Entrainment for distinguishing atypical AVNRT from Septal AP with long RP relationship (pitfall to VOD)

1. In all pts. With typical septal AP:  PPI – TCL = <115ms and SA-VA = <85ms

2. 6/12 with slowly conducting AP:  PPI – TCL >115ms and SA-VA = >85ms   

3. Slowly conducting AP frequently give entrainment criteria     similar to AVNRT

Bennett M/Klein G. Circ Arrhythm 4:506, 2011

Do HRPVC => in septal AP you have continuous reset of tachycardia. If you pace near exit of tach you wil see minimal
fusion (in HPS) you should always pace away from area to see maximal fusion

If captured first fused beat pulls in the A => you know V is part of circuit => ORT
In AVNRT if you capture the A QRS will not be fused cause when you capture V you have to go all the way up
so V paced beat will look like pacing in SR once it captures the A

A capture with fusion early during V pacing = ORT
Fused beat with termination and no A = ORT
up to 4 beats to capture A when V is not fused = AVNRT
For this maneuver to work APacing should be at same CL of SVT and right afterwards to rule out autonomous influences
In atypical AVNRT AH is short cause you are not activating A from HRA, it's going around AVN and activating A
In contrast in ORT and AT you have to traverse the entire A to get to His
If PP changes, PR stays the same, RP changes, then think AT
AVNRT or AP usually RP is fixed (exception is beginning of tachycardia)

If adenosine works it excludes AVRT
If during adenosine P is upright in II cannot be AVNRT
P negative in V1 is coming from the HRA (Crista AT)
20-25% of ATs are adenosine sensitive (usually near septal ATs, coming from the CS)

VAAV

If during LRPT you begin RV Pacing and it terminates SVT with no A, this excludes AT
Only way you can terminate AT with V pacing is if you pull the A

aAVNRT
CHARACTERISTICS OF ATYPICAL AVNRT

1. Negative P waves in 2,3,F and V6, positive in V1 (negative P in V1 is PJRT)
2. Usually initiated by ventricular pacing
3. PPI-TCL > 115 ms (110 if you correct for AH), S-VA-VAT       => 85 ms
4. V on His no effect on succeeding A
5. Parahisian pacing to exclude septal AP
6. During VOD fused V never advances succeeding A


RV apex is farther away from circuit
have to go through AVN twice
1. Atypical AVNRT

2. Atrial tachycardia

3. Decremental AP (PJRT)
misnomer by kumel thought it involved the AVN called it junctional but we know it's an AP

4. N-F tachycardia


AT: Diagnosis pearls and pitfalls
• Surface P wave & intracardiac atrial activation sequence during AT  different from that in sinus rhythm, warm up phenomena
• AH interval with atrial pacing same as AH during AT
• Initiation independent of a critical AV nodal or AV conduction delay
• AA drives VV during Tachycardia in AT but also decremental AVN and decr AP (may be mimicked by change in VA interval in AVNRT or
PJRT) . But if VV drives AA cannot be AT
• A and V not hooked (AT)
• Initiation from ventricles alone excludes AT
• Single V terms without change in A cycle length excludes A
• V-A-A-V response to ventricular extrastimuli
• AV dissociation (• Spontaneous • Pharmacologically-induced • Pacing-induced )

                                       Gradual onset,PP drives VV, PR constant,RP varies, independent of any change in PR








Mid-Long RPT
RV apex closer to circuit have to go
through AVN once
PJRT
1. Incessant tachycardia (50% of time on Holter)
2. P waves inverted in 2,3,F, positive in V1 (negative V1 is AVNRT)
3. PPI-TCL < 115ms, S-VA-VAT < 85 ms
4. V on His affect (advances or delays the next A)
5. V on His delivered to ventricular site opposite atrial insertion site always affects next A (put HRPVC at site of earliest
atrial activation, if earliest A is prox CS put V closer to that area ilke basal septum. You have to activate the A when the His
is engaged, if you pace far away from circuit you might miss it)
6. Parahisian pacing to prove presence of septal  accessory pathway ?? (can be a problem cause decrementap pathways
can simulate AVN)
7. Ipsilateral BBB or prolonged HV with VA interval prolongation PJRT

It lives around the CS Os
RP is long (as long as in sinus)
HRPVC from basal septum can terminate it or pull in A (you are close to the circuit)
Look for  a little "blip" or AP signal on CS 9,10
You have to kill it proximally. If you ablate on the distal part of the CS you will get some fibers of it cause it branches but you have
to get the proximal insertion
PITFALLS in V PACING

Change in A activation sequence when no AP (FP -> SP)
No change cause RVA is too far from AP (L ant Lat AP) in which case you should do RVOT Stim
Fusion beat VES coming from LV (L AP)
RVA decr despite AP (L Lat AP)


A PACING
L AP => slightly increasing preexcitation less marked than R AP with HRA fast pacing, in this case CS pacing will show more
preexcitation

HRPVC (measure TCL and deliver at 20 ms shorter)
in AVNRT you are excluding the V not affecting A showing V is no part of SVT
In RAP brings A closer
In LAP A earlier 15 ms (CS q,2 has earliest A, His A is late)

BBB
LBBB in SVT prolongs TCL = LAP
RBBB in SVT prolongs TCL = RAP

AOP in WCT
AVVA = VT
AVA could be antidromic AVRT or AVNRT with aberrancy