Arrhythmias in Children

On this page
  1. Direct answer
  2. What you must remember
  3. Working through a tachycardic infant
  4. How the examiner frames it
  5. Frequently asked questions
  6. Related topics

Direct answer

Supraventricular tachycardia is the commonest symptomatic tachyarrhythmia of childhood: a narrow-complex, regular tachycardia at 220-300 in infants and above about 180 in older children, usually re-entrant, terminated by vagal manoeuvres or adenosine at 0.1 mg/kg rapid intravenous push (maximum first dose 6 mg), repeated at 0.2 mg/kg (maximum 12 mg) if needed. The other pillars are congenital complete heart block, linked to maternal anti-Ro and anti-La antibodies with neonatal lupus, and the channelopathies, chiefly long QT syndrome, in which a corrected QT beyond roughly 460-480 milliseconds with exertional syncope demands beta-blockade and defibrillator assessment. In cardiac arrest, defibrillation for shockable rhythms starts at 2 joules/kg then 4 joules/kg, with adrenaline 0.01 mg/kg every three to five minutes.

What you must remember

  • Adenosine protocol: 0.1 mg/kg by rapid bolus with a saline flush (first dose maximum 6 mg); if it fails, 0.2 mg/kg (maximum 12 mg); continuous ECG recording during the attempt, because the response is diagnostic, not merely therapeutic.
  • Infant presentation: infants may simply look pale and feed poorly for hours before heart failure appears — rate 220-300, narrow QRS, no variability.
  • Wolff-Parkinson-White: short PR, slurred upstroke (delta wave), wide QRS in sinus rhythm; risk of sudden death is why radiofrequency ablation is considered, and why accessory-pathway atrial fibrillation must never receive AV-node blockers alone.
  • Congenital atrioventricular block: maternal anti-Ro (SSA) and anti-La (SSB) antibodies crossing the placenta; pacing is indicated for rates persistently below about 50-55 per minute, ventricular ectopy, wide-complex escape or hydrops.
  • Long QT syndrome: QTc beyond approximately 460-480 milliseconds, syncope with exertion, swimming or emotion, and torsades treated with intravenous magnesium; beta-blockers are first-line therapy.
  • Arrest energies and drugs: defibrillate ventricular fibrillation or pulseless ventricular tachycardia at 2 J/kg, then 4 J/kg; adrenaline 0.01 mg/kg (0.1 mL/kg of 1 in 10,000) every 3-5 minutes; amiodarone 5 mg/kg for refractory shockable rhythms.
  • Red flags in "syncope": exertional or supine episodes, family history of sudden death under forty, and deafness (Jervell and Lange-Nielsen) all push toward arrhythmic rather than vasovagal.

Working through a tachycardic infant

A three-month-old, previously healthy, is irritable and breathing fast with a heart rate monitor reading 290. The rhythm strip shows a regular narrow-complex tachycardia with no visible P waves. First confirm perfusion — if shocked, synchronised cardioversion at 0.5-1 J/kg is the route, not drugs. If stable, apply ice to the face for up to 15 seconds (the diving reflex) while drawing up adenosine and a saline flush through a good proximal line. Give 0.1 mg/kg as the fastest push the line allows, flush immediately, and record continuously: abrupt termination confirms re-entrant supraventricular tachycardia; a transient slowing revealing flutter waves changes the diagnosis entirely. Failure at 0.1 means 0.2 mg/kg once, and if the rhythm persists, move to an infusion of amiodarone 5 mg/kg over 20-60 minutes or propranolol/esmolol and consult cardiology, searching for the infant triggers — fever, dehydration, medication, or an unsuspected Wolff-Parkinson-White.

The older child with documented pre-excitation deserves electrophysiology study and ablation, but the infant who converts cleanly usually outgrows the pathway, so ablation is deferred beyond about age four to five.

How the examiner frames it

Two patterns recur. First, the recognition stem — a wide-complex tachycardia in a child is ventricular tachycardia until proven otherwise, and treating it as supraventricular tachycardia with aberrancy, with verapamil avoided in infants altogether, is the scripted error. Second, the syncope stem with a family history of drowning or unexplained death — the expected answer is an ECG with QTc measurement, not a tilt table. The congenital block question usually carries a mother with systemic lupus erythematosus or Sjögren antibodies; the anti-Ro link and the pacing threshold (roughly 50-55 per minute in a neonate) are the scored facts. Adenosine's dose ceiling — 6 mg then 12 mg — is among the most reliably examined paediatric numbers.

Frequently asked questions

How is adenosine given and at what dose?

As an extremely rapid intravenous bolus of 0.1 mg/kg (maximum 6 mg) followed by a saline flush, repeated once at 0.2 mg/kg (maximum 12 mg), with the ECG running throughout.

What ECG features define Wolff-Parkinson-White syndrome?

A short PR interval, a delta wave slurring the QRS upstroke and a widened QRS in sinus rhythm, indicating an accessory pathway capable of re-entrant tachycardia.

Why is congenital complete heart block linked to maternal antibodies?

Maternal anti-Ro and anti-La antibodies cross the placenta and injure fetal conduction tissue; pacing is needed if the rate falls below about 50-55 per minute.

Which children with syncope need an ECG urgently?

Any child with exertional or supine syncope, deafness, or a family history of sudden cardiac death — long QT and other channelopathies must be excluded before labelling episodes vasovagal.

What energy is used for paediatric defibrillation?

An initial 2 joules per kilogram for ventricular fibrillation or pulseless ventricular tachycardia, escalating to 4 joules per kilogram for subsequent shocks.

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