Supraventricular Tachycardia

Meet the patient

A 28-year-old nurse feels her heart "switch on" to a fast, regular pound as she walks to her car — lightheaded, breathless, her neck thumping in time. Twenty minutes later it "switches off" just as suddenly, and the first thing she does is pass a large volume of urine.^[7][16]

The three questions that decide her next ten minutes are the three that decide every SVT: is the QRS narrow? (the gate to the whole algorithm), is she stable? (electricity or adenosine), and is this really SVT — or flutter at 150, pre-excited AF, or VT in a broad-QRS disguise? Hold those three and the ladder below slots straight in.^[7][16]

What SVT is — one umbrella, one gatekeeper, three traps

Supraventricular tachycardia (SVT) is an umbrella term for any abnormally rapid tachyarrhythmia that originates at or above the AV node (the bundle of His).^[7] At the bedside it means a regular tachycardia with a narrow QRS complex (under 120 ms — under three small squares) and a rate usually between 150 and 250 bpm — explicitly excluding sinus tachycardia and atrial fibrillation, which are narrow-complex but irregular with a clear mechanism.^[16]

The clinical skill in SVT is threefold and is what examiners probe: (1) recognise that a regular narrow-complex tachycardia is SVT until proven otherwise; (2) distinguish the AV-node-dependent re-entrant tachycardias (AVNRT, AVRT) — which respond to vagal manoeuvres and adenosine — from the AV-node-independent atrial tachycardias (focal atrial tachycardia, multifocal atrial tachycardia); and (3) never miss the two life-threatening mimics: pre-excited atrial fibrillation in WPW (where AV-nodal blockers kill) and ventricular tachycardia masquerading as SVT with aberrancy.^[7][16]

The dominant mechanism of the AV-node-dependent tachycardias is re-entry: a self-perpetuating circuit in which an impulse repeatedly re-enters and re-excites tissue faster than the sinus node. Re-entry requires three conditions — a circuit of two interconnected pathways, different conduction velocities and refractory periods between them, and a unidirectional block in one limb that initiates the loop. AVNRT is the commonest regular supraventricular tachyarrhythmia;^[7] AVRT uses an accessory pathway. Intra-atrial re-entrant tachycardia is an AV-node-independent atrial circuit — adenosine and verapamil had no effect on atrial cycle length in 13 of 14 and 9 of 9 patients respectively, despite inducing second-degree AV block.^[17]

Classification

SVT is best classified by the anatomical substrate of the circuit, because this determines the ECG, the response to manoeuvres and the long-term treatment.^[7][16]

By mechanism and AV-node dependence: ^[7]

• AV-node-dependent (terminating with vagal manoeuvres/adenosine):
  • AV nodal re-entrant tachycardia (AVNRT) — re-entry within the AV node using dual pathways. The commonest regular supraventricular tachyarrhythmia. Typical (slow-fast) vs atypical (fast-slow, slow-slow) is conventional teaching.
  • AV re-entrant tachycardia (AVRT) — re-entry using the AV node plus an accessory pathway connecting atrium to ventricle (the bundle of Kent). Subdivided into orthodromic (narrow QRS) and antidromic (broad QRS). In a 17-country registry, orthodromic AVRT was the most prevalent arrhythmia among WPW patients (55%).^[15]
• AV-node-independent (atrial origin, adenosine reveals the diagnosis rather than terminating):
  • Intra-atrial / focal atrial tachycardia — adenosine and verapamil had no effect on atrial cycle length in 13 of 14 and 9 of 9 patients respectively, despite inducing second-degree AV block.^[17]
  • Multifocal atrial tachycardia (MAT) — three or more distinct P-wave morphologies; classically in COPD.
  • Sinus node re-entrant tachycardia — re-entry within the sinus node; sudden onset/offset unlike sinus tachycardia. ^[7]

By accessory-pathway (pre-excitation) syndromes: ^[7]

• Wolff-Parkinson-White (WPW) syndrome — manifest accessory pathway (bundle of Kent): short PR, delta wave (slurred upstroke), widened QRS in sinus rhythm. Syndrome = pathway plus symptomatic tachyarrhythmia. Community sudden-death rate was 0.0015 per patient-year; no SCD occurred in patients asymptomatic at diagnosis.^[9]
• Concealed accessory pathway — pathway conducts only retrogradely (ventricle to atrium); no delta wave in sinus rhythm, but causes orthodromic AVRT.
• Permanent junctional reciprocating tachycardia (PJRT) — a slowly-conducting concealed accessory pathway near the AV node causing an incessant long-RP tachycardia; a classic cause of tachycardiomyopathy.
• Lown-Ganong-Levine (LGL) — short PR with normal QRS (no delta); historically attributed to a James fibre bypass tract; now regarded as a AV-nodal-conduction variant rather than a true accessory pathway. ^[7]

