1. Ventricular Tachyarrhythmias
An Electrophysiologic Overview
Welcome to VENTRICULAR TACHYARRHYTHMIAS – AN ELECTROPHYSIOLOGIC OVERVIEW. This module contains a discussion of the various characteristics and classifications of ventricular tachycardia (VT). ECG recognition and treatment of the various tachycardias will be explored. Focus is given to the use of RF ablation as a treatment for certain VTs.

2. Module Objectives – Ventricular Tachyarrhythmias
After completion of this module, the participant should be able to:
Identify the mechanisms for ventricular tachycardias
Differentiate types of ventricular tachycardias using ECG and intracardiac electrogram recordings
Discuss treatment options for ventricular tachycardias
Participant objectives, for this module, are as listed.

3. Module Outline – Ventricular Tachyarrhythmias
Description
Characteristics
Mechanisms
Sustained vs. nonsustained
Premature ventricular contractions
This module will start by discussing the characteristics of VT.

4. Module Outline – Ventricular Tachyarrhythmias
Classification
Monomorphic
Idiopathic
Description
ECG recognition
Treatment – ablation
Bundle branch
Treatment –ablation
VTs are generally classified as being either monomorphic or polymorphic. Detailed discussions of monomorphic VTs, (idiopathic, bundle branch, ventricular flutter,and ventricular fibrillation) will include a description of the rhythm, ECG characteristics, and treatment options.

5. Module Outline – Ventricular Tachyarrhythmias
Classifications - continued
Ventricular flutter
ECG recognition
Ventricular fibrillation
Polymorphic
Torsades de pointes
Description
Treatment
Summary
The presentation will conclude with a discussion of Torsades de pointes.

6. Ventricular Tachycardia (VT)
Originates in the ventricles
Can be life threatening
Most patients have significant heart disease
Coronary artery disease
A previous myocardial infarction
Cardiomyopathy
Sudden death affects approximately 250,000 or more Americans annually according to the AHA. Most causes of sudden death can be attributed to VT or ventricular fibrillation (VF).
As the name implies, ventricular tachycardia, originates in the ventricles. Rates can range from 110 – 250 bpm.
Ventricular tachyarrhythmias are often, life threatening and require immediate intervention. Occasionally, slower VTs may be relatively well tolerated.
While most ventricular arrhythmias occur in patients with a history of heart disease, they have also been seen in patients with healthy hearts.

7. Mechanisms of VT Reentrant Automatic Triggered activity
Reentry circuit (fast and slow pathway) is confined to the ventricles and/or bundle branches
Automatic
Automatic focus occurs within the ventricles
Triggered activity
Early afterdepolarizations (phase 3)
Delayed afterdepolarizations (phase 4)
Ventricular tachycardia can be attributed to one of three mechanisms.

8. Reentrant Reentrant ventricular arrhythmias
Premature ventricular complexes
Idiopathic left ventricular tachycardia
Bundle branch reentry
Ventricular tachycardia and fibrillation when associated with chronic heart disease:
Previous myocardial infarction
Cardiomyopathy
Reentry is a common cause of ventricular tachyarrhythmias. It is the mechanism that is responsible for the arrhythmias listed on this slide.
Left idiopathic ventricular tachycardia is rare.

9. Automatic Automatic ventricular arrhythmias
Premature ventricular complexes
Ischemic ventricular tachycardia
Ventricular tachycardia and fibrillation when associated with acute medical conditions:
Acute myocardial infarction or ischemia
Electrolyte and acid-base disturbances, hypoxemia
Increased sympathetic tone
Automaticity enables the cell to spontaneously produce an electrical impulse without an external stimulus. It is the mechanism for arrhythmias listed on this slide.
Of note, hypoxemia is deficient oxygenation of the blood.

