Supraventricular Tachycardia, Atrioventricular Node Reentry 

  • Author: Glenn T Wetzel, MD, PhD; Chief Editor: Stuart Berger, MD   more...
 
Updated: Jun 28, 2010
 

Background

Atrioventricular node reentrant tachycardia (AVNRT) is a reentrant rhythm within the atrioventricular (AV) node. Reentrant rhythms account for most episodes of supraventricular tachycardia (SVT) in children. A reentrant rhythm involves the presence of 2 distinct pathways, a zone of slow conduction and unidirectional block in one limb, allowing an electrical impulse to travel down the second limb and reenter the blocked pathway from the other direction. Reentrant rhythms can usually be initiated and terminated by pacing or premature beats. During AVNRT, the circuit typically involves both a fast and a slow pathway within the region of the AV node, which allows the impulses to reenter the node in a retrograde fashion as the depolarization simultaneously proceeds to the ventricles.

The patient's heart rate is approximately 146 beatThe patient's heart rate is approximately 146 beats per minute with a normal axis. Note the pseudo S waves in leads II, III, and aVF. Also note the pseudo R' waves in V1 and aVR. These deflections represent retrograde atrial activation.

The relative incidence of AVNRT appears to increase with age. AVNRT is the predominant mechanism of SVT in adults. It occurs somewhat more commonly in adult females than in males and is usually not associated with structural heart disease.[1]

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Pathophysiology

Often, 2 or more functionally and (usually) anatomically distinct pathways are located within the AV node; they are known as the fast and the slow pathways and have different electrophysiologic characteristics. The fast pathway is identified by its relatively shorter conduction time and longer effective refractory period (ERP), whereas the slow pathway has a relatively longer conduction time and an ERP that typically is short when compared to fast pathway ERP. These separate pathways are anatomically discrete.

Conduction during sinus rhythm usually occurs over the fast pathway, and the PR interval is normal. A premature atrial beat may block in the fast pathway (because of its longer ERP) but conduct by the slow pathway. The slow pathway has a longer conduction time than the fast pathway, providing a delay of the impulse; therefore, when it reaches the distal end of the fast pathway (which has recovered from refractoriness), the impulse is conducted retrograde in the fast pathway. After traversing a short portion of the low septal right atrium, it reenters the slow pathway again, creating a circus movement tachycardia.

The 2 forms of AV node reentry (AVNR) that usually are described are the typical form (ie, slow-fast) and the atypical form (ie, fast-slow), referring to the characteristic of antegrade-retrograde conduction during tachyarrhythmia. In the typical form, which represents 90% of clinical AVNRT episodes, the conduction moves in antegrade direction through the slow pathway and in retrograde direction through the fast pathway. In the atypical form, the conduction moves antegradely in the fast pathway and retrogradely in the slow pathway, resulting in a long RP interval. A third form also has been identified in which the conduction appears to be antegrade and retrograde through 2 slow pathways.[2]

The natural history of AVNRT is unknown, but some infants appear to exhibit spontaneous resolution. The substrate for atrioventricular tachycardia is not fully understood, but cell-to-cell interactions may play a role.[3]

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Epidemiology

Frequency

United States

AVNRT is the most common cause of paroxysmal supraventricular tachycardia (PSVT). Approximately 89,000 new cases are reported each year, and 570,000 persons with PSVT live in the United States.

International

PSVT has a prevalence of 2.25 per 1000 population and an incidence of 35 per 100,000 person-years.

Mortality/Morbidity

Episodes of SVT caused by any mechanism, including AVNRT, have a minimal impact on mortality rates in children, although SVT may lead to some degree of morbidity. Rare cases of AVNRT in young infants may be associated with more significant morbidity and possible mortality. The presence of dual AV node physiology per se does not necessarily indicate morbidity. Discontinuous AV nodal conduction curves on the electrophysiologic study that suggest the presence of dual AV nodal pathways have been encountered in patients without SVT and occur in approximately 63% of children. However, the presence of dual AV node physiology with associated AVNRT is a common mechanism for SVT in children and adults. Thapar and Gillette's publication showed that dual AV node physiology was the mechanism in 46% of children who presented for evaluation of arrhythmias.[4]

Sex

Prevalence of AVNRT is more common in females than in males, particularly in adults.

Age

AVNR is uncommon in newborns and increases in prevalence throughout childhood. The relative incidence of AVNRT appears to increase with age in children, and AVNRT is the predominant mechanism (accounting for 40-50% of cases) of SVT in adults.

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Proceed to Clinical Presentation
 
 
Contributor Information and Disclosures
Author

Glenn T Wetzel, MD, PhD  Professor of Pediatrics, University of Tennessee College of Medicine; Director, Pediatric Arrhythmia Service, Le Bonheur Children's Medical Center

Glenn T Wetzel, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Heart Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Coauthor(s)

Ryan Jones, MD  Fellow, Division of Pediatric Cardiology, Department of Pediatrics, University of Tennessee Health Science Center, Memphis

Ryan Jones, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Cardiology

Disclosure: Nothing to disclose.

Specialty Editor Board

Charles I Berul, MD  Professor of Pediatrics, George Washington University School of Medicine; Chief, Division of Cardiology, Children's National Medical Center

Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, Pediatric and Congential Electrophysiology Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Hugh D Allen, MD  Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine

Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, and Western Society for Pediatric Research

Disclosure: Nothing to disclose.

Gilbert Z Herzberg, MD  Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center

Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD  Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

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The patient's heart rate is approximately 146 beats per minute with a normal axis. Note the pseudo S waves in leads II, III, and aVF. Also note the pseudo R' waves in V1 and aVR. These deflections represent retrograde atrial activation.
 
 
 
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