Cerebral Vascular Resistance is Dysregulated Following Resuscitation from Cardiac Arrest

Cardiac arrest (CA) is a public health crisis in the United States. CA results in a severely hypoxic insult to the brain, damaging it and causing devastating neurological outcomes even after successful resuscitation. Here, we characterized the cerebral vascular function post-CA as a means of evaluating CA-induced brain injury. Specifically, using a carefully developed experimental model that induced CA in rodents via asphyxia, we quantified metrics of cerebral vascular resistance (CVR) during the first sixty minutes after hyperemia following resuscitation from CA. This time period would generally coincide with the earliest time point clinicians have access to patients rushed to the hospital following an out-of-hospital CA. Using our model, we find that CVR is dysregulated post-CA. Specifically, CVR was significantly elevated, and its changes were not tightly coupled to changes in mean arterial pressure. Moreover, indices of CVR failed to establish a consistent correlation to metrics of cerebrovascular autoregulation. Our observations suggest that CVR-based indices could quantify the dysregulation of cerebral vascular function post-CA and provide complementary information to the status of cerebrovascular autoregulation. We believe our characterizations will pave way to improved real time indicators of cerebrovascular injury following CA and help calibrate clinical interventions to maximize neurological outcomes in CA survivors.