hemochromatosis, and progressive calcification related to mitral or aortic valve annular calcification. Endocarditis and other infections of the myocardium, such as Lyme disease with active infiltration of the AV conduction system, may lead to varying degrees of AV block. Systemic diseases, such as ankylosing spondylitis and Reiter syndrome, may affect the AV nodal conducting tissue.

Surgical procedures (eg, aortic valve replacement and congenital defect repair) may cause AV block, as may other therapeutic procedures (eg, AV node ablation and alcohol septal ablation in patients with obstructive hypertrophic cardiomyopathy). Patients with corrected transposition of the great vessels have anterior displacement of the AVN and are prone to develop complete heart block during right heart catheterization or surgical manipulation.

A variety of drugs may affect AV conduction. The most common of these include digitalis glycosides, beta-blockers, calcium channel blockers, adenosine, and other antiarrhythmic agents.

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Epidemiology

First-degree AV block can be found in healthy adults, and its incidence increases with age. At 20 years of age, the PR interval may exceed 0.20 seconds in 0.5-2% of healthy people. At age 60 years, more than 5% of healthy individuals have PR intervals exceeding 0.20 seconds.

Mobitz II second-degree AV block (Mobitz II) is rare in healthy individuals, whereas Mobitz I (Wenckebach) second-degree AV block is observed in 1-2% of healthy young people, especially during sleep.

Congenital third-degree AV block is rare, at 1 case per 20,000 births. This form of heart block, in the absence of major structural abnormalities, is associated with maternal antibodies to Ro (SS-A) and La (SS-B) and secondary to maternal lupus. It is most commonly diagnosed between 18 and 24 weeks’ gestation and may be first, second, or third degree (complete). Mortality approaches approximately 20%; most surviving children require pacemakers. Recent advances in diagnostics and pacing therapies have led to improved outcomes for children with AV block.[5]

AV blocks occur more frequently in people older than 70 years, especially in those who have structural heart disease. Approximately 5% of patients with heart disease have first-degree AV block, and about 2% have second-degree AV block.

The international incidence is similar to that of the United States.

Age-, sex-, and race-related demographics

The incidence of AV block increases with age. The incidence of third-degree AV block is highest in people older than 70 years (approximately 5-10% of patients with heart disease). A 60% female preponderance exists in congenital third-degree AV block. For acquired third-degree AV block, a 60% male preponderance exists. No racial proclivity exists in AV blocks.

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Prognosis

Patients treated with permanent pacing to treat AV blocks have an excellent prognosis. Patients with advanced AV blocks who are not treated with permanent pacing remain at high risk of sudden cardiac death.

Although AV block generally is not associated with major morbidity, progressive degrees of AV block carry increasing morbidity and mortality.

Cheng et al found that first-degree AV block (ie, PR interval >200 msec) is associated with an increased risk of atrial fibrillation, pacemaker implantation, and all-cause mortality.[6] In a prospective, community-based cohort of 7,575 individuals from the Framingham Heart Study (mean age, 47 y; 54% women) who underwent routine 12-lead ECG in 1968-1974, 124 individuals had PR intervals >200 msec on the baseline examination.

On follow-up of the cohort through 2007, individuals with first-degree AV block had a 2-fold adjusted risk of atrial fibrillation, a 3-fold adjusted risk of pacemaker implantation, and a 1.4-fold adjusted risk of all-cause mortality.[6] For all 3 outcomes, each 20-msec increment in PR was associated with an increase in risk.

A prospective cohort study of 938 patients with stable coronary artery disease were examined to assess if first-degree AV block was associated with an increased risk of heart failure and mortality.[7] Patients were classified as a PR interval of 220 ms or less. Patients with first-degree AV block were at increased risk for heart failure hospitalization (age-adjusted heart rate, 2.33; 95% CI, 1.49-3.65; P = 0.0002), mortality (age-adjusted heart rate, 1.58; 95% CI, 1.13-2.20; P = 0.008], cardiovascular mortality (age-adjusted heart rate 2.33; 95% CI, 1.28-4.22; P = 0.005], and the combined endpoint of heart failure hospitalization or cardiovascular mortality (age-adjusted heart rate, 2.43: 95% CI, 1.64–3.61; P ≤0.0001).

These associations persisted after multivariable adjustment for heart rate, medication use, ischemic burden, and QRS duration. Despite adjusting for systolic and diastolic dysfunction, first-degree AV block was associated with an increased risk for heart failure or cardiovascular death (heart rate, 1.61; 95% CI, 1.02–2.54; P = 0.04).[7]

The low heart rate observed in third-degree or Mobitz II second-degree AV block may lead to syncopal episodes with major injuries (eg, head trauma, hip fracture), exacerbation of congestive heart failure, or exacerbation of ischemic heart disease symptoms due to low cardiac output.