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Epidemiology & Risk Factors

In a defined US population, PSVT prevalence was 2.25/1,000 persons and incidence 35/100,000 person-years. There are two distinct subsets: lone PSVT (younger, mean 37 years, faster rates mean 186 bpm, more often first documented in the emergency room) versus PSVT with other cardiovascular disease (mean 69 years, 155 bpm). Other cardiovascular disease was present in 90% of males and 48% of females. Onset of symptoms occurred during the childbearing years in 58% of females with lone PSVT versus 9% of females with other cardiovascular disease.^[8]

AVNRT is the commonest regular supraventricular tachyarrhythmia.^[7] In one electrophysiology series, AVNRT patients were older (50 vs 37 years), predominantly female (71% vs 53%), and slower (175 vs 186 bpm) than AVRT patients.^[6] Newly diagnosed WPW occurred at about four per 100,000 per year in Olmsted County; about 50% were asymptomatic at diagnosis, with 30% later developing arrhythmia symptoms. Two sudden deaths occurred over 1,338 patient-years (0.0015 per patient-year); no SCD occurred in patients asymptomatic at diagnosis.^[9]

Risk factors and predisposing substrates: ^[7]

Pathophysiology

All clinically important SVT mechanisms converge on one principle: a wave-front that does not extinguish but instead circles repeatedly, re-exciting myocardium faster than the sinus node. The two dominant substrates — dual AV-nodal pathways and an accessory pathway — both satisfy the three classical conditions for re-entry: (1) an anatomical or functional circuit of two interconnected limbs; (2) different conduction velocities and refractory periods in the two limbs; and (3) a unidirectional block in one limb that allows the wave-front to travel only one way around the loop, returning to its origin after the first limb has recovered excitability.^[16]

AVNRT — dual AV-nodal physiology. In most people the AV node has a single effective conduction route. In patients with AVNRT there are functionally two pathways through or around the AV node: ^[7]

• The slow pathway (alpha) — slower conduction, shorter refractory period.
• The fast pathway (beta) — faster conduction, longer refractory period. ^[7]

In sinus rhythm the impulse travels down the fast pathway and reaches the bundle of His first. A premature atrial beat (the trigger) arrives when the fast pathway is still refractory but the slow pathway has recovered — the beat therefore conducts down the slow pathway, reaching the lower common pathway late enough that the fast pathway has now recovered. The impulse then conducts retrogradely up the fast pathway back to the atrium, and if it arrives back at the top of the slow pathway after the slow pathway has recovered, the circuit self-perpetuates: this is typical (slow-fast) AVNRT. The atria and ventricles are activated almost simultaneously (the circuit is tiny), so retrograde P waves are buried in or just after the QRS — producing the classic pseudo R-prime in V1 and pseudo S in the inferior leads. An RP interval at or under 90 ms favours AVNRT.^[5] In the rarer atypical forms the circuit runs in reverse: fast-slow (long RP with inverted P waves) and slow-slow.

AVRT — the accessory pathway. An accessory pathway (bundle of Kent) is a congenital muscular bridge connecting atrial myocardium directly to ventricular myocardium, bypassing the AV node. Because accessory-pathway tissue conducts faster than the AV node (and, unlike the AV node, conducts faster as heart rate rises), in sinus rhythm the impulse reaches the ventricle partly through the Kent bundle, pre-exciting a portion of the ventricle — this produces the delta wave (a slurred initial QRS upstroke), a short PR interval (under 120 ms), and a widened QRS (fusion of pre-excited and normally-conducted activation). This is Wolff-Parkinson-White pattern. WPW syndrome = the pattern plus symptomatic tachyarrhythmia. ^[7]

In orthodromic AVRT (narrow QRS) the re-entrant circuit runs anterogradely down the AV node (normal, narrow QRS activation) and retrogradely up the accessory pathway back to the atrium — so the QRS is narrow and a visible P wave with RP of 100 ms or more favours AVRT over AVNRT.^[6] In antidromic AVRT (broad QRS) the impulse travels anterogradely down the accessory pathway (the whole ventricle is pre-excited, giving a broad QRS that mimics VT) and retrogradely up the AV node. Electrical cardioversion is the first-line treatment for pre-excited atrial fibrillation and antidromic AVRT.^[15]

