Persistently Altered Brain Mitochondrial Bioenergetics After Apparently Successful Resuscitation From Cardiac Arrest

Background Although advances in cardiopulmonary resuscitation have improved survival from cardiac arrest (CA), neurologic injury persists and impaired mitochondrial bioenergetics may be critical for targeted neuroresuscitation. The authors sought to determine if excellent cardiopulmonary resuscitation and postresuscitation care and good traditional survival rates result in persistently disordered cerebral mitochondrial bioenergetics in a porcine pediatric model of asphyxia‐associated ventricular fibrillation CA. Methods and Results After 7 minutes of asphyxia, followed by ventricular fibrillation, 5 female 1‐month‐old swine (4 sham) received blood pressure–targeted care: titration of compression depth to systolic blood pressure of 90 mm Hg and vasopressor administration to a coronary perfusion pressure \u3e20 mm Hg. All animals received protocol‐based vasopressor support after return of spontaneous circulation for 4 hours before they were killed. The primary outcome was integrated mitochondrial electron transport system (ETS) function. CA animals displayed significantly decreased maximal, coupled oxidative phosphorylating respiration (OXPHOSCI+CII) in cortex (PPPPCI PCII PCIPCII PCI+CII), as well as a 30% reduction in citrate synthase activity (P\u3c0.04). Conclusions Mitochondria in both the cortex and hippocampus displayed significant alterations in respiratory function after CA despite excellent cardiopulmonary resuscitation and postresuscitation care in asphyxia‐associated ventricular fibrillation CA. Analysis of integrated ETS function identifies mitochondrial bioenergetic failure as a target for goal‐directed neuroresuscitation after CA. IACUC Protocol: IAC 13‐001023

MOESM1 of Developing a kinematic understanding of chest compressions: the impact of depth and release time on blood flow during cardiopulmonary resuscitation

Additional file 1: Figure S1. Schematic of the chest compression parameters controlled to generate the 6 distinct waveforms tested in these experiments. The two parameters that were changed were #1: Depth and #4, release time

MOESM2 of Developing a kinematic understanding of chest compressions: the impact of depth and release time on blood flow during cardiopulmonary resuscitation

Additional file 2: Figure S2. This figure shows the six measured blood flows approximately 10 min after the initiation of CPR. Several aspects of the flow should be noted. First, there is a transition between waveforms at ~1632 s. Second, all flow are traveling in the physiologically normal (positive) direction and the physiologically abnormal (negative) direction. These data confirm that CPR generates oscillatory flow as opposed to directional flow