Rhythm disturbance with a rate greater than 100 beats/ min and a QRS complex duration of 0.12 seconds or more.
The most important (“until proven otherwise”) cause of wide complex tachycardia (WCT) is ventricular tachycardia (VT).
Most wide-complex tachycardias (referring to the width of the QRS complex >120 ms) are in fact VTs (approximately 80-90%). There are features and algorithms using these features that can be used to differentiate between a VT and a SVT.
Broad QRS tachycardia can be divided into several groups
VT
SVT with bundle branch block (BBB)
BBB may be pre-existing or can occur when the refractory period of one of the bundle branches is reached because of the heart rate of the SVT
BBB can also occur because of retrograde invasion in one of the bundle branches
SVT with AV conduction over an accessory AV pathway
atrial tachycardia, atrial flutter, atrial fibrillation, AV nodal tachycardia, etc.
Class I antiarrhythmic agents (e.g., procainamide, flecainide) - can cause rate-related aberrant conduction of an SVT because of a slowing of conduction through the His-Purkinje system that is most pronounced at faster heart rates
Drug related- tricyclic antidepressants (sodium channel blockade and tachycardia due to the anticholinergic effects)
hyperkalemia
Wide QRS complex generated by ventricular paging
Typical features of VTs
Fusion beats and capture beats are most indicative of a VT, however they are not present frequently
- Fusion beats - have a different morphology than other QRS complexes and are a result of a fusion of a supraventricular beat and a ventricular beat - Capture beats - have a normal morphology as they are a supraventricular beat(s) interposed between the QRS complexes with abnormal morphology
AV dissociation is highly indicative of a VT, however, it does not have to be clearly demonstrated as well
AV dissociation represents independent electrical activity of the atria and the ventricles and manifests on the ECG as p waves occurring at different rates from the ventricular rate. Some of the QRS complexes can thus be altered in their appearance by the p waves. In approx. 25 % of VTs the AV dissociation is not present because of a retrograde activation of the atria from the ventricles (VA dissociation)
Extreme axis deviation (-90° to +180°)
Very broad complexes (such as >140 ms) are likely to be a VT. There are exceptions to this rule as fascicular VTs and VTs originating in the ventricular septum can have QRS complexes of a normal duration (<120 ms)
Absence of a typical RBBB or LBBB morphology
RS duration of >100 ms in the precordial leads = Brugada sign
Concordance of QRS complexes in the precordial leads - all QRS complexes in precordial leads have either positive or negative deflection (positive or negative concordance)
Specific criteria in RBBB morphology such as: - R taller than R’ or r’ in V1 - monophasic or biphasic QRS complex in V1 with an initial deflection different than that in sinus rhythm - small R and a large S wave or a QS pattern in V6
Specific criteria in LBBB morphology such as: - rightward axis, negative deflections deeper in V1 than in V6 - broad R wave (>40 ms) in V1
Picture 1 Signs of ventricular tachycardia
Anestesia.TK.
Typical features of a SVT
previous ECG with an aberrant conduction showing the same morphology as the wide complex tachycardia
Termination of the tachycardia with vagal manoeuvres or adenosine is indicative of a SVT, however RVOT VTs can also be terminated.
Algorithms
Several algorithms have been proposed to differentiate between a SVT conducted with aberrancy and a VT
Presented are two if the frequently used - Brugada criteria/algorithm and Vereckei criteria/algorithm
Brugada algorithm as well as Vereckei criteria are stepwise algorithms:
In each step a criteria for VT must be assessed and only after ruling out each of the criteria/going through all of the steps a diagnosis of SVT can be made.
In practice, applying Brugada criteria may be difficult for inexperienced doctors as in step 3, morphology criteria must be assessed. The original overall accuracy was reported to be 98%, although subsequent analysis found the accuracy to be lower at approximately 80%.
Vereckei criteria use only one lead to differentiate VT and SVT - aVR. It uses morphologic criteria in a stepwise approach. The most difficult step in this algorithm is the last one as well as voltage change in time must be assessed.
Picture 2 Brugada criteria
Picture 3 Vereckei criteria (lead aVR)
Picture 4 Overview of all useful information about how to differentiate between VT and SVT.
Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 11th ed, Zipes DP, Libby P, Bonow RO, et al, W.B. Saunders Company, Philadelphia 2018.
Garner, John B, and John M Miller. 2013. “Wide Complex Tachycardia – Ventricular Tachycardia Or Not Ventricular Tachycardia, That Remains The Question” 2 (1). https://doi.org/10.15420/aer.2013.2.1.23.
Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991 May;83(5):1649-59.
Vereckei A, Duray G, Szénási G, Altemose GT, Miller JM. Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia. Eur Heart J. 2007 Mar;28(5):589-600.
Wellens, H. Ventricular Tachycardia: Diagnosis of Broad QRS Complex Tachycardia. Heart (British Cardiac Society). 86. 579-85. 10.1136/heart.86.5.579.
