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Paeds Vivascardiology

Paeds Vivas · cardiology

Supraventricular tachycardia — branching viva

Branching viva on paediatric supraventricular tachycardia: the mechanisms and classification, the acute termination ladder, the ECG hallmarks of AVNRT and WPW, long-term management and catheter ablation, and the risk stratification of Wolff-Parkinson-White syndrome.

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Target exams

RACP DCEMRCPCH Clinical

Target exams

RACP DCEMRCPCH Clinical
Prompt
Emergency department: a four-month-old pale and irritable infant with a heart rate of 250 per minute on the monitor and a regular narrow-complex tachycardia on ECG with no visible P waves.

Examiner opening (Examiner)

You are the general paediatric registrar in the emergency department. A four-month-old boy is brought in pale and irritable with a heart rate of 250 per minute on the monitor. The 12-lead ECG shows a regular narrow-complex tachycardia with no visible P waves. Talk me through your assessment and management. [1]

Exemplar opening (Candidate)

This infant is in supraventricular tachycardia — the commonest significant arrhythmia of childhood — and he is showing early signs of haemodynamic compromise with pallor, irritability, and poor feeding. I will treat this as a time-critical presentation. First I confirm the airway, breathing, and circulation, attach continuous cardiac monitoring, and obtain intravenous access. Because he is pale and poorly perfused but not in overt shock, I will proceed with the stepwise termination ladder: a vagal manoeuvre first, then adenosine if needed, with a defibrillator at the bedside throughout. If he were unstable — hypotensive, in overt heart failure, or with altered consciousness — I would proceed directly to synchronised DC cardioversion without waiting for adenosine. [1] [5]

Branch 1 — the underlying mechanism (Examiner)

What is SVT, and what are the two dominant mechanisms in children? [3]

Exemplar (Candidate)

Supraventricular tachycardia is a rapid, regular tachycardia originating above the His bundle, with a rate typically 220 to 280 per minute in infants and 180 to 240 in older children. The mechanism is usually re-entry — a self-sustaining electrical loop — and there are two dominant reentrant circuits. AVRT, or atrioventricular re-entry tachycardia, uses an accessory pathway connecting the atrium to the ventricle in addition to the normal AV nodal pathway; the circuit runs from atrium through the AV node to the ventricle and back via the accessory pathway. AVRT is the commonest mechanism in infants, accounting for roughly 90 per cent of infant SVT. AVNRT, or atrioventricular nodal re-entry tachycardia, uses dual pathways within the compact AV node — a slow pathway and a fast pathway — and is the commonest mechanism in adolescents. A third category, focal atrial tachycardia, is driven by an automatic focus and accounts for 5 to 10 per cent. [3]

Branch 2 — acute termination (Examiner)

Describe the acute termination ladder step by step, including the adenosine dose and technique. [1] [5]

Exemplar (Candidate)

For the stable child, the ladder starts with vagal manoeuvres. In an infant, the most reliable technique is the diving reflex — a sealed ice pack or cold gel pack applied to the face for 15 to 30 seconds. In an older cooperative child, a modified Valsalva manoeuvre is used. If the vagal manoeuvre fails, adenosine is the first-line drug. The dose is 0.1 milligramme per kilogramme as a rapid intravenous bolus, maximum 6 milligrammes for the first dose, followed immediately by a 5 to 10 millilitre saline flush through the largest-bore cannula closest to the heart. If the first dose fails, the second dose is 0.2 milligramme per kilogramme, maximum 12 milligrammes. The rapid technique is essential because adenosine is metabolised within seconds by endothelial adenosine deaminase — a slow push will be inactivated before it reaches the AV node. If adenosine fails, intravenous amiodarone at 5 milligrammes per kilogramme or procainamide are the next agents. For the unstable child, the first-line treatment is synchronised DC cardioversion at 0.5 to 1 joule per kilogramme, escalating to 2 joules per kilogramme, without delay for adenosine. [1] [5]

Branch 3 — post-termination ECG and WPW (Examiner)

After you terminate the SVT, what do you look for on the resting ECG, and why does it matter? [4]

Exemplar (Candidate)

The post-termination resting ECG is critical because it may reveal the Wolff-Parkinson-White pattern — a delta wave, short PR interval, and widened QRS — indicating an accessory pathway capable of antegrade conduction. This matters because the WPW pattern carries a small but real risk of sudden cardiac death. During atrial fibrillation, the accessory pathway can conduct very rapidly to the ventricles, producing ventricular rates above 300 per minute that may degenerate to ventricular fibrillation. The shortest pre-excited RR interval during atrial fibrillation predicts this risk: a value below 250 milliseconds is high-risk and warrants catheter ablation. Risk stratification begins non-invasively with exercise testing — if pre-excitation disappears at peak exercise, the pathway has a long refractory period and is low-risk. If pre-excitation persists, an invasive electrophysiological study is offered to measure the antegrade effective refractory period of the pathway. [4]

Branch 4 — PJRT and tachycardiomyopathy (Examiner)

