Supraventricular tachycardia — formative SAQs

SAQ 1 (10 marks)

A four-month-old boy is brought to the emergency department by his mother, who says he has been "fussy and not feeding well" for a day. On examination he is pale and irritable, with a respiratory rate of 50 and capillary refill of three seconds. The nurse reports a heart rate of 250 per minute on the monitor. A 12-lead ECG shows a regular narrow-complex tachycardia at 250 per minute with no visible P waves. [3] [5]

1. Describe your immediate assessment and management of this infant, including the specific technique and dose of each pharmacological agent. (5) [1] [5]
2. Explain how you would distinguish this rhythm from sinus tachycardia, and why that distinction matters for management. (2) [1] [3]
3. Outline the long-term management plan after the acute episode, including medication choices and the expected natural history. (3) [3] [5]

Model answer — SAQ 1

(1) Immediate management (5). This infant is in SVT and is showing early signs of haemodynamic compromise — pallor, poor perfusion, irritability — but is not yet in overt shock with hypotension. He is stable enough for a stepwise approach. First, apply a 12-lead ECG and cardiac monitoring, establish intravenous access, and give high-flow oxygen. Attempt a vagal manoeuvre: the diving reflex, using a sealed ice pack or cold gel pack applied to the face for 15 to 30 seconds, is the most reliable technique in an infant. If the vagal manoeuvre fails, administer adenosine at 0.1 milligramme per kilogramme as a rapid intravenous bolus through the largest-bore cannula closest to the heart, followed immediately by a 5 to 10 millilitre saline flush. The maximum first dose is 6 milligrammes. If the first dose does not terminate the tachycardia, give 0.2 milligramme per kilogramme (maximum 12 milligrammes) by the same rapid technique. If adenosine fails or the infant deteriorates, proceed to synchronised DC cardioversion at 0.5 to 1 joule per kilogramme. A defibrillator must be available at the bedside throughout. [1] [5]

(2) Distinguishing SVT from sinus tachycardia (2). Sinus tachycardia has a normal P wave axis with visible P waves preceding each QRS, and the rate varies with stimulation — crying, fever, pain. The infant heart rate in sinus tachycardia is usually below 220 per minute, and a treatable cause (fever, dehydration, sepsis, anaemia) is present. SVT has a fixed rate that does not vary, absent or retrograde P waves, and a rate typically above 220 in infants. The distinction matters because sinus tachycardia is managed by treating the underlying cause, while SVT requires active termination with vagal manoeuvres or adenosine. Giving adenosine to a child in sinus tachycardia is unnecessary and may cause transient asystole. [1] [3]

(3) Long-term management (3). After successful termination, obtain a 12-lead ECG in sinus rhythm to check for the Wolff-Parkinson-White pattern (delta wave, short PR interval). Start prophylactic antiarrhythmic therapy because recurrence is common — first-line is propranolol at 2 to 4 milligrammes per kilogramme per day in three divided doses, or digoxin at 10 microgrammes per kilogramme per day. An echocardiogram excludes structural heart disease. The family is educated on recognising recurrence and performing simple vagal manoeuvres. Most infants (60 to 80 per cent) have spontaneous resolution by one year of age, so medication is typically weaned at 12 months with monitoring for recurrence. [3] [5]

SAQ 2 (10 marks)

A 14-year-old girl presents to the emergency department with sudden-onset palpitations that started 30 minutes ago while watching television. She describes a rapid, pounding sensation in her chest with mild breathlessness. Her pulse is 190 per minute and regular, blood pressure 110/70, and oxygen saturation 99 per cent in air. The ECG shows a regular narrow-complex tachycardia with a pseudo R-prime in V1 and no visible P waves. The tachycardia terminates with a modified Valsalva manoeuvre. The post-termination ECG is normal with no delta wave. [1] [6]

1. Interpret the ECG findings during and after tachycardia, and state the most likely mechanism. (3) [1] [2]
2. Describe the role and technique of the modified Valsalva manoeuvre, including the evidence supporting it. (3) [6]
3. Outline the long-term management options for this adolescent, including the role of catheter ablation and the factors that would favour it. (4) [2] [3]

Model answer — SAQ 2

(1) ECG interpretation and mechanism (3). During tachycardia, the ECG shows a regular narrow-complex tachycardia at 190 per minute with a pseudo R-prime (an rSr' or notched R wave) in V1 and no visible P waves — the classic ECG signature of typical slow-fast AVNRT. The pseudo R-prime in V1 reflects retrograde atrial activation occurring immediately after ventricular depolarisation, producing a small terminal positivity in the right precordial lead. The post-termination ECG is normal with no delta wave or short PR interval, excluding manifest Wolff-Parkinson-White syndrome and confirming that the mechanism is AVNRT rather than AVRT. AVNRT is the commonest SVT mechanism in adolescents, which is concordant with this presentation. [1] [2]

(2) Modified Valsalva and the REVERT evidence (3). The modified Valsalva manoeuvre, validated in the REVERT randomised controlled trial, involves the child lying semi-recumbent and performing a forced expiration against a closed glottis for 15 seconds (blowing into a 10 mL syringe so the plunger moves is one practical method), then being immediately repositioned supine with passive leg elevation for 15 seconds. The forced expiration increases intrathoracic pressure, which stimulates baroreceptors to produce vagal tone and transient AV nodal block; the repositioning enhances venous return and augments the vagal response. The REVERT trial in adults showed that the modified technique achieved a 43 per cent termination rate compared with 17 per cent for the standard Valsalva, with no increase in adverse events, and this technique is now adopted in paediatric SVT guidelines for cooperative children. [6]

(3) Long-term management and catheter ablation (4). For this adolescent with infrequent, well-tolerated episodes, a "pill in the pocket" strategy is a reasonable first approach — a single dose of a short-acting beta-blocker taken at the onset of an episode, combined with self-administered vagal manoeuvres. If episodes are frequent, poorly tolerated, or associated with pre-syncope, daily prophylactic medication with a beta-blocker is appropriate. Catheter ablation is curative and is the definitive treatment for AVNRT in adolescents. The procedure uses cryoablation (preferred over radiofrequency in young patients because of the lower risk of AV nodal injury) to modify the slow pathway of the AV node. Factors favouring ablation include frequent or severe episodes limiting daily activities, failure of or non-adherence with medication, pre-syncope or syncope during episodes, and patient preference for a definitive cure. Acute success rates exceed 95 per cent, recurrence is 5 to 10 per cent, and the risk of complete heart block requiring pacemaker is under 1 per cent with cryoablation. The procedure is generally offered from approximately five years of age, and this 14-year-old is well within the appropriate age range. [2] [3]