AP Advanced Svt&Vt

7/31/2019 AP Advanced Svt&Vt

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Supraventricular Tachycardias


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AV Nodal Reentrant

Tachycardia (AVNRT)


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Pts usually young to middle aged adults

More common in females

Concentric (septal) retrograde atrial activation low to high

Pseudo R wave in V1

Dual AV Nodal physiology common (fast and slow pathways)

Tachycardia is AV nodal dependent and is usually 1:1 AV conduction

AVNRTAVNRTAVNRT Features

Shortest VA during tachycardia is < 60 ms


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Baseline ECG


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AVNRT 12 Lead: Pseudo R Wave


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AVNRT

Sinus

Rhythm


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AV Nodal Jump With an Echo

echo

(FPWERP and jump to SPW)

A A A

A

H H HV V V A H V

S1(A1) S2(A2)S1(A1)

230 ms increase in AH to 450 msjump


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Sustained AVNRTSustained AVNRT


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AVNRT Terminates with Adenosine


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Exercise: What is happening here? Which catheter is being paced? Is it capturing? Howmany extras are given? Is an arrhythmia induced? What happens to the AH interval?

Atrial Pacing Protocol


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Atrioventricular ReciprocatingTachycardia (AVRT)-

Concealed Bypass Tracts and WPW


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Accessory AV Pathways APs represent an extra connection outside

the AV Node

Concealed pathways have only retrogradeconduction and do not have pre-excitation (NOdelta wave in SR)

Manifest show antegrade conduction(delta wave in SR)

These patients represent 30% of all SVTs.


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Hx of tachycardia typically beginning in childhood to youngadult

More common in males

Concentric (septal) or eccentric retrograde atrial activationlow to high

Tachycardia dependent on the AV node and the ventricles;cannot continue in the presence of AV nodal or VA block

Atrial preexcitation when his refractory proves AP

AVRT Features

VA during tachycardia is > 60 ms

AVRT

APs do not typically exhibit decremental conduction


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AVRTAVRT


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Nature of AVRT

May be antedromic: down the AP and up the AVnode resulting in wide complex (10%)

May be orthodromic: down the AV node andup the accessory pathway resulting in narrow

complex (90%)


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AVRT: Manifest AP


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AVRT: Manifest AP ERP


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AVRT: Orthodromic

Down AV

Node Up AP

Down AV

Node Up AP

Down AV

Node Up AP* * *


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Anatomic LocationsAccessory Pathways

Septal

Free Wall

Lateral


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AVRT: Orthodromic via L sided AP


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AVRT: AF With Pre-excitation


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AVRT: Ablation of Manifest AP


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AVRT: Manifest AP Delta AlgorithmAVRT: Manifest AP Delta Algorithm

*

**

**

*


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Algorithm for AP Identification

I + andAVF -

II, III,

AVF +

*

* *

**** *


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Algorithm for AP IdentificationGeneral Concepts for Manifest Pathways

If Delta Wave Is ThenPositive in V1 Pathway is L sidedNegative in V1 Pathway is R sidedPositive in the inferior leads (II, III, AVF) Pathway is anteriorNegative in the inferior leads (II, II, AVF) Pathway is posteriorNegative in lead II In a vein (CS) or epicardial

Negative in the lateral leads (I and AVL) Pathway is left lateralMaking a to + transition V1 to V2 Pathway is septalNot meeting the above criteria Multiple pathways may be

present

The analysis of the delta wave polarity should occur during thefirst 25 ms of the manifest QRS complex.

********


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AVRTAVRT

What is happening here? What is the rhythm? Where is theshortest VA time? Where is the AP?


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AVRT

Using the delta wave algorithm, where is this AP located?


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Diagnosing Septal Pathways

Why and How

Para-Hisian Pacing:


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Why

Used to distinguish mid or anteroseptalaccessory pathway from AV node whenretrograde conduction is concentric.

Is that over the node or pathway?


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How Pacing outputrather than mere electrode

location is used to capture different

structures.particularly the HIS bundle.

Stimuli delivered to the RV septum, distal tothe Hisrecording and proximal to the right

bundle recording.

