Broad Complex Tachycardia

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

• In broad complex tachycardias the QRS complex is longer than 120ms (3 small squares on the ECG).
• In narrow complex tachycardias the QRS complex is shorter than 120ms.

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

• Ventricular tachycardias
• Broad complex tachycardias of supraventricular origin:
  • With aberrant conduction or ventricular pre-excitation, any supraventricular tachycardia may present as a broad complex tachycardia and mimic ventricular tachycardia.
  • 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. Atrial fibrillation occurring with an aberrant conduction and a rapid ventricular response, produces an irregular broad complex tachycardia.
  • Wolff-Parkinson-White syndrome: broad complex tachycardias may occur, either as an atrioventricular re-entrant tachycardia or in association with atrial flutter or atrial fibrillation.
  • Atrial fibrillation: 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 (see below).

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.

Symptoms

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

Signs

• In ventricular tachycardia 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 atrio-ventricular dissociation, i.e. cannon waves in the jugular venous pulse or variable intensity of the first heart sound, indicates a ventricular tachycardia.
• Physical signs will also vary according to the haemodynamic effects of the tachycardia.

Varieties of broad complex tachycardia:¹

• Ventricular:
  • Regular:
    • Monomorphic ventricular tachycardia
    • Fascicular tachycardia
    • Right ventricular outflow tract tachycardia
  • Irregular:
    • Torsades de pointes tachycardia
    • Polymorphic ventricular tachycardia
• Supraventricular:
  • Bundle branch block with aberrant conduction
  • Atrial tachycardia with pre-excitation

ECG²

• Usually shows monomorphic QRS complexes as seen in most common forms of sustained ventricular tachycardia.³
• QRS complex shape is unusual and of prolonged duration (usually > 0.12s). Normally, the longer the duration of the QRS complex the more likely it is to be ventricular tachycardia (particularly if > 0.16s). 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 beats per minute.
• Rhythm: regular or approximately regular unless affected by capture or fusion beats. A clearly irregular rhythm it most likely to be due to atrial fibrillation.
• Diagnostic features (absence of these does not exclude VT):
  • Capture beats: occasional narrow QRS complexes appearing sooner than normal place in the trace, these show normal AV conduction so SVT is unlikely.
  • 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 treatment of a broad complex tachycardia depends on the origin of the tachycardia.
• A broad complex tachycardia should be treated as sustained ventricular tachycardia until proven otherwise.
• If adverse signs (systolic blood pressure less than 90, chest pain, heart failure, rate above 150 per minute), give synchronised DC shock, then intravenous amiodarone and further cardioversion as necessary. For refractory cases, consider additional pharmacological agents, e.g. lignocaine or sotalol, or overdrive pacing. Caution is required because pharmacological agents may cause myocardial depression.⁴
• If no adverse signs, give intravenous amiodarone or lignocaine, followed if necessary by synchronised DC shock and further amiodarone if required.
• Monitor potassium and if low, start infusions of potassium chloride and magnesium sulphate.
• Vagal stimulation, e.g. carotid sinus massage or the valsalva manoeuvre, does not usually affect a ventricular tachycardia but may affect arrhythmias of supraventricular origin. By transiently slowing or blocking conduction through the atrioventricular 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.

Initial management

Resuscitation: support ABCs, basic life support and advanced life support may be required. Give oxygen and gain venous access. The following guidance is taken from the Resuscitation Council algorithm for the treatment of tachycardias.⁵

• Monitor ECG, BP, oxygen saturation
• Record 12-lead ECG if possible; if not, record rhythm strip
• Identify and treat reversible causes (e.g. electrolyte abnormalities)
• If patient is unstable (signs of instability include reduced conscious level, chest pain, systolic BP below 90 mmHg, heart failure (rate-related symptoms are uncommon at less than 150 beats per minute):
  • Synchronised DC Shock; up to 3 attempts; attempted electrical cardioversion is always undertaken under sedation or general anaesthesia.
  • Amiodarone 300 mg IV over 10-20 min and repeat shock; followed by amiodarone 900 mg over 24 hours.
• If patient is stable:
  • Irregular:
    • Seek expert help; possibilities include:
    • AF with bundle branch block: treat as for narrow complex
    • Pre-excited AF: consider amiodarone
    • Polymorphic VT (e.g. torsade de pointes): give magnesium 2 g over 10 min)
  • Regular:
    • If Ventricular Tachycardia (or uncertain rhythm): amiodarone 300 mg IV over 20-60 min; then 900 mg over 24 h.
    • If previously confirmed SVT with bundle branch block: give adenosine as for regular narrow complex tachycardia.

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