In fetuses with congenital second- or third-degree AV block, the most important prognostic factor may be an association with a congenital heart defect, according to a retrospective study by Kuleva et al.[8] The investigators evaluated data from 62 cases of prenatally diagnosed fetal AV block, in which 45 (73%) were isolated AV blocks (42 of the 45 were related to maternal antibodies) and 17 (27%) were associated with a congenital heart defect. There were 5 deaths in 9 infants (55%) born live among those with AV block and a congenital heart defect; 1 death occurred in 40 infants (2.5%) born live with isolated AV block, and 36 (90%) of these infants underwent permanent pacemaker placement. In utero treatment or nontreatment of AV block appeared to result no difference in outcome for placement of a permanent pacemaker, postnatal death, or development of dilated cardiomyopathy.[8]

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Patient Education

Patients with implanted pacemakers require additional education, with particular emphasis on situations involving exposure to magnetic and electrical fields (eg, airport security gates) and training regarding transtelephonic monitoring of pacemaker function.

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Contributor Information and Disclosures
Author

Chirag M Sandesara, MD Virginia Cardiovascular Associates, Cardiac Rhythm Care

Chirag M Sandesara, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Medical Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Coauthor(s)

Brian Olshansky, MD Professor Emeritus of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, Heart Rhythm Society, Cardiac Electrophysiology Society, American Heart Association

Disclosure: Received honoraria from Guidant/Boston Scientific for speaking and teaching; Received honoraria from Medtronic for speaking and teaching; Received consulting fee from Guidant/Boston Scientific for consulting; Received consulting fee from BioControl for consulting; Received consulting fee from Boehringer Ingelheim for consulting; Received consulting fee from Amarin for review panel membership; Received consulting fee from sanofi aventis for review panel membership.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Steven J Compton, MD, FACC, FACP, FHRS Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Physicians, American Heart Association, American Medical Association, Heart Rhythm Society, Alaska State Medical Association, American College of Cardiology

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Wojciech Zareba, MD, PhD, FACC, and Stacy D Fisher, MD, to the development and writing of the source article.

References
  1. [Guideline] Epstein AE, Dimarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: executive summary. Heart Rhythm. 2008 Jun. 5(6):934-55. [Medline].

  2. [Guideline] Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA 3rd, Freedman RA, Gettes LS, et al. 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2013 Jan 22. 61(3):e6-75. [Medline].

  3. Schott JJ, Alshinawi C, Kyndt F, et al. Cardiac conduction defects associate with mutations in SCN5A. Nat Genet. 1999 Sep. 23(1):20-1. [Medline].

  4. Nery PB, Beanlands RS, Nair GM, Green M, Yang J, McArdle BA, et al. Atrioventricular block as the initial manifestation of cardiac sarcoidosis in middle-aged adults. J Cardiovasc Electrophysiol. 2014 Aug. 25(8):875-81. [Medline].

  5. Saleh F, Greene EA, Mathison D. Evaluation and management of atrioventricular block in children. Curr Opin Pediatr. 2014 Jun. 26(3):279-85. [Medline].

  6. Cheng S, Keyes MJ, Larson MG, et al. Long-term outcomes in individuals with prolonged PR interval or first-degree atrioventricular block. JAMA. 2009 Jun 24. 301(24):2571-7. [Medline]. [Full Text].

  7. Crisel RK, Farzaneh-Far R, Na B, Whooley MA. First-degree atrioventricular block is associated with heart failure and death in persons with stable coronary artery disease: data from the Heart and Soul Study. Eur Heart J. 2011 Aug. 32(15):1875-80. [Medline].

  8. Kuleva M, Le Bidois J, Decaudin A, et al. Clinical course and outcome of antenatally detected atrioventricular block: experience of a single tertiary centre and review of the literature. Prenat Diagn. 2014 Dec 8. [Medline].

  9. Stiles S. BLOCK-HF: replace RV pacing with BiV in AV-block heart failure. Heartwire. Nov 8, 2012. [Full Text].

 
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First-degree atrioventricular block. PR interval is constant and is 280 msec.
Second-degree atrioventricular block, Mobitz type I (Wenckebach). Note the prolongation of the PR interval preceding the dropped beat and the shortened PR interval following the dropped beat.
Second-degree atrioventricular block, Mobitz type II. A constant PR interval in conducted beats is present. Intraventricular conduction delay also is present.
Third-degree atrioventricular block (complete heart block). The atrial rate is faster than the ventricular rate, and no association exists between the atrial and ventricular activity.
 
 
 
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