OTVT

Transition of R wave in V4 or greater is suggestive of RVOT

When transition is in V3:


V2S / V3R ratio > 1.5 = RVOT

R/S amplitude index: R/S (V2) < 0.3 = RVOT

R wave duration index (tallest R in V1 or V2/S wave) < 0.5 = RVOT

R wave transition in PVC later than R wave transition in sinus = RVOT



S wave in I: ASCs or RVOT

Notching in QRS complex: free wall of RVOT

S in V6: endocardial LV

qRS right precordial leads: junction between LCC and RCC

EPI

Slurring of initial portion of QRS
V1 Left Bundle, V3 Transition
Inferior Axis, RII>RIII
Abrupt Transition from V2 to V3
Long MDI (Max Deflection index) >0.55ms
Pseudodelta >34ms
QS in aVR, aVL, Q aVR > Q aVL

MDI Maximum Deflection Index: shortest time to a deflection in any precordial
lead / QRS duration > 0.55 = epi

QaVL/QaVR > 1.4 = epi

R II> R III = epi

RVOT more fq in women
LVOT more fq in males

RVOT: abnormal automaticity (enhanced by exercise and Isuprel), suppressed by
BB
LVOT: triggered activity, induced by V stim


MAPPING

-Record 12 lead ECG before sedation

-3 sheaths in 3 FV. 1 arterial sheath. IV heparin ACT > 250

-His Quad
-CS decapolar advanced as far as possible even into the AIVV (anterior InterVentricular Vein)
When this is not possible use a 2.3 Fr micro multi-electrode catheter (pathfinder, Cardima,
fremont, CA)

-If no PVCs - burst pace from RVOT or RV apex and Isuprel

-Map in RVOT first in all PVCs with LBBB pattern
earliest bipolar activation mapping and/or local unipolar QS pattern
-When PVCs infrequent pace mapping (500 ms and minimum stim amplitude required to capture
consistently, up to max 20 mA and PW 2 ms) esp for RVOT less helpful in ASC (preferential
conduction or inability to capture). Pace stim to QRS is longer when pacing LCC for example and
the pace map at the site of success was not as good as in the RVOT site
when an earlier precordial transition can be reproduced by pace mapping in RVOT consider LVOT

When MDI during ventricular arrhythmias is closer to pace map from GCV than that from ASCs
and LVOT consider epicardial origin
ABLATION

When earliest V activation is > 20 ms and earlier than that recorded in GCV RFA can be performed at
site where there is a great confirmation of the pace map.
If not successful in RVOT move to LVOT and ASC
-PVC exhibiting R in I and local activation from HB precedes QRS onset then map RCC, NCC (just
superior to HB catheter and exhibits A>V)
Pacing in the ASCs exhibits a long stim to QRS interval whereas it does not in the LVOT below the
valve

CATHETERS
-RVOT, ASCs and endocardial LVOT: non irrigated catheter
.Cooling effect through OT is enough to deliver desirable RF energy
.Irrigated may cause perforation of RVOT free wall and destroy aortic valves

55-60 degrees
Max power output 50 W
Never deliver within 5 mm of a coronary. coronary contrast Q 15 secs

-CS: irrigated catheter (20W - 30 mL/min). Can go up to 30 W, temp < 41 degrees


If acceleration or reduction in rate of PVCs seen first 10 seconds continue for 30-60 sec otherwise
stop if no effect after 10 sec

ENDPOINT
Non inducibility with Isuprel 2-4 mcg/min adn burst pacing from RV CL < 240 ms

Reverse with protamine to ACT < 170 sec
Bedrest 6 hours
ASA 81 after LVOT and ASCs ablation for 6 weeks

COMPLICATIONS
Aortic insufficiency
Damage to coronaries
AV conduction system damage cause HB runs in central fibrous body located underneath RCC and
NCC
VF induced during RFA in RVOT
RVOT pericardial effusion (thin mb): quick pericardiocentesis +/- surgical repair
CS
Attempt at mapping GCV/AIV.  Will start with 4 or 6 fr inquiry catheter through SR0 or agilis sheath.  
Contrasted balloon venogram, then mapping via ablation or 4 fr inquiry or 0.14 vision wire or 3.3 Fr
Mapit Catheter through angled hydrophilic catheter or covered 0.18 micro catheter for improved
sensitivity.  If septal perforator visible then will attempt to cannulate