A broad complex tachycardia has a QRS complex greater than 0.12 seconds. They are usually ventricular in origin, but can also be supraventricular with aberrant conduction. Other possible causes for broad complex tachycardias include atrial fibrillation with ventricular pre-excitation, i.e. patients with Wolff–Parkinson–White (WPW) syndrome, or torsades de pointes (polymorphic VT).

Broad complex tachycardia is therefore due to SVT with aberrancy or Ventricular Tachycardia (VT), and differentiating between the two can be challenging. However, there are a few pathognomonic ECG features that diagnose VT

1.Atrio-ventricular (AV) dissociation. There is a higher ventricular rate than atrial rate (more QRS complexes than P-waves). This can only occur if the ventricular rate is autonomous and no longer under control of the SA node.

2.Capture beats: There is an isolated narrow complex amongst a train of broad complexes. This represents a normally conducted P-wave via the AV node and an intact His-Purkinje system indicating there is no underlying bundle branch block. Therefore, the train of broad complexes are ventricular in origin (i.e. VT).

3.Fusion beats: A normally conducted P-wave may fuse with a simultaneous ventricular beat causing a complex halfway between the appearance of a normal QRS and a broad complex.

4.VT is more likely in patients with a prior history of MI.

5.VT complexes are usually very broad (> 160 ms) due to a very abnormal path taken by the depolarisation wave from the VT focus.

6.The time from R-wave onset to the nadir of the S-wave is prolonged (> 100 ms) in VT, again representing an abnormal activation path through the ventricle.

7.Extreme left axis deviation and positive aVR are more common in VT, as the ventricles are depolarised in the opposite direction to normal conduction.

8.Failure to respond to iv adenosine

9.The absence of typical RBBB or LBBB patterns suggests VT. For example, an RSR pattern in V1 with a taller first R-wave suggests VT (in RBBB the first R-wave is caused by septal depolarisation and is therefore smaller than the second R-wave, which is caused by depolarisation of the RV).

SVT with aberrancy is more likely if previous ECGs demonstrate an accessory pathway or a bundle branch block with identical morphology to the broad complex tachycardia. When in doubt, treat as VT

TORSADES DE POINTES

Is a specific variant of ventricular tachycardia (VT). It has a classic undulating pattern with variation in the size of QRS complex. It is caused by a prolonged QT interval and can precipitate VF and sudden death

QT PROLONGATION: CAUSES

Tricyclic antidepressants, flecainide and quinidine; Hypocalcemia; Acute myocarditis

VENTRICULAR TACHYCARDIA(VT) AND VENTRICULAR FIBRILLATION (VF)

VT is a broad complex tachycardia, defined as a run of at least three consecutive ventricular ectopic beats, at a rate of >120 bpm. Can arise from a single or multiple foci or from a reentry circuit. There may be capture or fusion beats, where a normally conducted beat will join an ectopic beat travelling in the opposite direction

CAUSES: Acute MI, degeneration of other arrhythmias, electrolyte abnormalities etc

VF describes an ECG which is random and chaotic with no identifiable QRS complexes that is incompatible with life and need immediate provision of ACLS with prompt delivery of DC shock. Others: Amiodarone, Lidocaine, beta blockers, Implantable cardioverter defibrillators

MANAGEMENT

For VT treat with amiodarone 300 mg IV followed by 900 mg over 24 hours. If the arrhythmia is known to be supraventricular, treat as a narrow complex tachycardia.

An irregular broad complex tachycardia is most likely to be atrial fibrillation with bundle branch block, and should be treated as narrow complex atrial fibrillation

In a stable patient who is known to have WPW, the use of amiodarone is probably safe. Adenosine, digoxin, verapamil and diltiazem must be avoided, as these drugs block the AV node and will cause a relative increase in pre-excitation

Torsades de pointes is treated by stopping all drugs known to prolong the QT interval and correcting electrolyte abnormalities. Magnesium sulphate (2 g IV over 10 minutes) should also be given. Such patients may require ventricular pacing. If the patient’s condition deteriorates proceed to synchronised electrical cardioversion or, if the patient is pulseless, commence the ALS algorithm

Ventricular bigeminy
Ventricular bigeminy is associated with endotracheal intubation (a sympathoadrenal response). Given time the bigeminy will disappear, but if it does not intravenous
lidocaine (50–100 mg) may be helpful