You mention accessory pathways. Tell me about permanent junctional reciprocating tachycardia and why it is important. [3]

Exemplar (Candidate)

Permanent junctional reciprocating tachycardia, or PJRT, is a specific form of orthodromic AVRT that uses a concealed, slowly conducting accessory pathway, usually near the coronary sinus or the septum. The tachycardia is incessant — it is present most or all of the time — and the ECG shows a long RP tachycardia with deeply inverted P waves in the inferior leads, II, III, and aVF. The rate is typically slower than typical SVT, often 130 to 200 per minute, which is why it is frequently mistaken for sinus tachycardia. The clinical importance is that the incessant tachycardia can cause a tachycardiomyopathy — a reversible form of ventricular dysfunction that can mimic a dilated cardiomyopathy but recovers completely after the arrhythmia is controlled. The definitive treatment is catheter ablation of the accessory pathway, which eliminates the substrate and allows ventricular function to normalise. [3]

Branch 5 — long-term management and ablation (Examiner)

What is the long-term management for this infant, and when would you offer catheter ablation? [3] [6]

Exemplar (Candidate)

For an infant with a first episode of SVT, prophylactic antiarrhythmic therapy is standard because recurrence is common. The first-line agent is propranolol at 2 to 4 milligrammes per kilogramme per day, or digoxin at 10 microgrammes per kilogramme per day. Flecainide is added for resistant or recurrent cases. Importantly, most infants — 60 to 80 per cent — have spontaneous resolution of their SVT by one year of age, likely due to maturation of the accessory pathway, so medication is typically weaned at 12 months with monitoring for recurrence. Catheter ablation is curative but is generally deferred until after approximately five years of age because of the small risk of coronary artery injury from radiofrequency lesions near the coronary sinus in very young children. The exception is medically refractory or life-threatening SVT at any age. In older children and adolescents, ablation is offered for recurrent or poorly tolerated SVT, with success rates exceeding 95 per cent. Cryoablation is preferred for AVNRT because of the lower risk of AV nodal injury. [3] [6]

Branch 6 — transition and family (Examiner)

What do you tell the family about the outlook, and what must happen before this child leaves paediatric care if SVT persists? [2]

Exemplar (Candidate)

The family should be reassured that the prognosis is excellent. Most infants outgrow SVT by one year, and even if it persists, catheter ablation is curative in over 95 per cent. They should be taught to recognise the signs — sudden pallor, poor feeding, irritability, fast breathing — and to bring the child in promptly. If SVT persists into adolescence, or if the child has a Wolff-Parkinson-White pattern, they need a structured transition to an adult electrophysiology service. The risks of non-adherence, recreational stimulant use, and the WPW sudden death risk converge in early adulthood, so education about triggers, self-management, and awareness of the arrhythmia history are part of standard transition care. A warm handover to the adult electrophysiologist prevents the lost-to-follow-up gap that accounts for many preventable events. [2]

Examiner wrap-up (Examiner)

Thank you. Summarise the three points you most want the examiner to remember. [1]

Exemplar (Candidate)

First, SVT is the commonest significant arrhythmia of childhood — recognise the fast, regular, narrow-complex tachycardia and terminate it with vagal manoeuvres and adenosine, or DC cardioversion if unstable. Second, the mechanism determines the management — AVRT in infants, AVNRT in adolescents — and the post-termination ECG must be checked for the Wolff-Parkinson-White pattern, which carries a small sudden death risk that demands risk stratification. Third, the prognosis is excellent — most infants outgrow SVT by one year, catheter ablation is curative in over 95 per cent of suitable children, and the main exception is the high-risk WPW pathway that warrants ablation. [1] [4]

References

  1. [1]Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society J Am Coll Cardiol, 2016.PMID 26409259
  2. [2]Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardiaThe Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC) Eur Heart J, 2020.PMID 31504425
  3. [3]Brugada J, Blom N, Sarquella-Brugada G, et al. Pharmacological and non-pharmacological therapy for arrhythmias in the pediatric population: EHRA and AEPC-Arrhythmia Working Group joint consensus statement Europace, 2013.PMID 23851511
  4. [4]Cohen MI, Triedman JK, Cannon BC, et al. PACES/HRS expert consensus statement on the management of the asymptomatic young patient with a Wolff-Parkinson-White (WPW, ventricular preexcitation) electrocardiographic pattern: developed in partnership between the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing bodies of PACES, HRS, the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), the American Academy of Pediatrics (AAP), and the Canadian Heart Rhythm Society (CHRS) Heart Rhythm, 2012.PMID 22579340
  5. [5]Losek JD, Endom E, Dietrich A, et al. Adenosine and pediatric supraventricular tachycardia in the emergency department: multicenter study and review Ann Emerg Med, 1999.PMID 9922414
  6. [6]Van Hare GF, Javitz H, Carmelli D, et al. Prospective assessment after pediatric cardiac ablation: demographics, medical profiles, and initial outcomes J Cardiovasc Electrophysiol, 2004.PMID 15250858