Transmural recording of shock potential gradient fields, early postshock activations, and refibrillation episodes associated with external defibrillation of long-duration ventricular fibrillation in swine.
BACKGROUND
Knowledge of the shock potential gradient (nablaV) and postshock activation is limited to internal defibrillation of short-duration ventricular fibrillation (SDVF).


OBJECTIVE
The purpose of this study was to determine these variables after external defibrillation of long-duration VF (LDVF).


METHODS
In six pigs, 115-20 plunge needles with three to six electrodes each were inserted to record throughout both ventricles. After the chest was closed, the biphasic defibrillation threshold (DFT) was determined after 20 seconds of SDVF with external defibrillation pads. After 7 minutes of LDVF, defibrillation shocks that were less than or equal to the SDVF DFT strength were given.


RESULTS
For DFT shocks (1632 +/- 429 V), the maximum minus minimum ventricular voltage (160 +/- 100 V) was 9.8% of the shock voltage. Maximum cardiac nablaV (28.7 +/- 17 V/cm) was 4.7 +/- 2.0 times the minimum nablaV (6.2 +/- 3.5 V/cm). Although LDVF did not increase the DFT in five of the six pigs, it significantly lengthened the time to earliest postshock activation following defibrillation (1.6 +/- 2.2 seconds for SDVF and 4.9 +/- 4.3 seconds for LDVF). After LDVF, 1.3 +/- 0.8 episodes of spontaneous refibrillation occurred per animal, but there was no refibrillation after SDVF.


CONCLUSIONS
Compared with previous studies of internal defibrillation, during external defibrillation much less of the shock voltage appears across the heart and the shock field is much more even; however, the minimum nablaV is similar. Compared with external defibrillation of SDVF, the biphasic external DFT for LDVF is not increased; however, time to earliest postshock activation triples. Refibrillation is common after LDVF but not after SDVF in these normal hearts, indicating that LDVF by itself can cause refibrillation without requiring preexisting heart disease.
Allred
James D
JD
Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Killingsworth
Cheryl R
CR
Allison
J Scott
JS
Dosdall
Derek J
DJ
Melnick
Sharon B
SB
Smith
William M
WM
Ideker
Raymond E
RE
Walcott
Gregory P
GP
D000818:Animals; D018780:Body Surface Potential Mapping; D004554:Electric Countershock; D008564:Membrane Potentials / Q000502:physiology*; D013552:Swine; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000503:physiopathology* / Q000628:therapy*