VT versus SVT with aberrancy

Look at this ECG:

There are three main diagnostic possibilities:

  • VT
  • SVT with aberrant conduction due to bundle branch block
  • SVT with aberrant conduction due to the Wolff-Parkinson-White syndrome

The most important distinction is whether the rhythm is ventricular (VT) or supraventricular (SVT with aberrancy), as this will significantly influence how you manage the patient. SVTs usually respond well to AV-nodal blocking drugs, whereas patients with VT may suffer precipitous haemodynamic deterioration if erroneously administered an AV-nodal blocking agent.

Unfortunately, the electrocardiographic differentiation of VT from SVT with aberrancy is not always possible.

There are several electrocardiographic features that increase the likelihood of VT:

  • Absence of typical RBBB or LBBB morphology
  • Extreme axis deviation (“northwest axis”) — QRS is positive in aVR and negative in I + aVF.
  • Very broad complexes (>160ms)
  • AV dissociation (P and QRS complexes at different rates)
  • Capture beats — occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.
  • Fusion beats — occur when a sinus and ventricular beat coincides to produce a hybrid complex.
  • Positive or negative concordance throughout the chest leads, i.e. leads V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen.
  • Brugada’s sign –  The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms
  • Josephson’s sign – Notching near the nadir of the S-wave
  • RSR’ complexes with a taller left rabbit ear. This is the most specific finding in favour of VT. This is in contrast to RBBB, where the right rabbit ear is taller.

Examples of these ECG features are shown below:

AV dissociation: P waves (arrowed) appear at a different rate to the QRS complexes

Capture beats

Capture beats

Fusion beats

Fusion beats – the first of the narrower complexes is a fusion beat (the next two are capture beats)

Positive concordance in VT

Positive concordance in VT

Negative concordance in VT

Negative concordance in VT

Brugada’s and Josephson’s signs

Brugada’s sign (red callipers) and Josephson’s sign (blue arrow)

Taller left rabbit ear in VT

Taller left rabbit ear in VT

Taller right rabbit ear in RBBB

Taller right rabbit ear in RBBB

The likelihood of VT is also increased with:

  • Age > 35 (positive predictive value of 85%)
  • Structural heart disease
  • Ischaemic heart disease
  • Previous MI
  • Congestive heart failure
  • Cardiomyopathy
  • Family history of sudden cardiac death (suggesting conditions such as HOCM, congenital long QT syndrome, Brugada syndrome or arrhythmogenic right ventricular dysplasia that are associated with episodes of VT)

The likelihood of SVT with aberrancy is increased if:

  • Previous ECGs show a bundle branch block pattern with identical morphology to the broad complex tachycardia.
  • Previous ECGs show evidence of WPW (short PR < 120ms, broad QRS, delta wave).
  • The patient has a history of paroxysmal tachycardias that have been successfully terminated with adenosine or vagal manoeuvres.


Advanced Tips for Diagnosing VT — The Brugada Criteria

  • For difficult cases, the Brugada algorithm can be used to distinguish between VT and SVT with aberrancy.
  • The algorithm is followed from top to bottom — if any of the criteria are satisfied then VT is diagnosed.

Reproduced from ECGpedia.com (click image for link)

1. Absence of an RS complex in all precordial leads

  • This is essentially the same as having positive or negative concordance.
  • If all the precordial leads consist of either monophasic R or S waves then VT is diagnosed.
  • If there are any RS complexes present in V1-6 –> move on to the next step of the algorithm.
Positive concordance in VT

Precordial R waves only -> VT

Negative concordance in VT

Precordial S waves only -> VT

RS complexes present –> go to step 2


2. RS interval > 100ms in one precordial lead

  • If RS complexes are present in V1-6 then the RS interval is measured.
  • This is the time from the onset of the R wave to the nadir of the S wave.
  • If the RS interval is > 100 ms –> VT is diagnosed.
  • If the RS interval is < 100 ms –> move on to step 3.

