Abstract Body: Introduction: Cardiac output and oxygen supply to vital organs cease after cardiac arrest, resulting in cellular damage with the brain being one of the most affected organs. From collapse to ROSC, no-flow and low-flow phases lead to primary injury due to ischemia. Then, at normal-flow phase after ROSC, reperfusion of the ischemic cerebrovascular bed triggers secondary injury. Both effects combined may cause post-cardiac arrest brain injury (approximately 2/3 of all deaths 48-72h after ROSC). Recently, standardization of ETCO₂ to constant ventilation rate and chest compression depth has been proposed as a potential indicator of the patient’s physiological status during resuscitation.

Aim: Retrospectively assess how the trend of standardized ETCO₂ during CPR in patients achieving ROSC may reflect an increment in cellular damage that could promote brain injury.

Methods: Out-of-hospital cardiac arrest cases of patients achieving sustained ROSC, with defibrillator and clinical data. ETCO₂ was standardized to 10 ventilations per minute and 50mm (ET_s). Trends were calculated as the percent variation between the initial and the final values of ET_s in the low-flow phase before the onset of ROSC and in the normal-flow phase after ROSC. We used the modified Rankin Score (mRS, from 0 to 6) to classify the patients into good (mRS ≤ 3) or poor functional outcome (mRS > 3)

Results: Forty-two sustained ROSC cases were included, 8 with good and 34 with poor functional outcome. The median (IQR) trend of ET_s was +0.9 (–3.9, +3.6) %/min in the low-flow phase, and –1.8 (–4.1, +0.3) %/min in the normal-flow phase (p = 0.03). The low-flow phase lasted 12.0 (11.2, 14.7) min in patients with good outcome, and 16.2 (14.1, 19.2) min in those with poor outcome (p = 0.02). The trend of ET_s in the normal-flow phase was +0.1 (–0.2, +1.2) %/min in patients with good outcome and –2.4 (–4.2, –1.0) %/min in those with poor outcome (p = 0.01).

Conclusion: The trend of standardized ETCO₂ was significantly different in the normal-flow phase after ROSC than in the low-flow phase before ROSC. The negative trend in the normal-flow phase combined with a longer low-flow phase may reflect an increment of cellular damage, with a major impact on the brain. This is possibly because reperfusion aggravates primary injury the longer the low-flow phase has lasted.