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AVNRT
AVNRT Features 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 Shortest VA during tachycardia is < 60 ms
Baseline ECG
AVNRT
Sinus Rhythm
AVNRT
S1(A1)
S1(A1)
S2(A2)
echo A
H V A H V
AVNRT Induction
ECHO
UF DS DS
UF
Sustained AVNRT
Sustained AVNRT
Exercise: What is happening here? Which catheter is being paced? Is it capturing? How many extras are given? Is an arrhythmia induced? What happens to the AH interval?
Accessory AV Pathways
APs represent an extra connection outside the AV Node Concealed pathways have only retrograde conduction and do not have pre-excitation (NO delta wave in SR) Manifest show antegrade conduction (delta wave in SR) These patients represent 30% of all SVTs.
AVRT
AVRT Features Hx of tachycardia typically beginning in childhood to young adult More common in males Concentric (septal) or eccentric retrograde atrial activation low 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 VA during tachycardia is > 60 ms APs do not typically exhibit decremental conduction
AVRT
Nature of AVRT
May be orthodromic: down the AV node and up the accessory pathway resulting in narrow complex (90%)
May be antedromic: down the AP and up the AV node resulting in wide complex (10%)
AVRT: Manifest AP
AVRT: Orthodromic
Down AV Node Up AP
Up AP
Septal
* * * * * *
* *
II, III, I + and AVF + AVF -
If Delta Wave Is
Then
Pathway is L sided Pathway is R sided Pathway is anterior Pathway is posterior In a vein (CS) or epicardial Pathway is left lateral Pathway is septal Multiple pathways may be present
* * * * * * * *
Positive in V1 Negative in V1 Positive in the inferior leads (II, III, AVF) Negative in the inferior leads (II, II, AVF) Negative in lead II Negative in the lateral leads (I and AVL) Making a to + transition V1 to V2 Not meeting the above criteria
The analysis of the delta wave polarity should occur during the first 25 ms of the manifest QRS complex.
AVRT
What is happening here? What is the rhythm? Where is the shortest VA time? Where is the AP?
AVRT
Why
Used to distinguish mid or anteroseptal accessory pathway from AV node when retrograde conduction is concentric. Is that over the node or pathway?
How
Pacing output rather than mere electrode location is used to capture different structures.particularly the HIS bundle. Stimuli delivered to the RV septum, distal to the His recording and proximal to the right bundle recording. Pacing with high output to capture the His bundle directly (narrower QRS), then decrease output to no longer capture the His bundle (wider QRS), but depolarize the ventricle from the high septum (capture only of local ventricular myocardium)
Pace
Pace
Pace
Narrower QRS: HB/RB activated; S-H shortens to 15 ms; H-A constant; 45 ms in S-H= 45 ms in S-A w/o change in atrial activation
Narrower QRS: HB/RB activated; S-H shortens to 15 ms; H-A constant; 45 ms in S-H= 45 ms in S-A w/o change in atrial activation
Wider QRS
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 dependent activation, not local V myocardium and no AP; retro SPW (CS early)
Wider QRS
HA 110
HA 110
Wider QRS: HB/RB not activated;Late His Activation; S-H + by 60 ms (10 to 70 ms); SA + by 60 ms (120 to 180 ms); Constant H-A (110) and A activation =His dependent activation, not local V myocardium and no AP; retro SPW (CS early)
AP Present (1)
Para-Hisian pacing demonstrating retrograde conduction only over an anteroseptal accessory AV pathway (AP/AP pattern). HB-RB capture in the left complex resulted in an S-H interval of 15 ms. Loss of HB-RB capture in the right complex resulted in a 55ms increase in S-H interval to 70 ms. The S-A interval remained fixed at 95 ms and the atrial activation sequence remained identical, indicating that retrograde conduction was dependent on the timing of ventricular activation and not on the timing of retrograde Hisbundle activation.
