Supraventricular tachycardia — structured viva

Stem

Practice viva. You are the cardiology registrar. The examiner shows you a 12-lead ECG of a regular narrow QRS tachycardia in a 40-year-old man who is alert with a normal blood pressure, and follows the case from the emergency department to the electrophysiology clinic.

Branch A — Reading the ECG

Examiner: How do you work out the mechanism from this ECG?

Strong answer: Narrow QRS complexes are due to rapid ventricular activation through the His–Purkinje system, which suggests that the origin is above or within the His bundle, although high septal VT can give relatively narrow QRS complexes (110–140 ms).^[1] I look at onset, regularity and the P/QRS relationship: short-RP SVTs have an RP shorter than half the RR interval, and long-RP SVTs show RP equal to or longer than PR.^[1] A fixed VA interval with variable RR intervals excludes AT, and AV block or dissociation rules out AVRT.^[1] When retrograde P waves can be identified, a pseudo r in V1 and a pseudo S in the inferior leads are more common in typical AVNRT than in AVRT or AT: specific (91–100%) but modestly sensitive (58% and 14%).^[1] However, in all the referenced studies, cases of AT or atypical AVNRT were limited or entirely absent.^[1]

Follow-up: And at a ventricular rate of about 150 b.p.m.? Answer: Consider atrial flutter with 2:1 conduction, because atrial activity in flutter is usually 250–330 b.p.m.^[1]

Branch B — Termination

Examiner: He remains stable. How do you terminate it?

Strong answer: For a stable narrow QRS tachycardia without an established diagnosis, ESC 2019 recommends a 12-lead ECG during tachycardia (Class I, level C).^[1] In this narrow QRS setting, vagal manoeuvres, preferably in the supine position with leg elevation, are recommended (Class I, level B), then adenosine 6–18 mg IV bolus if vagal manoeuvres fail (Class I, level B).^[1] If vagal manoeuvres and adenosine fail, IV verapamil or diltiazem (Class IIa, level B) or IV esmolol or metoprolol (Class IIa, level C) should be considered for the narrow QRS tachycardia.^[1] The narrow QRS table footnotes add that IV verapamil and diltiazem are contraindicated in hypotension or HFrEF, and IV beta-blockers in decompensated heart failure.^[1] Synchronised DC cardioversion is recommended when drug therapy fails to convert or control the narrow QRS tachycardia (Class I, level B).^[1]

Follow-up: Why the modified Valsalva? Answer: REVERT randomised adults with SVT (excluding AF and flutter) in English emergency departments to a modified Valsalva or a standard semi-recumbent Valsalva.^[4] The modified manoeuvre adds supine repositioning and passive leg raise immediately after a semi-recumbent strain, and both groups used a 40 mm Hg, 15 s strain.^[4] Sinus rhythm at 1 min was achieved in 43% with the modified manoeuvre vs 17% with the standard manoeuvre (adjusted OR 3.7).^[4]

Follow-up: He presented to an Australian emergency department. What does ANZCOR say? Answer: Under its heading for regular narrow-complex tachycardia, ANZCOR Guideline 11.9 (adult advanced life support) says that in the absence of adverse features, start with vagal manoeuvres.^[3] If the arrhythmia persists and is not atrial flutter, give adenosine 6 mg as a rapid IV bolus followed by a minimum 20 mL flush; if there is no response, give a 12 mg bolus, which may be repeated.^[3]

Branch C — Adenosine

Examiner: How does adenosine work, and what do you warn the patient about?

