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Ventricular Tachycardia

Ventricular tachycardia (VT)

Ventricular Tachycardia

• Ventricular Tachycardia (VT) is a ventricular rhythm with a frequency > 100/min.
• Impulses are generated in the ventricles beneath the His bundle
• It is a wide-complex tachycardia (QRS width > 0.12s)
• The most common cause is
• Re-entry in a scar after a myocardial infarction
• which generates impulses with a frequency > 100/min.
• 50% of VT cases have preserved retrograde conduction
• Impulses from the ventricles spread retrogradely through the AV node to the atria
• Because the AV node at that time is not in the refractory period
• The SA node is reset and does not generate impulses (overdrive suppression)

Mechanism of Ventricular Tachycardia Formation

• An ectopic focus activates in the ventricle
• which starts generating impulses with a frequency > 100/min.
• The focus takes over the role of the pacemaker (overdrive suppression)
• The focus can generate impulses through 3 mechanisms:
• Re-entry
• Increased automaticity
• Trigger activity
  
  
• The most common mechanism is re-entry
• which occurs in a scar after a myocardial infarction

Duration of Ventricular Tachycardia

• Ventricular tachycardia is classified based on duration into:
• Non-sustained VT (Non-sustained VT)
• Sustained VT (Sustained VT)

Non-sustained Ventricular Tachycardia

• Consists of at least 3 ventricular QRS complexes in a row
• If there are fewer QRS complexes, it is a ventricular extrasystole
• Ends spontaneously within 30 seconds
• Non-sustained VT "does not persist" and terminates on its own within 30s

Sustained Ventricular Tachycardia

• Lasts for more than 30 seconds
• Ends spontaneously, or can be terminated with treatment such as electrical cardioversion

Morphology of Ventricular Tachycardia

• Every ventricular tachycardia (VT) has
• Frequency > 100/min.
• Wide QRS complexes (> 0.12s)
• Very rarely, QRS complexes can be narrow (VT from the ventricular septum, Fascicular VT)
• Active ectopic ventricular focus (foci)
  
  
• There is no uniform classification of VT because there are many criteria:
• Structural heart damage, number and location of foci, mechanism of VT, response of VT to treatment, hemodynamic stability, shape of the ECG curve...
  
  
• The shape of the VT ECG curve depends mainly on:
• Location of the ectopic focus
• Septal, Apical, Basal, in the Outflow Tract, in the Left Ventricle, in the Right Ventricle
• Mechanism of VT
• Re-entry, Increased automaticity, Trigger activity
  
  
• Based on the morphology of the ECG curve, ventricular tachycardia is classified into:
• Monomorphic VT (the most common form of VT)
• Polymorphic VT
• Torsades de Pointes
• VT of the Right Ventricular Outflow Tract
• VT of the Left Ventricular Outflow Tract
• Fascicular VT
• Bundle Re-entry VT
• Bidirectional VT
• Ventricular Flutter
• Ventricular Fibrillation

ECG and Ventricular Tachycardia

• Frequency > 100/min.
• Wide QRS complexes (≥ 0.12s, most often > 0.16s)
• Very rarely, QRS complexes are narrow (VT from the ventricular septum, Fascicular VT)
• Absence of typical ECG pattern of bundle branch block in leads V1, V6 (LBBB, RBBB)
• RSr configuration in V1 (Left bunny ear is larger)
• Extreme right axis deviation "north-west"
  • QRS is positive in aVR
  • QRS is negative in I, aVF
• AV dissociation
• Capture beats
• Fusion beats
• Precordial concordance (Positive or negative)
• Brugada sign
• Josephson sign
• R wave duration in lead II ≥ 50ms
  
  
• Each ECG finding can be logically derived
• VT does not always present all ECG findings
• Each finding has a certain sensitivity and specificity in diagnosing VT
• Diagnostic algorithms are used for diagnosing VT

Absence of Typical Tawar Bundle Branch Block EKG Pattern (V1, V6)

