title: Transmural recording of shock potential gradient fields, early postshock activations, and refibrillation episodes associated with external defibrillation of long-duration ventricular fibrillation in swine.
abstract: 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.
authors.affiliation: Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama, USA.
authors.forename: James D
authors.initials: JD
authors.lastname: Allred
authors.forename: Cheryl R
authors.initials: CR
authors.lastname: Killingsworth
authors.forename: J Scott
authors.initials: JS
authors.lastname: Allison
authors.forename: Derek J
authors.initials: DJ
authors.lastname: Dosdall
authors.forename: Sharon B
authors.initials: SB
authors.lastname: Melnick
authors.forename: William M
authors.initials: WM
authors.lastname: Smith
authors.forename: Raymond E
authors.initials: RE
authors.lastname: Ideker
authors.forename: Gregory P
authors.initials: GP
authors.lastname: Walcott
mesh_terms: 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*