AVRT : TREATMENT AND ABLATION

IYAN SOLIHIN
DIVISI ARRHYTHMIA PJN HARAPAN KITA,
JAKARTA
 Required accessory pathways and AV
Node
 Macroreentry circuit
 WPW syndrome is relatively common
abnormality
 Orthodromic & Antidromic
 Acut phase treatment
- Vagal Manouvre
- Pharmacological : ATP, verapamil iv

 Long Term treatment

- Use drugs which rise ERP of AVN : Verapamil,
Ca++ Blocker, Sotalol, Beta blockers
- Narrowing tachycardia zone/windows
 Rationale of Ablation
For every arrhythmias there is a critical
anatomic region of abnormal impulse
generation or propagation required for
arrhythmia to be sustained.

If this substrate is altered or destroyed, the

arrhythmia should not occur
 Patient intolerant to
pharmacological approach
 Ablation now is primary therapy =>
success rate > 95%, recurrence < 5%
and complication < 2%
RFA CRYO ABLATION
 Bleeding
 Tromboemboli
 Tamponade
 Heart structure damage
 AV block
 Pneumothorax
 TIA / Stroke
 Death
 Fasting at least 6 hrs prior the procedure
 Cease antiarrhytmic medication at least
5 half lives prior the procedure
 IV line
 Administration
 2 Quadripolar diagnostic catheters
 1 Decapolar ( CS) catheter
 4 mm ablation catheter

 It can be vary during procedure => change to

another catheters if necessary
HRA
HIS
RVA
CS
A) Normal: Seen when
conduction occurs via
normal AV conduction or
septal tract.
B) Right sided bypass
C) Left sided bypass.
Left atrium activated first.
Conduction of atrial
septum and RA are
activated later.
 Eccentric retro conduction

Earliest at cs 1,2

During spontaneous SVT seen the earliest signal at CS1,2 with eccentric atrial
retrograde conduction suggest orthodromic AVRT with left side AP
 AH<HA interval

with eccentric retrograde atrial acticiy ( earliaest at cs 1,2) Va interval during SVT 165
ms, AH<HA during SVT, NCT => orthodromic AVRT with left side AP
It takes 1 fully RVp beat to accelerate the SVT CL to the pacing CL, this
suggest AVRT as the SVT mechanism beacause impuls of RVp directly
traverse retrogradely via AP and no need more time to accelerate TCL
since AP has faster conduction velocity , AVNRTor AT is unlikely .
 A

V V

RVp result atria entraiment with an AV return sequence immediately following the
last RV p beat, this suggest AVN dependent reentrant mechanism like
AVNRT/AVRT wich is impulse traverse from ventricle to atrial via PF or Ap
depolarised atrial and retrogadely return via SF or AVN create AV sequence, A non
AVN mechanism like AT/AFL is unlikely
 12 ECG during SVT showing narrow complex
tachycardia with normal axis and visible p
wave at inferior leads
 VA interval>70 ms during SVT
 AH<HA interval during SVT
 1:1 AV conduction during SVT
 VA post RA p = VA during SVT
 Eccentric retrograde atrial activation at CS1,2
 ORTHODROMIC AVRT WITH LEFT SIDE
AP
 Transeptal needle
 8 F Mullin catheter
 SL1 long sheath
his Long sheath
ABL

RV
CS
 Power achieved

VA signal

temperature achieved

VA block during RFA

with RV pacing
10 ohm initial drop

With good signal of RV paving AP mapping, ablation commence with all RF parameter
achieved. After a few second of ablation, VA block occurred while RV pacing , it’s a sign of AP
destruction, another RFA continued until 60 second to make it sure of AP termination
VA dissociation during RV pacing showing destruction of AP
 Should wait 15-30 mnts post confirmation of
pathway elimination
 Check again end point of ablation
 If still successful  Consider procedure
ended