• A: r wave > 0.03s
• B: Josephson sign
• C: Brugada sign

• In the case of bundle branch block (left or right):
  • The ventricles first activate through the non-blocked bundle branch
  • Then, the other ventricle activates with delay through the myocardium, making the QRS complex wide (>0.12s)
• If the VT focus is lateral in the ventricle, both ventricles are activated through the myocardium from the focus
  • The QRS will resemble bundle branch block and does not meet the EKG criteria for bundle branch block
• VT with Right Bundle Branch Block Pattern (Right Bundle Branch Block)
  • In V1, the QRS complex is bifasic (R, qR, QR, RS)
  • If V1 shows a trifasic QRS (Rsr), then the left rabbit ear is larger
  • In V6, the R/S ratio is < 1
  • Extreme right axis deviation (180° to -90°)
    • Negative QRS in I, aVF
• VT with Left Bundle Branch Block Pattern (Left Bundle Branch Block)
  • In V1, the initial r wave is wider than 0.03s
  • In V1, there is a notch on the descending part of the S wave (Slurring or notching of S wave)
    • Josephson sign
  • In V1, the RS interval is > 0.1s
    • Brugada sign
  • In V6, there is a q (Q) wave
  • Right axis deviation (90° to 180°)
    • Negative QRS in I
    • Positive QRS in aVF

Ventricular Tachycardia with RBBB Pattern

• Heart rate: 150/min
• Wide QRS > 0.12s
• In V1, there is a wide, high R wave
• Does not have the typical RBBB configuration (in RBBB, the right rabbit ear is larger - rsR')
• Leads V1 and V6 do not resemble RBBB

Ventricular Tachycardia with RBBB Pattern

• Heart Rate 143/min
• Wide QRS > 0.12s
• QRS are borderline widened approximately 0.13s
• In V1 rsR (right rabbit ear is larger)
• This is the RBBB pattern (but it is ventricular tachycardia)
• Extreme right axis deviation (180° to -90°)
• Negative QRS (I, aVF)
Supraventricular tachycardia with RBBB does not have such an extremely deviated axis
• This is a rare fascicular ventricular tachycardia with the focus in the left posterior fascicle

Ventricular Tachycardia with LBBB Morphology

• Heart rate 150/min
• Wide QRS > 0.12s
• Brugada sign (V1)
• V1 RS interval > 100ms (From the beginning of the QRS complex to the peak of the S wave is > 100ms)
• Right axis deviation (90° to 180°)
• Negative QRS (I)
• Positive QRS (aVF)
• VA association
• Preserved retrograde conduction (arrows indicate retrograde P waves)
• Physiological P wave is never positive in inferior leads (II, III, aVF)

Left Rabbit Ear (V1)

• In right bundle branch block, the V1 rsR configuration appears
• The right rabbit ear is larger
• If ventricular tachycardia produces a positive Rsr in V1 (ectopic focus is in the left ventricle)
• Then there is a larger left rabbit ear
• VT has a different direction of cardiac vectors compared to right bundle branch block
• This does not apply to fascicular ventricular tachycardia

Right Bundle Branch Block

• Wide QRS > 0.12s
• "M" rsR configuration (V1) - The right rabbit ear is larger
• "W" configuration (V6) - Deep S wave

Ventricular Tachycardia with BPTR Pattern

• Wide monophasic QRS (V1) > 0.12s
• Left bunny ear is larger (blue arrow - It is not a typical "bunny ear")

AV Dissociation and VA Association

• 50% of VT cases have preserved retrograde conduction (This is VA association)
• Ventricular impulses activate the ventricles and then retrogradely spread through the AV node to the atria
• They reset the SA node, which does not generate impulses (overdrive suppression)
• The impulse passes through the AV junction because it is not in the refractory period
• The atria are activated retrogradely (bottom to top)
• VA association (Ventriculoatrial association) means there is an "association" between the ventricles and the atria
• The impulse first activates the ventricles and then retrogradely activates the atria
• Retrograde conduction gradually disappears with increasing VT frequency
  
  
• 50% of VT cases have AV dissociation
• Impulses originate in the ventricle and simultaneously in the SA node
• Ventricular impulses have a higher frequency (> 100/min.)
• Impulses from the SA node create a P wave, but are then blocked in the AV junction
• Because in the AV junction two impulses meet in the refractory period (one from the ventricles and the other from the SA node)
• AV dissociation is seen on EKG as the independence of P waves from QRS complexes
• Note that AV dissociation is not AV block III degree, but AV block III degree will show AV dissociation on EKG
• P waves are often not seen during VT because they are embedded within wide QRS complexes
• Therefore, AV dissociation is not visible
• To better visualize AV dissociation during ventricular tachycardia, a Lewis lead may be used

