The correct diagnosis of a wide complex tachycardia (WCT)—QRS duration > 120 ms—remains a challenge despite numerous established criteria for the differentiation of ventricular from supraventricular tachycardia (SVT) with aberrant conduction. Making the correct diagnosis is important for the acute as well as long term management of patients with WCT. The objective of the present review is to discuss the major causes as well as clinical and electrophysiologic criteria of WCT (table 1) in patients without structural heart disease.

Broad categories of WCTs include ventricular tachycardia (VT), SVT with abnormal intraventricular conduction, and ventricular paced rhythms. A lack of underlying structural heart disease does neither exclude a VT nor imply a benign prognosis. However, if a patient has had similar episodes during previous years, SVT is more likely than VT. Termination of a tachycardia by the Valsalva manoeuvre or adenosine injection also suggests a supraventricular origin, although some VT can also be terminated by these manoeuvres (for example, fascicular VT).

A WCT in a patient who is alert and haemodynamically stable is not necessarily of supraventricular origin. The clinical presentation depends on the haemodynamic consequences it produces. These depend partly on tachycardia rate, the degree of myocardial dysfunction, the circumstances and suddenness of initiation, and autonomic factors. Physical examination in a patient presenting with WCT may indicate haemodynamic distress (low blood pressure, heart failure or cardiogenic shock). When cardiac output and blood pressure are maintained and/or when the tachycardia is short lived, the arrhythmia may present as palpitations, breathlessness or just discomfort.

WIDE COMPLEX SUPRAVENTRICULAR TACHYCARDIAS

Intraventricular conduction delay can result from heart rate changes, as well as from fixed pathological lesions in the conduction system. In patients with pre-existing or “fixed” (present during the normal baseline rhythm) bundle branch block (BBB), …