The WPW danger — pre-excited atrial fibrillation. The real lethality of WPW is not the orthodromic circuit but atrial fibrillation conducting down the accessory pathway. Unlike the AV node (which slows and blocks at high rates), accessory-pathway tissue conducts very fast and without decrement, so AF impulses can bombard the ventricles at very high rates with broad QRS complexes, generating an irregular broad-complex tachycardia that can degenerate into ventricular fibrillation and sudden death. Blocking the AV node in pre-excited AF may increase the ventricular rate and has resulted in VF after administration of AV-nodal blockers.^[10] Electrical cardioversion is the first-line treatment for pre-excited AF and antidromic AVRT.^[15]

Focal atrial tachycardia arises from enhanced automaticity or triggered activity (delayed after-depolarisations) in a single atrial focus, firing faster than the sinus node. It is AV-node-independent: the focus continues to fire regardless of what the AV node does, so adenosine produces transient AV block but does not terminate the atrial tachycardia — a diagnostic clue. Incessant focal atrial tachycardia is a leading cause of tachycardiomyopathy. Multifocal atrial tachycardia (MAT) is driven by multiple competing atrial foci, classically in the hypoxic, theophylline-treated COPD patient, and is recognised by three or more distinct P-wave morphologies in one lead with irregular RR intervals. ^[7]

The polyuria pearl. During SVT the atria contract against closed AV valves (the atrial and ventricular cycles nearly coincide), generating raised atrial pressure and atrial stretch. This releases atrial natriuretic peptide (ANP), producing the polyuria that classically follows termination of an episode — a high-yield exam clue to SVT (and absent in sinus tachycardia).^[16]

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Clinical Presentation

The hallmark of paroxysmal SVT is palpitations of abrupt onset and abrupt offset — patients often remember the exact second the episode began and the exact second it stopped (often with urination, a vagal trigger, or after a manoeuvre). Episodes last minutes to hours and recur unpredictably over years.^[7]

Typical symptoms: ^[7]

• Palpitations — rapid, regular, "fluttering" or "pounding"; the patient may feel it in the neck.
• Lightheadedness, presyncope, frank syncope — from reduced cerebral perfusion; syncope suggests haemodynamic compromise or, in WPW, is a warning sign for sudden-death risk.
• Dyspnoea / air hunger.
• Chest tightness or chest pain — common even with normal coronaries (demand ischaemia from rapid rate); ischaemic-type pain mandates a lower threshold to cardiovert.
• Anxiety, sense of impending doom.
• Neck pulsations — the frog sign (prominent regular cannon A waves) visible in the neck when atria contract against closed AV valves; highly suggestive of AVNRT.
• Polyuria after termination — ANP release from atrial stretch; a classic discriminator from sinus tachycardia. ^[7]

During the episode the examination findings are: ^[7]

• A rapid, regular pulse (lone PSVT mean 186 bpm in one population series).
• A normal or low blood pressure; hypotension indicates instability.
• Jugular venous pulsations — in AVNRT, regular, prominent "cannon" A waves (the frog sign) as the atria beat against closed tricuspid valve.
• Heart sounds may be normal; the first heart sound can vary in intensity. ^[7]

Atypical presentations (must-know for examiners): ^[7]

• Elderly — may present with syncope, falls, dyspnoea, or exacerbation of heart failure rather than typical palpitations; rates can be higher and tolerance lower. Atrial tachycardia and AF are proportionally more common in older patients; AVNRT less so.
• Pregnancy — SVT frequency increases; episodes are poorly tolerated (higher circulating volume, cardiovascular stress); the safe drugs differ (see Special Populations).
• Children / infants — present with poor feeding, irritability, pallor, tachypnoea, and in infants heart failure if the tachycardia is incessant (think PJRT or concealed accessory pathway).
• Incessant SVT (focal atrial tachycardia, PJRT) — the patient may be unaware of "paroxysms"; presents insidiously with new heart failure or a reduced ejection fraction = tachycardiomyopathy, which is reversible with rate control or ablation.
• WPW with AF — irregular palpitations, pre-syncope, or collapse; the ECG shows an irregular broad-complex tachycardia — a medical emergency. ^[7]

