Eighteen swine were randomized to three treatment arms in two phases. VF was electrically induced and untreated for 4 min. The animals then received 6 min of mechanical CPR. Blinded investigators infused two study medicines peripherally during this interval. One group received 1.5 mEq/kg KCl with CPR initiation followed 3 min later by CaCl 10% infusion 0.12 cm3/kg, the second group received 1.5 mEq/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 30 min if ROSC. AMSA change from before to 5 min 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 1.8 mm Hg (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.