Ventricular Arrhythmias EP Overview Medtronic

8/14/2019 Ventricular Arrhythmias EP Overview Medtronic

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An Electrophysiologic Overview

Ventricular Tachyarrhythmias


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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:


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Module Outline Ventricular Tachyarrhythmias

I. Description

II. Characteristics

A. MechanismsB. Sustained vs. nonsustained

C. Premature ventricular contractions


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Module Outline Ventricular Tachyarrhythmias

III. ClassificationA. Monomorphic

1. Idiopathic

a. Description

b. ECG recognition

c. Treatment ablation

2. Bundle branch

a. Descriptionb. ECG recognition

c. Treatment ablation


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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


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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)


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Reentrant

Reentrant ventricular arrhythmias Premature ventricular complexes

Idiopathic left ventricular tachycardia

Bundle branch reentry

Ventricular tachycardia and fibrillation whenassociated with chronic heart disease:

Previous myocardial infarction

Cardiomyopathy


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Automatic

Automatic ventricular arrhythmias Premature ventricular complexes

Ischemic ventricular tachycardia

Ventricular tachycardia and fibrillation whenassociated with acute medical conditions:

Acute myocardial infarction or ischemia

Electrolyte and acid-base disturbances, hypoxemia

Increased sympathetic tone


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Automaticity

Abnormal Acceleration of Phase 4

Fogoros: Electrophysiologic Testing. 3 rd ed. Blackwell Scientific 1999; 16.


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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


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Triggered

Fogoros: Electrophysiologic Testing. 3rd

ed. Blackwell Scientific 1999; 158.


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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


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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


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Classification

Ventricular Tachycardia Monomorphic

Idiopathic VT

Bundle branch reentry tachycardia

Ventricular flutter

Ventricular fibrillation

Polymorphic Torsades de pointes (TdP)


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Monomorphic VTs


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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


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ECG Recognition

ECG used with permission of Dr. Brian Olshansky.


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Intracardiac Recording of VT

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


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Idiopathic RightVentricular 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


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Kay NG. Am J Med 1996; 100: 344-356.

ECG Recognition


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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 palpitationsat airport In ER, converted with IV lidocaine

Patient underwent EP study

39 y.o. female with no prior cardiac history


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At EP study, tachycardia focus was mappedand localized to right ventricular outflow tract

The focus was successfully ablatedusing radiofrequency energy, with nosubsequent inducible or clinical VT


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EndocardialActivation Mapping

Using an ablation catheter, map the areaaround 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


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Pace Mapping

Pace mapping helps to localize the siteof origin after endocardial mapping hasbeen performed

If the heart is paced from this region, the resultingECG should be identical to the ECG taken duringtachycardia

Delivering RF energy to this site usually eliminates

ventricular tachycardia


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Idiopathic VT Ablation in RVOT

RAO RAO


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Idiopathic LeftVentricular Tachycardia

RBBB/LAFB Involves the Purkinje network

Treatment options: RF ablation

Pharmacologic therapy (verapamil, beta blockers)


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ECG used with permission of Kay NG.

ECG Recognition


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Bundle Branch Reentry

Reentry circuit is confined to the left and rightbundle branches

Usually LBBB, during sinus rhythm

Presents with: Syncope

Palpitations

Sudden cardiac death

Treatment: RF ablation of right bundle


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VT Due to BundleBranch Reentry


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Catheter Ablation of RightBundle Branch

Courtesy of Dr. Warren Jackman

IIIV1

RA

Current

Voltage


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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


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Ventricular Fibrillation

Heart rate: Chaotic, random and asynchronous

Rhythm: Irregular

Mechanism: Multiple wavelets of reentry

Recognition: No discrete QRS complexes

Treatment: Defibrillation


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ECG Recognition

P waves and QRS complexes not present

Heart rhythm highly irregular Heart rate not defined


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Polymorphic VT


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Polymorphic VT

Heart rate: Variable

Rhythm: Irregular

Mechanism: Reentry

Triggered activity

Recognition: Wide QRS with phasic variation

Torsades de pointes


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ECG Recognition

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


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Torsades de Pointes (TdP)

Heart rate: 200 - 250 bpm

Rhythm: Irregular

Recognition: Long QT interval

Wide QRS

Continuously changing QRS morphology


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Mechanism

Events leading to TdP are: Hypokalemia

Prolongation of the action potential duration

Early afterdepolarizations

Critically slow conduction that contributes to reentry


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ECG Recognition

QRS morphology continuously changes

Complexes alternates from positive to negative


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Possible Causes

Drugs that lengthen the QT: Quinidine

Procainamide

Sotalol

Ibutilide

Physical Ischemia Electrolyte abnormalities


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Treatment

Pharmacologic therapy: Potassium

Magnesium

Isoproterenol

Possibly class Ib drugs (lidocaine) to decreaserefractoriness/shorten length of action potential

Overdrive ventricular pacing Cardioversion


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Summary

VT ablation is not an FDA-approved indication

RF catheter ablation can be a useful techniquein patients with ventricular tachycardia

Success largely depends on the etiologyof the arrhythmia

Unstable sustained VT, polymorphic VT and

ventricular fibrillation are not ablatable Improved catheters and imaging techniques

may change this in the future

Ventricular Arrhythmias EP Overview Medtronic

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