부산대학교 도서관

Background: Cardiac rearrest after return of spontaneous circulation (ROSC) is a significant barrier to successful resuscitation, making it a high priority for emergency care research. Regardless of initial arrest rhythm, rearrest is commonly due to pulseless electrical activity (PEA). However, mechanisms underlying PEA rearrest are poorly understood. Previously, myocardial contractile function during ischemia-reperfusion has been tied to alterations in extracellular sodium (Na+) and calcium (Ca2+) concentrations.Objective: To determine physiological predictors and explore potential mechanisms underlying susceptibility to PEA rearrest.Methods: Acute myocardial infarction (AMI) induced by left anterior descending artery (LAD) occlusion was followed by 8 min of VF, then pigs were resuscitated (defibrillation, CPR, epinephrine) to ROSC and the LAD was reperfused. Pigs were instrumented to measure metabolic variables from arterial and coronary sinus venous blood gases, electrolytes, and hemodynamics. Subjects that had PEA rearrest (n=7) were compared to those that did not rearrest (n=4).Results: Hemodynamic and primary arrest characteristics were similar between PEA and no rearrest groups, including ischemia duration, time to ROSC, CPR events, and epinephrine administration. At ROSC, hemodynamic and metabolic variables including pH, myocardial lactate consumption, myocardial arterial/venous oxygen difference were also similar between groups. Importantly, post-ROSC myocardial lactate consumption was significantly increased in the PEA group (3.9 vs. 0.5 mmol, p<0.03) as was coronary sinus Na+ (147 vs. 135 mEq/L, p<.03); however, coronary sinus Ca2+ was significantly reduced (1.9 vs. 2.3 mEq/L, p<.01 ). Taken together, these data suggest that metabolic substrate depletion may promote local electrolyte shifts contributing to mechanical dysfunction underlying PEA.Conclusion: PEA rearrest was associated with increased myocardial lactate consumption and derangements in cardiac Na+ and Ca2+ in a translational model with well controlled arrest characteristics. Improved understanding of mechanisms underlying post-ROSC electrolyte shifts may identify novel mechanisms and therapeutic approaches to prevent and treat PEA.