normal ep study - pacemapping entrainment -...

Normal EP study

Pacemapping

Entrainment

Jesus Almendral, Madrid, Spain

NORMAL EP STUDY

Angelo Auricchio

Normal EP study

Tricks to measure AV intervals

Abnormalities in AV intervals

False signals

Reponses to atrial stimulation: AV physiology

Reponses to ventricular stimul.: VA physiology

HV=50 ms

Usual antegrade behavior in response to atrial extrastimuli: delay in AV node, HV remains constant

RB-V=25 ms

Continuous atrial pacing, cycle length 350 ms

V1

HRA

HBE

RV

Wenckeback phenomenon at the AV node:

This is normal AV nodal physiology

Continuous A pacing, CL 520 ms: intra-His block

*

An elo Auricchio

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Continuous A pacing, CL 520 ms: intra-His block

Note: 1) presence of H on the blocked beat; 2) narrow QRS in

conducted beats; 3) HV a little over normal; 4) lack of change in AH or

HV before/after block; 5) prolonged intra-His conduction time

HV=65HV=65

Atrial prematures reproducibly produced 2 signals between A and V

600 330

H? H’?

I

II

V1

HRAd

His p

His d

RVA

Induced AVNRT: the 2 signals between A and V persist during tachycardia

I

II

V1

HRAd

His p

His d

RVA

Sometimes the interval between the 2 signals changed during tachycardia

I

II

V1

HRAd

His p

His d

RVA

QUESTION What is the most likely mechanism for the 2 signals?

1) Rate-related intra-His conduction delay

2) Rate-related His-RB conduction delay

3) Artifact, because AVNRT cycle length remains constant despite variable pseudo HH’ interval

4) Artifact, because VA interval remains constant during AVNRT despite variable pseudo HH’ interval

5) None of the above is likely

Variable intra-His delay is not expected to occur without a change in VA interval during tachyacardia

VA=80 VA=80 VA=80

I

II

V1

HRAd

His p

His d

RVA

A

AVN

H

HP

V

SCHEMATIC REPRESENTATION OF AVNRT

A

AVN

H

HP

V

AVNRT WITH INTRA-HIS DELAY: same TCL, shorter VA

The most likely explanation is an electronic artifact producing the 1st component, the second being a real H

VA=80 VA=80 VA=80

* H * H * H

I

II

V1

HRAd

His p

His d

RVA

600/300 VH 131, VA 180

600/250 VH 180, VA 236

I II

V1

V4

HBE p

HBE d

RV 380 300 250

Retrograde physiology in response to extrastimuli

A A A A

H H H H

600/380 H precedes V electrogram

400/290 VH ?, VA 138

Retrograde physiology in response to extrastimuli 400/280

VH 180, VA 225

I II

V1

V4

HBE p

HBE d

RV

A A A *

H H? H *

400/270 VH block

Retrograde physiology in response to continuous pacing CL 320 ms, block occurs in the AV node

I II

V1

V4

HBE p

HBE d

RV

A A *

H H H

Summary of retrograde physiology

In response to ventricular extrastimuli, as CI decreases:- VH interval increases: sudden increase: retrograde block

in the right bundle, goes up the left bundle - VH interval increases: progressive increase: retrograde

delay in right/left bundle, delay in m-P junction - HA tends to remain constant: delay in H-P system

prevents the AV node to “see” shorter CI

In response to continuous ventricular pacing: - VH tends to remain constant - Block tends to occur in the AV node

Angelo Auricchio

If at the tricuspid annulus there is a deflection right after the atrial deflection, how could you distinguish between a double atrial potential and an atrial and His bundle potential?

1. Rapid atrial pacing 2. Atrial extrastimuli 3. Moving the catheter to a more ventricular position 4. Injection of a bolus of adenosine 5. All the above

Regarding retrograde VA conduction in physiologic conditions?

1. Block in the AV node is more common than in the His-Purkinje system during continuous ventricular pacing

2. Block in the AV node is more common than in the His-Purkinje system during ventricular extrastimuli

3. Block in the AV node is more common than in the His-Purkinje system regardless the mode of ventricular pacing

4. It is not usually possible to identify the site of retrograde block because of inability to record retrograde His deflection

5. If there is VA conduction at slow pacing rates block in the AV node does not occur at fast pacing rates

The most common mechanism of a sudden increase in S2-A2 in response to ventricular extrastimuli under physiologic conditions is:

1. Conduction delay in the AV node 2. Conduction block in the AV node 3. Conduction delay in the right bundle 4. Conduction block in the right bundle 5. Conduction delay in the ventricular muscle to Purkinje junction

PACEMAPPING

Angelo Auricchio

Principles of pacemapping

If a rhythm originates from a certain spot, pacing from that site will originate electrical activation in an identical fashion, as recorded from the 12-lead ECG

A number of considerations: 1. Is the rhythm focal or reentrant? Better for focal 2. Is pacing performed during SR or during tachycardia?3. Is pacing unipolar or bipolar 4. What is the output in relation to threshold? Virtual

electrode 5. What is the spatial resolution? 6. How is morphology approximation evaluated?

