Supraventricular tachycardia

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

SVT generally arises above the ventricles, but the clinically useful acute split is regular versus irregular and narrow versus broad. The label should never overrule haemodynamic state.

The March 2026 RCUK algorithm is the current UK peri-arrest source. Its adenosine sequence differs from several UK product licences, so local resuscitation and medicines governance must explicitly support the regimen being used.

Long-term therapy is mechanism- and patient-specific: episodic AVNRT, AVRT, focal atrial tachycardia and flutter do not share one rigid drug ladder.

Key points

SVT is a mechanism group, not one ECG diagnosis: common regular narrow-complex causes are AVNRT, orthodromic AVRT, atrial tachycardia and flutter with fixed conduction.
An abrupt-onset, very regular narrow tachycardia with hidden or retrograde P waves suggests AVNRT/AVRT, but obtain a 12-lead during symptoms whenever this does not delay emergency care.
Classify first by stability, QRS width below or at least 120 ms, and regularity.
Stable regular narrow SVT: modified Valsalva is a good first manoeuvre; avoid carotid massage when carotid disease/bruit or prior TIA/stroke makes it unsafe.
Current RCUK 2026 adenosine regimen is 6 mg, then 12 mg, then 18 mg as rapid IV boluses if unsuccessful and if there is no pre-excitation.
Important UK discrepancy: several current adenosine SmPCs license 3 mg, then 6 mg after 1-2 minutes, then 12 mg after another 1-2 minutes and state that higher doses are not recommended.
Adenosine may terminate AV-node-dependent SVT or transiently expose flutter/atrial tachycardia; record continuous/multilead ECG through each dose.
Treat an undifferentiated regular broad-complex tachycardia as VT. Adenosine is considered only for regular monomorphic suspected SVT with aberrancy and no pre-excitation.
Irregular broad pre-excited AF is a cardioversion/procainamide problem, not an adenosine, verapamil, beta-blocker or digoxin problem.
Recurrent symptomatic AVNRT/AVRT merits electrophysiology discussion; catheter ablation is potentially curative.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

AV nodal re-entry

Dual pathways within or near the atrioventricular node permit a premature atrial impulse to circulate repeatedly. This commonly produces AVNRT in people without demonstrable structural heart disease.

Accessory-pathway re-entry

A congenital atrioventricular connection can complete a circuit with the normal conduction system. Orthodromic AVRT is usually narrow, while antegrade accessory-pathway conduction may broaden the QRS.

Atrial tachycardia or flutter

A focal atrial source or an atrial re-entry circuit may drive the ventricles rapidly. Structural atrial disease, previous cardiac procedures and atrial enlargement make these mechanisms more likely.

Reversible precipitants

Acute illness, adrenergic stimulation, stimulants, thyroid disturbance or electrolyte imbalance can increase atrial ectopy and conduction, exposing a susceptible re-entry circuit or automatic focus.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Susceptible circuit or focus
An AV nodal pathway, accessory connection or abnormal atrial focus provides the substrate for rapid activation arising above the ventricular myocardium.
2
Initiating impulse
A premature atrial or ventricular impulse may encounter conduction tissue with differing refractory periods, allowing unidirectional block and slow conduction into a potential re-entry loop.
3
Sustained rapid activation
In re-entry, the returning impulse repeatedly re-excites recovered tissue, usually producing abrupt, very regular tachycardia. An automatic atrial focus may instead accelerate more gradually and show some rate variation.
4
Ventricular conduction pattern
Normal His–Purkinje activation produces a narrow QRS. Rate-related bundle-branch block or antegrade accessory-pathway conduction broadens it, creating an important mimic of ventricular tachycardia.
5
Haemodynamic effect
Shortened diastole reduces ventricular filling and coronary perfusion. Very rapid or prolonged episodes can therefore cause hypotension, ischaemia, pulmonary congestion or transient loss of consciousness.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Regular narrow-complex tachycardia

QRS below 120 ms and highly regular. Abrupt onset/offset favours re-entry. P waves may be absent within QRS, appear just after QRS (retrograde), or precede QRS in atrial tachycardia; 2:1 flutter near 150/min is an important mimic.

Life-threatening adverse featuresRed flag

Shock, syncope with severe/ongoing hypotension, myocardial ischaemia, severe heart failure with pulmonary oedema, or immediately post-ROSC.

Regular broad-complex tachycardiaRed flag

Assume VT unless an expert/known prior ECG securely establishes SVT with aberrancy. AV dissociation, capture/fusion beats or extreme axis support VT but their absence does not prove SVT.