Differential Diagnosis

A regular narrow-complex tachycardia narrows the differential, but several conditions must be distinguished because treatment diverges sharply.^[7][16]

The three "do-not-miss" mimics in any SVT assessment: ^[7]

1. Sinus tachycardia from a serious cause (sepsis, hypovolaemia, pulmonary embolism, thyrotoxicosis) — giving adenosine is harmless but useless; find and treat the cause.
2. Atrial flutter with 2:1 block at 150 bpm — adenosine transiently slows AV conduction and reveals the sawtooth waves, confirming the diagnosis; definitive treatment is rate control, rhythm control, anticoagulation as indicated, and often isthmus ablation.
3. Pre-excited AF / antidromic AVRT (WPW) — irregular or broad-complex tachycardia where AV-nodal blockers are lethal; electrical cardioversion is first-line.^[10][15]

Clinical & Bedside Assessment

The bedside management of a stable SVT follows a fixed ladder. ABCDE first: secure the airway, give high-flow oxygen if hypoxic, attach monitoring, set up IV access, and take bloods.^[7]

Assess stability — the single decision that branches management: ^[7]

• Unstable (any of): hypotension / shock, syncope or reduced GCS, ischaemic chest pain, acute heart failure, or very rapid rate compromising perfusion -> synchronised DC cardioversion (do not delay for adenosine).
• Stable: proceed to vagal manoeuvres then adenosine. ^[7]

Vagal manoeuvres increase vagal (parasympathetic) tone, transiently slowing AV-nodal conduction and breaking AVNRT and AVRT circuits: ^[7]

• Modified Valsalva manoeuvre (first-line, per the REVERT trial^[2]): a 40 mm Hg pressure, 15 s standardised strain performed semi-recumbent, followed immediately by supine repositioning with a passive leg raise. In REVERT this postural modification returned 43% (93 of 214) to sinus rhythm at 1 minute versus 17% (37 of 214) with a standard semi-recumbent Valsalva, and should be considered a routine first treatment.^[2]
• Carotid sinus massage and the standard Valsalva are the classical vagal manoeuvres used as the initial treatment of stable SVT.^[13]

The frog sign — prominent regular cannon A waves in the jugular venous pulse — is a bedside clue highly suggestive of AVNRT (atria contracting against closed AV valves).^[16]

Record a 12-lead ECG during any manoeuvre — vagal manoeuvres and adenosine may transiently slow AV conduction and unmask atrial activity (flutter waves, P-wave morphology), establishing the diagnosis even if they do not terminate the arrhythmia. ^[7]

Investigations

First-line (during the tachycardia): ^[7]

• 12-lead ECG — the single most important test. Assess rate, regularity, QRS width (under or over 120 ms), P-wave position and morphology, and the RP interval.^[7]
• Continuous cardiac monitoring and a rhythm strip during adenosine.
• IV access and a 12-lead ECG printed before, during, and after termination.
• Bloods: U&E (potassium, magnesium), FBC, digoxin level if relevant, TSH to exclude thyrotoxicosis, and a troponin if there is chest pain or a prolonged episode (it will be demand-positive; do not attribute SVT to an ACS unless ST changes persist).

ECG analysis of a regular narrow-complex tachycardia — the RP interval method (RP interval = from onset of QRS to the next P wave):^[16]

• Short RP tachycardia (RP at or under 90 ms favours AVNRT): the P wave is buried in or just after the QRS.^[5]
  • AVNRT (commonest) — look for pseudo R-prime in V1 and pseudo S in inferior leads (II, III, aVF); these disappear in sinus rhythm.
  • Orthodromic AVRT with a rapidly-conducting retrograde pathway (occasionally short RP).
  • Junctional tachycardia.
• Long RP tachycardia (a visible P with RP of 100 ms or more favours AVRT): the P wave is clearly separated from the preceding QRS.^[6]
  • Atypical AVNRT (fast-slow) — inverted P waves, long RP.
  • Orthodromic AVRT / PJRT — the classic long-RP tachycardia; PJRT is incessant.
  • Focal atrial tachycardia.
  • Sinus node re-entrant tachycardia. ^[7]

ECG in sinus rhythm (after termination) — look for the substrate: ^[7]

