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Atrioventricular Node Reentry Supraventricular Tachycardia Workup

  • Author: Glenn T Wetzel, MD, PhD; Chief Editor: Stuart Berger, MD  more...
Updated: May 30, 2014

Laboratory Studies

Upon initial presentation of atrioventricular node reentrant tachycardia (AVNRT), assessments of serum electrolyte levels, thyroid function, and hemoglobin are often performed.

Other laboratory studies may be performed to monitor serum levels and adverse effects in children receiving antiarrhythmic medications.



The ECG obtained during normal sinus rhythm shows a normal PR interval and the absence of preexcitation. Some patients may exhibit a slightly shortened PR interval or increased beat-to-beat variability of the PR interval, reflecting conduction through the fast or slow pathways. The typical AVNRT is characterized as a narrow complex regular tachycardia with rates that vary from 150-300 beats per minute.[14] Unlike AV reentrant tachycardia (WPW or accessory pathway mediated tachycardia), AVNRT may exhibit AV dissociation with block to either the atrium (1:2 conduction) or to the ventricle (2:1 conduction).[15]

Slow-fast form of AVNRT

Note the following:

  • The slow-fast form of AVNRT is typical.
  • Initiation of tachycardia usually occurs suddenly with a premature atrial beat. Sometimes, sudden sinus slowing is followed by a junctional escape beat as a trigger for the tachyarrhythmia.
  • The termination usually occurs with atrioventricular (AV) block, which is spontaneous or induced by vagal maneuvers or medications.
  • The rhythm may terminate with a P wave or QRS complex, depending on the site of block.
  • Little variability in RR intervals is usually noted.
  • The time that the impulse takes to reach the atrium and the ventricle from the distal node is approximately the same, which causes the retrograde P waves to be buried within the QRS or appear immediately preceding or at the terminal end of the QRS.
  • The RP interval is usually less than 50-70 milliseconds, which often results in the P wave being hidden in the QRS complex.
  • When the P wave is visible at the end of the QRS, it exhibits a characteristic late-positive component in ECG lead V1 (ie, pseudo-r' wave), or the retrograde P waves may simulate an S wave in the inferior leads.

Fast-slow form of AVNRT

Note the following:

  • The fast-slow form of AVNRT is atypical.[16]
  • The trigger is usually a premature ventricular beat that blocks in the fast pathway and is conducted in a retrograde fashion through the slow pathway and then in an antegrade fashion through the fast pathway.
  • In this form, conduction to the atria takes longer than conduction to the ventricles, and the RP interval is longer than the PR interval.
  • Another characteristic is that the P wave axis is superior (ie, negative P waves in inferior leads), because the impulse is retrograde and originates in the AV node.
  • Distinguishing this tachycardia from permanent form of junctional reciprocating tachycardia (PJRT) is difficult, although PJRT usually presents with a more incessant rather than paroxysmal pattern.[12]

Imaging Studies

Chest radiography and echocardiography are often performed to evaluate the degree of cardiopulmonary dysfunction associated with the tachyarrhythmia and to assess for structural abnormalities.

Clinical and experimental studies using electrophysiological and electroanatomical mapping are adding to the understanding of the anatomy and physiology of this disorder.

The coronary sinus, imaged at the time of electrophysiologic study, may have a broader opening in patients with AVNRT.[17] This has not been confirmed.



The electrophysiological characteristics of AVNRT include initiation and termination of tachycardia by extrastimulus or rapid pacing; normal antegrade and retrograde AV conduction (with earliest retrograde activation at the His bundle); and termination with AV block that, although uncommon, may allow the AVNRT to persist. These characteristics can be evaluated in patients through the electrophysiological study (EPS), which may be semi-invasive (eg, esophageal electrode behind the heart) or intracardiac.

Note the following:

  • During the EPS, the presence of the 2 functional pathways in adult patients can usually be demonstrated with atrial extrastimulus testing.
  • As the atrial extrastimulus-coupling interval (A1-A2) is shortened by 10-millisecond decrements, the AV nodal conduction time following the atrial extrastimulus (A2-H2) increases gradually.
  • At a critical atrial-coupling interval, a 10-millisecond decrease in A1-A2 results in a marked increase (>50 ms) in A2-H2. This abrupt increase in AV nodal conduction time is termed a jump in conduction (discontinuous AH conduction curve), and it often is associated with the appearance of atrial echo beats or initiation of AVNRT.
  • Further 10-millisecond decreases in the A1-A2 interval result in small additional increases (< 50 ms) in the A2-H2 interval, or, less commonly, additional AH jumps are evident.

Some data indicate that AV nodal physiology in children is different than in adults. Based on the traditional definition of a 50-millisecond AH jump after a decrement of 10 milliseconds in the extrastimulus coupling interval, only 62% of the children in one study met criteria for dual AV node physiology.[18] However, all patients had inducible AVNRT, and most of them were successfully ablated. The clinical importance of this finding is that children may not always fit the classic electrophysiologic criteria as it applies to adults; therefore, the endpoints for catheter ablation need to be readdressed and redefined in the pediatric population.

Contributor Information and Disclosures

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

Glenn T Wetzel, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, Heart Rhythm Society

Disclosure: Nothing to disclose.


Ryan Jones, MD Assistant Professor, 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, American College of Cardiology

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

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 Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, Western Society for Pediatric Research, American College of Cardiology, American Heart Association, American Pediatric Society

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD Medical Director of The Heart Center, Children's Hospital of Wisconsin; Associate Professor, Department of Pediatrics, Section of Pediatric Cardiology, Medical College 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, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Additional Contributors

Charles I Berul, MD Professor of Pediatrics and Integrative Systems Biology, 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, Heart Rhythm Society, Cardiac Electrophysiology Society, Pediatric and Congenital Electrophysiology Society, American College of Cardiology, American Heart Association, Society for Pediatric Research

Disclosure: Received grant/research funds from Medtronic for consulting.


The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous authors Robert Hamilton, MD, and Rejane Dillenburg, MD, to the development and writing of this article.

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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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