Broad Complex Tachycardias

Authored by , Reviewed by Dr John Cox | Last edited | Meets Patient’s editorial guidelines

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Treatment of almost all medical conditions has been affected by the COVID-19 pandemic. NICE has issued rapid update guidelines in relation to many of these. This guidance is changing frequently. Please visit to see if there is temporary guidance issued by NICE in relation to the management of this condition, which may vary from the information given below.

A tachycardia is defined as a heart rate greater than 100 beats per minute (bpm).

  • In broad complex tachycardias the QRS complex is longer than 120 ms (three small squares on the ECG).[1]

A broad QRS complex is either caused by the ventricular conducting system not working (bundle branch block) or the electrical circuit not involving the atrioventricular (AV) node correctly. Broad complex tachycardias may be ventricular or supraventricular in origin.

  • Ventricular tachycardias (VTs).
  • Broad complex tachycardias of supraventricular origin:
    • With aberrant conduction or ventricular pre-excitation, any supraventricular tachycardia (SVT) may present as a broad complex tachycardia and mimic VT.
    • Atrial tachycardia with aberrant conduction:
      • Aberrant conduction usually manifests as either left or right bundle branch block and the bundle branch block may predate the tachycardia.
      • It may be a rate-related functional block, occurring when atrial impulses arrive too rapidly for a bundle branch to conduct normally.
    • Wolff-Parkinson-White syndrome: in the Wolff-Parkinson-White syndrome the atrial impulses are conducted down the accessory pathway, which may allow rapid conduction and consequently very fast ventricular rates with broad QRS complexes. The QRS pattern is fairly constant, except for occasional normal complexes and fusion beats.
    • Atrial fibrillation: broad complex tachycardias may occur, either as an atrioventricular re-entrant tachycardia or in association with atrial flutter or atrial fibrillation.

A ventricular origin for a broad complex tachycardia is suggested if the patient is aged over 35 years and has a history of ischaemic heart disease or congestive cardiac failure.


  • Depend on the haemodynamic consequences of the arrhythmia rather than the origin of the arrhythmia.
  • In some patients with VT, they may not be in a state of collapse, but present with dizziness, palpitations, syncope, chest pain or heart failure.
  • Some patients with SVT and poor ventricular function may present in a state of haemodynamic collapse.


  • In VT the rhythm is regular or almost regular.
  • An obviously irregular rhythm is most likely due to atrial fibrillation with either aberrant conduction or pre-excitation.
  • Clinical evidence of atrioventricular dissociation, ie cannon waves in the jugular venous pulse or variable intensity of the first heart sound, indicates a VT.
  • Physical signs will also vary according to the haemodynamic effects of the tachycardia.

The ECG differential diagnosis includes VT, SVT with functional aberration, pre-existing bundle branch block, intraventricular conduction disturbances and or pre-excitation.[2]


  • Regular:
    • Monomorphic VT
    • Fascicular tachycardia
    • Right ventricular outflow tract tachycardia
  • Irregular:


  • Bundle branch block with aberrant conduction.
  • Atrial tachycardia with pre-excitation.


  • Usually shows monomorphic QRS complexes as seen in most common forms of sustained VT.
  • QRS complex shape is unusual and of prolonged duration (usually >0.12 seconds). Normally, the longer the duration of the QRS complex the more likely it is to be VT (particularly if >0.16 seconds). Changing QRS morphology during the tachycardia also indicates a ventricular origin.
  • Evidence of AV dissociation through presence of P waves independent of the QRS complex is common but not always present.
  • Rate: usually 120-300 bpm.
  • Rhythm: regular or approximately regular unless affected by capture or fusion beats. A clearly irregular rhythm it most likely to be due to AF.
  • Diagnostic features (absence of these does not exclude VT):
    • Capture beats: the sinoatrial node transiently ‘captures’ the ventricles during AV dissociation; the resulting QRS complex is of normal duration.
    • Fusion beats: QRS complexes somewhere between a standard QRS and the others present on the trace. They occur when a normal AV node beat fuses with a beat originating from the ventricles.
    • QRS concordance: all QRS complexes in chest leads either mainly positive or negative.


The following guidance is taken from the Resuscitation Council guideline for Peri-Arrest Arrhythmias:[4]

  • Monitor ECG, BP, oxygen saturation.
  • Record 12-lead ECG if possible; if not, record rhythm strip.
  • Identify and treat reversible causes (eg, electrolyte abnormalities - monitor potassium and, if low, start infusions of potassium chloride and magnesium sulfate).
  • If the patient is unstable (signs of instability include reduced conscious level, chest pain, systolic BP below 90 mm Hg, heart failure (rate-related symptoms are uncommon at less than 150 bpm):
    • Synchronised direct current (DC) shock; up to three attempts; attempted electrical cardioversion is always undertaken under sedation or general anaesthesia.
    • Amiodarone 300 mg IV over 10-20 minutes and repeat shock; followed by amiodarone 900 mg over 24 hours.
  • If the patient is stable:
    • Irregular:
      • Seek expert help; possibilities include:
      • Atrial fibrillation with bundle branch block: treat as for narrow complex.
      • Pre-excited atrial fibrillation: consider amiodarone.
      • Polymorphic VT (eg, torsades de pointes): give magnesium 2 g over 10 minutes).
    • Regular:
      • If VT - or uncertain rhythm: amiodarone 300 mg IV over 20-60 minutes; then 900 mg over 24 hours.
      • If previously confirmed SVT with bundle branch block: give adenosine as for regular narrow complex tachycardia.
      • For refractory cases, consider additional pharmacological agents (eg, lidocaine or sotalol) or overdrive pacing. Caution is required because pharmacological agents may cause myocardial depression.

The treatment of a broad complex tachycardia depends on the origin of the tachycardia and should be treated as sustained VT until proven otherwise.

Vagal stimulation (eg, carotid sinus massage or the Valsalva manoeuvre) does not usually affect a VT but may affect arrhythmias of supraventricular origin. By transiently slowing or blocking conduction through the AV node, an atrioventricular nodal re-entrant tachycardia or atrioventricular re-entrant tachycardia may be terminated. In atrial flutter, transient block may reveal the underlying flutter waves.

Monomorphic VT usually occurs after myocardial infarction and is a sign of extensive myocardial damage; there is a high mortality, often resulting from impaired ventricular function.

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Further reading and references

  1. van de Swaluw JE, van Mechelen R; Saturday night broad QRS complex tachycardia in a young male. Neth Heart J. 2014 Jan22(1):42-3. doi: 10.1007/s12471-013-0489-5.

  2. Alzand BS, Crijns HJ; Diagnostic criteria of broad QRS complex tachycardia: decades of evolution. Europace. 2011 Apr13(4):465-72. doi: 10.1093/europace/euq430. Epub 2010 Dec 3.

  3. ECG Library

  4. Peri-arrest Arrhythmias Guideline; Resuscitation Council UK, 2010

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