Broad-complex tachycardia

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

Broad-complex tachycardia is a high-risk ECG phenotype rather than one diagnosis. The major possibilities are VT, SVT with bundle-branch aberrancy or pre-excitation, pre-excited AF and polymorphic ventricular tachycardia.

Stability determines the first action. Do not spend time applying a complex ECG algorithm to a patient with shock or pulmonary oedema; prepare synchronised cardioversion while correcting immediately reversible causes.

The March 2026 RCUK algorithm favours cardioversion for regular broad tachycardia and narrows drug treatment to circumstances where sedation/anaesthesia risk is high, with procainamide preferred and amiodarone conditional.

Key points

A tachycardia with QRS duration 120 ms or more is broad complex; sustained regular broad tachycardia should be treated as VT when uncertain.
Structural heart disease, previous myocardial infarction and older age increase the prior probability of VT.
AV dissociation, capture beats, fusion beats and precordial concordance strongly support VT, but their absence does not exclude it.
Unstable VT with a pulse: synchronised 120-150 J shock, escalating if needed; pulseless VT: unsynchronised defibrillation under ALS.
Current RCUK also recommends electrical cardioversion for stable monomorphic VT with structural heart disease or uncertain myocardial status.
If sedation or anaesthesia is judged unusually hazardous in stable monomorphic VT, IV procainamide is the drug option; IV amiodarone is the alternative when procainamide is unavailable or contraindicated.
An irregular broad rhythm may be pre-excited AF or polymorphic VT; AV nodal blockers can be dangerous in the former and amiodarone should be avoided in torsades.
Adenosine is reserved for a regular broad rhythm suspected to be SVT with aberrancy; if it fails, treat as VT.

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

Scar-related ventricular tachycardia

Previous myocardial infarction or other structural heart disease creates electrically heterogeneous scar around which a re-entry circuit can form. This is a common substrate for sustained regular monomorphic ventricular tachycardia.

Acute myocardial and metabolic stress

Acute ischaemia, hypoxia, acid–base disturbance and abnormalities of potassium, magnesium or calcium alter ventricular conduction and excitability, precipitating monomorphic or polymorphic ventricular rhythms.

Medicines, toxins and prolonged repolarisation

QT-prolonging medicines, sodium-channel blockers, digoxin toxicity and stimulants can create broad tachyarrhythmias through different electrical mechanisms. A careful exposure history directs cause-specific treatment beyond the generic algorithm.

Supraventricular activation with broad conduction

A supraventricular tachycardia may appear broad when conducted through bundle-branch block or an accessory pathway. Pre-excited atrial fibrillation may produce an especially irregular, variable broad rhythm.

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

1
Ventricular re-entry
Slow conduction through or around myocardial scar permits an electrical wavefront to circulate repeatedly. Activation begins in ventricular myocardium rather than the specialised conduction system, producing broad, often uniform complexes.
2
Triggered or unstable ventricular activity
Ischaemia, metabolic disturbance or abnormal repolarisation can generate premature ventricular activity and changing activation pathways. Beat-to-beat variation in QRS morphology during ventricular tachycardia defines a polymorphic pattern; twisting around the baseline suggests torsades when repolarisation is prolonged.
3
Abnormal supraventricular conduction
An atrial or junctional tachycardia remains supraventricular but reaches the ventricles through bundle-branch aberrancy or an accessory pathway. The resulting depolarisation is broad despite a different origin.
4
Haemodynamic compromise
Rapid ventricular activation shortens filling time and may abolish coordinated atrial contribution. Stroke volume, coronary perfusion and cardiac output fall, especially when ventricular function is already impaired.
5
Electrical degeneration
Persistent ventricular tachycardia may become more disorganised and deteriorate into ventricular fibrillation. Loss of effective contraction then converts a perfusing tachycardia into cardiac arrest.

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

VT until proven otherwise

A regular broad-complex tachycardia in an adult, especially with structural heart disease or prior infarction, should be managed as VT if doubt remains.

AV dissociation

Atrial activity marching independently from ventricular complexes indicates separate atrial and ventricular rhythms and strongly favours VT.

Capture and fusion

A capture beat is a near-normal QRS produced when a sinus impulse reaches the ventricle; a fusion beat is a hybrid of sinus and ventricular activation. Both support VT.

Concordance or extreme axis

All precordial QRS complexes in one direction, an extreme axis or morphology incompatible with typical bundle-branch block raises the probability of VT.

Irregular broad rhythmRed flag

Consider pre-excited AF, AF with bundle-branch block, frequent ventricular ectopy and polymorphic VT; inspect QT and beat-to-beat QRS morphology before giving drugs.

Life-threatening featuresRed flag

Shock, syncope with severe or ongoing hypotension, myocardial ischaemia, severe pulmonary oedema or immediately post-ROSC triggers the unstable route.