Pacing with high output to capture the Hisbundle directly (narrower QRS), then

decrease output to no longer capture the Hisbundle (wider QRS), but depolarize theventricle from the high septum (capture only

of local ventricular myocardium)


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High Output His Capture (No AP)

Capture of the HISbundle directlywillspread the impulseto the AV noderetrograde and tothe ventricles overthe HPS=narrower

QRS

Pace


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Lower output: No His Capture (No AP)

His not captured asoutput reduced, butventricle is depolarizedfrom the high septumyielding a left bundlebranch block QRSmorphology(widerQRS). Impulse travelsto apex then retrograde

to His-purkinje systemto the atrium so the stimto atrial depolarizationtime is increased(no

AP present)

Pace


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Anteroseptal AccessoryPathway

In the presence ofan AP, theretrograde activationis rapid regardless

of the activation ofthe HPS system orventricular septum(occurs withnarrower or widerQRS)

Pace


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Para-Hisian pacing - No AP (1) Para-Hisian pacing demonstrating

retrograde conduction over the fast AV

nodal pathway (AVN/AVN pattern) in a

patient with AVNRT.

The pacing stimulus (S) in the leftcomplex did not produce HB-RB

capture, reflected by the wide QRS

complex and relatively late His bundle

activation (S-H=60 ms).

HB-RB capture was achieved in the rightcomplex reflected by narrowing of the

QRS complex and shortening of the S-H

interval to 15 ms. The 45-ms shortening

in S-H interval was matched by a 45 ms

shortening in the S-A interval from 90 to

45 ms, without a change in the atrial

activation sequence. The constant H-A

interval (35 ms) and atrial activation

sequence indicate that retrograde

conduction was dependent on activation

of the His bundle and not on the local

ventricular myocardium and thus no APWider QRS: HB/RB not

activated;Late HisActivation S-H=60 ms

Narrower QRS: HB/RB activated; S-Hshortens to 15 ms; H-A constant; 45 ms

in S-H= 45 ms in S-A w/o change inatrial activation


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Para-Hisian pacing - No AP (1)

Wider QRS: HB/RB notactivated;Late His Activation S-H=60 ms

Narrower QRS: HB/RB activated; S-H shortens to 15 ms; H-A constant; 45ms in S-H= 45 ms in S-A w/o change in atrial activation

Wider QRS Narrower QRS


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Para-Hisian Pacing No AP (2) Para-Hisian pacing demonstrating retrogradeconduction over the slow AV nodal pathway(AVN/AVN pattern).

The pacing stimulus (S) in the left complexresulted in ventricular capture and HB-RB

capture, producing a relatively narrow QRScomplex and early activation of the His bundle(H).

HB-RB capture was lost in the right complex,resulting in widening of the QRS complex and a60-ms increase in the S-H interval from 10 to70 ms. This was also associated with a 60-ms

increase in the S-A interval from 120 to 180ms, without a change in the retrograde atrialactivation sequence. The constant H-A interval(110 ms) and atrial activation sequenceindicate that retrograde conduction wasdependent on His bundle activation and not onlocal ventricular activation, indicating retrogradeconduction exclusively over the AV node.

Earlier atrial activation in the proximal coronarysinus electrogram (CS

p) than in the His bundle

electrogram (HBp) suggests retrograde

conduction over the slow AV nodal pathway.This tracing was recorded after ablation of a leftlateral accessory AV pathway.

Wider QRS: HB/RB not activated;Late His Activation;S-H + by 60 ms (10 to 70 ms); S-A + by 60 ms (120 to180 ms); Constant H-A (110) and A activation =Hisdependent activation, not local V myocardium and noAP; retro SPW (CS early)

Narrower QRS: HB/RBactivated; S-H short=10ms; S-A=120 ms

Narrower QRS Wider QRS


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Para-Hisian Pacing No AP (2)

Wider QRS: HB/RB not activated;Late His Activation; S-H + by 60 ms (10 to 70 ms); S-

A + by 60 ms (120 to 180 ms); Constant H-A (110) and A activation =His dependentactivation, not local V myocardium and no AP; retro SPW (CS early)

Narrower QRS: HB/RB

activated; S-H short=10ms; S-A=120 ms


HA 110HA 110


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AP Present (1) Para-Hisian pacingdemonstrating retrogradeconduction only over ananteroseptal accessory AVpathway (AP/AP pattern).

HB-RB capture in the leftcomplex resulted in an S-Hinterval of 15 ms.

