Paroxysmal supraventricular tachycardia (PSVT) is the most frequent form of arrhythmia in the paediatric age group following sinus tachycardia.1 The underlying mechanisms of PSVT involve a pattern of reentry or the presence of arrhythmias due to enhanced abnormal automaticity, which are referred to as ectopic or focal tachycardias. In young children, tachycardias due to accessory pathways are most frequent (80%), but in adolescence the proportion is reversed, and nodal reentrant tachycardias become more frequent.2,3 In the group of reentrant tachycardias, we ought to specifically mention permanent junctional reciprocating tachycardia (PJRT), also known as Coumel’s tachycardia, because while it is a reentrant tachycardia it is caused by an occult accessory pathway typically located in the posterior septal portion of the tricuspid ring with properties of decremental conduction that produce a characteristic electrocardiographic pattern with a prolonged RP interval and negative P waves in the inferior leads. This form of tachycardia is relevant because it is particularly frequent in infants and usually has onset with tachycardiomyopathy.4 Ectopic atrial tachycardias (ATs) are relatively infrequent in children,2 amounting to approximately 10% of the total cases of PSVT according to some authors.5 Due to its abrupt onset, older patients usually can identify the exact time of onset of the tachycardia, but it may go undetected in younger patients, especially in newborns and infants, and eventually present as severe acute heart failure secondary to tachymyocardiopathy.3,6 Acute care of the episode varies depending on the level of haemodynamic instability of the patient and focuses on terminating the tachycardia and initiating supportive care to revert the haemodynamic effects of the episode, which may require mechanical ventilation, use of inotropic/diuretic agents and administration of antiarrhythmic drugs to stabilize the patient, and in some cases even cardiopulmonary resuscitation (CPR) manoeuvres. The interventions used to terminate PSVT may include vagal manoeuvres, treatment with antiarrhythmic drugs and electrical cardioversion based on the severity and mechanism of the tachycardia.7,8

The aetiology, presentation, treatment and outcomes of PSVT in paediatric patients are thoroughly described in books on paediatrics and paediatric cardiology.9,10 In the current scientific literature, there are articles on the subject of the prehospital care of PSVT in adults,11 but none specifically focused on the paediatric population. The available literature includes some prospective studies that report outcomes of PSVT management in the emergency department1,12 and others that describe the outcomes of using adenosine for its management.13,14 The Paediatric Medical Emergency System (P-MES) of Catalonia is responsible for paediatric and neonatal interhospital transport and covers the entire regions of Catalonia and Andorra, with a maximum range of action of 4 h and a radius of 300 km. It comprises 3 units: 2 land units and 1 air unit (helicopter). All units are based off the city of Barcelona. Each transport team (TT) consists of a paediatrician, a paediatric nurse and a medical transport technician.

The objectives of our study were to establish the frequency of PSVT as a reason for interhospital transport, describe the clinical presentation of PSVT, its outcomes, and its management, and analyse the risk factors associated with haemodynamic instability, with the purpose of proposing a specific protocol for the management of these patients during interhospital transport.

We conducted a retrospective observational study of all patients given a final diagnosis of PSVT between January 2005 and June 2017. We retrieved data from the database of the P-MES of the Hospital Universitari Vall d’Hebron, which stores data collected prospectively in a structured and systematic fashion, collecting information for the following variables: age (newborn, ≤30 days, or child >30 days), weight, sex, previous history of tachycardia, current ongoing treatment, presence of congenital heart defects, symptoms and haemodynamic instability, mechanism of the tachycardia, type and effectiveness of treatment used to terminate the episode, severity of episode based on need for mechanical ventilation, administration of volume expanders or inotropic agents, type of vascular access, performance of CPR, time to stabilization, duration of transport and complications during transport. We did not include patients with other types of arrhythmia.

We defined haemodynamic instability as the presence of poor general condition, respiratory distress, decreased peripheral perfusion, systemic hypotension and metabolic acidosis (pH <7.35 and base excess <−5). We defined the time to stabilization as the time elapsed from the departure of the P-MES team from the referring hospital to arrival to the receiving hospital.

The descriptive analysis of the data was performed with the software SPSS® version 18.0. We expressed continuous data as mean ± standard deviation (SD) or median and range depending on whether or not they followed a normal distribution, and compared proportions with the Fisher exact test, considering differences corresponding to p-values of less than 0.05 statistically significant. To assess potential risk factors for haemodynamic instability, we performed a multivariate logistic regression with backward stepwise removal based on likelihood ratios (LRs) by applying the BSTEP-LR method.

Of a total of 7348 transports, 67 corresponded to patients with PSVT (0.9%). Table 1 summarises the demographic, clinical and aetiological characteristics of included cases. Most patients were aged 1 year or less (42; 62.7%), the male-to-female ratio was 1:1.16, and the median weight of patients was 4.8 kg (2.2–80). For most patients, this was the first episode of PSVT (64.2%).

