Atrioventricular Node Reentry Supraventricular Tachycardia Clinical Presentation

Updated: Dec 09, 2020
  • Author: Glenn T Wetzel, MD, PhD; Chief Editor: Stuart Berger, MD  more...
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Presentation

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. [8, 9]

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 A 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.

Note the following:

  • 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. [10]

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