Management of oxygen and carbon dioxide pressure after cardiac arrest

Experimental evidence shows that derangements of arterial partial pressures of either oxygen (PaO2) and carbon dioxide (PaCO2) immediately after resuscitation from cardiac arrest may increase the severity of organ dysfunction due to whole body ischemia and subsequent reperfusion. Hyperoxia is believed to increase reperfusion injury, especially to mitochondrial membrane due to increased production of reactive oxygen species. Two large observational studies in human adults showed that hyperoxia (defined as a PaO2≥300 mmHg) in the first 24 h after hospital admission was associated with increased mortality or lower likelihood of independent functional status at hospital discharge. Evidence of the effects of hyperoxia in children were less consistent. A reduction of PaCO2 below normal values may cause cerebral vasoconstriction and increase the severity of delayed brain hypopefusion which usually occurs within 24h from resuscitation. Cerebrovascular reactivity to CO2 is preserved during therapeutic hypothermia. According to recent clinical studies, a low PaCO2 after resuscitation is associated with increased mortality and higher rates of poor neurological outcome both in children and in adults, while the effects of a PaCO2 above 45 mmHg are less clear. The PaCO2 derangements are very common in resuscitated patients. Maintaining normal levels of both PaO2 and PaCO2 and in particular avoiding both hyperoxia and hypocapnia may reduce morbidity and improve survival of cardiac arrest survivors. Available clinical evidence is however almost exclusively limited to observational studies which may be biased by potential uncontrolled confounders.