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 post cardiac 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 to track neurovascular oxygenation and cardiac function trajectories in a murine model of cardiac arrest and resuscitation. We report preservation of brain oxygenation is greater compared to that in peripheral tissues during arrest. Furthermore, distinct patterns of cerebral oxygen decay may relate to the support of vital brain functions. Additionally, we followed trajectories of cerebral perfusion and cardiac function longitudinally after induced cardiac arrest and resuscitation. Volumetric cerebral oxygen saturation decreased 24 hours post arrest, 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 photoacoustic imaging in preclinical models, could provide new insights in understanding the physiopathology of cardiac arrest and resuscitation.