title: Energy conserving chemical defibrillation of ventricular fibrillation: A randomized two phase controlled blinded trial.
abstract: Potassium cardioplegia-induced transient asystole may conserve myocardial energy, foster chemical defribrillation, and improve VF arrest outcome. A trial of potassium infusion with or without calcium reversal was conducted to test for improvement in intra-arrest VF waveform and post-ROSC hemodynamics.
  
  
  
  Eighteen swine were randomized to three treatment arms in two phases. VF was electrically induced and untreated for 4min. The animals then received 6min of mechanical CPR. Blinded investigators infused two study medicines peripherally during this interval. One group received 1.5mEq/kg KCl with CPR initiation followed 3min later by CaCl 10% infusion 0.12cm(3)/kg, the second group received 1.5mEq/kg KCl without CaCl, and the third group received placebo infusions. Ten minutes post VF initiation, defibrillation was performed, as appropriate, followed by ACLS for continued arrest or observation for 30min if ROSC. AMSA change from before to 5min post study drug infusion was compared with nonparametric statistics. MAP post ROSC was compared using mixed linear regression analysis.
  
  
  
  Average normalized AMSA change was -0.15, -0.63, and +0.27 in the KCl, KCl+CaCl, and placebo groups, respectively (p=0.01). Three KCl+CaCl animals developed on organized rhythm chemically without electrical defibrillation. One, 3, and 4 animals in the KCl, KCl+CaCl, and placebo groups, respectively, survived post ROSC. Post ROSC, MAP decreased 1.8mmHg (95% CI -1.4 to 5.1) min(-1) less in the KCl+CaCl group compared to placebo.
  
  
  
  Chemical defibrillation and ROSC are possible post potassium-induced asystole. Potassium followed by calcium reversal, but not potassium alone, led to ROSC and post-ROSC hemodynamics comparable to recommended therapy.
authors.affiliation: Department of Emergency Medicine, University of Pittsburgh School of Medicine, United States. Electronic address: kmarill@partners.org.
authors.forename: Keith A
authors.initials: KA
authors.lastname: Marill
authors.affiliation: Department of Emergency Medicine, University of Pittsburgh School of Medicine, United States.
authors.forename: David D
authors.initials: DD
authors.lastname: Salcido
authors.affiliation: Department of Emergency Medicine, University of Pittsburgh School of Medicine, United States.
authors.forename: Matthew L
authors.initials: ML
authors.lastname: Sundermann
authors.affiliation: Department of Emergency Medicine, University of Pittsburgh School of Medicine, United States.
authors.forename: Allison C
authors.initials: AC
authors.lastname: Koller
authors.affiliation: Department of Emergency Medicine, University of Pittsburgh School of Medicine, United States.
authors.forename: James J
authors.initials: JJ
authors.lastname: Menegazzi
mesh_terms: D000818:Animals; D002122:Calcium Chloride / Q000008:administration & dosage*; D004195:Disease Models, Animal; D005260:Female; D006323:Heart Arrest / Q000628:therapy; D007036:Hypothermia, Induced / Q000379:methods*; D017680:Potassium Compounds / Q000008:administration & dosage*; D011897:Random Allocation; D034421:Sus scrofa; D013552:Swine; D014693:Ventricular Fibrillation / Q000628:therapy*
chemical_list: D017680:Potassium Compounds; C018369:potassium cardioplegic solution; D002122:Calcium Chloride
keywords: Calcium; Heart arrest; Potassium; Sudden cardiac death; Ventricular fibrillation