Wide complex tachycardia

Introduction

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
  • Onset of a tachycardia with a premature P wave
  • Very short RP interval (<100ms)
  • P-P interval changes preceding R-R interval changes
  • 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.

https://www.aerjournal.com/articles/wide-complex-tachycardia-ventricular


References

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. Wellens, H. Ventricular Tachycardia: Diagnosis of Broad QRS Complex Tachycardia. Heart (British Cardiac Society). 86. 579-85. 10.1136/heart.86.5.579.
  6. https://litfl.com/vt-versus-svt-ecg-library/
  7. Anestesia.TK. http://lnx.mednemo.it/?p=1217
  8. https://www.aerjournal.com/articles/wide-complex-tachycardia-ventricular