Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Treat broad-complex tachycardia safely as ventricular tachycardia unless a more secure diagnosis supports a specific alternative.
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.
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 ischaemia, hypoxia, acid–base disturbance and abnormalities of potassium, magnesium or calcium alter ventricular conduction and excitability, precipitating monomorphic or polymorphic ventricular rhythms.
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.
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.
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.
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.
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.
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.
Persistent ventricular tachycardia may become more disorganised and deteriorate into ventricular fibrillation. Loss of effective contraction then converts a perfusing tachycardia into cardiac arrest.
A regular broad-complex tachycardia in an adult, especially with structural heart disease or prior infarction, should be managed as VT if doubt remains.
Atrial activity marching independently from ventricular complexes indicates separate atrial and ventricular rhythms and strongly favours VT.
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.
All precordial QRS complexes in one direction, an extreme axis or morphology incompatible with typical bundle-branch block raises the probability of VT.
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.
Shock, syncope with severe or ongoing hypotension, myocardial ischaemia, severe pulmonary oedema or immediately post-ROSC triggers the unstable route.
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.
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.
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.
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.
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.
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.
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.
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 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.
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.
Mis-treating VT as SVT can be catastrophic; treating an uncertain regular broad tachycardia as VT is the safer asymmetry.
With a pulse, synchronisation avoids delivering energy on the T wave. Pulseless VT requires unsynchronised defibrillation.
A single relatively narrow complex amid broad tachycardia may represent sinus capture and strongly supports AV dissociation and VT.
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.
Before giving adenosine or amiodarone, exclude pre-excited AF and torsades because both require different treatment.
Use the resuscitation algorithm for peri-arrest arrhythmia; cite the product SmPC regimen when prescribing amiodarone outside that algorithm.
Delaying cardioversion in an unstable patient while seeking a perfect ECG diagnosis.
Giving verapamil to an undifferentiated broad-complex tachycardia.
Using adenosine for an irregular broad rhythm.
Giving amiodarone to torsades or pre-excited AF.
Forgetting to re-enable synchronisation before a repeat shock.
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During a regular broad-complex tachycardia, one near-normal narrow QRS appears at the expected time of a sinus impulse. What does this finding most strongly support?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem ·
Continuous ECG and blood-pressure monitoring; slow or stop for hypotension, marked QRS widening or QT prolongation.
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.
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.
Monitor blood pressure, respiration and renal function; do not substitute amiodarone in torsades.