Ventricular Tachycardia – Monomorphic

• Ventricular Tachycardia (VT) is a broad complex tachycardia originating in the ventricles.
• There are several different varieties of VT — the most being Monomorphic VT.

• Ventricular tachycardia may impair cardiac output with consequent hypotension, collapse, and acute cardiac failure. This is due to extreme heart rates and lack of coordinated atrial contraction (loss of “atrial kick”).
• The presence of pre-existing poor ventricular function is strongly associated with cardiovascular compromise.
• Decreased cardiac output may result in decreased myocardial perfusion with degeneration to VF.
• Prompt recognition and initiation of treatment (e.g. electrical cardioversion) is required in all cases of VT.

• Monomorphic
• Polymorphic VT
• Torsades De Pointes (Polymorphic with QT prolongation)
• Right Ventricular Outflow Tract Tachycardia
• Fascicular Tachycardia
• Bidirectional VT
• Ventricular Flutter
• Ventricular Fibrillation

• Sustained = Duration > 30 seconds or requiring intervention due to hemodynamic compromise.
• Non-sustained = Three or more consecutive ventricular complexes terminating spontaneously in < 30 seconds.

• Haemodynamically stable.
• Haemodynamically unstable — e.g hypotension, chest pain, cardiac failure, decreased conscious level.

• Commonest mechanism.
• Requires two distinct conduction pathways with a conduction block in one pathway, and a region of slow conduction in the other.
• Develops due to abnormal myocardial scarring usually due to prior ischemia or infarction.

• Occurs due to early or late after-depolarisations.
• Examples include Torsades and digitalis toxicity.

• Accelerated abnormal impulse generation by a region of ventricular cells.

Ventricular tachycardia can be difficult to differentiate from other causes of broad complex tachycardia. The following characteristics aid in the identification of VT.Features common to any broad complex tachycardia

• Rapid heart rate (> 100 bpm).
• Broad QRS complexes (> 120 ms).

Features suggestive of VT

• Very broad complexes (>160ms).
• Absence of typical RBBB or LBBB morphology.
• Extreme axis deviation (“northwest axis”) — QRS is positive in aVR and negative in I + aVF.
• 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 coincide to produce a hybrid complex of intermediate morphology.
• 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.

Additional morphological criteria for VT can be found on ECGpedia

• Regular rhythm.
• Originates from a single focus within the ventricles.
• Produces uniform QRS complexes within each lead — each QRS is identical (except for fusion/capture beats).

• Ischaemic Heart Disease
• Dilated cardiomyopathy
• Hypertrophic cardiomyopathy
• Chaga’s Disease

Monomorphic VT:

• Classic monomorphic VT with uniform QRS complexes.
• Indeterminate axis.
• Very broad QRS (~200 ms).
• Notching near the nadir of the S wave in lead III = Josephson’s sign.

Monomorphic VT:

• Very broad QRS complexes (~ 200 ms) with uniform morphology.
• Fusion and capture beats are seen in the rhythm strip.
• Brugada’s sign is present: the time from the onset of the QRS complex to nadir of S wave is > 100 ms (best seen in V6).

NB. The rhythm strip is recorded after the other 12 leads rather than simultaneously. 

Monomorphic VT:

• Very broad complexes (~ 200 ms in V5-6).
• Northwest axis (-120 degrees).
• Brugada’s sign – The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms.
• Joesphson’s sign – Notching near the nadir of the S wave is seen in leads II, III, aVF.
• Possibly some superimposed P waves in aVF.

Monomorphic VT alternates withventricularbigeminy. The ventricular complexes have the following features:

• Very broad QRS duration (> 160 bpm).
• Positive concordance in the precordial leads (dominant R waves in V1-6).
• Brugada’s sign – time from onset of QRS to nadir of S wave > 100 ms; best seen in leads aVR and aVL.

The presence of normal sinus beats (capture beats) in the second half of the ECG further supports the diagnosis of VT.

Monomorphic VT:

• Extreme axis deviation / northwest axis is present
  • -150 degree; QRS positive in aVR, negative in I + aVF
• There is a RBBB-like pattern in V1 with a taller left rabbit ear – this is very specific for VT.

Monomorphic VT:

• Northwest axis.
• Tall monophasic R wave in V1 with an rS complex in V6 (small R wave, big S wave)  – this pattern is also very specific for VT.

This ECG fulfils the Brugada Morphology Criteria for 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 rS complex in V6 (tiny R wave, deep S wave) indicate that this is VT.

Several arrhythmias can present as a wide-complex tachycardia (QRS > 120 ms) including:

• Ventricular Tachycardia
• SVT with aberrant conduction due to bundle branch block
• SVT with aberrant conduction due to the Wolff-Parkinson-White syndrome
• Pace-maker mediated tachycardia
• Metabolic derangements e.g. hyperkalaemia
• Poisoning with sodium-channel blocking agents (e.g. tricyclic antidepressants)

Differentiating between the various causes of wide-complex tachycardia is challenging and not always possible.

• 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)

• A number of diagnostic algorithms exist to help aid in the diagnosis of VT.
• No algorithm is 100% accurate in predicating VT
• Algorithms can be complex and require specific and unfamiliar measurements to be calculated
• Flow charts for the four commonly used algorithms (ACC, Brugada, Ultra-simple Brugada, Vereckei ) can be found over at ECGpedia.org.

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

• VT versus SVT with aberrancy
• Right Ventricular Outflow Tract Tachycardia
• Polymorphic VT / Torsades De Pointes
• Fascicular VT
• Bidirectional VT
• Ventricular Flutter
• ECG Exigency 004 – a case of broad complex tachycardia.

• Brady WJ, Truwit JD. Critical Decisions in Emergency and Acute Care Electrocardiography
• Hampton, JR. The ECG In Practice, 6e
• Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric, 6e
• Wagner, GS. Marriott’s Practical Electrocardiography 12e
• Chan, TC. ECG in Emergency Medicine and Acute Care
• Mattu, A. ECG’s for the Emergency Physician