Effect of pacing site on ventricular fibrillation initiation by shocks during the vulnerable period

The critical point hypothesis for the upper limit of vulnerability (ULV) st ates that the site of S1 pacing should not affect the ULV S2 shock strength for a single S2 shock electrode configuration but may affect the S1-S2 int erval at which sub-ULV shocks induce ventricular fibrillation (VF). Further more, early post-S2 activations leading to VF should arise in areas with lo w potential gradients of similar magnitude, regardless of the S1 site. This hypothesis was tested in 10 pigs by determining ULVs for three SI sites [l eft ventricular apex (LVA), LV base (LVB), and right ventricular outflow tr act (RVOT)] with one 52 configuration (LVA patch to superior vena cava cath eter). T-wave scanning was performed with biphasic S2 shocks incremented fr om 60 V in 40-V steps and stepped up or down in 20- and 10-V steps. Activat ions and S2 potential gradients were recorded at 528 epicardial sites. Alth ough shocks just below the ULV induced VF significantly earlier in the T wa ve when the S1 site was the RVOT than when it was the LVA or LVB, ULVs were not significantly different for the three S1 pacing sites. Early post-S2 a ctivations arose closer to the S2 electrode for weak S2s but moved to dista nt low potential gradient areas as the S2 strengthened. Just below the ULV, early post-S2 activations arose in the RVOT when the S1 site was the LVA o r LVB but arose along the RV base when the SI site was the RVOT. Early site potential gradients were not significantly different just below the ULV (L VA: 8.2 +/- 4.1 V/cm; LVB: 8.6 +/- 4.9 V/cm; RVOT: 8.7 +/- 4.4 V/cm). At th e ULV, early post-S2 activations arose from the same areas but did not indu ce VE: The results support the critical point hypothesis for the ULV. For t his S2 configuration, no single point in the T wave could be used to determ ine the ULV for all S1 sites.