title: Ascending-ramp biphasic waveform has a lower defibrillation threshold and releases less troponin I than a truncated exponential biphasic waveform.
abstract: BACKGROUND
  We tested the hypothesis that the shape of the shock waveform affects not only the defibrillation threshold but also the amount of cardiac damage.
  
  
  RESULTS
  Defibrillation thresholds were determined for 11 waveforms-3 ascending-ramp waveforms, 3 descending-ramp waveforms, 3 rectilinear first-phase biphasic waveforms, a Gurvich waveform, and a truncated exponential biphasic waveform-in 6 pigs with electrodes in the right ventricular apex and superior vena cava. The ascending, descending, and rectilinear waveforms had 4-, 8-, and 16-millisecond first phases and a 3.5-millisecond rectilinear second phase that was half the voltage of the first phase. The exponential biphasic waveform had a 60% first-phase and a 50% second-phase tilt. In a second study, we attempted to defibrillate after 10 seconds of ventricular fibrillation with a single ≈30-J shock (6 pigs successfully defibrillated with 8-millisecond ascending, 8-millisecond rectilinear, and truncated exponential biphasic waveforms). Troponin I blood levels were determined before and 2 to 10 hours after the shock. The lowest-energy defibrillation threshold was for the 8-milliseconds ascending ramp (14.6±7.3 J [mean±SD]), which was significantly less than for the truncated exponential (19.6±6.3 J). Six hours after shock, troponin I was significantly less for the ascending-ramp waveform (0.80±0.54 ng/mL) than for the truncated exponential (1.92±0.47 ng/mL) or the rectilinear waveform (1.17±0.45 ng/mL).
  
  
  CONCLUSIONS
  The ascending ramp has a significantly lower defibrillation threshold and at ≈30 J causes 58% less troponin I release than the truncated exponential biphasic shock. Therefore, the shock waveform affects both the defibrillation threshold and the amount of cardiac damage.
authors.affiliation: University of Alabama-Birmingham, 1670 University Blvd, Room B140 Volker Hall, Birmingham, AL 35294-0019, USA. jh@crml.uab.edu
authors.forename: Jian
authors.initials: J
authors.lastname: Huang
authors.forename: Gregory P
authors.initials: GP
authors.lastname: Walcott
authors.forename: Richard B
authors.initials: RB
authors.lastname: Ruse
authors.forename: Scott J
authors.initials: SJ
authors.lastname: Bohanan
authors.forename: Cheryl R
authors.initials: CR
authors.lastname: Killingsworth
authors.forename: Raymond E
authors.initials: RE
authors.lastname: Ideker
mesh_terms: D000818:Animals; D017147:Defibrillators, Implantable / Q000009:adverse effects; D004554:Electric Countershock / Q000295:instrumentation* / Q000379:methods; D004566:Electrodes; D060733:Electromagnetic Radiation / Q000145:classification*; D005260:Female; D006335:Heart Injuries / Q000209:etiology; D006352:Heart Ventricles / Q000503:physiopathology; D008297:Male; D023421:Models, Animal; D013552:Swine; D013997:Time Factors; D019210:Troponin I / Q000097:blood*; D014683:Vena Cava, Superior / Q000503:physiopathology; D014693:Ventricular Fibrillation / Q000503:physiopathology / Q000628:therapy*
chemical_list: D019210:Troponin I