Narrower QRS
Wider QRS
Narrower QRS: HB/RB Wider QRS: Loss of HB/RB; S-H + by 55 ms to capture; S-H=15 ms 70 ms; S-A remains constant at 95 ms (if S-A
dependent on H, S-A would also + by 55 ms not the case here; A activation unchanged; A activation dependent on V activation, not retro H activation; thus AP present
AP Present (1)
Narrower QRS
Wider QRS
HA 65
HA 25
Wider QRS: Loss of HB/RB; S-H + by 55 ms to 70 ms; S-A remains constant at 95 ms (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
AP Present (2)
Narrower QRS
Wider QRS
The SA intervals and retrograde atrial activation sequence are unchanged, indicating retrograde conduction over a single accessory pathway.
AP Present (2)
Narrower QRS
Wider QRS
The SA intervals and retrograde atrial activation sequence are unchanged, indicating retrograde conduction over a single accessory pathway.
In orthodromic AVRT with a LBBB and a left sided (here left lateral) AP, the circuit can only return to the AP 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 the AP-otherwise known as ipsilateral BBB.
Normal Orthodromic
LBBB
In orthodromic AVRT and a RBBB, neither the V-A time, nor the tachycardia cycle length is affected in the 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, while a contralateral (opposite side) BBB does not.
Netter Images
RBBB during orthodromic AVRT using a R sided AP influences the VA interval and tachycardia cycle length. Panel (A) shows SVT with a narrow complex QRS, VA=105 ms, and a TCL=350 ms. Panel (B) shows tachycardia with a RBBB, VA increases to 180 ms, and the TCL to 425 ms.
A.
B.
105
180
Atrial Flutter
What is it? Atrial flutter is a cardiac arrhythmia characterized by beat-to-beat uniformity of cycle length, polarity, and amplitude of the electrogram recordings. Atrial rates usually 200-300 beats/min.
C S T A
C. R. Bard, Inc.
C. R. Bard, Inc.
C. R. Bard, Inc.
C. R. Bard, Inc.
C. R. Bard, Inc.
C. R. Bard, Inc.
General Definition of Entrainment: A premature impulse invades the circuit during tachycardia
With correct timing, a paced impulse will divide in two, with the antidromic wavefront colliding with and extinguishing one portion of the original circuit, and the orthodromic creating a new wavefront propagating via the tachycardia pathway, and resetting it. Consists of a continuous pacing train, slightly faster than the tachycardia cycle length. Each paced impulse will advance the circuit otherwise known as entrainment.
Entrainment
The goal of entrainment is to determine the relationship of a given site to the reentrant circuit There are two types of entrainment: Concealed Entrainment: entrainment without fusion (No change in P wave, QRS, or IC morphology) Manifest Entrainment: entrainment with fusion (A change in P wave, QRS, or IC morphology)
Concealed Entrainment
No change in the morphology
ECG 1 ECG 2 ECG 3 LEAD 1 LEAD 2
Entrainment
Concealed:
Pacing Site
Entrainment
With Fusion:
Pacing Site
Pacing lateral to the ablation line will confirm bidirectional conduction block.
Counterclockwise block
C. R. Bard, Inc.
What is happening? What is the activation sequence? What is the rhythm? What do you think of the surface EKG?
What is happening? What rhythm is on the left hand side of the tracing? What is happening to the right of the tracing?
Atrial Tachycardia
Atrial Tachycardia
a tach
sinus
Atrial Tachycardia
45ms
Atrial Tachycardia
What rhythm is shown here? Which a is earliest? Where may this tachycardia be coming from?
Atrial Fibrillation
LSPV Mapping
PV Mapping CS Pacing
S A and PVP Fusion A PVP
CS 3/4
Atrial Fibrillation
What is this rhythm? What is the activation sequence? Where is the earliest a?