The main presenting symptom that led to diagnosis of tachycardia varied by age group. In the group of 51 patients aged less than 5 years, the most frequent symptoms were irritability with poor general health (25, 49.0%), followed by chest pain (4, 7.8%) and syncope (1, 1.9%). In the remaining 21, the diagnosis was made following incidental finding of a high heart rate (HR) in absence of any other symptoms, and in 4 cases the diagnosis was made after detection of an increased HR during a bronchitis episode. In the group of 16 patients aged more than 5 years, the symptoms that led to diagnosis were palpitation in 13 cases (81.2%), abdominal pain in 1 (6.2%), and incidental finding of increased HR in 2 (12.5%). Of all 67 patients, 14 (20.9%) presented with haemodynamic instability at the time of diagnosis. Only 6 patients (8.9%) had an underlying congenital heart defect. The underlying mechanism of PSVT was a reentrant pattern with a short RP interval in 56 (83.6%), PJRT in 3 (4.5%) and ectopic/automatic AT in 7 (10.4%). One patient had atrial fibrillation (1.5%).

This article is the first to present the experience of a paediatric transport team in the management of PSVT in the paediatric age group. There are articles in the literature on the prehospital management of adults with PSVT by paramedics,11 which is a different situation from the one analysed in our study.

Our findings show that PSVT corresponds to a small percentage of the total transports (about 1% of all interhospital transports). The predominant age groups were newborns, infants and toddlers, with no differences based on sex. Previous studies have reported an incidence of PSVT in children of 0.1%–0.4%,15 with a predominance of boys and onset before age 4 months.10 A relevant finding of our study is that 19.4% of patients had haemodynamic instability at the time of transport, with age equal or less than 1 year being the sole independent risk factor for this condition, with an OR of 10.2 (95% confidence interval, 1.2–89.9; p = 0.004), which demonstrates that adequate management of these patients may involve advanced life support throughout transport. Other possible risk factors like sex, pre-existing heart disease, a history of previous episodes, an electrical mechanism of tachycardia and whether the patient still had tachycardia when the TT arrived to the referring hospital were not statistically significant in our analysis.

The high percentage of patients with haemodynamic instability in our cohort may result from selection bias in our sample, as we only included patients that the RH decided to transfer to a specialised hospital, and it would be logical to assume that these were the most severely ill patients. The treatment patients received at the RH in transport did not deviate from published guidelines,15 and the transport team was able to maintain a sinus rhythm without recurrence of tachycardia in most patients, with no relevant complications and no deaths occurring during transport. Although previous studies have reported that the time elapsed from onset of tachycardia to reversion to sinus rhythm is associated with the risk of haemodynamic instability, the time of onset of tachycardia is often not known in children.

We ought to highlight that both the clinical diagnosis and treatment of the patients were mostly established by RHs. Decision-making by the TT predominated only in patients with haemodynamic instability in relation to the use of advanced life support measures like intubation or cardioversion. The time to stabilization and the duration of transport did not differ significantly from the corresponding median times recorded for the overall population served by our transport team.

As concerns the treatments used to terminate the tachycardia, we ought to highlight that only 29.7% of vagal manoeuvres were effective. In contrast, administration of adenosine was successful in 53% of cases. Patients received a median of 3 doses of adenosine. The mean initial dose of 100 µg/kg, but the mean effective dose was nearly twice as high. Guidelines on the management of PSVT in the neonatal period recommend initial doses of 50 µg/kg,16 but data from our study suggest that doses of less than 100 µg/kg are ineffective, so it seems appropriate to recommend an initial dose of 100 µg/kg and escalating to 200 and 300 µg/kg if the initial dose is not effective.

There is sufficient evidence in the literature,2 further supported by our findings, to recommend transport of all patients aged less than 1 year with a first episode of PSVT to a paediatric cardiology specialty centre for monitoring, assessment and treatment given the high percentage of patients in this age group that develop haemodynamic instability. Only in case of older children with tachycardia that reverts with basic measures it would be appropriate to refer the patient to an outpatient paediatric cardiology clinic with indications on when to seek attention at the RH and education on how to perform vagal manoeuvres,1,10 as is done with adult patients.8 None of the patients in our study met these criteria, and therefore the transfer was justified in every case.

Some of the limitations of our study are the selection bias implied in including patients requiring intrahospital transport by a specialised team and the difficulty in making a comprehensive evaluation of the outcomes of all transported patients due to the large number of receiving hospitals.

Transport of paediatric patients with PSVT to a tertiary care hospital is infrequent and may require highly specialised care, especially in infants aged 1 year or less. In our case series, 20% of patients had haemodynamic instability at the time of transport, the probability of which was 10.2 times greater in the group aged 1 year or less. Adequate management and treatment of these patients allows transport with maintenance of a sinus rhythm, which is associated with a lower morbidity and mortality.

The authors have no conflicts of interest to declare.