Irregular broad-complex tachycardiaRed flag

Consider pre-excited AF or polymorphic VT. Varying QRS shape with very short R-R intervals in WPW is particularly dangerous; avoid AV-nodal blockers.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
ABCDE, ECG/BP/SpO2 monitoring, IV access and defibrillator availabilityFirst step
Why
Identify instability and make deterioration immediately treatable.
Interpretation and limitations
Do not delay synchronised cardioversion for a full diagnostic work-up when adverse features are due to the tachyarrhythmia.
02
12-lead ECG during tachycardia and after termination
Why
Classify width/regularity, P-QRS relation and possible accessory pathway; compare baseline PR/QRS/ST-T after conversion.
Interpretation and limitations
A short PR and delta wave in sinus rhythm supports pre-excitation; adenosine-induced transient AV block can reveal continuing flutter or atrial tachycardia.
03
Focused trigger/structural history and prior ECGs
Why
Assess abruptness, previous identical episodes, syncope, congenital/structural disease, family sudden death, pregnancy, stimulant/recreational drugs and medication interactions.
Interpretation and limitations
A known identical SVT with documented aberrancy may follow the narrow-complex branch; uncertainty should default to VT-safe management.
04
U&E/creatinine, potassium, magnesium, calcium, glucose; FBC/TFT/troponin when clinically indicated
Why
Find reversible triggers and establish safe antiarrhythmic prescribing.
Interpretation and limitations
Troponin can rise from tachycardia itself; interpret it with symptoms, serial change and ECG rather than diagnosing ACS from an isolated value.
05
Echocardiography
Why
Assess structural disease/LV function after a first significant presentation, broad tachycardia, heart failure signs or abnormal baseline ECG.
Interpretation and limitations
Structural disease changes the safety of drug therapy and lowers the threshold for specialist inpatient review.
06
Ambulatory ECG or patient-activated recording
Why
Capture intermittent symptoms when ED/clinic ECG is normal.
Interpretation and limitations
Choose duration by symptom frequency and insist on symptom-rhythm correlation before labelling recurrent palpitations as SVT.
07
Electrophysiology assessment
Why
Define mechanism and offer ablation for recurrent, poorly tolerated or high-risk accessory-pathway tachycardia.
Interpretation and limitations
Ablation decisions depend on mechanism, burden, occupation, preference and procedural risk, not simply episode count.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Sinus tachycardia

The rate usually changes gradually with fever, pain, hypovolaemia or anxiety, and each QRS is preceded by a normal sinus P wave rather than abrupt re-entry.

Atrial flutter

Fixed atrioventricular conduction can look like regular SVT. Flutter waves, a ventricular rate near half the atrial rate, or continuing atrial activity during transient AV block discriminate it.

Atrial fibrillation

Beat-to-beat RR variability and absent organised P waves favour atrial fibrillation. Apparent regularity on a short rhythm strip should be checked on a longer tracing.

Ventricular tachycardia

A regular broad-complex rhythm, especially with structural disease, is ventricular tachycardia until securely shown otherwise. AV dissociation or capture and fusion beats support the diagnosis.

Pre-excited atrial fibrillation

An irregular broad rhythm with rapidly changing QRS morphology suggests atrial fibrillation conducted through an accessory pathway, rather than regular AVRT, and carries a distinct acute risk.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01UnstableTachyarrhythmia with life-threatening featuresFirst stepAdverse features attributable to SVT/tachyarrhythmia.

1Call expert/resuscitation help, attach pads, treat reversible causes and prepare careful sedation/anaesthesia if conscious without delaying shock.
2Deliver synchronised cardioversion: RCUK initial 70-120 J for atrial flutter or paroxysmal SVT, with stepwise energy increases and up to three attempts.
3If unsuccessful and instability persists, the RCUK pathway uses either procainamide 10–15 mg/kg IV (maximum 1 g) over 20 minutes or amiodarone 300 mg IV over 10–20 minutes, selected for rhythm, contraindications and product availability; then repeat synchronised cardioversion.
4If the patient becomes pulseless, switch immediately to the cardiac-arrest algorithm; do not continue synchronised shocks.

02Stable narrow regularVagal manoeuvre then adenosineRegular QRS below 120 ms without life-threatening features and no evidence of pre-excitation.

