A 6-year-old girl was brought by her parents to the emergency department (ED) with an elevated heart rate. According to the parents, the girl was carrying her younger sister when they both fell, landing on their buttocks. The child told them that her heart was beating fast, and the parents said she appeared to be on the verge of fainting.
They stated that their daughter was healthy and active; they denied previous episodes of shortness of breath, headache, weakness, tachycardia, syncope, or fatigue with exercise. Her caffeine intake, they claimed, was limited to one small cup of soda they allowed her each week.
Initial evaluation in the ED revealed an anxious child with tachycardia and shortness of breath. She presented with a temperature of 98.3°F (36.8°C); pulse, 210 beats/min; respirations, 33 breaths/min; blood pressure, 100/72 mm Hg; weight, 78 lb; height, 45 in; and BMI, 27.1. ECG revealed a heart rate exceeding 210 beats/min, and a pediatric cardiologist made a diagnosis of supraventricular tachycardia (SVT).
The pediatric cardiologist prescribed an adenosine IV drip, which successfully stabilized the child’s heart to sinus rhythm. After three hours in the ED, the patient was discharged with a stable heart rate of 100 beats/min. (It is well known that heart rate regulation changes significantly during development; this is most obvious in higher basal rates in infants and children, compared with adults.1)
The parents were advised to administer atenolol 12.5 mg (one tablet) twice daily and to make a follow-up appointment with a pediatric electrophysiologist. (Although atenolol is not currently FDA approved for this use, a multicenter prospective randomized controlled trial comparing digoxin with beta-blockers for the treatment of SVT in children is presently under way.2)
At that appointment, the pediatric electrophysiologist provided information to the parents regarding the therapeutic options for SVT. The parents continued to administer atenolol to the child, as was deemed necessary until any accessory electrical pathway could be identified and, if so, an ablation procedure could be performed. They were uncertain how to proceed so long as their daughter experienced no recurrent episodes of SVT while receiving pharmacologic therapy.
However, six months after the initial episode, the child (then age 7) presented to the ED once again with recurrent SVT. The pediatric cardiologist ordered an adenosine IV drip, which resulted in successful conversion to sinus rhythm. The parents were instructed to increase the child’s atenolol dosage to 25 mg twice a day.
Six months later, after extensive research and consultation, the parents agreed to an ablation procedure in order to prevent further episodes of SVT. Upon their informed consent, the child was sent to a cardiac catheterization laboratory for an electrophysiology study (EPS), which confirmed the presence of an accessory pathway, as well as the diagnosis of atrioventricular reciprocating tachycardia (AVRT). The procedure was followed by radiofrequency catheter ablation to correct the 7-year-old patient’s accessory pathway–mediated reentry tachycardia.
Discussion
SVT, also known as paroxysmal supraventricular tachycardia (PSVT), is one of the most common symptomatic pediatric arrhythmias, affecting between one in 25,000 and one in 250 children.3 It is defined as rapid heart rhythm (140 to 240 beats/min) that is caused by the presence of additional electrical connections and/or congenital muscle fibers between the atrium and the ventricle or within the atrioventricular (AV) node that did not, for unknown reasons, separate completely during development.4 SVT can be triggered by physical or psychological stress automaticity.3
Approximately 50% of children with SVT present with a first episode before age 1. SVT usually occurs in early childhood, between ages 6 and 9.4 Almost 90% of pediatric patients with SVT are diagnosed with a reentry mechanism.3 The symptoms experienced may be resolved pharmacologically or by means of an invasive therapy. Serious sequelae associated with SVT include heart failure and cardiac arrest.
For children with rare and mildly symptomatic episodes in whom SVT is easily terminated, the SVT may not warrant treatment. However, it may be advisable to offer medical therapy or transcatheter ablation as therapeutic options for children with episodes that are difficult to terminate, occur frequently, or occur during participation in athletics.4
Pathophysiology
SVT generally presents as one of three types: AVRT, which is also known as Wolff-Parkinson-White syndrome; atrioventricular nodal reentry tachycardia (AVNRT); and automatic tachycardia (AT).
AVRT, the most common type of SVT, comprises about 90% of pediatric cases. It is defined by the presence of one or more accessory conduction pathways that are anatomically separated from the normal cardiac conduction system.5 AVRT may be orthodromic (that is, the arrhythmia circuit proceeds down the AV node and retrograde up the accessory conduction pathway) or antedromic (ie, proceeding down the accessory pathway and up the AV node5; see figure.6,7)