3. AV dissociation

  • The ECG is scrutinised for hidden P waves; these are often superimposed on the QRS complexes and may be difficult to see.
  • If P waves are present at a different rate to the QRS complexes –> AV dissociation is present and VT is diagnosed.
  • If no evidence of AV dissociation can be seen –> go to step 4.

AV dissociation: P waves can be spotted in between QRS complexes (circled) and superimposed upon the T wave causing a peaked appearance (arrow)

4. Morphological Criteria for VT

Leads V1-2 and V6 are assessed for characteristic features of VT. There are two sets of morphological criteria depending on the appearance of the QRS complex in V1:

  • If there is a dominant R wave in V1  –> see criteria for RBBB-like morphology.
  • If there is a dominant S wave in V1  –> see criteria for LBBB-like morphology.

RBBB-like morphology

LBBB-like morphology

Broad complex tachycardia with RBBB morphology

Appearance in V1-2

With a positive R wave in V1, three patterns are indicative of VT:

  • Smooth monophasic R wave
  • Notched downslope to the R wave — the taller left rabbit ear (= Marriott’s sign)
  • A qR complex (small Q wave, tall R wave) in V1

Smooth monophasic R wave –> VT

Taller left rabbit ear –> VT

qR pattern –> VT

In contrast, an RSR’ pattern is suggestive of SVT with RBBB.

Typical RSR’ pattern of RBBB

Appearance in V6

In V6, the following patterns are consistent with VT:

  • QS complex — a completely negative complex with no R wave (= strongly suggestive of VT).
  • R/S ratio < 1 — small R wave, deep S wave (indicates VT only if LAD is also present).

QS waves in V6 –> VT

R/S ratio < 1 in V6 –> probably VT

Broad complex tachycardia with LBBB morphology

Appearance in V1-2

With a dominant S wave in V1, the following three features are diagnostic of VT:

  • Initial R wave > 30-40 ms duration.
  • Notching or slurring of the S wave (Josephson’s sign).
  • RS interval (time from R wave onset to S wave nadir) > 60-70 ms.

Image reproduced from Wellens (2001). See references for link.

Appearance in V6

With a LBBB-like pattern, the presence of Q waves in V6 is indicative of VT. There are two possible patterns:

  • QS waves in V6 (as with RBBB-like patterns, this finding is very specific for VT).
  • qR pattern = small Q wave, large R wave.

QS waves in V6 –> VT

qR complex in V6 –> VT

Conversely, SVT with LBBB is associated with absent Q waves in V6.

Absent Q waves in V6 with LBBB

More Advanced Tips — The Vereckei Algorithm

There is some overlap between the Vereckei and Brugada algorithms, but one of the most useful tips from the Vereckei algorithm is to examine the QRS complex in lead aVR.

  • A dominant initial R wave in aVR is indicative of VT.
  • A dominant terminal R’ wave in aVR (i.e. following a Q/S wave) is more likely SVT with aberrancy — this pattern is most commonly seen in tricyclic poisoning.

Dominant initial R wave in aVR -> VT

Dominant secondary R’ wave in aVR -> TCA toxicity

Other diagnostic algorithms

Flow charts for the other three commonly used diagnostic algorithms (ACC, Ultra-simple Brugada, Vereckei ) can be found here.


  • Most of the published criteria have high specificities but very low sensitivities (e.g. 20-50%) for diagnosing VT.
  • This means that even in the absence of diagnostic features for VT, there is no way to be 100% certain that the rhythm is SVT with aberrancy…
  • If in doubt, treat as VT!


Broad Complex Tachycardia Quiz

Test your skills with these broad complex rhythms…

Example 1


AV-nodal re-entry tachycardia (AVNRT) with LBBB

  • Typical LBBB morphology.
  • No positive Brugada criteria.
  • This patient had LBBB with identical morphology on their previous ECGs.

Read more about AVNRT here

Read more about LBBB here.