Loss of HB-RB capture in theright complex resulted in a 55-ms increase in S-H interval to70 ms. The S-A intervalremained fixed at 95 ms andthe atrial activation sequence

remained identical, indicatingthat retrograde conduction wasdependent on the timing ofventricular activation and not onthe timing of retrograde His-bundle activation.

Narrower QRS: HB/RBcapture; S-H=15 ms

Wider QRS: Loss of HB/RB; S-H + by 55 ms to70 ms; S-A remains constant at 95ms (if S-Adependent on H, S-A would also + by 55 msnot the case here; A activation unchanged; A

activation dependent on V activation, not retroH activation; thus AP present

Narrower QRSWider QRS


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AP Present (1)

Narrower QRS: HB/RBcapture; S-H=15 ms

Wider QRS: Loss of HB/RB; S-H + by 55 ms to 70 ms; S-A remains constant at 95ms (if

S-A dependent on H, S-A would also + by 55 msnot the case here; A activation unchanged;A activation dependent on V activation, not retro H activation; thus AP present


HA 65 HA 25


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AP Present (2)

The SA intervals and retrograde atrial activationsequence are unchanged, indicating retrograde

conduction over a single accessory pathway.



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Diagnosing Septal Pathways

Summary:

Wider QRS/Long S-H= Local Ventricular Capture Only

Narrower QRS/Short S-H= His/RB Capture

Shortening of S-H interval reflects His/RB capture

S-A changes which follow S-H changes= Retro AV Node

conduction

S-A intervals which are short regardless of a narrower orwider QRS and which do not follow changes in the S-H interval

are indicative of an AP

Para-Hisian Pacing:


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Effects of Bundle BranchBlock During OrthodromicTachycardia


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In orthodromic AVRT with a LBBB and a left sided (here left lateral) AP, the circuit can only return to theAP via the right bundle and conduction via the left ventricular septumtherefore the VA time and the

cycle length of the tachycardia is increased. This occurs only when the block is on the same side as theAP-otherwise known as ipsilateral BBB.

Normal Orthodromic LBBB

L Lat AP=Fixed TCL and VA Time w/ Narrow QRS L Lat AP= + TCL and VA Time w/ LBBB

Netter Images


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In orthodromic AVRT and a RBBB, neither the V-A time, nor the tachycardia cycle length is affected inthe case of a left sided (here left lateral) AP. Only a right sided pathway would be affected by a RBBB.

Ipsilateral (same side) bundle branch blocks increase the VA time and tachycardia cycle length, whilea contralateral (opposite side) BBB does not.

L Lat AP= No

change in TCL andVA Time w/ RBBB

Netter Images


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RBBB duringorthodromic

AVRT using a Rsided AP

influences the V-A interval andtachycardia

cycle length.Panel (A) shows

SVT with anarrow complexQRS, VA=105ms, and a

TCL=350 ms.Panel (B) showstachycardia with

a RBBB, VAincreases to 180ms, and the TCL

to 425 ms.

A. B.

105 180

RFW AP=Fixed TCL and VATime w/ Narrow QRS RFW AP= +TCL and VATime w/ RBBB


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Effects of Bundle Branch BlockDuring Orthodromic Tachycardia

Summary:Narrow QRS (HPS)= BL TCL and VA time

Ipsilateral (same side) BBB= + TCL and VA time

Contralateral (opposite side BBB)= no change TCL orVA time

LBBB: RBBB:


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Classic Atrial Flutter


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Atrial Flutter

Atrial rates usually 200-300 beats/min.

Atrial flutter is a cardiac arrhythmia

characterized by beat-to-beat uniformity ofcycle length, polarity, and amplitude of theelectrogram recordings..

What is it?What is it?


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Typical Atrial Flutter Mechanism: Reentry, involving a largereentrant circuit localized within the right

atrium, around anatomical obstacles.

May be counterclockwise Or clockwise

CST

A

CSTA

Involves the TVA, CS, ER and CSTA


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Counterclockwise Typical Atrial Flutter

Typical SawtoothFlutter Waves


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Intracardiac Electrograms of Typical

Counterclockwise Atrial Flutter


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C. R. Bard, Inc.


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C. R. Bard, Inc.


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C. R. Bard, Inc.


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C. R. Bard, Inc.


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C. R. Bard, Inc.


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C. R. Bard, Inc.


