Neurovascular Hypoxia Trajectories Assessed by Photoacoustic Imaging in a Murine Model of Cardiac Arrest and Resuscitation

Cardiac arrest is a common cause of death annually mainly due to postcardiac arrest syndrome that leads to multiple organ global hypoxia and dysfunction after resuscitation. The ability to quantify vasculature changes and tissue oxygenation is crucial to adapt patient treatment in order to minimize major outcomes after resuscitation. For the first time, we applied high-resolution ultrasound associated with photoacoustic imaging (PAI) to track neurovascular oxygenation and cardiac function trajectories in a murine model of cardiac arrest and resuscitation. We report the preservation of brain oxygenation is greater compared to that in peripheral tissues during the arrest. Furthermore, distinct patterns of cerebral oxygen decay may relate to the support of vital brain functions. In addition, we followed trajectories of cerebral perfusion and cardiac function longitudinally after induced cardiac arrest and resuscitation. Volumetric cerebral oxygen saturation (sO2) decreased 24 h postarrest, but these levels rebounded at one week. However, systolic and diastolic cardiac dysfunction persisted throughout and correlated with cerebral hypoxia. Pathophysiologic biomarker trends, identified via cerebral PAI in preclinical models, could provide new insights into understanding the pathophysiology of cardiac arrest and resuscitation.