Tachycardias (4.10). Wide complex tachycardia differentiation

There are three possible mechanisms of wide complex tachycardia: supraventricular tachycardia with bundle branch block, ventricular tachycardia; and supraventricular tachycardia with conduction via an accessory pathway.
Despite the presence of multiple differentiation criteria, sometimes an exact diagnosis cannot be made. In such cases, patients should be managed according to the guidelines for ventricular tachycardia management.
And now we talk about the most common differential features of wide complex tachycardia.
The first feature is atrioventricular dissociation. It is the absence of a relationship between P waves and QRS complexes. This is an exact feature of ventricular tachycardia. P waves are arrowed. There is no relationship between P waves and QRS complexes. Pay attention to regular PP intervals. Note, that absence of AV dissociation does not mean that it is not ventricular tachycardia.
The second feature is fusion beats. They are QRS complexes of intermediate morphology between supraventricular and ventricular complexes. This means that ventricles are depolarized simultaneously by two impulses: supraventricular and ventricular ones. So, certain portion of ventricles is depolarized by the ventricular ectopic impulse, while another one are depolarized by impulse of supraventricular origin. Fusion beats are highly specific for ventricular tachycardia.
The third feature is capture beats. They are QRS complexes of the same morphology as those in the sinus rhythm. They occur due to ventricular capture of the supraventricular impulse conducted over the atrioventricular node – His bundle pathway. It’s highly specific for ventricular tachycardia as well.
The fourth feature is positive or negative precordial concordance. It means that all QRS complexes during the tachycardia are either positive or negative in all precordial leads. This is more typical of ventricular tachycardia than supraventricular tachycardia. However, this is not seen in the right ventricular outflow tract ventricular tachycardia and bundle branch reentrant ventricular tachycardia.
The fifth feature is QRS complex width. If it’s more than 160 milliseconds ventricular tachycardia is more probable. However, it’s not seen in fascicular tachycardia and may be absent in outflow tract ventricular tachycardia, in which QRS complexes may be only slightly widened.
The sixth feature is presence or absence of typical right or left bundle branch block pattern. The absence of a typical right bundle branch block pattern is more typical of most forms of ventricular tachycardia (except fascicular ventricular tachycardia).
Atypical patterns in the right bundle branch block morphology include:
- R wave taller than R-prime wave (straight left rabbit ear) in lead V1;
- tiny Q wave with high R wave in lead V1;
- Monophasic R wave in lead V1;
- Absence of R wave in lead V6 or R wave is smaller than S wave in lead V6.
Atypical patterns in the left bundle branch block pattern morphology include QS in lead V6 or tiny Q wave with high R wave in lead V6 and dominant S wave in lead V1 with following features:
- Width of initial R wave more than 30 ms;
- Time from onset of the R wave to nadir of S wave more than 70 ms;
- Slurred or notched S wave.
The seventh feature is Josephson’s sign which denotes notch near the S wave nadir. It favours ventricular tachycardia.
The eightth sign is Brugada’s sign. If time from R wave onset to S wave nadir is more than 100 ms, ventricular tachycardia is more probable.
The nineth sign is extreme axis deviation (so-called “undetermined axis”) means the cardiac axis from minus 90 degrees to minus 180 degrees and favours ventricular tachycardia (except fascicular and outflow tract ventricular tachycardia). QRS complexes are negative in leads one, II, III and aVF.
The tenth feature is positive initial R wave in lead aVR. It favours ventricular tachycardia.
Other clinical factors that increase likelihood of ventricular tachycardia include: myocardial infarction (acute or previous), diseases associated with sudden cardiac death (such as long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular dysplasia, hypertrophic cardiomyopathy), dilated cardiomyopathy, severe valvular heart disease, reduced ejection fraction from any cause, elderly patients.
Clinical factors that increase likelihood of supraventricular tachycardia include: previous ECGs in sinus rhythm showed a wide QRS complex with pattern identical to one during wide complex tachycardia, history of tachycardia responding to vagal manoeuvres or adenosine, WPW pattern on previous ECGs, newborn and childhood (antidromic atrioventricular reentrant tachycardia is the most common tachycardia in childhood in the absence of structural heart disease).