Oxygen administration during cardiac arrest is primarily supported by scientific evidence, though the strength and nuance of that evidence have evolved over time. Cardiac arrest results in the cessation of effective blood circulation, depriving vital organs, especially the brain and heart, of oxygen. Early guidelines and clinical practice have long advocated for supplemental oxygen during resuscitation efforts, aiming to restore oxygen delivery once circulation is re-established with chest compressions or return of spontaneous circulation (ROSC).

Scientific studies and consensus guidelines (such as those from the American Heart Association and European Resuscitation Council) indicate that hypoxemia (low blood oxygen levels) during and after cardiac arrest is associated with worse outcomes, including brain injury and poor survival. Thus, oxygen is administered to mitigate the risk of hypoxic injury during resuscitation. However, more recent evidence suggests that hyperoxia (excessively high oxygen levels) after ROSC may also be harmful, possibly due to oxidative stress and reperfusion injury. As a result, while 100% oxygen is typically provided during active resuscitation, current guidelines recommend titrating oxygen to maintain normal oxygen saturation (94–98%) once ROSC is achieved.

In summary, the use of oxygen in cardiac arrest is grounded in scientific understanding of the pathophysiology of hypoxia during arrest, and is supported by both experimental and clinical data. Ongoing research continues to refine best practices regarding optimal oxygen levels during and after resuscitation.