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
Continuous monitoring and 12-lead ECGFirst step
Why
Define regularity, QRS morphology and adverse evolution while preserving a diagnostic tracing.
Interpretation and limitations
Do not delay shock for a 12-lead in instability; capture one before conversion only if immediately available.
02
Previous ECG
Why
Compare baseline bundle-branch block, pre-excitation and QRS morphology.
Interpretation and limitations
An identical baseline bundle pattern supports SVT with aberrancy but does not by itself exclude VT.
03
U&Es, magnesium, calcium and blood gas
Why
Find potassium, magnesium, calcium, pH and oxygen abnormalities.
Interpretation and limitations
Correct abnormalities promptly, particularly with polymorphic VT or drug toxicity.
04
Troponin and ischaemia assessment
Why
Evaluate acute coronary syndrome when clinically suspected.
Interpretation and limitations
Tachycardia itself can elevate troponin; interpret dynamically with symptoms, ECG and coronary context.
05
Bedside echo after immediate stabilisation
Why
Assess ventricular function, gross structural disease and complications.
Interpretation and limitations
Structural disease strengthens the VT diagnosis and informs cardioversion, antiarrhythmic and longer-term ICD decisions.
06
Drug and toxicology review
Why
Identify digoxin toxicity, sodium-channel blockers, QT-prolonging drugs or stimulants.
Interpretation and limitations
The toxic mechanism may require specific antidotal treatment beyond the generic tachycardia algorithm.

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

Monomorphic ventricular tachycardia

A regular broad rhythm with atrioventricular dissociation, capture or fusion beats, precordial concordance or an extreme axis strongly supports ventricular tachycardia. Structural disease further raises its prior probability.

SVT with bundle-branch aberrancy

A regular tachycardia matching a documented baseline bundle-branch pattern supports supraventricular tachycardia with aberrancy. This comparison is helpful but does not safely exclude ventricular tachycardia when uncertainty remains.

Atrial fibrillation with aberrancy

An irregularly irregular ventricular response with a consistent bundle-branch morphology suggests atrial fibrillation with aberrant conduction. Marked beat-to-beat variation in QRS width or morphology, particularly with very short RR intervals, raises concern for pre-excitation but is not diagnostic on its own.

Pre-excited atrial fibrillation

A very irregular broad rhythm with changing QRS width and morphology suggests conduction through an accessory pathway. Atrioventricular-nodal blockers may increase ventricular conduction through the accessory pathway and should be avoided when this is suspected.

Polymorphic ventricular tachycardia

A continuously changing QRS axis and morphology during a rapid ventricular rhythm suggest polymorphic ventricular tachycardia. Reviewing the preceding QT interval, medicines and electrolytes helps identify torsades physiology and avoid inappropriate antiarrhythmic treatment.

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

01pulselessPulseless broad tachycardiaFirst stepNo signs of life or definite pulse.

1Call the cardiac-arrest team, start high-quality CPR and attach a defibrillator.
2Treat VF/pulseless VT with unsynchronised shocks under the 2025 RCUK ALS algorithm, resuming CPR immediately after each shock.
3Give adrenaline and amiodarone at the shock points specified by ALS and treat reversible causes.
4After ROSC, obtain a 12-lead ECG and investigate the precipitant and secondary-prevention needs.

02unstable-pulseBroad tachycardia with a pulse and adverse featuresShock, severe hypotensive syncope, myocardial ischaemia, pulmonary oedema or post-ROSC state.

1Perform ABCDE assessment, attach pads, obtain IV access and call expert/anaesthetic help.
2Use carefully titrated sedation or anaesthesia in a conscious patient if it does not delay life-saving treatment.
3EscalationDeliver synchronised cardioversion at 120-150 J, escalating stepwise and re-enabling synchronisation before each shock.
4After up to three unsuccessful shocks, give procainamide 10-15 mg/kg IV over 20 minutes (maximum 1 g) or amiodarone 300 mg IV over 10-20 minutes, then repeat the synchronised shock.

03stable-regularStable regular broad-complex tachycardiaA pulse is present and no life-threatening adverse feature is identified.

1Seek expert help, treat as VT and favour synchronised cardioversion when structural heart disease is present or myocardial status is uncertain.
2If sedation/anaesthesia risk is too high, give procainamide 10-15 mg/kg IV over 20 minutes with continuous ECG and blood pressure monitoring.
3If procainamide is unavailable or contraindicated, give amiodarone 300 mg IV over 10-60 minutes, followed by 900 mg IV over 24 hours.
4If a regular SVT with aberrancy is genuinely suspected, monitored rapid-bolus adenosine may be tried; if ineffective, revert immediately to the VT route.

04irregularIrregular broad-complex tachycardiaQRS complexes or RR intervals vary beat to beat.

1Assess for instability and cardiovert immediately when adverse features are present.
2If QT is prolonged and the rhythm is polymorphic, give magnesium 8 mmol IV over 10 minutes, stop QT-prolonging drugs, correct electrolytes and consider isoprenaline or temporary pacing to raise heart rate; avoid amiodarone.
3If pre-excited AF is suspected, use procainamide or cardioversion and avoid AV nodal blockers and amiodarone.
4If AF with fixed bundle-branch block is confirmed, manage AF according to ventricular function, duration and stroke risk rather than applying the regular-VT drug pathway.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

RCUK first drug option for stable monomorphic VT when cardioversion sedation/anaesthesia risk is high; also an option after failed shocks in persistent instability and for stable pre-excited AF.

