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Broad complex tachycardia: a diagnostic dilemma

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Q1: What is the diagnosis?

The ECG shows a broad complex tachycardia, atrioventricular (AV) dissociation, fusion beats, andcapture beats. P waves are seen throughout the tracings, but have no consistent relation to the QRS complexes and are occasionally followed by fusion beats. Capture beats are recognised by narrow QRS complexes followed by upright T waves. Fusion beats are slightly wider complexes followed by inverted T waves, which are of lesser magnitude compared with the deeply inverted T waves following ventricular complexes. In the rhythm strip on the lower trace, complexes suggesting capture beats and fusion beats are labelled C and F, respectively. These findings are consistent with ventricular tachycardia.

Q2: What is the most important differential diagnosis?

The differential diagnosis is supraventricular tachycardia with aberrant conduction. These may be difficult to distinguish on a surface ECG. However, the presence of fusion beats and capture beats provides support for the diagnosis of ventricular tachycardia. The presence of ischaemic heart disease, increased age, and very wide QRS complexes makes the diagnosis of ventricular tachycardia more likely.1

Q3: How would you treat this condition?

Ventricular tachycardia or supraventricular tachycardia associated with haemodynamic decompensation should be treated with electrical cardioversion.2 If the patient is otherwise well ventricular tachycardia can be treated medically by various antiarrhythmic drugs, including intravenous lignocaine (lidocaine), amiodarone, disopyramide, and flecainide. Bretylium can be used in life threatening situations when other antiarrhythmic agents have failed. Overdrive pacing may be useful in patients with recurrent ventricular tachycardia not responding to drug treatment.


It is important to differentiate between supraventricular and ventricular tachycardia, as the optimal treatment is different. The haemodynamic state should not be used as a guide for making the diagnosis, as this depends on the ventricular rate and left ventricular function; supraventricular tachycardia is often assumed to be the diagnosis in patients who are clinically well.3 At times it may be impossible to differentiate between these two based on the surface ECG, but the following features aid in the differential diagnosis:

  • Wide and bizarre QRS complexes, AV dissociation, and the presence of fusion beats and capture beats support the diagnosis of ventricular tachycardia. Ventricular complexes with bizarre or prolonged configuration indicate only that conduction through the ventricle is abnormal, and such complexes can occur in supraventricular tachycardias because of pre-existing bundle branch, aberrant conduction, or conduction over accessory pathways. AV dissociation has long been considered a hallmark of ventricular tachycardia, but at times it is difficult to determine whether the P wave is conducted anterogradely (supraventricular tachycardia) or retrogradely (ventricular tachycardia). As a general rule, the presence of AV dissociation during a wide QRS tachycardia is strong presumptive evidence that it is of ventricular origin.1

  • Fusion beats indicate the activation of the ventricle from two foci, implying that one is of ventricular origin. When two impulses invade the ventricle simultaneously, each impulse activates the part of the ventricle, and the resulting QRS complex has a configuration that is between that of a QRS complex of the ectopic beat and the QRS complex of a sinus beat. Also the modification of the QRS complex by fusion will depend upon the relative contribution of the supraventricular and ventricular impulse to ventricular activation.4

  • A capture beat is the momentary activation of the ventricles by the sinus impulse during AV dissociation. During ventricular tachycardia, the slower sinus impulse cannot be conducted anterogradely to the ventricles, as a result of the lower AV nodal refractoriness reflecting partial retrograde penetration of the ventricular impulse. However, as the two pacemakers discharge asynchronously, the slower sinus discharge occurs progressively later in relation to ventricular discharge. The sinus impulse eventually reaches the AV node when it is no longer refractory, and is able to penetrate and capture the ventricles, resulting in a capture beat.5 A capture beat resembles the QRS complex of a normal sinus impulse and is preceded by a P wave (which is clearly shown in lead I). The presence of fusion beat and capture beats provides the maximum support for the diagnosis of ventricular tachycardia, although they are not very common.

  • Vagal manoeuvres or intravenous adenosine may terminate or slow down supraventricular tachycardia. Adenosine has an important role as a diagnostic and therapeutic agent in the emergency management of broad complex tachycardia. The ability to block AV conduction allows diagnosis and treatment for most supraventricular tachycardias, and its short half life and absence of negative inotropic effects makes it safe if given during ventricular tachycardia.6 Verapamil should only be used if the diagnosis of supraventricular tachycardia is established as it may cause haemodynamic collapse in some patients with ventricular tachycardia.7

After the immediate management, further treatment depends on the underlying diagnosis, and a specialist opinion may be needed to choose the correct option to prevent any further attacks.

Final diagnosis

Ventricular tachycardia.


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