title: Heterogeneity of ventricular fibrillation dominant frequency during global ischemia in isolated rabbit hearts.
abstract: BACKGROUND
  Ventricular fibrillation (VF) studies show that ECG-dominant frequency (DF) decreases as ischemia develops. This study investigates the contribution of the principle ischemic metabolic components to this decline.
  
  
  RESULTS
  Rabbit hearts were Langendorff-perfused at 40 mL/min with Tyrode's solution and loaded with RH237. Epicardial optical action potentials were recorded with a photodiode array (256 sites, 15 x 15 mm). After 60 seconds of VF (induced by burst pacing), global ischemia was produced by low flow (6 mL/min), or the solution changed to impose hypoxia (95% N2/5% CO2), low pH(o) (6.7, 80% O2/20% CO2), or raised [K+](o) (8 mM). DF of the optical signals was determined at each site. Conduction velocity (CV), action potential duration (APD90), effective refractory period (ERP), activation threshold, dV/dt(max), and membrane potential were measured in separate experiments during ventricular pacing. During VF, ischemia decreased DF in the left ventricle (LV) (to [58 +/- 6]%, P < 0.001), but not the right (RV) ([93 +/- 5]%). Raised [K+](o) reproduced this DF pattern (LV: [67 +/- 12]%, P < 0.001; RV: [95 +/- 9]%). LV DF remained elevated in hypoxia or low pH(o). During ventricular pacing, ischemia decreased CV in LV but not RV. Raised [K+](o) did not change CV in either ventricle. Ischemia and raised [K+](o) shortened APD90 without altering ERP. LV activation threshold increased in both ischemia and raised [K+](o) and was associated with diastolic depolarization and decreased dV/dt(max).
  
  
  CONCLUSIONS
  These results suggest that during VF, decreased ECG DF in global ischemia is largely due to elevated [K+](o) affecting the activation thresholds in the LV rather than RV.
authors.affiliation: Division of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.
authors.forename: Jane
authors.initials: J
authors.lastname: Caldwell
authors.forename: Francis L
authors.initials: FL
authors.lastname: Burton
authors.forename: Godfrey L
authors.initials: GL
authors.lastname: Smith
authors.forename: Stuart M
authors.initials: SM
authors.lastname: Cobbe
mesh_terms: D000200:Action Potentials; D000818:Animals; D006329:Heart Conduction System / Q000503:physiopathology*; D006339:Heart Rate; D066298:In Vitro Techniques; D017202:Myocardial Ischemia / Q000503:physiopathology*; D011188:Potassium / Q000378:metabolism*; D011817:Rabbits; D014693:Ventricular Fibrillation / Q000503:physiopathology*
chemical_list: D011188:Potassium