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Typical Atrial Flutter A zone of slow conduction existsbetween the tricuspid annulus,coronary sinus ostium, and

inferior vena cava (the isthmus)

These conduction barriers areused as a guide to ablation.

Pacing from this area will entrainthe tachycardia and prove themechanism. If the activationsequence during pacing is thesame as flutter and the postpacing interval equals thetachycardia CL, then this isconcealed entrainment.


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Principles of entrainment toidentify reentry circuit An electrophysiologic technique in which pacing is

used to continuously reset a reentrant circuit

Identifies a wavefront that rotates around aninexcitable obstacle which, in the case of flutter, is

the tricuspid valve, IVC and area of functional blockalong the crista terminalis

Requires area of slow conduction that delays theimpulse sufficiently such that it does not catch up with

refractory tail of the preceding beat.


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General Definition of Entrainment: A prematureimpulse invades the circuit during tachycardia With correct timing, a paced

impulse will divide in two,

with the antidromicwavefront colliding with andextinguishing one portion ofthe original circuit, and theorthodromic creating a new

wavefront propagating viathe tachycardia pathway,and resetting it.

Consists of a continuouspacing train, slightly faster

than the tachycardia cyclelength. Each paced impulsewill advance the circuitotherwise known as

entrainment.

New circuit started here


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Entrainment The goal of entrainment is to

determine the relationship of agiven site to the reentrant circuit

There are two types ofentrainment:

Concealed Entrainment:entrainment without fusion (Nochange in P wave, QRS, or ICmorphology)

Manifest Entrainment:entrainment with fusion (A changein P wave, QRS, or IC

morphology)


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Criteria for concealed entrainment

P wave, QRS, or IC morphologies andactivation sequences during pacing resemblethose in tachycardia

A post-pacing interval within 20-30 msec ofthe tachycardia cycle length recorded at thepacing site

A stimulus to P, QRS, or IC signal intervalequal to the electrogram to P, QRS or ICinterval during tachycardia

Typical Atrial Flutter: Concealed Entrainment


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Typical Atrial Flutter: Concealed Entrainment

Pacing during flutterPost pacing interval=tachycardia

cycle length

Concealed Entrainment PPI


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Concealed Entrainment -PPI


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Pacing at a slightly faster rate

No change in the morphology

ECG 1

ECG 2

ECG 3

LEAD 1

LEAD 2

Pacing at the critical site of the tachycardia

Concealed Entrainment


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Criteria for manifest entrainment(with fusion)

P wave, QRS, or intracardiac morphologies

and activation sequences during pacing donot resemble that of tachycardia

A post-pacing interval greater than the

tachycardia cycle length by more than 20-30msec recorded at the pacing site (the greaterthe PPI above the TCL, the farther from thecircuit)

A stimulus to P, QRS, or IC electrograminterval during pacing is not equal to the localelectrogram to P, QRS, or IC interval in

tachycardia


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Entrainment With Fusion:

2

3

Pacing Site

1

Manifest Entrainment (with fusion)


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( )


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ECG 1

ECG 2

ECG 3

LEAD 1

LEAD 2

Pacing at a slightly faster rate

Change in the morphology

Pacing at site non-critical to the tachycardia

Entrainment With Fusion


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Atrial flutter is cured by

performing a drag ablationfrom the tricuspid annulusto the eustachian ridge(IVC)

Typical Atrial Flutter

May also make additionalline from TVA to CS or CSto ER

The goal is to connect nonconducting tissues to form abarrier across the isthmus.


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Pacing from the CSostium is done after

ablation to showunidirectionalconduction block.

Counterclockwise block

Clockwise block


Pacing lateral to theablation line will

confirm bidirectionalconduction block.


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Atrial Tachycardia

Atrial tachycardia: More A signals than V


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Atrial Tachycardia


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What rhythm is shown here? Which a is earliest? Where may this

tach cardia be comin from?


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Atrial Fibrillation (A Fib)


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Among the most prevalent SVTs

Chaotic electrical pattern in the atria

Negates the physiologic benefit of AV synchrony

Foci from the pulmonary veins, SVC, Vein of Marshall, and othersources may serve as triggers for AF


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PV Mapping CS Pacing


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A

CS3/4

SPVP

A and PVP Fusion


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Atrial Fibrillation


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What is this rhythm? What is the activation sequence? Where is

the earliest a?