10. Abnormal Acceleration of Phase 4
Automaticity
This graphic illustrates the cause of automaticity: abnormal acceleration of phase 4 of the action potential in a cardiac cell. This reduces the time of repolarization, and allows the cell to depolarize again.
Automaticity enables some cardiac cells (ectopic cells) to act as backup pacemakers when the SA node malfunctions. Ectopic sites may generate impulses in addition to the impulses generated by the SA node, or the ectopic sites may generate impulses out of sync with the normal heart rhythm. Enhanced automaticity occurs when the SA node or ectopic sites generate electrical impulses too quickly, which may affect heart rhythm or rate. Ectopic sites may be located in the atria, AV node, or in the ventricles and can produce tachycardias reflective of the site of origination.
Abnormal Acceleration of Phase 4
Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 16.

11. Triggered Triggered activity ventricular arrhythmias
Pause-dependent triggered activity
Early afterdepolarization (phase 3)
Polymorphic ventricular tachycardia
Catechol-dependent triggered activity
Late afterdepolarizations (phase 4)
Idiopathic right ventricular tachycardia
Characteristically, triggered activity resembles both automaticity and reentry. Triggered activity can be divided into two different categories: pause-dependent and catechol-dependent. Pause-dependent triggered activity is caused by early afterdepolarizations in phase 3 of the action potential. These VTs are usually polymorphic.
Catechol-dependent triggered activity is caused by late afterdepolarizations in phase 4 of the action potential. They may be seen in patients with digitoxicity, cardiac ischemia, or congenitally prolonged QT intervals. Increased sympathetic tone also plays a part in these arrhythmias. Idiopathic right ventricular tachycardia is attributed to this mechanism.

12. Triggered
Figure A illustrates the early afterdepolarizations in phase 3 of the action potential, responsible for pause-dependent triggered activity.
Figure B illustrates late afterdepolarizations seen in late phase 3 or phase 4 of the action potential, responsible for catechol-dependent triggered activity.
Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 158.

13. Sustained vs. Nonsustained
Sustained VT
Episodes last at least 30 seconds
Commonly seen in adults with prior:
Myocardial infarction
Chronic coronary artery disease
Dilated cardiomyopathy
Non-sustained VT
Episodes last at least 6 beats but < 30 seconds
Another characteristic, used to describe VT, is whether it is sustained or non-sustained.

14. Premature Ventricular Contraction
PVC
Ectopic beat in the ventricle that can occur singly or in clusters
Caused by electrical irritability
Factors influencing electrical irritability
Ischemia
Electrolyte imbalances
Drug intoxication
PVC’s can lead to ventricular tachycardia or fibrillation in individuals with ischemic or damaged hearts.
PVCs can occur in many combinations (e.g., bigeminal, trigeminal, couplets) or from many ectopic foci, (e.g., multifocal PVCs).

15. Classification Ventricular Tachycardia Monomorphic Polymorphic
Idiopathic VT
Bundle branch reentry tachycardia
Ventricular flutter
Ventricular fibrillation
Polymorphic
Torsades de pointes (TdP)
Ventricular tachycardia can be classified as being either monomorphic or polymorphic. The following slides present a discussion for each rhythm listed, along with EGC identification and treatment options.
Ventricular flutter is rarely seen, and may be seen just prior to the onset of ventricular fibrillation.
Torsades de pointes is associated with a long QT interval.

16. Monomorphic VTs

17. Monomorphic VT Heart rate: 100 bpm or greater Rhythm: Regular
Mechanism
Reentry
Abnormal automaticity
Triggered activity
Recognition
Broad QRS
Stable and uniform beat-to-beat appearance
Monomorphic VT is regular, with uniform beat-to-beat morphology. It can be sustained, nonsustained, idiopathic or caused by bundle branch reentry.

18. ECG Recognition ECG used with permission of Dr. Brian Olshansky.
ECG characteristics that help define VTs are:
The QRS complexes are rapid, wide, and distorted.
The T waves are large with deflections opposite the QRS complexes.
The ventricular rhythm is usually regular.
P waves are usually not visible.
The PR interval is not measurable.
A-V dissociation may be present.
V-A conduction may or may not be present.
It may be difficult to distinguish VT from SVT with aberrancy from a surface ECG. Many texts offer tips for distinguishing these rhythms. The presence of capture and fusion beats generally occur in VT.
ECG used with permission of Dr. Brian Olshansky.

