What activates the systemic ischaemia/reperfusion response after cardiac arrest?

The systemic ischaemia/reperfusion response is primarily activated by the resuscitation process after cardiac arrest. When cardiopulmonary resuscitation (CPR) and other resuscitation efforts are initiated, there is a restoration of blood flow to tissues that had previously been deprived of oxygen. This sudden influx of blood, rich in oxygen and nutrients, can lead to a cascade of physiological responses.

During cardiac arrest, the body experiences a state of ischaemia as the heart is not pumping effectively, causing tissues to suffer from a lack of oxygen. When resuscitation restores blood flow, there is a risk of reperfusion injury, which can lead to systemic inflammation, oxidative stress, and potential damage to various organs. This process highlights the importance of understanding the dual nature of reperfusion, where restoration of blood flow saves lives but also poses risks due to the inflammatory response it triggers.

In contrast, while medications, defibrillation, and the patient's underlying health condition can influence outcomes after cardiac arrest, they do not directly initiate the systemic ischaemia/reperfusion response. Medications might assist in stabilizing heart rhythms or supporting circulation, defibrillation aims to restore a viable heart rhythm, and a patient's history can certainly impact recovery,