title: The effect of cardiac compression on defibrillation efficacy and the upper limit of vulnerability.
abstract: BACKGROUND
  We determined the effects of decreasing the ventricular blood volume and altering cardiac geometry on defibrillation, the upper limit of vulnerability (ULV), and the relationship between them.
  
  
  RESULTS
  In six pigs, fibrillation/defibrillation trials were performed with a left ventricular apex patch to a superior vena cava catheter electrode configuration and a biphasic waveform. Thirty trials each were performed on a compressed versus noncompressed (normal) heart. Compression was achieved using direct mechanical ventricular actuation. Dose-response curves were constructed, and the 50% probability points (ED50) were compared for leading edge voltage (LEV), leading edge current (LEI), and total energy (TE). In another 12 pigs, triplicate defibrillation thresholds (DFTs) and ULVs were determined for each heart state. The T wave was scanned with shocks in 10-msec steps for determining the ULV. Compression resulted in decreased ED50s for LEV (delta = 138 +/- 77 V, P < 0.05, mean +/- SD), LEI (delta = 1.57 +/- 0.7 A, P < 0.05), and TE (delta = 4.9 +/- 3.6 J, P < 0.05) compared to normal. In the second study, compression significantly reduced DFT (P < 0.02) and ULV (P < 0.02) for LEV, LEI, and TE compared to normal. The ULV tended to be lower than the DFT for the normal heart state (delta = 23 +/- 46 V LEV: P = NS). However, the ULV was significantly greater than the DFT for the compressed heart state (delta = 19 +/- 25 V LEV; P < 0.03).
  
  
  CONCLUSIONS
  Shock delivery during cardiac compression improves defibrillation efficacy. Additionally, cardiac compression decreases both DFT and ULV, which supports the ULV hypothesis of defibrillation. Finally, maintaining the heart's geometric and volumetric state during ULV testing in paced rhythm and DFT testing in ventricular fibrillation moves the ULV higher than the DFT-the position predicted by the ULV hypothesis for defibrillation.
authors.affiliation: Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA.
authors.forename: S F
authors.initials: SF
authors.lastname: Idriss
authors.forename: M P
authors.initials: MP
authors.lastname: Anstadt
authors.forename: G L
authors.initials: GL
authors.lastname: Anstadt
authors.forename: R E
authors.initials: RE
authors.lastname: Ideker
mesh_terms: D000818:Animals; D002306:Cardiac Volume / Q000502:physiology; D004554:Electric Countershock; D004566:Electrodes; D004597:Electroshock; D006321:Heart / Q000033:anatomy & histology / Q000502:physiology*; D066298:In Vitro Techniques; D013552:Swine; D016276:Ventricular Function