Ventricular Tachycardias
Macroreentry
Intra myocardial Re entry Ablate Critical Pathway
-Analysis of 12 lead ECG -Analysis of 12 lead ECG of VT of VT -Pace mapping -Pace mapping Response to pacing (PPI and
CE)
-Activation mapping
Idiopathic VT
Most commonly from RVOT; other sites also possible Associated with a normal heart; usually benign Reproducibility unpredictable with pacing: burst pacing may trigger as this is primarily an automatic rhythm, not reentrant Pts typically receive ablation or medical therapy
RIGHT VENTRICLE
LEFT VENTRICLE
RVOT
80%
PAROXYS MAL EXERCISE INDUCED
FASCICLES
15%
NON-SUSTAINED
ANTERIOR
POSTERIOR
VT
SUSTAINED VT
RBBB RIGHT AXIS NARROW QRS RBBB LEFT AXIS NARROW QRS
5% other locations
Idiopathic RVOT VT from a young male with a normal heart. The QRS is wide, and regular (.14 sec). There is a left bundle branch pattern (QRS negative in V1) and an inferior axis (QRS positive in II, III, and AVF). Independent P waves are not apparent.
Pacemapping RVOT VT. Clinical VT is on left. A-E show single paced complexes from five different sites attempting to match VT QRS. In A-D, the QRS appears progressively more similar to the target morphology: successful ablation occurred at site E, where pacing creates a perfect 12/12 perfect EKG pace map.
VT
In a pt with a normal heart, this VT is induced. Where in the heart do you think it is coming from?
LVOT VT. CL=290 ms; RBBB morphology (+) V1. Inferior Axis (+) II, II, and AVF. Precordial leads are concordant with a positive, peaked QRS.
Ventricular ectopy arising from the base of the left coronary cusp.
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 a diastolic Purkinje potential or at the VT exit site guided by a fused pre-systolic Purkinje potential
Right bundle (positive (+) V1) superior axis (II, III, and AVF negative (-))
Ischemic VT
Induced with PES Re-entry in nature RF is second line therapy Stable Vs Unstable VT
Ischemic VT
What is happening here? What is the rhythm? Is there association between the A and V? What is the activation sequence?
Ischemic VT
Ischemic VT
v v v
Ischemic VT
Associated with scar from a myocardial infarction through which a reentry circuit rotates 90% inducible in EP lab with programmed stimulation Pts typically receive ICD/ablation is 2nd line therapy for patients receiving frequent shocks
VT circuit in scar
LV - RAO
>1.5mV
LV - LAO
< 0.50mV
LV - PA
LV - BOTTOM
980528RM
Endocardial Scar / Infarct Size: Magnetic Mapping - 37% Vs SPECT Imaging - 36%
Ventricular Tachycardia
Ischemic VT
Most common type of VT Usually LV; life threatening if EF is low Associated with scar from a myocardial infarction through which a reentry circuit rotates 90% inducible in EP lab with programmed stimulation Pts typically receive ICD/ablation is 2nd line therapy for patients receiving frequent shocks
VT circuit in scar
Ischemic VT
Ischemic VT
v v v
Electrogram recorded from the LV endocardium during VT in a patient with a prior MI. A isolated low amplitude mid-diastolic potential precedes local ventricular activation by approximately 150-160 ms. This potential presumably reflects activation of a zone of slow conduction. Ablation in such a site may successfully result in VT termination.
Ischemic VT
What is happening here? What is the rhythm? Is there association between the A and V? What is the activation sequence?
Idiopathic VT
Represents the minority of all VTs Most commonly from RVOT; other sites also possible Associated with a normal heart; usually benign Reproducibility unpredictable with pacing: burst pacing may trigger as this is primarily an automatic rhythm, not reentrant Pts typically receive ablation or medical therapy
RVOT RVOT
80%
PAROXYS MAL PAROXYS MAL EXERCISE INDUCED EXERCISE INDUCED
FASCICLES FASCICLES
15%
NON-SUSTAINED NON-SUSTAINED
RMVT RMVT
ANTERIOR ANTERIOR
POSTERIOR POSTERIOR
SUSTAINED VT SUSTAINED VT
RBBB RBBB RIGHT AXIS RIGHT AXIS NARROW QRS NARROW QRS
RBBB RBBB LEFT AXIS LEFT AXIS NARROW QRS NARROW QRS
5% other locations
Idiopathic RVOT VT from a young male with a normal heart. The QRS is wide, and regular (.14 sec). There is a left bundle branch pattern (QRS negative in V1) and an inferior axis (QRS positive in II, III, and AVF). Independent P waves are not apparent.