19. Intracardiac Recording of VT
This slide contains an intracardiac recording of VT. Note the morphology changes slightly during the tracing. Nice VA dissociation is seen (His A is small).
EGM used with permission of Texas Cardiac Arrhythmia, P.A.

20. Idiopathic Right Ventricular Tachycardia
Right ventricular idiopathic VT
Focus originates within the right ventricular outflow tract
Ventricular function is usually normal
Usually LBBB, inferior axis
Treatment options:
Pharmacologic therapy (beta blockers, verapamil)
RF ablation
This tachycardia may terminate with adenosine. It is catecholamine sensitive and usually inducible with isoproterenol.

21. ECG Recognition Kay NG. Am J Med 1996; 100: 344-356.
This slide is a recording of RVOT VT.
Kay NG. Am J Med 1996; 100:

22. Case History: Idiopathic VT
39 y.o. female with no prior cardiac history
First episode
9 hours of palpitations
In ER, found to be in wide-complex tachycardia of LBBB, inferior axis, at 205 bpm
Converted with IV lidocaine; placed on tenormin
Second episode
While on tenormin, patient had onset of palpitations at airport
In ER, converted with IV lidocaine
Patient underwent EP study
The following slides discuss the case of a 39 year old white female, who presented with idiopathic VT.

23. Case History: Idiopathic VT
This recording was taken during the patient’s EP study.

24. Case History: Idiopathic VT
At EP study, tachycardia focus was mapped and localized to right ventricular outflow tract
The focus was successfully ablated using radiofrequency energy, with no subsequent inducible or clinical VT

25. Endocardial Activation Mapping
Using an ablation catheter, map the area around and inside of the right ventricular outflow tract
Find the electrograms that precede the onset of the QRS complex during tachycardia
This area identifies the site of earliest activation, and possibly the “site of origin” of the arrhythmia
In the case of reentrant tachycardias, activation mapping identifies the exit. Furthermore, it looks for the earliest activation site compared to the other sites sampled. If the tachycardia arises from another chamber, it may not be detected with this technique.

26. Pace Mapping
Pace mapping helps to localize the “site of origin” after endocardial mapping has been performed
If the heart is paced from this region, the resulting ECG should be identical to the ECG taken during tachycardia
Delivering RF energy to this site usually eliminates ventricular tachycardia
These statements are true, especially if pacing unipolar.

27. Idiopathic VT Ablation in RVOT
RAO
RAO

28. Idiopathic Left Ventricular Tachycardia
RBBB/LAFB
Involves the Purkinje network
Treatment options:
RF ablation
Pharmacologic therapy (verapamil, beta blockers)
Idiopathic left ventricular tachycardia has been seen in younger patients with normal hearts.

29. ECG Recognition ECG used with permission of Kay NG.
This ECG is left ventricular tachycardia.
ECG used with permission of Kay NG.

30. Bundle Branch Reentry
Reentry circuit is confined to the left and right bundle branches
Usually LBBB, during sinus rhythm
Presents with:
Syncope
Palpitations
Sudden cardiac death
Treatment: RF ablation of right bundle
Bundle branch reentry tachycardia is another VT that is treatable with RF ablation. With this type of tachycardia, the HV interval is increased.
Ablation of the right bundle does cure this form of reentry. However, given the underlying LBBB, ablation of the RBBB results in either very impaired His/Purkinje function or in complete heart block. A pacer is usually required.

31. VT Due to Bundle Branch Reentry
The most helpful criteria to consider when diagnosing VT due to bundle branch reentry is the comparison of this LBBB morphology to the LBBB seen in sinus. The morphology does not have to be exactly the same (if there is some conduction down the left bundle) but it should be really similar.