• Wolff-Parkinson-White pattern: short PR (under 120 ms), delta wave (slurred upstroke of the QRS), broadened QRS, and repolarisation abnormalities (T-wave changes opposite to the delta-wave direction). Localise the accessory pathway by the delta-wave vector (e.g. left-sided pathways have a positive delta in V1; right-sided, negative).
• Concealed pathway — sinus-rhythm ECG is normal (pathway conducts only retrogradely); diagnosis is made at electrophysiology study. ^[7]

Advanced / confirmatory investigations: ^[7]

• Ambulatory ECG / event monitor / implantable loop recorder — to capture infrequent paroxysms and correlate symptoms with rhythm.
• Echocardiogram — to exclude structural heart disease (Ebstein anomaly, hypertrophic cardiomyopathy) and assess ventricular function (tachycardiomyopathy in incessant SVT).
• Electrophysiological study (EPS) — the gold standard: it maps the circuit, localises an accessory pathway, confirms dual AV-nodal physiology, and is performed immediately before catheter ablation in the same procedure.^[16]

Severity / risk in WPW: community sudden death was 0.0015 per patient-year, and no SCD occurred in patients asymptomatic at diagnosis — arguing against routine electrophysiological testing in asymptomatic patients.^[9] In a 17-country registry, radiofrequency ablation was the first long-term therapy option for 88% of patients.^[15]

Management — Resuscitation

ABCDE first. Give high-flow oxygen only if hypoxic. Establish IV access, attach continuous cardiac monitoring and a defibrillator, and ensure resuscitation equipment (including atropine and a temporary pacemaker) is at the bedside before giving adenosine.^[7][7]

The stability decision — unstable SVT needs electricity, not drugs: ^[7]

Synchronised DC cardioversion is first-line if the patient is haemodynamically unstable (any of: systolic BP under 90 mmHg / shock, syncope or reduced consciousness, ischaemic chest pain, acute heart failure, or signs of end-organ hypoperfusion). ^[7]

• Synchronised shock (sync to the R wave to avoid delivering energy on the T wave, which would cause VF).
• For paroxysmal SVT/AF with haemodynamic compromise, direct current cardioversion is the therapy of choice.^[12]
• Sedate the conscious patient where circumstances allow — but do not delay cardioversion in the genuinely unstable patient.
• Before cardioversion: vagal manoeuvres and adenosine come first only in the stable patient; in the unstable patient electricity is not delayed for drugs.^[2][1]

For stable SVT, proceed directly to the vagal-manoeeuvre then adenosine ladder (below). If broad-complex or pre-excited AF, see Specific Subtypes — the ladder differs. ^[7]

Management — Definitive & Stepwise

The stable narrow-complex SVT ladder is fixed and examinable verbatim:^[2][1]

Step 1 — Vagal manoeuvres (modified Valsalva first-line).

• Modified Valsalva: semi-recumbent 40 mm Hg, 15-second standardised strain, then immediate supine repositioning with passive leg raise (REVERT protocol — 43% vs 17% return to sinus rhythm).^[2]

Step 2 — Adenosine (if vagal manoeuvres fail).^[1]

• Adenosine 6 mg rapid IV bolus; if necessary, adenosine 12 mg — the regimen of the randomised dose-ranging trials.^[1]
• Efficacy: cumulative response 57.4% after 6 mg, rising to 93.4% after 12 mg; the average time from injection to termination was 30 seconds.^[1]
• Warn the patient before each dose: adenosine caused adverse effects in 36% of patients, but they lasted less than 1 minute and were usually mild.^[1]
• Asthma: adenosine caused bronchoconstriction in the only two asthmatics among 26 patients treated — alternative treatments should be considered in asthmatics.^[11]
• Mechanism: adenosine terminates acute PSVT "in which the atrioventricular node is an integral part of the re-entrant circuit" — with more rapid onset than verapamil.^[1]

Step 3 — If adenosine is contraindicated or fails — a second-line agent: ^[1]

• IV verapamil 5 mg, with a further 7.5 mg if necessary, was the comparator regimen in the randomised trials — cumulative response 81.3% then 91.4%, efficacy similar to adenosine but with slower onset.^[1] Never give an AV-nodal blocker in WPW with pre-excited AF — AV-nodal blockade can increase the ventricular rate and has precipitated VF.^[10]
• IV beta-blockers are an alternative where adenosine is contraindicated or fails.^[1]

Step 4 — If pharmacological cardioversion fails and the patient is stable — seek expert cardiology input. For refractory paroxysmal tachyarrhythmias, IV amiodarone terminated PSVT in 61% of a coronary-care series after a median of two failed agents (mean dose to conversion 220 mg; mean time 1.2 hours) with no proarrhythmia or heart-failure aggravation — or proceed to synchronised DC cardioversion under sedation. ^[12]

