Abstract 9: Role of Hyperkalemia in the Transmural Activation Rate Gradient and Asystole During Long-Duration Ventricular Fibrillation (LDVF) in Isolated Canine Heart
During LDVF in globally ischemic hearts, a transmurally heterogeneous decrease in VF rate (VFR) occurs culminating in asystole. While hyperkalemia is considered to be a major modulator of excitability during ischemia, the magnitude of extracellular potassium ([K+]o) accumulation during LDVF and its role in the transmural VFR gradient and asystole remain unknown. Twelve isolated, blood perfused canine hearts underwent 20 min of global ischemia and VF; and an additional 4 hearts were subjected to VF during normoxic perfusion with varying [K+]o (2 - 15 mM). Plunge needle electrodes with electrical and K+ sensors were used for left ventricular endocardial (ENDO) and epicardial (EPI) measurements of VFR and [K+]o. Cluster analysis revealed a dichotomy in the timing of asystole (Figure A, Inset): 6/12 hearts experienced asystole at 7.2 ± 1.0 min of ischemia (EARLY ASYS), while the remaining 6/12 hearts were still in VF at 20 min of ischemia (LATE ASYS). EARLY ASYS showed significantly faster K+ accumulation in ENDO and EPI than LATE ASYS; neither group developed a gradient in [K+]o (Figure A). Nevertheless, a prominent ENDO-EPI VFR gradient developed during LDVF in both groups (not shown). Compared to normoxic VF, LDVF exhibited a marked decrease in VFR as a function of [K+]o. In addition, there was a significant difference in K+ sensitivity of VFR between ENDO and EPI which was not observed during normoxic VF (Figure B). We conclude that during LDVF enhanced K+ leak predicts early asystole, but the level of [K+]o per se cannot explain VFR decline either in EPI or ENDO. Thus, hyperkalemia is not the main determinant of electrical depression and asystole during LDVF.
- © 2011 by American Heart Association, Inc.