Management of acute supraventricular tachycardia in children

Vagal maneuvers

Vagal maneuvers are considered non-invasive first-line treatment of children with SVT who are hemodynamically stable.⁵ These maneuvers work by increasing parasympathetic tone, which can increase the refractory period of the AV node and terminate SVT.⁶ Some commonly used maneuvers include the Valsalva maneuver (eg, squatting, forced expiration against a closed glottis), stimulating the diving reflex in infants (eg, placing a bag of ice over the face), and carotid sinus massage (important to do it unilaterally only).³ In one study, the Valsalva maneuver demonstrated the highest success rate at 47%, followed by diving reflex stimulation at 5%, while carotid sinus massage had the lowest success rate at 1.5%.⁷ Furthermore, the Valsalva maneuver induced the longest prolongation of the R-R interval during sinus rhythm and paroxysmal SVT.⁷ Overall, these maneuvers were effective at terminating SVT up to 53% of the time.³

Pharmacologic therapy

Primary pharmacologic treatment of SVT often involves intravenous (IV) adenosine, which has an extremely short half-life of 2 to 5 seconds and is known for its rapid onset and minimal side effects.² Adenosine, a naturally occurring rapidly metabolized purine nucleoside, is formed from the degeneration of adenosine triphosphate.⁸ In a study published in 1929, researchers at the University of Cambridge in England extracted adenosine from a bull’s heart and injected it into a guinea pig to elicit a transient high-grade heart block.⁹ Adenosine works by prolonging AV conduction, resulting in a transient block in myocardial conduction at the AV node, thus slowing down the heart rate.¹⁰ The most commonly reported dosage via rapid peripheral IV line is 0.1 mg/kg, with repetitive doses of 0.2 and 0.3 mg/kg, and in children younger than 1 year the initial dose is usually reported to be up-titrated to 0.15 mg/kg.¹¹ Electrophysiologic effects may not take place if adenosine is administered slowly due to the rapid metabolism by endothelial and red blood cells.¹⁰ Effects of adenosine manifest within a few seconds for up to a maximum of 30 seconds.⁸ As adenosine can cause atrial fibrillation, it is preferable to have a defibrillator available when administering the medication.

Adenosine is administered using a rapid bolus with an immediate normal saline solution flush through a large vein within 1 to 2 seconds; this technique is known as the double-syringe technique.¹⁰ It requires an IV line and a 2-way stopcock with 2 syringes to ensure effective administration of the adenosine and saline.¹⁰ In practical application in rural practice, this may not be feasible due to a shortage of medical staff. A more convenient single-syringe technique requires mixing a bolus of adenosine with saline and administering it intravenously.¹⁰

In a pilot multicentre randomized controlled trial conducted in Thailand by Kotruchin et al¹⁰ comparing a single-syringe technique with a double-syringe technique, the termination rate of stable SVT in adult patients (average age 54 years) was 93.3% using the double-syringe technique and 100% using the single-syringe technique (n=15 in each group). The total dosing required to terminate SVT was slightly lower in the single-syringe technique group (7.6 mg vs 8.6 mg, respectively), but this difference was not statistically significant (P=.608). Although the single-syringe technique had a higher success rate, this was also not a statistically significant difference.

A 2-way or 3-way stopcock is typically used for the administration of IV adenosine. However, one study investigated the impact of the dead space in these stopcocks when administering adenosine to infants of low weight.¹² Doses prepared for a 5.5-kg and a 12.5-kg infant (95th percentile weights for a 1-month-old and a 1-year-old infant, respectively) showed 56% and 21% of the doses were lost, respectively, due to the 0.1-mL dead space in the stopcock.¹² In a retrospective study in the United Kingdom, the advised dose of 0.1 mg/kg was effective in less than 25% of infants (age range 1 to 72 days) and less than 50% of children (age range 17 months to 15 years), whereas a dose of 0.15 mg/kg was effective in 35% of infants and 80% of children.¹³ These results may be caused by the loss of a certain amount of the dose due to the technique of administration.¹⁴ To prevent loss, the dose could be injected into the IV line directly or the dead space in the stopcock could be accounted for when calculating the dose.

For patients with acute SVT, alternative medications include esmolol, a quick-acting β₁-blocker (onset: 2 to 10 minutes via IV administration), and procainamide, a class IA antiarrhythmic (sodium-channel blocker; onset: 5 to 10 minutes via IV administration). Liver metabolism of procainamide yields a cardioactive metabolite (N-acetylprocainamide) with class III antiarrhythmic properties.⁶ Caution is warranted for both drugs. Esmolol may cause severe ventricular dysfunction and should be used with caution in patients with asthma.⁶ Similarly, procainamide may cause ventricular dysfunction with hypotension, may further prolong QT interval among those with long QT syndrome, or may cause renal impairment.⁶ It is ideal to consult a pediatric cardiologist when considering second-line medications.

Drug therapy options for long-term management of SVT include digoxin, propranolol, and amiodarone. Digoxin, a cardiac glycoside (onset: 5 to 60 minutes via IV administration), is often considered first-line prophylactic monotherapy for when SVT is detected.⁶ It has a narrow therapeutic index and can lead to substantial bradycardia or arrhythmia in neonates and infants. It is important to note that it is contraindicated in patients with Wolff-Parkinson-White syndrome, as it may worsen symptoms.⁶ Propranolol is a nonselective β-blocker and is a first-line monotherapy in its oral form to treat infants with SVT. Amiodarone is a class III antiarrhythmic (onset: 2 to 21 days via oral administration). Oral amiodarone use has been associated with photosensitivity, thyroid dysfunction, and hepatic dysfunction.⁶

When adenosine does not work

The short half-life of adenosine is advantageous when considering the transient nature of adverse effects. However, there are certain situations in which adenosine is not advised, such as in patients with asthma or non–AV-node-dependent SVT.

Traditionally, caution has been exercised when administering adenosine to patients with asthma, patients with chronic obstructive pulmonary disease, or patients regularly taking methylxanthine, owing to adenosine’s propensity to cause bronchospasm.¹⁵ However, in individuals with normal airway function adenosine-induced bronchoconstriction is infrequent and is often misinterpreted as dyspnea.¹⁵ It is advisable to exercise caution when administering adenosine in this cohort of patients.

In certain cases, the arrhythmia does not respond to adenosine. These are usually cases of non–AV-node-dependent SVT, including atrial tachycardia, atrial fibrillation, and atrial flutter.¹⁶ These arrhythmias are not dependent on the AV node, and adenosine therefore would not target the underlying pathogenesis.¹⁶