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Ventricular Tachycardias

Diff ti l Di i f VT


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His-Purkinje System Tachycardias

oBundle Branch Reentry Ventricular TachycardiaoVerapamil-Sensitive Left Ventricular TachycardiaoFocal His-Purkinje Tachycardia

Arrhythmogenic Right Ventricular DysplasiaRVOT Ventricular TachycardiaRight ventricular scar after surgical repair of congenital heart diseaseCoronary artery disease with previous myocardial infarctionLVOT Ventricular TachycardiaVerapamil-Sensitive Left Ventricular Tachycardia

VT associated with Tetralogy of Fallot Repair

Differential Diagnosis for VT


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Strategy for Catheter Ablation of VT


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-Analysis of 12 lead ECG of VT

-Pace mapping

Response to pacing (PPI and

CE)

-Activation mapping

-Substrate Mapping (VoltageMapping)

-Analysis of 12 lead ECGof VT

-Pace mapping

-Activation mapping

Tools

Ablate Critical PathwayAblate FocusTarget

Intra myocardial Re entryTriggered Activity

Automaticity

Mechanism

MacroreentryFocalStrategy for Catheter Ablation of VT


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RVOT VT: Mapping Catheter in RVOTRVOT VT: Mapping Catheter in RVOT


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VA Dissociation Proves VT MechanismVA Dissociation Proves VT Mechanism

RVOT VT: Mapping EGMRVOT VT: Mapping EGM3333


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Early site in RVOTEarly site in RVOT


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Pacemapping RVOT VT. Clinical VT is on left. A-E show single paced complexesfrom five different sites attempting to match VT QRS. In A-D, the QRS appearsprogressively more similar to the target morphology: successful ablation occurredat site E, where pacing creates a perfect 12/12 perfect EKG pace map.

12/12 Pace Map: Side By Side Comparison


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Perfect Pace Map


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Idiopathic Left VentricularTachycardia


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Tachycardia

Left Fascicular VT

-reentry or triggered

Left Ventricular Outflow Tract VT-automatic


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LVOT VT. CL=290 ms; RBBB morphology (+) V1. Inferior Axis (+) II, II, and AVF.Precordial leads are concordant with a positive, peaked QRS.


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Left Fascicular VT


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Left Fascicular VT Also known as verapamil sensitive VT Left Posterior fascicular VT with a RBBB and superior

axis(common) Left Anterior fascicular VT with a RBBB and right

axis(uncommon)

Upper septal fascicular VT with a narrow QRS and normal

axis(rare

Young patients without heart disease

Posterior and anterior fascicular VT can be

successfully ablated at the mid-septum guided by adiastolic Purkinje potential or at the VT exit siteguided by a fused pre-systolic Purkinje potential

Left Posterior Fascicular VTLeft Posterior Fascicular VT


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Left Posterior Fascicular VTLeft Posterior Fascicular VT

Right bundle (positive (+) V1) superior axis (II, III, and AVF negative (-))


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Ischemic VTIschemic VT


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What is happening here? What is the rhythm? Is there associatiWhat is happening here? What is the rhythm? Is there associationon

between the A and V? What is the activation sequence?between the A and V? What is the activation sequence?


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Ischemic VTIschemic VT


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v v v

a a


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LV - RAO LV - LAO

>1.5mV


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LV - BOTTOMLV - PA

980528RM

< 0.50mV

Endocardial Scar / Infarct Size: Magnetic Mapping - 37% Vs SPECT Imaging - 36%

Ischemic VT: Scar Voltage Mapping


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Electrically Unexcitable Scar


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Pace at 10 mA unipolar from map catheter

If there is failure to capture, then the area istagged as scar

Can be used to identify borders of low voltage

infarct regions and borders of infarct zones

Can identify areas that will NOT respond toRF as they are already electrically inert


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Ischemic VT

Most common type of VT

Usually LV; life threatening if EF is low


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VT circuit in scar

90% inducible in EP lab with programmed stimulation

Usually LV; life threatening if EF is low

Associated with scar from a myocardial infarction through which a

reentry circuit rotates

Pts typically receive ICD/ablation is 2nd line therapy for patients

receiving frequent shocks

Ischemic VT


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Ischemic VT


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v v v

a a

Ischemic VT: Scar Voltage Mapping


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Idiopathic VT Represents the minority of all VTs

Most commonly from RVOT; other sites also possible


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Reproducibility unpredictable with pacing: burst pacing may triggeras this is primarily an automatic rhythm, not reentrant

Associated with a normal heart; usually benign

Pts typically receive ablation or medical therapy


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RVOT VT and Automaticity


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RVOT VT: Mapping Catheter in RVOT


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VA Dissociation Proves VT Mechanism


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Pacemapping RVOT VT. Clinical VT is on left. A-E show single paced complexesfrom five different sites attempting to match VT QRS. In A-D, the QRS appearsprogressively more similar to the target morphology: successful ablation occurredat site E, where pacing creates a perfect 12/12 perfect EKG pace map.