Long-term management — definitive therapy:^[7][16]

• Catheter ablation is curative and first-line for recurrent AVNRT: in a 359-patient series, acute success was 95% with long-term efficacy 93% over a mean follow-up of nearly 53 months.^[7] For WPW patients who have survived sudden cardiac death, accessory-pathway ablation is the treatment of choice.^[10]
• Pharmacological prophylaxis is reserved for patients who decline or fail ablation: oral agents are chosen on safety profile and structural-heart status.
• Avoidance of triggers: caffeine, alcohol, nicotine, recreational stimulants; manage stress, anxiety, and sleep.

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Specific Subtypes & Scenarios

• Typical AVNRT (slow-fast) — the commonest regular supraventricular tachyarrhythmia.^[7] Pseudo R-prime in V1 and pseudo S waves in the inferior leads indicate AVNRT with very high accuracy.^[16] Vagal manoeuvres and adenosine terminate it reliably; definitive: slow-pathway catheter ablation (acute success 95%, long-term efficacy 93%).^[7]
• Orthodromic AVRT — narrow QRS; with a visible P wave, an RP interval of 100 ms or more favours AVRT over AVNRT.^[6] Treatment identical to AVNRT acutely; ablation of the accessory pathway is curative.
• Antidromic AVRT — broad QRS (all ventricles pre-excited); easily confused with ventricular tachycardia. Electrical cardioversion is the first-line treatment for pre-excited atrial fibrillation and antidromic AVRT.^[15] Ablation is definitive.
• Wolff-Parkinson-White syndrome with atrial fibrillation (pre-excited AF) — medical emergency. Never give AV-nodal blockers: blocking the AV node in pre-excited AF may increase the ventricular rate and has caused ventricular fibrillation.^[10] Treat with synchronised DC cardioversion^[15]; long-term: accessory-pathway ablation, the treatment of choice.^[10]
• Focal atrial tachycardia — discrete abnormal P waves; AV-node-independent — adenosine and verapamil had no effect on atrial tachycardia cycle length in 13 of 14 and 9 of 9 patients respectively, despite inducing second-degree AV block (a diagnostic clue).^[17] Acute: beta-blocker or verapamil. Long-term: catheter ablation of the focus.
• Multifocal atrial tachycardia (MAT) — a heart rate over 100 bpm with three or more different non-sinus P-wave morphologies in the same lead, irregular PP intervals, and an isoelectric baseline; typically seen with COPD. For most patients no treatment is required beyond treating the underlying condition.^[18]
• Permanent junctional reciprocating tachycardia (PJRT) — a concealed, slowly-conducting accessory pathway near the AV node causing an incessant long-RP tachycardia, often presenting in children/young adults with tachycardiomyopathy. Treatment: catheter ablation of the pathway, after which the cardiomyopathy reverses.
• Sinus node re-entrant tachycardia — sudden onset/offset unlike sinus tachycardia; terminates with vagal manoeuvres/adenosine. Often in structural heart disease.
• SVT with aberrancy vs VT — any broad-complex tachycardia (QRS over 120 ms) in a patient with structural heart disease is VT until proven otherwise. Do not give verapamil (haemodynamic collapse). If uncertain, treat as VT (amiodarone or DC cardioversion).^[16]

Complications & Pitfalls

Complications: ^[7]

• Syncope and falls — from transient cerebral hypoperfusion during episodes.
• Tachycardiomyopathy — reversible ventricular dysfunction from incessant SVT (focal atrial tachycardia, PJRT); resolves with rate control or ablation. The key teaching: always look for an incessant tachycardia in unexplained heart failure.^[16]
• Sudden cardiac death — rare; occurs in WPW when pre-excited AF degenerates to VF. This is the rationale for offering ablation to symptomatic and selected high-risk asymptomatic WPW patients.
• Thromboembolism — rare in pure re-entrant SVT (atria contract), but rises if SVT degenerates to AF (anticoagulate by CHA2DS2-VASc).
• Demand ischaemia / infarction — a rapid SVT in coronary disease can precipitate type-2 MI; do not reflexively cath-lab a patient whose ST changes resolve with termination.
• Psychological — anxiety, avoidance behaviour, and impaired quality of life from unpredictable episodes.

