Ace your next case.

Answer for Medical student – Science focus

Supraventricular tachycardia (SVT) is any tachyarrhythmia (heart rate over 100 beats/min) whose mechanism relies on tissue at or above the bifurcation of the bundle of His. In clinical usage, “SVT” commonly refers to paroxysmal supraventricular tachycardias — arrhythmias with abrupt onset and termination.

The mechanism is re-entry. Two anatomically or functionally distinct pathways join proximally and distally to form a loop. A premature beat blocks one pathway while it is refractory, then conducts slowly down the other, so the blocked limb has repolarised by the time the impulse reaches the distal junction.

Subtypes. AVNRT (about 60%) re-enters within or adjacent to the AV node. AVRT (about 30%) uses an accessory pathway, as in the bundle of Kent of Wolff–Parkinson–White. Atrial tachycardia (about 10%) arises from an ectopic focus or micro-re-entry confined to atrial myocardium.

Answer for Medical student – Clinical focus

Supraventricular tachycardia (SVT) refers broadly to tachyarrhythmias originating at or above the bundle of His that require atrial tissue or the atrioventricular (AV) junction for their initiation and maintenance. In clinical and OSCE contexts, paroxysmal SVT most often means a regular, narrow-complex tachycardia: AVNRT, AVRT or atrial tachycardia.

At the bedside. Palpitations are sudden-onset and sudden-termination — the “light switch” phenomenon — typically regular and rapid at 150–250 bpm. The frog sign is caused by cannon a-waves in the JVP when atrial and ventricular contraction coincide, and polyuria follows atrial natriuretic peptide release.

The branch point is haemodynamic stability. Hypotension, altered conscious state, acute pulmonary oedema or ongoing ischaemic chest pain means synchronised DC cardioversion. If stable: confirm on a 12-lead ECG, then modified Valsalva, then IV adenosine 6 mg rapid push escalating to 12 mg, then an AV-nodal blocking agent.

Answer for General Practice

Supraventricular tachycardia (SVT) is any tachyarrhythmia originating above the bundle of His bifurcation. In primary care, the term most commonly refers to paroxysmal narrow-complex regular tachycardias involving re-entry, predominantly AV nodal re-entrant tachycardia (AVNRT) or AV re-entrant tachycardia (AVRT, including Wolff–Parkinson–White).

Clinical features. Sudden-onset, regular palpitations often described as a “flutter” or racing heart, with abrupt termination. Associated presyncope, lightheadedness, mild chest tightness, dyspnoea or polyuria. Syncope, severe chest pain, hypotension or heart failure signs suggest haemodynamic compromise or structural heart disease.

Initial management. For a stable episode, the modified Valsalva (40 mmHg strain for 15 seconds followed immediately by passive leg elevation) has the highest conversion rate. Cardiology referral is recommended for all newly diagnosed patients: EPS and catheter ablation have high cure rates and are typically the preferred long-term treatment.

Answer for Junior doctor

What it is. Supraventricular tachycardia (SVT) is an umbrella term for tachyarrhythmias originating above the bundle of His, most commonly AV nodal re-entrant tachycardia (AVNRT) or AV re-entrant tachycardia (AVRT).

How to confirm. Obtain an immediate 12-lead ECG: a regular, narrow-complex tachycardia (QRS under 120 ms) typically at 140–220 bpm, often with absent or retrograde P waves. Check stability first — BP, conscious state, ongoing chest pain, acute pulmonary oedema.

If unstable, call a MET or code and prepare for urgent synchronised DC cardioversion under senior guidance.

If stable, modified Valsalva, then IV adenosine 6 mg via a large proximal cannula with a rapid 20 mL saline flush, escalating to 12 mg, with continuous ECG monitoring. Discuss second-line AV-nodal blockers with your registrar first.