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VT


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In a pt with a normal heart, this VT is induced. Is is ischemic or idiopathic? Where in

the heart do you think it is coming from?


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VT From Bundle Branch Reentry Dependent on both bundles for reentry


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p y

Baseline EKG usually will demonstratesigns of underlying conduction delay(bundle branch block) and signs of

cardiac dilatation (atrial enlargement)

Goals:

Ablate right bundle and abolish reentry

Baseline Sinus EKG in BBRVT

The baseline sinus rhythm EKG demonstrates a classic LBBB (wide negative QRS in

V1>120 ms) with left atrial enlargement as seen with a large negative component to theP wave in V1 and a very broad P wave in lead II.


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VT Due to Bundle Branch Reentry

The typical induction method for BBRVT is with single premature beats from the right

ventricle. Here, a single premature beat (S) blocks retrograde in the right bundlebranch, but conducts up the left bundle branch into the His Bundle.


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RightBundleBranch

Left BundleBranch

His Bundle


Often, by the time the impulse gets up the left bundle and through the His, the right

bundle has recovered and the impulse then travels antegrade down the right bundlebranch, then back up the left bundle, initiating the reentry circuit of bundle branch reentry

with a LBBB pattern. The His is part of the circuit and a 1:1 relationship is observed

between the His and V during VT


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RightBundleBranch

Left BundleBranch

His Bundle

between the His and V during VT.

In rare instances, the premature beat may block in the left bundle retrogradeand set up a circuit in the reverse direction with a RBB pattern (wide positive QRS in V1


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VT EKG in BBRVT

Interestingly, the EKG during BBRVT shows a similar QRS morphology as compared tothe baseline sinus EKG: a classic LBBB. With careful inspection, VA dissociation may

also be observed at the rhythm strip on the bottom as P waves march through the QRS.


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V-His Association in BBRVT

While the A is dissociated, each V is preceded by a His signal denoting the His is part of the circuit.

This is diagnostic for BBRVT. In addition, the HV in BBRVT, as seen here, is classically > 100 ms.


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HRA

Each V is preceded by aHis The third His is obscured by the dissociated A

HV Interval=110 ms

Site of Ablation in BBRVTThe ablation catheter is positioned at the right bundle branch during sinus rhythm, which is the site of ablation for this tachycardia.Note that the RBB spike occurs well after the His spike. In this patient, elimination of the RBB will eliminate the VT, but leaves the

patient with AV conduction totally relying on the LBB. Given this patients underlying LBBB, they may likely need a pacer postablation.


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I

II

V1

Post RBB Ablation

Successful ablation of the right bundle in another patient does not cause complete heart block, butrather, leaves the patient with a permanent right bundle branch block (wide positive QRS in V1) in

sinus rhythm. Now that the the right bundle is ablated, this patient can no longer have BBRVT.This patient will probably not require a pacemaker


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V1

RA

Current

Voltage

Bundle Branch Reentry andCARTO XP System

Bundle branch reentry VT ablation


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y

with CARTO XP System isanatomical.

The site of the RBB potential can bedemarcated for ablation.


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Right Bundle Branch Location

The right bundle branch lies just distal to the His Bundle below the tricuspid valve on the superior

aspect of the interventricular septum.


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Site of RBB for BBRVT Ablation (with CARTOXP System) in RAO

RVOT


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TVA

RVA

RBB Site onInterventricular

Septum justdistal to the His

(SuccessfulAblation)

His

RV RAO for anatomicrepresentation of the right bundle

branch location

RBB Potential

His Potential

Idiopathic Left Ventricular Tachycardia

Left Fascicular VT


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-reentry or triggered

Left Ventricular Outflow Tract VT-automatic

Left Fascicular VT Also known as verapamil sensitive VT Left Posterior fascicular VT with a RBBB and superior axis(common)


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Left Posterior fascicular VT with a RBBB and superior axis(common)

Left Anterior fascicular VT with a RBBB and right axis(uncommon)

Upper septal fascicular VT with a narrow QRS and normal axis(rare)

Young patients without heart disease Posterior and anterior fascicular VT can be

successfully ablated at the mid-septum guided by adiastolic Purkinje potential or at the VT exit site

guided by a fused pre-systolic Purkinje potential.