Classic pitfalls (examiner favourites): ^[7]

• Treating a broad-complex tachycardia as "SVT with aberrancy" and giving verapamil — in VT this causes haemodynamic collapse. Broad-complex = treat as VT unless you can prove otherwise.
• Giving adenosine to an asthmatic — can precipitate severe bronchospasm.
• Giving AV-nodal blockers in pre-excited AF (WPW) — accelerates the accessory pathway and precipitates VF.
• Forgetting the adenosine saline flush / arm raise — adenosine is metabolised in seconds; without a rapid flush it never reaches the heart in effective concentration, and is wrongly declared "ineffective."
• Misdiagnosing atrial flutter (2:1, 150 bpm) as SVT — adenosine will unmask the sawtooth waves; definitive treatment differs.
• Missing WPW on the sinus-rhythm ECG after termination — always look for the delta wave and short PR, which dictate long-term strategy.
• Ignoring incessant tachycardia in a patient with new heart failure.
• Not reducing the adenosine dose in a patient on dipyridamole is conventional teaching (profound asystole risk) — not verified from the papers fetched for this topic.

Prognosis & Disposition

SVT is, in the great majority of cases, a benign arrhythmia with an excellent prognosis. Most patients are otherwise structurally normal; quality-of-life impairment (rather than mortality) drives treatment decisions.^[7][16]

Disposition after an acute episode: ^[7]

• Terminated, stable, no red flags — can be discharged with ambulatory ECG monitoring, a clear safety-net, an outpatient ECG to look for WPW, and a cardiology referral to consider ablation.
• WPW pattern found — refer for cardiology / EPS and ablation (curative, eliminates sudden-death risk).
• Incessant SVT / tachycardiomyopathy — admit for rhythm/rate control and urgent ablation planning.
• Pre-excited AF / haemodynamic instability / failed cardioversion — admit (CCU/HDU), cardiology input.
• Inappropriate sinus tachycardia of uncertain cause — investigate and treat the underlying cause before discharge. ^[7]

Prognostic points: catheter ablation of AVNRT had 95% acute success and 93% long-term efficacy over a mean 53 months.^[7] Community WPW sudden death was 0.0015 per patient-year, with no SCD among patients asymptomatic at diagnosis.^[9] Pharmacological therapy controls but does not cure. After sudden-death survival in WPW, accessory-pathway ablation is the treatment of choice.^[10]

Special Populations

• Pregnancy — SVT is the most common tachyarrhythmia of pregnancy. For stable patients: vagal manoeuvres (carotid sinus massage or Valsalva), then adenosine (first-line in the first trimester; half-life about 10 seconds) or beta-blockers (propranolol, metoprolol). Atenolol and verapamil are contraindicated in the first trimester (atenolol: intrauterine growth restriction; verapamil: fetal arrhythmias/heart block) but may be used in the second and third trimesters. Synchronised cardioversion is safe in any trimester if drugs fail or the patient is unstable.^[13]
• Children — adenosine administration is the recommended treatment for paediatric acute SVT, dosed at 0.1 mg/kg; note that delivery through a stopcock under-doses infants under 10 kg (mean delivered 0.08 mg/kg), which may explain failed first doses.^[14]
• Elderly — atypical presentations (syncope, falls, dyspnoea, heart failure); atrial tachycardia and AF proportionally more common. Auscultate for carotid bruits before carotid sinus massage (embolic risk); consider modified Valsalva first. Lower starting doses of adenosine/verapamil; beware polypharmacy (digoxin toxicity -> atrial tachycardia with block).
• Asthma / severe COPD — adenosine caused bronchoconstriction in both asthmatics of a 26-patient series; consider alternatives (verapamil). Modified Valsalva is safe.^[11]
• Heart-transplant patients — denervation hypersensitivity to adenosine is conventional teaching (reduce the dose or use verapamil); a numeric starting dose was not verified from the papers fetched here.
• Patients on dipyridamole or theophylline — dose-interaction rules are conventional teaching and were not verified from the papers fetched here.
• Structural heart disease — intra-atrial re-entrant tachycardia is often associated with structural disease and atrial enlargement (17 of 19); left ventricular dysfunction is not required.^[17]

Evidence, Guidelines & Regional Differences

Landmark trials and guidance: ^[7]

• REVERT trial (Appelboam et al., Lancet 2015)^[2] — the modified Valsalva (semi-recumbent strain + immediate supine repositioning with passive leg raise) returned 43% vs 17% to sinus rhythm — it should be considered a routine first treatment. Chen et al., 2020^[3] conducted a further multicentre randomised trial of a modified Valsalva in a Chinese population (numeric results not in the PubMed abstract).

