Less oxygen for cardiac arrest patients is better
There is no doubt that oxygen is necessary to sustain life. We have been using oxygen since the late 19th century with its use taken for granted. However, administering oxygen above atmospheric concentration should be prescribed as a medication accounting for potential adverse effects. Exposure to high dose of supplemental oxygen has been associated with pulmonary and cardiac toxicity. Moreover, an increase in oxygen radicals was found to be involved in cell death after cerebral ischemia. Cardiac arrest, both in and out of hospital, is a major cause of death worldwide. Brain injury, myocardial dysfunction and multi-organ failure comprise post cardiac arrest syndrome and reactive oxygen species play a central role in initiating and exacerbating the damage. Studies in animal models of cardiac arrest have found that the administration of 100% oxygen following return of spontaneous circulation (ROSC) may cause neurological harm in comparison to low-dose oxygen. Hyperoxia (PaO2>300 mmHg) is not uncommon among patients after ROSC however, since oxygen therapy is considered integral during resuscitation and post resuscitation care there are no large randomized controlled trials in humans. The existing data from retrospective studies demonstrates correlation between hyperoxia after ROSC and increased in-hospital mortality as well as poor neurological outcome. Hence, we should regard oxygen therapy carefully and use the lowest fraction of inspired oxygen to ensure adequate arterial saturation while avoiding hyperoxia and hypoxia.