Principles of pacemapping

Pacing characteristics

Unipolar vs bipolar: Unipolar theoretically better, but stimulus artifact distorts QRS: bipolar more practical

High output in relation to threshold: can product direct capture of a big zone: stimulate as closer to threshold as possible

What is the spatial resolution? With diagnostic catheters in normal heart: 15 mm (a difference detected in all patients in a mean of 8.4 leads). With ablation catheters in sick hearts using computerized analysis: 10 mm

Big infarct / anatomic obstacle

Infarcted tissueNormal

myocardium

Normal

myocardium

During VT

VT

Pacemapping in reentrant rhythms

Big infarct / anatomic obstacle

Infarcted tissueNormal

myocardium

Normal

myocardium

During VT

VT

Pacemapping in reentrant rhythms

Pacing during sinus rhythm: change in morphology

St

Big infarct / anatomic obstacle

Infarcted tissueNormal

myocardium

Normal

myocardium

During VT

VT

Pacemapping in reentrant rhythms

Pacing during tachycardia: identical morphology

St

Pacemapping: evaluation of morphology approximation

The X out of 12 method: Number of ECG leads without major/minor changes:

- Major: app, disapp or change in amplitude of a component >50% QRS amplitude

- Minor: app/disapp notch or Q, R or S <25% QRS amplitude, ch in amplitude individual components >25 <50% QRS, change in shape of a major component

The score method: each lead evaluated as having major differences (score 0), minor diff (score 1), or no diff (score 2): Best pacemap=24 points

VPC PM-1 PM-2 PM-3

Angelo Auricchio

ENTRAINMENT

Angelo Auricchio

The essence of the concept of transient entrainment

• During pacing

–All the tissue of the paced chamber and the

tachycardia origin is activated at the pacing rate:

interaction pacing wavefront – tachycardia

mechanism

• At cessation of pacing

–Tachycardia continues unaltered

• The “tachycardia clock”

– Permanently altered: easier to analyze with resetting

Resetting of VT

Pause after stimulus (RC) is less than compensatory

Tachycardia remains unaltered

Tachycardia “clock” is permanently changed

RC RV

Tachycardia

ENTRY

EXIT

Resetting

Pacing

Entrainment = continuous resetting

PS

ENTRY

EXIT

Pacing site: at the circuit. PPI = VTCL

PS

Pacing site: at a distance from the circuit. PPI > VTCL

The recognition of entrainment: entrainment criteria

• Constant fusion

• Progressive fusion

• Shorter conduction time associated with

termination

• Fusion at the local electrograms

Tachycardia

ENTRY

EXIT

Resetting

Pacing

Exiting wavefront

F U S I O N

I II

V1

V6

LV

RVOT

RVA

S S S S S VT VT VT

F F F F VT VT VT

End of rapid ventricular pacing during VT: Transient entrainment: progressive surface ECG fusion (V1 less positive),

intracavitary fusion (LV orthodromic, RVOT antidromic)

330 330 330 330 430 430

I

II

V1

V6

LV

RVOT

RVA

S S S S S S S S

F F F F F No F No F

Rapid ventricular pacing during VT: Block of one impulse is followed by conduction with shorter CT and different morph. Waldo’s 3rd criterion. Indicates tachycardia termination. Indicates reentry

290 290 290 290 290 290 290

I

II V1

V6

LV

RVOT

RVA

S S S S

End of rapid ventricular pacing

290 290 290

Utility as a diagnostic tool

• Entrainment + fusion = reentry

• Entrainment + fusion: differential diagnosis

between AVNR & AVR with a septal pathway

• FPPI – TCL = proximity to circuit

• FPPI: rapid DD right vs left atrial tach

• Adjusted FPPI: rapid DD among SVT

Tachycardia

ENTRY

EXIT

Entrainment

Pacing

Exiting wavefront

F U S I O N

FPPI – TCL – (AH FPPI – AH tach) = 650 – 440 – (270-235) = 175

Corrected first post-pacing interval

FPPI – TCL – (AH FPPI – AH tach) = 405 – 310 – (250-178) = 23 ms

Corrected first post-pacing interval