AI Article Synopsis

  • Cardiac arrest often leads to postcardiac arrest syndrome, causing severe oxygen deprivation and organ dysfunction after resuscitation.
  • Researchers used high-resolution ultrasound and photoacoustic imaging to monitor brain oxygen levels and heart function in a mouse model of cardiac arrest, discovering that brain oxygenation is better preserved than in other tissues during the event.
  • Post-arrest, brain oxygen levels dropped for 24 hours but improved by week one, while heart function issues persisted and were linked to ongoing brain oxygen deprivation.

Article Abstract

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.

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Source
http://dx.doi.org/10.1109/TUFFC.2023.3265800DOI Listing

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