Atrioventricular Node Reentry Supraventricular Tachycardia Clinical Presentation

  • Author: Glenn T Wetzel, MD, PhD; Chief Editor: Stuart Berger, MD   more...
 
Updated: Apr 12, 2012
 

History

Presenting symptoms vary with factors such as age, heart rate, duration, and underlying heart condition. Tachycardia rates can be very dependent on the adrenergic state. Children presenting with tachycardia during exercise may have much faster rates.

  • Patients with atrioventricular node reentrant tachycardia (AVNRT) may be more symptomatic than those with other mechanisms of supraventricular tachycardia (SVT); this is because of the simultaneous depolarization of atrial and ventricular myocardium, causing the occurrence of atrial contraction against a closed atrioventricular (AV) valve and loss of the atrial contribution to a complete diastolic filling.[5, 6]
  • Symptoms of congestive heart failure in the infant may include restlessness, feeding problems, and diaphoresis. Shock may occur when a tachyarrhythmia goes unrecognized during variable amounts of time, from a few hours to days.
  • In the older child, symptoms may include chest pain, palpitations, shortness of breath, lightheadedness, and fatigue.
  • Occasionally, adult patients may present with syncope or severe presyncope. A pounding sensation in the neck (ie, neck pulsations) is fairly unique to the presence of AVNRT and considered to be the result of cannon waves when the atrium contracts against a simultaneously contracting ventricle.
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Physical

Promptly evaluate the hemodynamic state of children presenting with tachyarrhythmia. As stated above, the degree of compromise is usually determined by numerous factors, including age, heart rate, duration of the arrhythmia, and the presence or absence of structural heart disease.

  • Evaluate infants for signs of congestive heart failure, such as tachypnea, retractions, rales, liver enlargement, decreased pulse, and perfusion.
  • Cardiogenic shock with hypotension, metabolic acidosis, ventricular dysfunction, and pulmonary edema may occur.
  • Physical examination findings of the older child without underlying heart disease may be normal except for the fast heart rate.
  • The patient may exhibit tachypnea, pallor, and evidence of jugular venous pulsations caused by asynchrony of atrial and ventricular contractions (ie, the atrium contracting against a closed AV valve).
  • Patients with structural heart disease and ventricular dysfunction may have more severe hemodynamic compromise upon presentation because they have limited myocardial reserves and do not tolerate tachycardia and the absence of AV synchrony for long periods.
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Causes

  • The incidence of AVNRT appears to be increased in the setting of congenital heart disease. In addition, related conditions, such as AV node-to-node reentry with a Mönckeberg sling, may occur in the setting of complex congenital heart disease. Finally, dual AV nodal physiology may be a bystander to accessory pathways, and accessory pathways, including Mahaim fibers, may be bystanders to AVNRT.
  • One report detailed evidence that AVNRT may have a familial inheritance in some cases, which is suggestive of a genetic mechanism.
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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 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, American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, Pediatric and Congenital Electrophysiology Society, and Society for Pediatric Research

Disclosure: Johnson & Johnson Consulting fee Consulting

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 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.

Additional Contributors

The authors and editors of eMedicine 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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