Electrocardiogram acquisition and interpretation in children — formative SAQs

SAQ 1 (10 marks)

A 14-year-old girl is referred by her GP after two episodes of syncope, the first during a school swimming lesson and the second on hearing sudden bad news. The GP arranged a 12-lead ECG, which is handed to you. The heart rate is 75 beats per minute, the rhythm is sinus, and the Bazett-corrected QT interval is 490 milliseconds. [1] [4]

1. Outline the systematic interpretation you would apply to this ECG, and state why the age-specific normal ranges matter. (3) [2]
2. Interpret the QTc of 490 milliseconds in this 14-year-old, and explain why Bazett may over-read or under-read the true value depending on the heart rate. (4) [4] [5]
3. What is the most likely diagnosis, what else must you ask about in the history, and what is the disposition? (3) [4]

Model answer — SAQ 1

(1) Systematic interpretation (3). I read the ECG in the same order every time — rate, rhythm, axis, intervals (PR, QRS, QTc), chamber size, repolarisation, clinical context — and at every step I compare the measurement with the value expected for the child's age. The age-specific normal ranges matter because the paediatric ECG evolves from a right-ventricular-dominant neonatal pattern to the adult pattern through childhood: the neonate has a rightward axis (+90 to +190 degrees), a dominant R in V1, an upright then inverted T in V1, and shorter intervals, and a QTc up to 480 milliseconds by Bazett is accepted in the infant under six months. Reading a child's ECG against adult ranges is the commonest cause of an unnecessary cardiology referral. [1] [2]

(2) Interpretation of the QTc (4). A Bazett-corrected QTc of 490 milliseconds in a 14-year-old at a heart rate of 75 is prolonged: the upper normal for an older child is 460 milliseconds in a female (450 in a male), and 490 is clearly above that threshold. Bazett's formula divides the QT by the square root of the RR interval in seconds, which overcorrects at fast heart rates and undercorrects at slow rates. At a heart rate of 75 (RR 0.8 seconds), the correction is close to accurate, so the 490 milliseconds is a reliable prolonged reading. If the heart rate had been 150, Bazett would have over-read the QTc and I would recheck at a slower rate; for drug-safety monitoring over time I would use the Fridericia correction (cube root of RR) to minimise the rate-dependent artefact. [4] [5]

(3) Diagnosis, history, and disposition (3). The most likely diagnosis is long QT syndrome, supported by the prolonged QTc and the two syncopal episodes with characteristic triggers (exertion with swimming, and a sudden emotional stimulus). I would ask specifically about a family history of sudden death before the age of 40, congenital deafness (the Jervell and Lange-Nielsen phenotype), and any QT-prolonging medication. The disposition is urgent paediatric cardiology referral the same day, with a Holter, an exercise test, genetic testing, and the institution of beta-blockade and activity modification; I would advise the family that the child should avoid swimming alone and competitive sport until the cardiology review. [4]

SAQ 2 (10 marks)

A three-month-old infant presents with poor feeding and irritability over 24 hours. On examination the child is pale and mottled, the heart rate is 250, the capillary refill is 4 seconds, and the oxygen saturation is 94 percent in air. A 12-lead ECG is acquired. [2] [3]

1. What rhythm is most likely, and what features on the ECG would support it? (3) [2]
2. Outline the immediate resuscitation and the pharmacological management of this child, with the doses you would use. (4) [2]
3. After the rhythm has been terminated, what features on the post-cardioversion ECG would you look for, and why? (3) [2] [3]

Model answer — SAQ 2

(1) Rhythm and ECG features (3). The most likely rhythm is supraventricular tachycardia, the commonest tachyarrhythmia of infancy and most often an accessory-pathway mechanism at this age. The ECG features in the arrhythmia are a narrow-complex, regular tachycardia with no discernible P waves, at a rate that is too fast for age (above 220 in an infant is the teaching threshold). The differential is sinus tachycardia (which is slower, variable, and shows a P wave preceding every QRS) and, less commonly, a junctional or atrial ectopic tachycardia; a wide-complex tachycardia in a sick infant would be treated as ventricular tachycardia until proven otherwise. [2]

(2) Resuscitation and pharmacology (4). This infant is haemodynamically compromised (mottled, capillary refill 4 seconds), so I follow the APLS pathway. I secure the airway and give high-flow oxygen, obtain intravenous access, and treat the SVT. Because the child is shocked, the first-line treatment is synchronised DC cardioversion at 0.5 to 1 joule per kilogram, escalating if needed, under sedation if time permits. If the child were stable, I would start with vagal manoeuvres appropriate to age (a cold pack to the face for the diving reflex in an infant) and, if unsuccessful, give intravenous adenosine at 100 micrograms per kilogram as a rapid bolus through a large cannula with a brisk saline flush, escalating to 200 then 300 micrograms per kilogram (max 12 mg) if the first dose fails. I would warn the family of the brief unpleasant sensation of the adenosine flush and have full resuscitation facilities available. [2]

(3) Post-cardioversion ECG (3). Once sinus rhythm is restored, the post-cardioversion 12-lead ECG is searched for the substrate of the SVT. I look specifically for a short PR interval and a delta wave with a widened QRS, the triad of ventricular pre-excitation (Wolff-Parkinson-White pattern), which is the commonest accessory-pathway substrate in infancy. I also re-measure the QTc in sinus rhythm, look for chamber hypertrophy and structural-heart-disease patterns, and request an echocardiogram. The disposition is paediatric cardiology referral for risk stratification of the accessory pathway, which may require electrophysiology study and catheter ablation in childhood. [2] [3]