Supraventricular tachycardia (SVT) remains the most common tachyarrhythmia in children, occurring in 1 in 250 to 1 in 1000 children.1
Although common, the presenting symptoms of SVT can vary dramatically, even within similar age groups, posing a tremendous challenge to quick and accurate diagnosis.
With non-specific complaints such as fussiness and irritability in infants as well as chest pain and trouble breathing in children and adolescents, it is important for physicians to keep SVT in the list of differentials when caring for a pediatric patient.
This article aims to provide an overview of the pathophysiology of SVT, common presenting symptoms, approach to emergent management, and post-intervention care.
SVT is defined as a narrow complex tachycardia with a heart rate greater than 180 bpm in children and adolescents and greater than 220 bpm in infants.2
Only 15% of children will have spontaneous resolution of SVT.3
SVT demonstrates a bimodal incidence, occurring most often in children aged 6-9, and then again peaking in adolescence.3 There are typically no congenital associations associated with SVT; however, Wolff-Parkinson-White syndrome (WPW), a subset of SVT, has been shown to have an association with Ebstein anomaly.3
SVT is divided into three categories based on their cause; however, there are essentially no differences in their emergency management:
1. Reentrant tachycardias with an accessory pathway
Atrioventricular reciprocating tachycardia (AVRT) involves an accessory pathway outside of the SA or AV node. Is it the most common type of SVT seen in children, representing 82% of arrhythmias occurring during infancy. WPW is an example of an accessory pathway resulting in a pre-excitation syndrome.
2. Reentrant tachycardias without an accessory pathway
This is the most common cause of SVT in adults; it accounts for ~15% of SVT in the pediatric age group, increases with age, and is rarely seen in infants.
3. Ectopic tachycardias
An ectopic focus outpaces the SA node.
Clinical presentation of SVT can vary greatly, especially between age groups. Infants will typically present with fussiness, irritability, restlessness, tachypnea, and ashen appearance, especially if the episode has lasted longer than a few hours.
Older children may present with complaints of fast heart rate, chest pain, shortness of breath, dizziness, lightheadedness, or syncope, or even just a “funny feeling” in their chest.4
Fortunately, most children compensate for SVT very well, notably with episodes of SVT that are fast on and off. Their ability to compensate can lead to delays in seeking medical attention. It is not uncommon for healthy infants to tolerate SVT for 24 hours before being recognized. However, infants with underlying congenital heart disease lack cardiac reserve and may present earlier and be more critical upon presentation.
Unrecognized SVT can progress to congestive heart failure in 50% of children with structurally normal hearts. Therefore, it is of extreme importance for clinicians to consider SVT as complaints may be so nonspecific and general that children may present in florid heart failure if symptoms go unrecognized.
Diagnosis of SVT is made with a 12 lead EKG. Typically, an EKG will reveal a narrow complex (QRS duration <0.09 seconds) tachycardia with a rate over 180 bpm in children and adolescents and over 220 bpm in infants.2 Roughly 50% of infants will present with a visible P-wave on EKG.4
It is important to distinguish sinus tachycardia vs SVT, especially in infants and younger children. Sinus tachycardia will typically have a varying heart rate, while SVT is generally steady and unvarying. Another clue to differentiation is if P-waves are visible on EKG, they will be normal and upright in lead I and aVF, while they will be abnormal in SVT.4 Due to baseline elevated heart rates in children, it can often be challenging to appreciate P-waves prior to QRS complexes. A good trick is to increase the speed of the EKG to 50mm/s to reveal P-waves that can get buried in QRS complexes.
As always, start with the ABCs, obtain access and obtain a rhythm strip as soon as possible. Due to the fast rate, consider speeding up the pace of the paper to help distinguish any P-waves. Per the PALS SVT algorithm, SVT should be quickly classified into stable or unstable SVT.
Approach to Unstable SVT
Although unstable SVT is relatively uncommon, the management is different than in a child with stable SVT. Unstable SVT is defined as the presence of hypotension, altered mental status, or evidence of shock during an episode of SVT. Monitor for prolonged capillary refill, lethargy, mottled skin.5 If a patient presents in unstable SVT, immediate synchronized cardioversion is required. Initial energy required for the first round of synchronized cardioversion is 0.5-1 J/kg. If unsuccessful, increase the energy to 2 J/kg. If a child continues with unstable SVT after this point, expert consultation is strongly advised to discuss alternative or additional antiarrhythmic medications.1
Approach to Stable SVT
Stable SVT is much more common. You may try vagal maneuvers while preparing for an IV. Valsalva, straining, breath-holding, blowing through a narrow straw (for older children), or asking children to attempt to blow the plunger in an empty syringe can be attempted. For infants, an ice slurry applied to the face, covering the eyes and bridge of the nose, is an acceptable method as an alternative to vagal maneuvers.