Left Posterior Fascicular VT


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Right bundle (positive (+) V1) superior axis (II, III, and AVF negative (-))

Left Posterior Fascicular VT


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Fused pre-systolic Purkinje potential

Left Ventricular Outflow Tract VT Three locations possible


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1. Endocardial 2. Coronary cusp

3. Epicardial


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LVOT VT. CL=290 ms; RBBB morphology (+) V1. Inferior Axis (+) II, II, and AVF.Precordial leads are concordant with a positive, peaked QRS.

Limitations of EUS Technique Many labs are unfamiliar with Unipolar


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pacing Requires a IVC electrode

Noise on Map catheter with Unipolar

pacing interferes with entrainmentpacing measurements

Requires significant confidence in

contact of catheter with myocardium

Pace Mapping Well established technique for


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Idiopathic VTs but less reliable forischemic VTs

A perfect pace match may not be

achievable with scar relatedtachycardia

12/12 pace map represents exit site of

arrhythmia Azegami et al, Pacing Clin Electrophysiol.2002

RAOVT # 1 (LBB LSa)

Best PMExample of Pace Mapping


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LV post/midseptum inferior

Bipolar voltagemap 1.5-.5mV


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Stim-QRS =

EGM-QRS

=


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Egm-QRS

Entrainment of ventricular tachycardia (VT) at a site with a double potential is shown


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Copyright 2003 American College of Cardiology Foundation. Restrictions may apply.

Tung, S. et al. J Am Coll Cardiol 2003;42:110-115

Stim to QRS During Pace Map

P id f l d i


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Provides a measure of slow conductionwhen Stim to QRS > 40 msec

Sites with long S-QRS delays are likelyin potential isthmus, infarct zone

Sites with short S-QRS are likely at exit

site C.Brunckhorst et al, Circ 2004


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anc

e

OuterLo

op

Pacing During VTEntrain with Concealed

Fusion (CF)

Entrain with QRS fusion (QRSchange)

PPI = VTCL 30 ms

orS QRS = EG-QRS 20 ms

PPI = VTCL 30 ms

No Yes

ENTRAINMENT MAPPING

* * *


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*Adjacent bystander

Isthm

us

Entranc

Exit

Inner Loop

**

*Adjacent Bystander S QRS / VTCL (%)

< 30% 31-50% 51-70% >70%

Exit Central Proximal Inner Loop

YesNo

Remote Bystander Outer Loop*Remote bystanders* * *

Targeting Late Potentials in NSR


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C.Hwang, Europace 2003


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Electrograms During VT


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Isthm

usEn

tran

ce

Exit

Inner Loop

OuterL

oop

* *

*

Mid Diastolic Potentials DuringVT

Map potentials which precede QRS by


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Map potentials which precede QRS by> 50 msec

Potentials must be shown to correlate

during NSR to VT potentials


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C.Hwang, Europace 2003


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Bundle Branch Reentrant


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Bundle Branch ReentrantVentricular Tachycardia

VT From Bundle BranchReentry Occurs in up to 30% of VT associated

with idiopathic dilated cardiomyopathy


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with idiopathic dilated cardiomyopathy

VT is usually left bundle branch block

(negative QRS in V1), superior axis(negative QRS in II, III, and AVF)morphology


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Baseline Sinus EKG in BBRVT


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VT EKG in BBRVT


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Hi B dl



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His Bundle

VT Due to Bundle Branch ReentryVT Due to Bundle Branch Reentry


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Right BundleBranch

Left BundleBranch

His Bundle


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VV--His Association in BBRVTHis Association in BBRVT


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HRA

Each V is preceded by aHis The third His is obscured by the dissociated A

HV Interval=110 ms

Site of Ablation in BBRVTSite of Ablation in BBRVT


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Post RBB AblationPost RBB Ablation


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Documents

AP Advanced Svt&Vt