An Electrophysiologic Overview Ventricular Tachyarrhythmias.
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Transcript of An Electrophysiologic Overview Ventricular Tachyarrhythmias.
An Electrophysiologic Overview
Ventricular Tachyarrhythmias
Module Objectives – Ventricular Tachyarrhythmias
• Identify the mechanisms for ventricular tachycardias
• Differentiate types of ventricular tachycardias using ECG and intracardiac electrogram recordings
• Discuss treatment options for ventricular tachycardias
After completion of this module, the participant should be able to:
Module Outline – Ventricular Tachyarrhythmias
I. Description
II. Characteristics
A. Mechanisms
B. Sustained vs. nonsustained
C. Premature ventricular contractions
Module Outline – Ventricular Tachyarrhythmias
III. ClassificationA. Monomorphic
1. Idiopathic
a. Description
b. ECG recognition
c. Treatment – ablation
2. Bundle branch
a. Description
b. ECG recognition
c. Treatment –ablation
Module Outline – Ventricular Tachyarrhythmias
III. Classifications - continued3. Ventricular flutter
a. ECG recognition
4. Ventricular fibrillationa. ECG recognition
B. Polymorphic1. Torsades de pointes
a. Description
b. ECG recognition
c. Treatment
IV. Summary
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
Kay NG. Am J Med 1996; 100: 344-356.
ECG Recognition
Case History: Idiopathic VT
• 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
39 y.o. female with no prior cardiac history
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 ablatedusing 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 used with permission of Kay NG.
ECG Recognition
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
Courtesy of Dr. Warren Jackman
IIIV1
RA
Current
Voltage
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