Abstract

Clinical studies have demonstrated that dynamic changes in regional cerebral oxygen saturation (rSO2) after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) have a role in predicting neurological outcomes after the return of spontaneous circulation (ROSC). Our study evaluated whether the timing of rSO2 decline shortly after CPR reflects the severity of brain injury in a rat model of CA. Rats were subjected to different durations of asphyxia to produce variable severities of brain injury, due to CA. Time from ROSC to achieving the initial minimum rSO2 was defined as Tnadir. A Tnadir cut-off of 24 min had optimal sensitivity and specificity for predicting good neurological outcomes at 72 h after ROSC (AUC, 0.88; sensitivity, 89%; specificity, 86%; p < 0.01). Immunohistochemistry at 72 h post-CA revealed that the number of Fluoro-Jade B positive degenerating neurons in the hippocampus CA1 sector were markedly higher in animals with Tnadir > 24 min than that in animals with Tnadir ≤ 24 min. There was no difference in the gene expressions of cytokines and mitochondrial fission proteins in the brain at 2 h after ROSC between rats with Tnadir > 24 min and with Tnadir ≤ 24 min. In conclusion, Tnadir can be a novel predictor of good neurological outcomes after CA/CPR.

Highlights

  • Sudden cardiac arrest (CA) is a major public health problem globally, which accounts for over 355,000 emergency medical, service-assessed, out-of-hospital cardiac arrest (OHCA)cases in the United States [1]

  • Adopting more effective methods of real-time brain monitoring may improve cognitive outcomes after return of spontaneous circulation (ROSC) [5] and optimize therapeutic interventions; no timely and reliable single prognostication marker is available for patients who remain comatose after CA/cardiopulmonary resuscitation (CPR) [6]

  • While animals subjected to 6 min CA did not exhibit a substantial difference in cerebral CO2 production over time, animals subjected to 12 min CA showed a marked increase in cerebral CO2 production, compared to that at baseline and 20 min post-ROSC (Figure 3)

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Summary

Introduction

Sudden cardiac arrest (CA) is a major public health problem globally, which accounts for over 355,000 emergency medical, service-assessed, out-of-hospital cardiac arrest (OHCA)cases in the United States [1]. Several studies have reported the trend of improved survival rates and favorable neurological outcomes in patients with OHCA who received cardiopulmonary resuscitation (CPR) [1,2,3], the global rate of hospital discharge, with intact neurocognitive function among these patients is still low [2,4]. Regional cerebral oxygen saturation (rSO2 ), measured using near-infrared spectroscopy (NIRS), has emerged as a monitoring system for predicting the probability of ROSC and/or favorable neurological outcomes after successful CPR [7,8,9]. More recent studies have suggested that dynamic assessments of rSO2 , obtained throughout resuscitation, are more appropriate than single-time assessments for predicting the outcomes in patients with OHCA [9,10,11,12,13]. The role of temporal changes in rSO2 shortly after

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