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Ventricular tachycardia (VT) is an imminently life-threatening arrhythmia that must be rapidly diagnosed and treated. Supraventricular tachycardia is a more benign arrhythmia that may also present as a wide complex tachycardia when combined with aberrant conduction; this can be difficult to distinguish from VT.This section contains a list of ECG findings that suggest a diagnosis of VT as opposed to SVT with aberrancy.
Narrow Complex Tachycardia
Wide Complex Tachycardia
VT vs SVT with Aberrancy
- Ventricular tachycardia (VT) is an imminently life-threatening arrhythmia that must be rapidly diagnosed and treated. Supraventricular tachycardia is a more benign arrhythmia that may also present as a wide complex tachycardia when combined with aberrant conduction; this can be difficult to distinguish from VT.
- This section contains a list of ECG findings that suggest a diagnosis of VT as opposed to SVT with aberrancy.
Factors favouring VT over SVT with Aberrancy
- Structural heart disease (95% of wide complex tachycardias in patients with heart disease will be VT)
- Normal baseline ECG - no bundle branch block or preexcitation
- Extreme axis deviation (-90 to 180°)
- Atypical LBBB or RBBB morphology
- QRS duration >140 with RBBB pattern or >160 with LBBB pattern
- AV dissociation - visible, regular P waves (Almost 100% specific for VT)
- Positive or negative concordance - precordial leads all positive or all negative
- RS interval >100ms in precordial leads - from onset of R wave to deepest point of S wave
- R wave peak time ≥50ms in lead II - from isoelectric line to peak of R wave
Onset and Offset
- Wide complex tachycardia initiated by a ventricular complex
- Fusion beats: a hybrid between a normal QRS complex and a ventricular ectopic
- Capture beats: a normal, narrow QRS complex produced during due to a conducted atrial beat
Extreme Axis Deviation
- Extreme axis deviation, also known as northwest axis, is highly suggestive of ventricular tachycardia.
- Negative lead I
- Negative lead aVF
- Wide QRS ≥120ms
- Broad R wave in lateral leads (I, aVL, V5, V6)
- Absent Q waves in I, V5 and V6
- Initial R wave >30ms
- Josephson’s sign - notching of the S wave
- RS interval >100ms in precordial leads
- Q waves in V6
- Wide QRS ≥120ms (complete BBB) or 110-120ms (incomplete BBB)
- Added R wave (R’) in right precordial leads - RSR’ pattern in leads V1 or V2 (R’ taller than R) (Due to delayed conduction to right ventricle)
- Slurred S wave in lateral leads - S wave duration > R wave duration (or >50ms) in leads I, V5 and V6
- Monophasic R wave
- R wave taller than R’ (taller left rabbit ear)
- Q wave in V1
- QS waves in V6
- R:S ratio <1 in V6 (S wave deeper than R wave is tall)
- The presence of P waves that are regular are not associated with QRS complexes is highly suggestive of VT.
- Positive concordance - all precordial leads are positive
- Negative concordance - all precordial leads are negative
- Positive concordance:
- Negative concordance:
- Concordance, and particularly negative concordance, is highly suggestive of VT.
RS Interval in Precordial Leads
- The time from the onset of the R wave to the deepest point of the S wave in the precordial leads.
- An RS interval >100ms in the precordial leads is suggestive of VT.
R Wave Peak Time in Lead II
- The time from the start of the depolarisation from the isoelectric line to the first deflection in the complex.
- An R wave peak time ≥50ms in lead II is suggestive of VT.
Fusion & Capture Beats
- Fusion beats are hybrid complexes that occur when a ventricular beat and a supraventricular beat coincide.
- A capture beat occurs when a sinus impulse is normally conducted down the AV node and ‘captured' by the ventricle, resulting in a normal QRS complex.
- If present in the context of a wide complex tachycardia, fusion and capture beats are suggestive of VT.
Last updated on December 29th, 2018
Cosío FG. Atrial Flutter, Typical and Atypical: A Review. Arrhythmia & electrophysiology review. 2017 Jun;6(2):55.Falk RH. Atrial Fibrillation. New England Journal of Medicine. 2001 Apr 5; 344: 1067-1078.Katritsis DG, Zareba W, Camm AJ. Nonsustained ventricular tachycardia. Journal of the American College of Cardiology. 2012 Nov 13;60(20):1993-2004.Kistler PM, Roberts-Thomson KC, Haqqani HM, Fynn SP, Singarayar S, Vohra JK, Morton JB, Sparks PB, Kalman JM. P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin. Journal of the American College of Cardiology. 2006 Sep 5;48(5):1010-7.Pava LF, Perafán P, Badiel M, Arango JJ, Mont L, Morillo CA, Brugada J. R-wave peak time at DII: a new criterion for differentiating between wide complex QRS tachycardias. Heart rhythm. 2010 Jul 1;7(7):922-6.Roberts-Thompson KC, Kistler PM, Kalman JM. Focal atrial tachycardia I: clinical features, diagnosis, mechanisms, and anatomic location. Pacing and clinical electrophysiology. 2006 Jun;29(6):643-52.Rosso R, Kistler PM. Focal atrial tachycardia. Heart. 2010 Feb 1;96(3):181-5.Schoonderwoerd BA, Smit MD, Pen L, Van Gelder IC. New risk factors for atrial fibrillation: causes of not-so-lone atrial fibrillation. Europace. 2008 Jun 1;10(6):668-73.