Abstract 19360: Potassium Infusion at the Onset of CPR Prevents Mitochondrial Impairment After Prolonged VF Arrest
Introduction: Potassium-based cardioplegia has been used for decades in cardiac surgery to preserve cardiac tissue while inducing cardiac standstill. Recent studies have also shown that animals can be successfully resuscitated after infusion of potassium at the beginning of cardiopulmonary resuscitation (CPR). This study tested the hypothesis that infusion of potassium at the onset of CPR prevents mitochondrial impairment caused by reperfusion injury after prolonged cardiac arrest.
Methods: After 15 minutes of untreated ventricular fibrillation (VF), 18 pigs were randomized to receive control saline, 50 mEq potassium (low-dose), or 100 mEq potassium (high-dose) via central venous catheter at the initiation of CPR. All animals received mechanical CPR with active compression/decompression, an impedance threshold device, and epinephrine per standard AHA protocols. Cardiac tissue was harvested after 4 minutes of CPR without defibrillation. Primary endpoints included mitochondrial respiratory control index (RCI) and mitochondrial calcium retention capacity (CRC). Secondary endpoints included the hemodynamic assessment.
Results: Infusion of potassium at the onset of CPR had no effect on hemodynamics including coronary perfusion pressure (25 vs. 28, p=0.7 for Control and low-dose KCl, respectively). Despite similar hemodynamics, potassium infusion improved RCI comparing control to low-dose KCl infusion using both complex I (4.3 vs. 6.1, p=0.01) and complex II (2.4 vs. 3.3, p=0.003) substrates. High-dose KCl did not provide additional respiration benefit. Potassium infusion also increased CRC. With complex I substrates, high-dose KCl enhanced CRC compared to controls [1361 vs. 1040, (in nmol), p=0.008, respectively]. Low-dose KCl increased CRC with complex II (1337 vs. 1597, p=0.02, for control and low-dose KCl, respectively) while high-dose KCl did not provide additional benefit.
Conclusions: Potassium infusion at the initiation of CPR prevents reperfusion-induced mitochondrial damage. This improvement was independent of the perfusion pressure achieved during CPR. Improvement of mitochondrial function and stability is observed within the first four minutes of CPR providing an improved substrate for establishing ROSC.
Author Disclosures: J.A. Bartos: None. T.R. Matsuura: None. A. Tsangaris: None. K. Chandra Shekar: None. S.H. McKnite: None. J.N. Rees: None. D. Yannopoulos: None.
- © 2015 by American Heart Association, Inc.