Broad complex tachycardias

What is broad complex tachycardia?

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.

Causes of broad complex tachycardias

• 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.

Presentation

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

Broad complex tachycardias symptoms

• 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.

Signs

• 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.
  

Differential diagnosis

The ECG differential diagnosis includes VT, SVT with functional aberration, pre-existing bundle branch block, intraventricular conduction disturbances, and pre-excitation¹ .

Ventricular

• Regular:
  

  • Monomorphic VT.

  • Fascicular tachycardia.

  • Right ventricular outflow tract tachycardia.

• Irregular:
  

  • Torsades de pointes tachycardia.

  • Polymorphic VT.

Supraventricular

• Bundle branch block with aberrant conduction.

• Atrial tachycardia with pre-excitation.

Investigations

ECG²

• 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.

Broad complex tachycardias treatment and management

Resuscitation

• Support ABCs.

• Basic life support and advanced life support may be required. Give oxygen and gain venous access.

Although mainly relevant to ambulance and immediate hospital care, the following guidance is taken from the Resuscitation Council guideline for peri-arrest tachycardias and is included for information³ :

The assessment and treatment of all arrhythmias addresses the condition of the patient (stable versus unstable) and the nature of the arrhythmia. Life-threatening features in an unstable patient include:

• Shock: hypotension (eg, systolic blood pressure <90 mm Hg) and symptoms of increased sympathetic activity and reduced cerebral blood flow.

• Syncope: reduced cerebral blood flow.

• Severe heart failure: pulmonary oedema and/or raised jugular venous pressure.

• Myocardial ischaemia: chest pain (angina) or without pain as an isolated finding on the 12-lead ECG (silent ischaemia).

Electrical cardioversion is the preferred treatment for tachyarrhythmia in an unstable patient displaying potentially life-threatening adverse signs. Conscious patients require anaesthesia or sedation, before attempting synchronised cardioversion

• To convert atrial or ventricular tachyarrhythmias, the shock must be synchronised to occur with the R wave of the electrocardiogram (ECG).

• For atrial fibrillation: an initial synchronised shock at maximum defibrillator output rather than an escalating approach.

• For atrial flutter and paroxysmal supraventricular tachycardia: an initial shock of 70-120 Joules. Give subsequent shocks using stepwise increases in energy.

• For ventricular tachycardia with a pulse: energy levels of 120-150 Joules for the initial shock. Consider stepwise increases if the first shock fails to achieve sinus rhythm.

If cardioversion fails to restore sinus rhythm and the patient remains unstable, give amiodarone 300 mg intravenously over 10-20 minutes (or procainamide 10-15 mg/kg over 20 minutes) and re-attempt electrical cardioversion. The loading dose of amiodarone can be followed by an infusion of 900 mg over 24 hours.

If the patient with tachycardia is stable (no life-threatening adverse signs or symptoms) and is not deteriorating, pharmacological treatment may be possible.

Consider amiodarone for acute heart rate control in AF patients with haemodynamic instability and severely reduced left ventricular ejection fraction (LVEF). For patients with LVEF <40%, consider the smallest dose of beta-blocker to achieve a heart rate less than 110 bpm. Add digoxin if necessary.

Prognosis

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.