normal ep study - pacemapping entrainment -...
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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