Orbital pressure should never be performed, as it is often performed incorrectly and can cause facial/orbital trauma and possible retinal detachment. Carotid massage is rarely effective.6
While vagal maneuvers are trialed, IV or IO access should be established, preferably in the right upper extremity- the rationale being that it is the closest vein to the heart. In the case of vagal maneuver failure, adenosine should be pushed through the IV or IO with an initial dose of 0.1 mg/kg (maximum dose 6 mg). If a second dose is required, increase the dose to 0.2 mg/kg (maximum dose 12 mg). Adenosine is an amino acid that is rapidly metabolized, with a half-life of 9 seconds. Therefore, adenosine must be delivered via a large-bore IV placed as close to the heart as possible and should quickly be followed by a normal saline flush. This is best accomplished by using a 3-way stop cock. Adenosine briefly blocks conduction in the AV node causing disruption of any tachycardia circuit that relies on the AV nodal conduction
Recent studies have suggested that a higher initial dose of adenosine (0.2 mg/kg) in both infants and children reduces the risk of unsuccessful cardioversion by 35% with a NNT: 3 (Quail 2012). However, the most recent PALS update still recommends a stratified dose. During adenosine administration, a rhythm strip should be running to capture termination of SVT and return to normal sinus rhythm or to reveal the underlying dysrhythmia.
If adenosine fails, consult pediatric cardiology. SVT refractory to adenosine usually either abates with procainamide or synchronized cardioversion. IV procainamide has been found to be more effective than IV amiodarone for refractory SVT.10 If requiring synchronized cardioversion, consider sedation and pain control as this is a very painful procedure.
If the clinician is successful in terminating an SVT, a decision must be made as to the next steps in management, specifically whether the patient is admitted to the telemetry unit or pediatric intensive care unit (PICU). Typically, patients with newly-diagnosed SVT should be admitted to the PICU for close observation. Those with known SVT may be able to be admitted to the telemetry unit, although consultation with a pediatric cardiologist is recommended. Although out of the scope of this review, long-term medical management of pediatric SVT may require daily antidysrhythmic medications.
- SVT is the most common pediatric arrhythmia, with a bimodal incidence peak in ages 6-9 and adolescents.
- SVT presentation varies greatly, especially between age groups. It is of vital importance for the clinician to always consider SVT with generalized, vague complaints.
- Rapid assessment of the patient is crucial, as is differentiating between stable and unstable SVT. Vagal maneuvers and adenosine are the initial resuscitative measures for patients in stable SVT, while synchronized cardioversion without delay is necessary for patients in unstable SVT.
- Maconochie IK, Aickin R, Hazinski MF, et al. Pediatric Life Support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation. 2020 Oct 20;142(16_suppl_1):S140-S184.
- Salerno JC, Seslar SP. Supraventricular Tachycardia. Arch Pediatr Adolesc Med. 2009;163(3):268–274.
- Wackel P, Cannon B. Heart Rate and Rhythm Disorders. Pediatrics in Review. 2017;38(6):243-253.
- Clausen H, Theophilos T, Jackno K, Babl FE. Paediatric arrhythmias in the emergency department. Emerg Med J. 2012;29(9):732.
- de Caen AR, Kleinman ME, Chameides L, et al. Part 10: paediatric basic and advanced life support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation. 2010;81(suppl 1):e213-59.
- Lewis J, Arora G, Tudorascu D, Hickey R, Saladino R, Manole M. Acute Management of Refractory and Unstable Pediatric Supraventricular Tachycardia. J Pediatr. 2017;181:177-182.e2.
- Dalal A, Van Hare G. Supraventricular Tachycardia. Nelson Textbook of Pediatrics. 21 Edition. 2020. Ch: 426.3 pp 2439-2444.
- Janoušek J, Kubuš P. What's new in cardiac pacing in children? Curr Opin Cardiol. 2014 Jan;29(1):76-82.
- Lee Pi-Chang, Chen Shih-Ann, Hwang B. Atrioventricular node anatomy and physiology: implications for ablation of atrioventricular nodal reentrant tachycardia. Curr Opin Cardiol. 2009;24(2):105-112.
- Chang PM, Silka MJ, Moromisato DY, Bar-Cohen Y. Amiodarone Versus Procainamide for the Acute Treatment of Recurrent Supraventricular Tachycardia in Pediatric Patients. Circulation: Arrhythmia and Electrophys. 2010;3:134–140.