Strong answer: It acts through cardiac A1 receptors, prolonging AV conduction through the AH interval, not the HV interval, until transient AV block terminates the tachycardia.^[1] Transient dyspnoea is common, facial flushing may occur, and chest pain may well be of cardiac origin.^[1] AF may follow adenosine and appears more commonly associated with AVRT than AVNRT, and adenosine may occasionally cause or accelerate pre-excited atrial arrhythmias.^[1]

Follow-up: Is calcium channel blockade any less effective? Answer: A Cochrane review of seven trials (622 emergency department participants) found moderate-quality evidence of no difference in reversion with adenosine or calcium channel antagonists (89.7% vs 92.9%; OR 1.51, 95% CI 0.85 to 2.68).^[6]

Branch D — Definitive therapy

Examiner: It was AVNRT. He has had four episodes this year, each with troublesome palpitations. What next?

Strong answer: Catheter ablation is recommended for symptomatic, recurrent AVNRT (Class I, level B).^[1] Slow-pathway ablation offers a success rate of 97%, a recurrence rate of about 1.3–4%, and a risk of AV block under 1% in previous reports. Recent experience indicates that in experienced centres it can be done in typical and atypical AVNRT with almost no risk of AV block, by targeting the inferior nodal extension and avoiding the mid-septum and the roof of the coronary sinus.^[1] For AVNRT, if ablation is not desirable or feasible, diltiazem or verapamil (in patients without HFrEF) or beta-blockers should be considered (Class IIa, level B).^[1]

Follow-up: He mentions his cousin was offered cryoablation. Is it better? Answer: Cryoablation may carry a lower risk of AV block but a significantly higher recurrence rate; it is especially attractive for children.^[1]

Branch E — Pre-excited AF

Examiner: A different patient has known WPW and an irregular wide QRS tachycardia. What do you avoid?

Strong answer: Any AV nodal modulating agent (adenosine, verapamil, diltiazem, beta-blockers or digoxin) should be avoided in pre-excited AF, because these drugs may contribute to a risk of ventricular fibrillation; in haemodynamically stable patients, IV amiodarone is not recommended (Class III, level B).^[1] Synchronised DC cardioversion is recommended if haemodynamically unstable (Class I, level B); if stable, IV ibutilide or procainamide should be considered (Class IIa, level B).^[1] IV ibutilide is contraindicated with a prolonged QTc, and procainamide prolongs the QTc, but much less than class III agents.^[1]

Follow-up: Why is it dangerous? Answer: AF with a fast ventricular response over an overt AP with a short anterograde refractory period is a potentially life-threatening arrhythmia in WPW syndrome, because of potential degeneration into VF.^[1]

Branch F — Asymptomatic pre-excitation

Examiner: A 20-year-old with an incidental WPW pattern asks whether he can keep playing competitive football.

Strong answer: ESC 2019 recommends an EPS with isoprenaline to risk-stratify asymptomatic pre-excitation in those who participate in competitive athletics or have high-risk occupations or hobbies (Class I, level B).^[1] Catheter ablation is recommended if electrophysiology testing with isoprenaline identifies high-risk properties such as SPERRI 250 ms or less, AP ERP 250 ms or less, multiple APs or an inducible AP-mediated tachycardia (Class I, level B).^[1]

Follow-up: What is his risk if untreated? Answer: About one in five people with asymptomatic pre-excitation develop an AP-related arrhythmia during follow-up, and the risk of cardiac arrest or VF has been estimated at 2.4 per 1000 person-years.^[1]

Branch G — Pregnancy

Examiner: A different patient is 24 weeks pregnant and in a stable narrow QRS tachycardia. What changes?

Strong answer: Under the 2025 ESC pregnancy guideline, vagal manoeuvres and IV adenosine are recommended for conversion of haemodynamically stable SVT (Class I, level C), and immediate electrical cardioversion is recommended for SVT with haemodynamic instability (Class I, level C).^[2] In pregnancy, beta-1-selective blockers (except atenolol) or verapamil are recommended for prevention of SVT in women without pre-excitation on the resting ECG (Class I, level C).^[2]

Follow-up: What adenosine dose does the pregnancy guideline give? Answer: The 2025 ESC pregnancy guideline’s Figure 14 (management of narrow QRS tachycardia in pregnant women) gives IV adenosine as a 6–18 mg bolus.^[2]