Effects of therapeutic hypothermia on brain function in a refractory cardiac arrest model treated with extracorporeal cardiopulmonary resuscitation.

backgroundCardiac arrest (CA) remains a leading cause of mortality and long-term neurological disability. In cases of refractory CA, extracorporeal cardiopulmonary resuscitation (ECPR) may be implemented as a salvage therapy to mitigate hypoxic-ischemic brain injury and improve outcomes. However, the optimal target temperature in the specific context of ECPR remains uncertain. The objective of this study was to evaluate the impact of hypothermia on brain function using a controlled experimental model of ECPR.

methodsTwelve pigs were subjected to 5 min of untreated ventricular fibrillation, followed by 25 min of conventional cardiopulmonary resuscitation (CPR). At 30 min, veno-arterial extracorporeal membrane oxygenation support was initiated, and defibrillation attempts were performed until the achievement of return of spontaneous circulation (ROSC). Following ROSC, animals were randomly assigned to one of two groups: hypothermia (HT), targeting a core body temperature of 33-34 °C, or controlled normothermia (NT), targeting 37-38 °C. All animals underwent continuous multimodal neurological and cardiovascular monitoring. Blood samples were collected at predefined time points to assess circulating biomarkers of organ injury. The primary outcome was the change of brain tissue oxygen tension (PbtO

resultsA total of 12 pigs were included in the study, with six animals allocated to each group. Baseline characteristics were comparable between the groups and ROSC was achieved in all animals. Throughout the experiment, PbtO₂ gradually declined and intracranial pressure (ICP) increased in both groups; however, no significant differences were observed between groups. Similarly, there were no significant differences in cerebral metabolites, cortical activity, or gene expression in either frontal or parietal brain tissues. Notably, neurofilament light chain (NfL) concentrations were significantly lower at the end of the observation period in the HT group compared to NT (p = 0.04), while neuron-specific enolase (NSE) and glial fibrillary acidic protein (GFAP) levels did not differ significantly between the two groups.

conclusionsHT did not improve cerebral perfusion or metabolic parameters in this refractory cardiac arrest ECPR model; the early decrease in NfL levels requires cautious interpretation and further investigation.