Pacemapping RVOT VT. Clinical VT is on left. A-E show single paced complexes from five different sites attempting to match VT QRS. In A-D, the QRS appears progressively more similar to the target morphology: successful ablation occurred at site E, where pacing creates a perfect 12/12 perfect EKG pace map.
VT
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?
In rare instances, the premature beat may block in the left bundle retrograde and set up a circuit in the reverse direction with a RBB pattern (wide positive QRS in V1)
Baseline HV in BBRVT
It is quite typical to observe a baseline prolonged HV interval in patients with BBRVT during sinus rhythm. In this example the baseline HV is slightly prolonged at 65 ms.
VT EKG in BBRVT
Interestingly, the EKG during BBRVT shows a similar QRS morphology as compared to the 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.
VA Dissociation in BBRVT
During BBRVT, there is a left bundle branch pattern and a dissociation between the V and A signals. The A signals are not only dissociated as they march through the VT, they are high to low, denoting a sinus origin.The atrial dissociation demonstrates the atrium is not part of the circuit.
HRA
HRA
HV Interval=110 ms
V1 RA
Current
Voltage
Bundle Branch Reentry and CARTO XP System Bundle branch reentry VT ablation with CARTO XP System is anatomical.
The site of the RBB potential can be demarcated for ablation.
His
His Potential
RBB Site on Interventricular Septum just distal to the His (Successful Ablation)
RVA
RV RAO for anatomic representation of the right bundle branch location
TVA
RBB Potential
Idiopathic Left Ventricular Tachycardia Left Fascicular VT -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) 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 a diastolic Purkinje potential or at the VT exit site guided by a fused pre-systolic Purkinje potential.
Right bundle (positive (+) V1) superior axis (II, III, and AVF negative (-))
Ventricular ectopy arising from the base of the left coronary cusp.
LVOT VT. CL=290 ms; RBBB morphology (+) V1. Inferior Axis (+) II, II, and AVF. Precordial leads are concordant with a positive, peaked QRS.
Pace Mapping
Well established technique for Idiopathic VTs but less reliable for ischemic VTs A perfect pace match may not be achievable with scar related tachycardia 12/12 pace map represents exit site of arrhythmia Azegami et al, Pacing Clin Electrophysiol.
2002
RAO
PACING - NSR Trans-barrier conduction during pacing. Barrier only present in AT SOO VT; QRS changes
200ms
520ms
460ms
460ms
Entrainment Mapping
Pace from map catheter during VT at slightly faster rate than VT rate Entrainment with Concealed fusion Vs Manifest fusion Stimulus to QRS should equal local EGM to QRS during VT (within 10 msec)
= Stim-QRS = EGM-QRS
Egm-QRS
Stim to QRS
ENTRAINMENT MAPPING
Pacing During VT
Entrain with QRS fusion (QRS change)
*
er L Out
*
oop
PPI = VTCL 30 ms
Is t
* mus h
r nt E
e nc a
Adjacent Bystander
Exit
< 30%
Inner Loop
31-50% Central
51-70% Proximal
*
Exit
* *Adjacent bystander * * *
No Remote Bystander
*Remote bystanders
Activation Map
Is useful to identify the entire circuit Can identify areas of slow conduction
Success of ablation is independent on speed of conduction through protected isthmus
Electrograms During VT
er L Out
o op
Is
*mus th
an tr En
ce
Exit
Inner Loop
VT EKG in BBRVT
His Bundle
Baseline HV in BBRVT
HRA
HV Interval=110 ms
Current
Voltage