Background:

Animal studies in post-ROSC management after cardiac arrest have repeatedly demonstrated poorer neurological outcomes with higher amounts of oxygen administration.¹ Studies in humans have also demonstrated dose-dependent associations between hyperoxia and poorer neurologic outcomes, as well as in-hospital mortality.^2,3

Recent Data

A retrospective analysis of prospectively-collected data in 187 OHCA patients undergoing postarrest care with targeted temperature management found worse neurologic outcomes in patients experiencing hyperoxia in the first 6 hours following ROSC.⁴

This association was dose-dependent, with worsening outcomes as with higher PaO2 levels >200.

• Adjusted OR 1.659 [95% CI, 1.194–2.305] at 200 mmHg
• Adjusted OR 3.969 [95% CI, 1.450–10.862] for 300 mmHg
• Trend towards worsening at 150 mmHg that did not reach statistical significance

Bottom Line:

• Our initial management of these patients in the ED is crucial
• In post-cardiac arrest patients, titrate immediate FiO2 to SpO2 ≥ 94% and PaO2 75 to 150/200 mmHg to avoid hyperoxia and worsening neurologic and survival outcomes. 

References

1. Pilcher J, Weatherall M, Shirtcliffe P, et al. The effect of hyperoxia following cardiac arrest - a systematic review and meta-analysis of animal trials. Resuscitation. 2012;83(4):417-22. 
2. Kilgannon JH, Jones AE, Parrillo JE, et al. Relationship between supranormal oxygen tension and outcome after resuscitation from cardiac arrest. Circulation. 2011;123(23):2717-22.
3. Janz DR, Hollenbeck RD, Pollock JS et al. Hyperoxia is associated with increased mortality in patients treated with mild therapeutic hypothermia after sudden cardiac arrest. Crit Care Med. 2012;40(12):3135-9. 
4. Youn CS, Park KN, Kim SH, et al. The cumulative partial pressure of arterial oxygen is associated with neurological outcoems after cardiac arrest treated with targeted temperature management. Crit Care Med. 2018;46(4):e279-85.