• Dose-ranging adenosine trials (DiMarco et al., Ann Intern Med 1990)^[1] — established the 6 mg then 12 mg adenosine escalation and the similar efficacy of verapamil 5 mg then 7.5 mg.

• Population and registry data (Orejarena 1998; Munger 1993; Allam 2025)^[8][9][15] — PSVT prevalence 2.25/1000 persons with incidence 35/100,000 person-years; the community natural history of WPW; and contemporary registry management of pre-excitation.

• Asymptomatic WPW (community data)^[9] — sudden cardiac death occurred at 0.0015 per patient-year, with no SCD among patients asymptomatic at diagnosis, arguing against routine electrophysiological testing in asymptomatic patients.

• Symptomatic WPW (registry practice)^[15] — in a 17-country registry, radiofrequency ablation was the first long-term therapy option for 88% of patients.

• India (tertiary practice) — adenosine availability and cardiac monitoring are universal in tertiary centres; in resource-limited settings vagal manoeuvres are emphasised as zero-cost first steps.

• Controversies: (1) management of asymptomatic WPW — conservative community data vs registry ablation practice; (2) the safety of adenosine in mild/moderate COPD vs asthma, where bronchoconstriction has been reported.^[11]

Exam Pearls

• Regular narrow-complex (QRS under 0.12 s) tachycardia = SVT until proven otherwise.^[16]
• Abrupt onset and abrupt offset + polyuria after termination — urine flow rose from 3.2 to 7.6 mL/min with a rise in atrial natriuretic peptide during induced SVT.^[4]
• Pseudo R-prime in V1 / pseudo S in inferior leads = AVNRT (with pseudo R-prime in lead aVR an even more accurate newer sign).^[5][6]
• RP interval at or under 90 ms favours AVNRT; a visible P wave with RP of 100 ms or more favours AVRT.^[5][6]
• Modified Valsalva first (semi-recumbent 40 mm Hg 15 s strain, then immediate supine repositioning with passive leg raise — 43% vs 17%) — then rapid IV adenosine 6 mg, then 12 mg if necessary.^[2][1]
• Adenosine: adverse effects in 36% of patients, under 1 minute, usually mild; caution in asthma (bronchoconstriction reported).^[1][11]
• Verapamil 5 mg (then 7.5 mg if needed) IV — similar efficacy to adenosine, slower onset.^[1]
• Haemodynamic compromise in SVT = synchronised DC cardioversion, not adenosine.^[12]
• WPW with pre-excited AF is an emergency: AV-nodal blockers can increase the ventricular rate and precipitate VF — use DC cardioversion, then ablation.^[10][15]
• WPW on sinus-rhythm ECG: short PR, delta wave, prolonged QRS — the classical triad.^[16]
• AVNRT is the commonest regular supraventricular tachyarrhythmia; AVNRT patients are more often female and older than AVRT patients (71% female, 175 vs 186 bpm in one series).^[7][6]
• Catheter ablation of AVNRT: 95% acute success, 93% long-term efficacy — curative.^[7]

Exam application bank (NEET-PG / INICET)

One-line answer

SVT is a rapid tachycardia originating at or above the AV node with a narrow QRS (under 0.12 s).^[16] AVNRT is the commonest regular supraventricular tachyarrhythmia.^[7] Induced SVT raised urine flow from 3.2 to 7.6 mL/min with a rise in ANP.^[4] If unstable — synchronised DC cardioversion;^[12] if stable — modified Valsalva (43% vs 17%), then IV adenosine 6 mg then 12 mg if necessary (57.4% then 93.4%).^[2][1] Verapamil 5 mg then 7.5 mg has similar efficacy, slower onset.^[1] WPW pre-excited AF: no AV-nodal blockers — electrical cardioversion, then ablation.^[10][15]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard. ^[7]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. ^[7]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. ^[7]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. ^[7]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory. ^[7]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Supraventricular Tachycardia.

The mantra, and the ward-round test

The mantra: narrow and regular is SVT until proven otherwise — Valsalva, then adenosine, then shock; but the moment the pathway is pre-excited, the blockers go away.^[7][16]

Ward-round test — three stems, thirty seconds each