1Record a 12-lead and start a continuous rhythm strip. Perform a modified Valsalva if safe: semi-recumbent 40 mmHg strain for 15 seconds, immediately lie flat and passively raise legs to 45 degrees for 15 seconds, then return semi-recumbent and assess at 1 minute; the REVERT trial permitted a repeat attempt.
2If unsuccessful, follow the current RCUK algorithm: adenosine 6 mg rapid IV bolus with immediate flush; if unsuccessful give 12 mg; if still unsuccessful give 18 mg. Warn the patient about brief flushing, chest discomfort and dyspnoea and record ECG through each dose.
3Use the current RCUK 6–12–18 mg sequence as the national peri-arrest algorithm. The cited UK SmPC instead licenses 3 mg over 2 seconds, then 6 mg after 1–2 minutes, then 12 mg after another 1–2 minutes and says no higher dose; the RCUK 18 mg step is therefore outside that product label and must be reconciled through organisational medicines governance.
4If adenosine is contraindicated or fails, seek expert help and choose verapamil OR a beta-blocker according to EF, BP, conduction, airway disease, interacting drugs and diagnostic certainty; these are conditional alternatives, not an automatic sequence.
5If drug therapy fails or the patient deteriorates, use synchronised cardioversion.

03Broad or irregularProtect against VT and pre-excited AFQRS at least 120 ms or irregular tachycardia.

1Regular broad tachycardia: treat as VT. If SVT with aberrancy is suspected, RCUK permits IV adenosine only when regular/monomorphic and there is no pre-excitation; if ineffective, revert to the VT pathway.
2Known, previously documented SVT with the same aberrancy can be treated like regular narrow SVT with expert oversight.
3Irregular narrow tachycardia is commonly AF/flutter with variable block and belongs in the AF pathway; do not use adenosine to cardiovert AF/flutter.
4Irregular broad pre-excited AF: urgent expert help; use cardioversion when unstable or procainamide when appropriate/available. Avoid adenosine, beta-blockers, verapamil/diltiazem and digoxin.
5Polymorphic broad tachycardia with long QT belongs in the ventricular-arrhythmia/torsades pathway.

04AftercareDocument mechanism and prevent recurrenceSinus rhythm restored or recurrent symptomatic episodes.

1Save the pre-, during- and post-treatment ECGs; document which manoeuvre/drug worked and any adverse effects.
2Correct triggers and arrange cardiology/electrophysiology follow-up after a first concerning episode, recurrent symptoms, syncope, broad tachycardia or pre-excitation.
3Discuss catheter ablation for recurrent symptomatic AVNRT/AVRT or a high-risk accessory pathway; long-term drug suppression is conditional on mechanism and patient preference.
4Give safety-netting for chest pain, syncope, breathlessness or prolonged recurrence; driving/occupational advice is diagnosis- and symptom-specific.

Key medicines and prescribing safety6 treatments · regimens, roles and cautions

Therapeutic and diagnostic treatment of stable regular narrow SVT without pre-excitation; selected regular monomorphic broad tachycardia only when SVT with aberrancy is suspected.

Adenosine—RCUK March 2026 algorithm regimen

6 mg rapid IV bolus with an immediate rapid saline flush; if unsuccessful, 12 mg rapid IV; if still unsuccessful, 18 mg rapid IV. RCUK does not mandate a fixed inter-dose interval on the algorithm: assess the immediate response and maintain continuous ECG.

Use in hospital with continuous ECG/BP and cardiorespiratory resuscitation equipment. Do not use for irregular broad tachycardia/pre-excited AF. Avoid in sick-sinus or second/third-degree AV block without a pacemaker, bronchospastic asthma/COPD, severe hypotension, decompensated heart failure and long-QT syndrome. Heart transplant/dipyridamole heighten effect; caffeine/theophylline antagonise it. The 18 mg step exceeds the cited UK SmPC maximum.

Licensed reference for the cited product, shown to make the discrepancy with the current RCUK national algorithm explicit—not as a co-equal default pathway.

Adenosine—product-label comparison

3 mg rapid IV bolus over 2 seconds; if SVT persists after 1-2 minutes, 6 mg rapid IV; if it persists after a further 1-2 minutes, 12 mg rapid IV. The cited SmPC says additional or higher doses are not recommended.

The current RCUK 6–12–18 mg sequence remains the national peri-arrest algorithm. State the chosen preparation and authority explicitly, and resolve the out-of-label 18 mg step through organisational medicines governance.

Conditional alternative after vagal manoeuvres and adenosine fail or adenosine is contraindicated in a stable, confidently narrow SVT.

Verapamil IV

5-10 mg slow IV over at least 2 minutes under continuous ECG/BP monitoring; if needed, a further 5 mg after 5-10 minutes.

