Ventricular Tachycardia

Definition

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

Monomorphic ventricular tachycardia

Clinical Significance

  • 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.

Classification of Ventricular Tachycardia

Ventricular tachycardia can be classified based on:

1. Morphology

2. Duration

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

3. Clinical Presentation

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

Mechanisms of Ventricular Tachycardia

Three mechanisms exist for initiation and propagation of ventricular tachycardia:

1. Reentry

  • 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.


2. Triggered Activity

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

3. Abnormal Automaticity

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

Electrocardiographic Features of Ventricular Tachycardia

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 are available here.

Monomorphic VT

  • 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).
AV dissociation in VT

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

Capture beats in VT

Capture beat: the sinus node “captures” the ventricles producing a narrow-complex beat

Fusion beats in VT

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 the precordial leads

Negative concordance in VT

NEGATIVE concordance in the precordial leads

Brugadas and Josephson’s signs

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

Causes of Monomorphic VT

ECG Examples – Monomorphic VT

Example 1

Monomorphic VT

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.

 

Example 2

Monomorphic VT

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. 

 

Example 3

Ventricular tachycardia

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.

 

Example 4

VT and bigeminy

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.

 

Example 5
Ventricular Tachycardia

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.

 

Example 6 

Ventricular Tachycardia

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.

NOTE: in the presence of a dominant R waveinV1 (“RBBB morphology”), VT is diagnosed if:

  • There is an RSR’ complex with a taller left rabbit ear
  • There is a tall monophasic R wave
  • There is an rS complex in V6 (R/S ratio < 1)

See “VT versus SVT with aberrancy” for more details.

 

Example 7

Ventricular Tachycardia

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.

AV dissociation: superimposed P waves at a different rate to the QRS complexes

 

Differential Diagnosis of Wide-Complex Tachycardia

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.

Clinical Features Suggestive of VT

  • 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)

Diagnostic Algorithms

  • 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 here.

Remember

  • If in doubt, treat as VT!

 

Related Topics

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

References

  • Surawicz B, Knilans TK. Chou’s Electrocardiography in Clinical Practice. 6th Edition. Saunders Elsevier 2008.
  • Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.
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