32. Catheter Ablation of Right Bundle BranchV1 II RA
Current
Voltage
Notice the abrupt transition from the LBBB to the RBBB during RF. Also note the significant PR prolongation both before and after RF. Severe His/Purkinje delay is required for this tachycardia to occur.
Courtesy of Dr. Warren Jackman

33. Ventricular Flutter Heart rate: 300 bpm Rhythm: Regular and uniform
Mechanism: Reentry
Recognition:
No isoelectric interval
No visible T wave
Degenerates to ventricular fibrillation
Treatment: Cardioversion
Rarely seen, ventricular flutter may occur just prior to the onset of ventricular fibrillation. It degenerates into ventricular fibrillation in a matter of seconds.

34. Ventricular Fibrillation
Heart rate: Chaotic, random and asynchronous
Rhythm: Irregular
Mechanism: Multiple wavelets of reentry
Recognition:
No discrete QRS complexes
Treatment:
Defibrillation
Ventricular fibrillation (VF) will convert to fine VF and then no electrical activity will be seen. Patients resuscitated from VF are deemed sudden cardiac death survivors.

35. ECG Recognition P waves and QRS complexes not present
Heart rhythm highly irregular
Heart rate not defined
The following ECG findings help electrophysiologists to diagnose VF:
P waves and QRS complexes are not present.
Heart rhythm is highly irregular.
The heart rate is not defined (without QRS complexes).

36. Polymorphic VT

37. Polymorphic VT Heart rate: Variable Rhythm: Irregular Mechanism:
Reentry
Triggered activity
Recognition:
Wide QRS with phasic variation
Torsades de pointes
A second classification of VT is polymorphic VT.

38. ECG Recognition
EGM used with permission of Texas Cardiac Arrhythmia, P.A.

39. Torsades de Pointes (TdP)
Heart rate: bpm
Rhythm: Irregular
Recognition:
Long QT interval
Wide QRS
Continuously changing QRS morphology
TdP is a rapid and distinct VT with a twisting configuration of the QRS morphology, associated with prolonged repolarization. It may be acquired or congenital. It is a very deadly form of VT.

40. Mechanism Events leading to TdP are: Hypokalemia
Prolongation of the action potential duration
Early afterdepolarizations
Critically slow conduction that contributes to reentry
The early afterdepolarizations initiate the tachycardia; reentry sustains it.

41. ECG Recognition QRS morphology continuously changes
Complexes alternates from positive to negative
Torsades de pointes (twists of points) is a unique VT in which the QRS complexes change from positive to negative and appear to twist around the isoelectric line.

42. Possible Causes Drugs that lengthen the QT: Physical Quinidine
Procainamide
Sotalol
Ibutilide
Physical
Ischemia
Electrolyte abnormalities
Possible causes of TdP can include drugs that lengthen the QT interval. Causes can also be physical in nature.

43. Treatment Pharmacologic therapy: Overdrive ventricular pacing
Potassium
Magnesium
Isoproterenol
Possibly class Ib drugs (lidocaine) to decrease refractoriness/shorten length of action potential
Overdrive ventricular pacing
Cardioversion
The treatment for TdP can be with drugs, overdrive pacing, or cardioversion.
Of note, isoproterenol is contraindicated in patients with hypertension or ischemic heart disease. Treatment with potassium is dependent on the potassium blood level and is only given if the patient is hypokalemic.
The treatment for congenital TdP is beta blockade and/or an ICD. The treatment for acquired TdP is avoiding pauses (acutely) and reversing the underlying cause.

44. Summary VT ablation is not an FDA-approved indication
RF catheter ablation can be a useful technique in patients with ventricular tachycardia
Success largely depends on the etiology of the arrhythmia
Unstable sustained VT, polymorphic VT and ventricular fibrillation are not ablatable
Improved catheters and imaging techniques may change this in the future
This concludes VENTRICULAR TACHYARRHYTHMIAS – AN ELECTROPHYSIOLOGIC OVERVIEW. As discussed, ablation is an effective therapy for selected VTs. Approximate success rates are as follows:
70% for patients with coronary artery disease
95% for patients with BBR VT
85% for RVOT VT
85% for Idiopathic left ventricular tachycardia