Avoid haemodynamic instability, EF below 40%/pulmonary congestion, broad-complex tachycardia, pre-excited AF, significant AV block/sick sinus without pacing, and IV beta-blocker co-administration.

Conditional alternative for stable narrow tachycardia when adenosine is unsuitable/ineffective and verapamil is not chosen.

Atenolol IV (one licensed beta-blocker option)

2.5 mg IV over 2.5 minutes; repeat at 5-minute intervals to response, maximum 10 mg. Alternative infusion 0.15 mg/kg over 20 minutes.

Avoid hypotension, bradycardia/high-grade block, acute decompensated heart failure and severe bronchospasm; do not combine with IV verapamil. Renal clearance requires dose consideration.

RCUK option after unsuccessful shocks in persistent unstable tachyarrhythmia, stable VT or pre-excited AF under expert care.

Procainamide IV

10-15 mg/kg IV over 20 minutes, maximum 1 g.

UK product availability varies. Use continuous ECG/BP monitoring; avoid or stop for marked hypotension, QRS prolongation, long QT or decompensated heart failure, and verify the available preparation before administration.

Conditional rescue after unsuccessful cardioversion; not routine treatment of stable regular narrow SVT.

Amiodarone IV

RCUK rescue after failed shocks: 300 mg IV over 10-20 minutes, followed when appropriate by 900 mg over 24 hours.

Monitor ECG/BP; can cause hypotension, bradycardia and QT prolongation. Avoid in torsades/long-QT polymorphic VT and use specialist oversight in thyroid/lung/liver disease.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Haemodynamic collapse

Extreme rate and abbreviated filling can sharply reduce cardiac output, producing hypotension, syncope or shock, particularly when ventricular function or valve reserve is already impaired.

Myocardial ischaemia and congestion

Increased oxygen demand combined with shortened coronary perfusion can cause chest pain or a troponin rise, while raised filling pressures may precipitate pulmonary oedema.

Tachycardia-induced cardiomyopathy

Frequent or incessant supraventricular tachycardia can progressively impair ventricular function. Recognising the rhythm mechanism matters because function may improve after durable rhythm control.

Recurrent syncope and injury

Abrupt recurrences may cause presyncope or loss of consciousness without warning, creating driving, occupational and trauma risks even when ventricular function is otherwise normal.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Continuous ECG and BP during IV adenosine, verapamil, beta-blocker, procainamide or amiodarone; defibrillation/pacing capability immediately available.
Record a multilead rhythm strip during adenosine because transient AV block may reveal flutter or atrial tachycardia even when it does not terminate the rhythm.
After conversion, repeat a 12-lead for pre-excitation, QT, conduction disease and ischaemia; check potassium/magnesium and address the trigger.
During procainamide monitor QRS, QT and BP; during amiodarone monitor QT/bradycardia and infusion-site/BP effects.
For recurrent symptoms, obtain objective rhythm correlation and assess LV function rather than escalating empirical drugs indefinitely.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Adenosine can diagnose without curing

A brief AV block that exposes continuing atrial activity suggests flutter or atrial tachycardia. Do not keep escalating adenosine when the mechanism is no longer AV-node dependent.

The RCUK/SmPC dose mismatch is real

The current resuscitation algorithm starts at 6 mg and reaches 18 mg; the cited UK SmPC starts at 3 mg and stops at 12 mg. A textbook should not silently merge them.

Modified Valsalva has primary UK trial evidence

REVERT used a 15-second, 40-mmHg strain followed by supine repositioning and 45-degree leg raise; 43% versus 17% were in sinus rhythm at one minute, with no serious adverse events.

Broad-complex certainty is asymmetric

Missing classic VT signs does not establish SVT. The harm from treating VT as SVT can be greater than treating uncertain regular broad tachycardia as VT.

Ablation is not merely a last drug step

For recurrent symptomatic AVNRT/AVRT, a mechanism-specific ablation discussion may be preferable to indefinite drug escalation, especially in younger people or high-risk occupations.

11Common pitfallsFrequent interpretation and management errors.

01
Calling every narrow tachycardia 'SVT' without checking regularity and atrial activity.
02
Giving serial drugs to an unstable patient instead of synchronised cardioversion.
03
Giving adenosine to irregular broad pre-excited AF or polymorphic VT.
04
Using verapamil in an undifferentiated broad-complex tachycardia or with IV beta-blockade.
05
Presenting 18 mg adenosine as universally licensed UK dosing without the SmPC discrepancy.
06
Failing to capture/save the tachycardia ECG before successful termination.