Ventricular Tachycardia

• The first QRS complex is a sinus beat
• Then follows ventricular tachycardia (wide QRS complexes >0.12s)
• The SA node still generates impulses (P waves) with a frequency of 60/min.
• An ectopic ventricular focus generates impulses (QRS) with a frequency of 150/min.
• Ventricular impulses do not pass to the atria, and atrial impulses do not pass to the ventricles
• Due to the refractory period of the AV node
• On the EKG, we see AV dissociation (independence of P waves from QRS complexes)

Ventricular Tachycardia

• Wide QRS complexes 0.18s
• Frequency: 130/min.
• AV Dissociation
• P waves are independent of QRS complexes
• P waves deform QRS complexes and T waves

Fusion Beat

• During VT, an impulse originates in the SA node and conducts to the ventricles at a time
• when two impulses meet in the ventricles (atrial + ventricular)
• A Fusion Beat occurs
• The result is a deformed QRS complex, which is
• Smaller than the ectopic ventricular QRS complex
• Larger than the sinus QRS complex (Capture Beat)

Capture Beat, Fusion Beat, Ventricular Beat

• Sinus Beat (Capture Beat)
• The ventricles are activated by an impulse from the SA node through the conduction system, resulting in a narrow QRS complex
• If a sinus beat occurs during VT, it is called a Capture Beat
• Ventricular Beat
• The ventricles are activated by an impulse from an ectopic ventricular focus through the myocardium, not through the conduction system, resulting in a wide QRS complex
• It is essentially a ventricular extrasystole (VES); 3 VES in a row is considered VT
• Fusion Beat
• The ventricular myocardium is activated by 2 impulses
• One from the atrium (SA node)
• The other from the ventricular ectopic focus
• The ectopic focus and the SA node generated impulses simultaneously, and did not reset in the AV junction
• A deformed QRS is produced (different from both sinus and ventricular)

Capture Beat and Fusion Beat

• Ventricular Extrasystoles (Couplet) (1st and 2nd wide QRS complexes)
• Capture Beat
• The SA node outpaced and deactivated the ventricular focus
• Fusion Beat
• Two impulses met in the ventricles:
• One from the SA node
• The other from a ventricular ectopic focus

Ventricular Tachycardia

• Frequency: 160/min.
• Wide QRS complexes 0.2s
• If the QRS is wide > 0.16s, it is almost always VT
• Negative Precordial Concordance
• All QRS complexes (V1-V6) are negative

Ventricular Tachycardia

• Frequency: 160/min.
• Wide QRS complexes 0.2s
• If the QRS is wider than 0.16s, it is almost always VT
• Negative Precordial Concordance
• All QRS complexes (V1-V6) are negative

Josephson Sign

• In VT, the ventricles are almost always structurally altered (due to infarction, cardiomyopathy, etc.)
• During the propagation of the impulse through the damaged myocardium, the vector may partially change direction
• which is seen as a notch on the descending part of the S wave (Notching near the nadir of the S-wave)
• The Josephson sign is evaluated in any lead

Josephson Sign and Brugada Sign

• Brugada Sign
• RS interval > 100ms
• Josephson Sign
• Notch on the descending part of the S wave (blue arrow)

Ventricular Tachycardia

• Wide QRS complexes 0.2s
• Extreme right axis deviation (180° to -90°)
• Negative QRS (I, aVF)
• Brugada Sign
• RS interval > 100ms
• Josephson Sign
• Notch on the descending part of the S wave (II, III, aVF)
• R (Q) wave peak time in lead II > 50ms

Ventricular Tachycardia

• Wide QRS Complexes: 0.2s
• In the second half of the continuous lead (rhythm strip), there are capture beats and fusion beats
• The continuous lead was recorded after the 12-lead ECG
• Therefore, the beats are not shown in the precordial and chest leads
• Brugada Sign
• RS interval > 100ms (V6)
• R (Q) wave peak time in lead II > 50ms