title: Effect of standard-dose versus high-dose epinephrine on myocardial high-energy phosphates during ventricular fibrillation and closed-chest CPR.
abstract: OBJECTIVE
  To evaluate the effects of standard-dose versus high-dose epinephrine on myocardial high-energy phosphate metabolism during resuscitation from cardiac arrest.
  
  
  METHODS
  Prospective, nonrandomized, controlled study using a swine model of cardiac arrest and resuscitation.
  
  
  METHODS
  After anesthesia, intravascular pressure instrumentation, and ten minutes of ventricular fibrillation arrest, closed-chest CPR was begun. After three minutes of CPR, animals were allocated to receive either 0.02 mg/kg i.v. standard-dose epinephrine (eight) or 0.2 mg/kg i.v. high-dose epinephrine (nine). The animals underwent thoracotomy and rapid-freezing transmural myocardial core biopsy for high-energy phosphate analysis 3.5 minutes after epinephrine administration. High-energy phosphate values were blindly determined using high-pressure liquid chromatography.
  
  
  RESULTS
  Intravascular pressure (mm Hg) and high-energy phosphate (nmol/mg protein) results for standard-dose epinephrine versus high-dose epinephrine are, respectively, coronary perfusion pressure, 15.3 +/- 7.8 versus 23.7 +/- 5.5 (P = .0009); phosphocreatine, 0.4 +/- 0.8 versus 6.2 +/- 4.4 (P = .0003); adenosine triphosphate, 9.8 +/- 4.8 versus 12.7 +/- 5.7 (P = .30); adenosine diphosphate, 5.4 +/- 2.1 versus 6.1 +/- 1.3 (P = .41); and adenylate charge, 0.68 +/- 0.12 versus 0.72 +/- 0.12 (P = .87).
  
  
  CONCLUSIONS
  High-dose epinephrine does not deplete myocardial high-energy phosphate when given in this model of prolonged ventricular fibrillation. High-dose epinephrine increases coronary perfusion pressure compared with standard-dose epinephrine. High-dose epinephrine administration repletes phosphocreatine during closed-chest CPR, thereby increasing myocardial energy stores.
authors.affiliation: Department of Emergency Medicine, Ohio State University, Columbus.
authors.forename: J W
authors.initials: JW
authors.lastname: Hoekstra
authors.forename: R
authors.initials: R
authors.lastname: Griffith
authors.forename: R
authors.initials: R
authors.lastname: Kelley
authors.forename: R J
authors.initials: RJ
authors.lastname: Cody
authors.forename: D
authors.initials: D
authors.lastname: Lewis
authors.forename: M
authors.initials: M
authors.lastname: Scheatzle
authors.forename: C G
authors.initials: CG
authors.lastname: Brown
mesh_terms: D000241:Adenosine / Q000032:analysis; D000244:Adenosine Diphosphate / Q000032:analysis*; D000249:Adenosine Monophosphate / Q000032:analysis; D000255:Adenosine Triphosphate / Q000032:analysis*; D000818:Animals; D001706:Biopsy; D001784:Blood Gas Analysis; D016887:Cardiopulmonary Resuscitation / Q000379:methods*; D002851:Chromatography, High Pressure Liquid; D002985:Clinical Protocols; D004195:Disease Models, Animal; D004353:Drug Evaluation, Preclinical; D004837:Epinephrine / Q000008:administration & dosage / Q000494:pharmacology*; D006160:Guanosine Triphosphate / Q000032:analysis; D006323:Heart Arrest / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects*; D007275:Injections, Intravenous; D007288:Inosine / Q000032:analysis; D007291:Inosine Monophosphate / Q000032:analysis; D009206:Myocardium / Q000737:chemistry* / Q000378:metabolism* / Q000473:pathology; D010725:Phosphocreatine / Q000032:analysis*; D013552:Swine; D014693:Ventricular Fibrillation / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
chemical_list: D010725:Phosphocreatine; D007291:Inosine Monophosphate; D000249:Adenosine Monophosphate; D007288:Inosine; D000244:Adenosine Diphosphate; D006160:Guanosine Triphosphate; D000255:Adenosine Triphosphate; D000241:Adenosine; D004837:Epinephrine