Procainamide

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

Continuous ECG and blood-pressure monitoring; slow or stop for hypotension, marked QRS widening or QT prolongation.

Conditional alternative when procainamide is unavailable or contraindicated.

Amiodarone

RCUK stable broad-tachycardia alternative: 300 mg IV over 10-60 minutes then 900 mg IV over 24 hours; after failed cardioversion in an unstable patient, 300 mg IV over 10-20 minutes before another shock.

Avoid in torsades/long-QT polymorphic VT and pre-excited AF. The eMC general SmPC regimen is different: 5 mg/kg over 20 minutes to 2 hours, up to 1200 mg/24 h; the RCUK doses above are the peri-arrest algorithm doses.

Only a regular broad tachycardia thought to be SVT with aberrancy, with defibrillation capability immediately available.

Adenosine

6 mg rapid IV bolus, then 12 mg, then 18 mg if required under the March 2026 RCUK sequence. This algorithm-specific sequence differs from the cited product SmPC's licensed 3 mg, 6 mg, then 12 mg sequence.

Do not use for irregular broad tachycardia or suspected pre-excited AF; if ineffective, treat as VT. The cited UK SmPC contraindicates bronchospastic chronic lung disease including asthma, long-QT syndrome, severe hypotension, decompensated heart failure, and sick-sinus or second-/third-degree AV block without a functioning pacemaker. Avoid concurrent dipyridamole unless an expert-adjusted strategy is essential.

Polymorphic VT with QT prolongation (torsades de pointes).

Magnesium sulfate

8 mmol IV over 10 minutes under the RCUK tachyarrhythmia algorithm.

Monitor blood pressure, respiration and renal function; do not substitute amiodarone in torsades.

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

Hypotension and syncope

Reduced filling and ineffective ventricular contraction lower cardiac output. Cerebral hypoperfusion causes presyncope or syncope, while persistent hypotension indicates an unstable rhythm requiring prompt electrical treatment.

Myocardial ischaemia

Tachycardia increases oxygen demand while reducing diastolic coronary perfusion. Chest pain and ischaemic ECG change may follow, and the resulting myocardial stress can further sustain ventricular arrhythmia.

Acute heart failure

Rapid uncoordinated ventricular activation raises filling pressures and reduces forward flow. Pulmonary oedema is a life-threatening feature and may develop particularly quickly in people with structural ventricular disease.

Ventricular fibrillation and arrest

Ventricular tachycardia can deteriorate into chaotic ventricular fibrillation or lose its pulse despite organised electrical activity. The treatment pathway then changes immediately from synchronised cardioversion to cardiac-arrest defibrillation.

Treatment-related deterioration

Misclassifying ventricular tachycardia or an irregular pre-excited rhythm can expose the patient to unsuitable atrioventricular nodal or antiarrhythmic drugs, worsening instability or delaying cardioversion.

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

Continuous ECG, blood pressure, oxygen saturation and consciousness during acute treatment.
Confirm synchronisation markers before every cardioversion shock and record delivered energy and response.
During procainamide, watch QRS, QT and blood pressure; during amiodarone infusion, watch for hypotension, bradycardia and QT effects.
Repeat potassium, magnesium, calcium and acid-base assessment after correction.
After conversion, monitor for recurrence and obtain echocardiography and specialist arrhythmia assessment before discharge.

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

Treat probability, not certainty

Mis-treating VT as SVT can be catastrophic; treating an uncertain regular broad tachycardia as VT is the safer asymmetry.

Synchronised is not defibrillation

With a pulse, synchronisation avoids delivering energy on the T wave. Pulseless VT requires unsynchronised defibrillation.

Capture beats are highly useful

A single relatively narrow complex amid broad tachycardia may represent sinus capture and strongly supports AV dissociation and VT.

Current RCUK favours electricity

Even stable monomorphic VT is cardioverted when structural heart disease exists or myocardial damage is uncertain; drugs are an alternative when sedation/anaesthesia risk is high.

Irregular changes the drug rules

Before giving adenosine or amiodarone, exclude pre-excited AF and torsades because both require different treatment.

RCUK and SmPC doses answer different contexts

Use the resuscitation algorithm for peri-arrest arrhythmia; cite the product SmPC regimen when prescribing amiodarone outside that algorithm.

11Common pitfallsFrequent interpretation and management errors.

01
Delaying cardioversion in an unstable patient while seeking a perfect ECG diagnosis.
02
Giving verapamil to an undifferentiated broad-complex tachycardia.
03
Using adenosine for an irregular broad rhythm.
04
Giving amiodarone to torsades or pre-excited AF.
05
Forgetting to re-enable synchronisation before a repeat shock.