Example 2

Monomorphic VT

Monomorphic VT:

  • This ECG is a difficult one!
  • Although there is a broad complex tachycardia (HR > 100, QRS > 120), the appearance in V1 is more suggestive of SVT with aberrancy, given that the the complexes are not that broad (< 160 ms) and the right rabbit ear is taller than the left.
  • However, on closer inspection there are signs of AV dissociation, with superimposed P waves visible in V1.
  • Also, the presence of a northwest axis and an R/S ratio < 1 in V6 (tiny R wave, deep S wave) indicate that this is VT.
  • This patient had a completely different QRS axis and morphology on his baseline ECG.

Read more about monomorphic VT here.


Example 3

Sinus tachycardia with incomplete RBBB

Sinus tachycardia with incomplete RBBB:

  • P waves are visible before each QRS complex.
  • There is a typical RBBB morphology with a RSR’ complex in V1 and wide S wave in the lateral leads I, V5-6.
  • In contrast to the previous example, there is a dominant R wave in V6 (RS ratio > 1), which is much more typical of RBBB.
  • QRS complexes are only slightly prolonged (110ms), making this an incomplete RBBB.
  • Q waves and T-wave inversions in III and aVF suggest prior inferior infarction.

Read more about RBBB here

Example 4

Massive TCA overdose

Tricyclic antidepressant toxicity:

  • QRS complexes are very broad (~200ms) — however, unlike with VT most of the broadening is in the terminal portion of the QRS (this can be best appreciated in leads V3-V6 where narrow R waves are followed by massively broad and deep S waves).
  • There are no positive Brugada criteria — in particular, the RS interval is < 100 ms.
  • No P waves can be seen.

The characteristic features of TCA toxicity are:

  • Tachycardia — this is often a sinus tachycardia with a grossly prolonged PR interval, such that the P wave is hidden in the previous T wave or QRS complex; may be difficult to differentiate from junctional tachycardia with aberrant conduction.
  • Broad QRS complexes.
  • Right axis deviation of the terminal QRS — positive R’ wave in aVR, deep S wave in lead I.

Read more about TCA toxicity here.

Example 5

Antidromic atrioventricular re-entry tachycardia in a 5-year old boy

The patient is 5 years old.

Antidromic atrioventricular re-entry tachycardia (AVRT) due to Wolff-Parkinson-White syndrome:

  • This is the one rhythm that may be impossible to distinguish from VT!
  • In this case the main clue is the history — more than 95% of broad complex tachycardias in children are SVT with aberrancy.

Read more about paediatric dysrhythmias here.  

Read more about WPW here

 Example 6

Rapid paced rhythm

Rapid ventricular paced rhythm (e.g. pacemaker-mediated tachycardia)

  • There are obvious pacing spikes before each QRS complex.
  • Ventricular paced rhythms have features in common with other ventricular rhythms — in this case the ECG demonstrates negative concordance in V1-6, initial R wave > 40ms in V1, RS interval > 70 ms in V1, QS complex in V6.
  • Remember that the pacing spikes may not always be as obvious as this!

Read more about pacemaker dysfunctions here.


For those of you wondering what the ECG at the top of the page is…. it is an example of right ventricular outflow tract tachycardia – a type of VT!

More on this Topic

Related Topics

Read more about the different types of VT by following these links: 

Author Credits

Further Reading


  • Alzand BS, Crijns HJ. Diagnostic criteria of broad QRS complex tachycardia: decades of evolution. Europace. 2011 Apr;13(4):465-72. Epub 2010 Dec 3. Review. PubMed PMID: 21131372.
  • Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.
  • Surawicz B, Knilans TK. Chou’s Electrocardiography in Clinical Practice. 6th Edition. Saunders Elsevier 2008.
  • Wagner, GS. Marriott’s Practical Electrocardiography (11th edition), Lippincott Williams & Wilkins 2007.
  • Wellens HJ. Electrophysiology: Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart. 2001 Nov;86(5):579-85. Review. PubMed PMID: 11602560; PubMed Central PMCID: PMC1729977Full text.
Print Friendly