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


III. ClassificationA. Monomorphic

1. Idiopathic

a. Description

b. ECG recognition

c. Treatment – ablation

2. Bundle branch

a. Description

b. ECG recognition

c. Treatment –ablation


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



• 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


• 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


• 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

Documents

An Electrophysiologic Overview Ventricular Tachyarrhythmias