Ventricular
Tachyarrhythmias
An Electrophysiologic Overview
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
Module Outline –
Ventricular Tachyarrhythmias
I.
Description
II.
Characteristics
A.
Mechanisms
B.
Sustained vs. nonsustained
C.
Premature ventricular contractions
Module Outline –
Ventricular Tachyarrhythmias
III. Classification
A.
Monomorphic
1.
2.
Idiopathic
a.
Description
b.
ECG recognition
c.
Treatment – ablation
Bundle branch
a.
Description
b.
ECG recognition
c.
Treatment –ablation
Module Outline –
Ventricular Tachyarrhythmias
III. Classifications - continued
3.
Ventricular flutter
a.
4.
Ventricular fibrillation
a.
B.
ECG recognition
ECG recognition
Polymorphic
1.
Torsades de pointes
a.
b.
c.
IV. Summary
Description
ECG recognition
Treatment
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
Mechanisms of VT
• Reentrant
–
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)
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
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
Abnormal Acceleration of Phase 4
Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 16.
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
Triggered
Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 158.
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
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
Classification
• Ventricular Tachycardia
–
–
Monomorphic
•
Idiopathic VT
•
Bundle branch reentry tachycardia
•
Ventricular flutter
•
Ventricular fibrillation
Polymorphic
•
Torsades de pointes (TdP)
Monomorphic VTs
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
ECG Recognition
ECG used with permission of Dr. Brian Olshansky.
Intracardiac Recording of VT
EGM used with permission of Texas Cardiac Arrhythmia, P.A.
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
ECG Recognition
Kay NG. Am J Med 1996; 100: 344-356.
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
Case History: Idiopathic VT
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
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
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
Idiopathic VT Ablation in RVOT
RAO
RAO
Idiopathic Left
Ventricular Tachycardia
• RBBB/LAFB
–
Involves the Purkinje network
• Treatment options:
–
RF ablation
–
Pharmacologic therapy (verapamil, beta blockers)
ECG Recognition
ECG used with permission of Kay NG.
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
VT Due to Bundle
Branch Reentry
Catheter Ablation of Right
Bundle Branch
V1
I
II
RA
Current
Voltage
Courtesy of Dr. Warren Jackman
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
Ventricular Fibrillation
• Heart rate: Chaotic, random and asynchronous
• Rhythm: Irregular
• Mechanism: Multiple wavelets of reentry
• Recognition:
–
No discrete QRS complexes
• Treatment:
–
Defibrillation
ECG Recognition
• P waves and QRS complexes not present
• Heart rhythm highly irregular
• Heart rate not defined
Polymorphic VT
Polymorphic VT
• Heart rate: Variable
• Rhythm: Irregular
• Mechanism:
–
Reentry
–
Triggered activity
• Recognition:
–
Wide QRS with phasic variation
–
Torsades de pointes
ECG Recognition
EGM used with permission of Texas Cardiac Arrhythmia, P.A.
Torsades de Pointes (TdP)
• Heart rate: 200 - 250 bpm
• Rhythm: Irregular
• Recognition:
–
Long QT interval
–
Wide QRS
–
Continuously changing QRS morphology
Mechanism
• Events leading to TdP are:
–
Hypokalemia
–
Prolongation of the action potential duration
–
Early afterdepolarizations
–
Critically slow conduction that contributes to reentry
ECG Recognition
• QRS morphology continuously changes
• Complexes alternates from positive to negative
Possible Causes
• Drugs that lengthen the QT:
–
Quinidine
–
Procainamide
–
Sotalol
–
Ibutilide
• Physical
–
Ischemia
–
Electrolyte abnormalities
Treatment
• Pharmacologic therapy:
–
Potassium
–
Magnesium
–
Isoproterenol
–
Possibly class Ib drugs (lidocaine) to decrease
refractoriness/shorten length of action potential
• Overdrive ventricular pacing
• Cardioversion
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