According to the author, “supplemental oxygen therapy in patients with STEMI but without hypoxia increased myocardial injury, recurrent myocardial infarction, and major cardiac arrhythmia, and was associated with larger myocardial infarct size assessed at six months.”

Although this article, presented at the American Heart Association Scientific Sessions in November 2014, received considerable attention, concern about the negative effects of hyperoxia is not new. The findings shouldn’t surprise us. What amazes me is that this concept is in some way a revelation. Many articles have reported this concern and have even expanded the concern to other clinical entities that are oxygen-sensitive. The surprise should be the gap between science and clinical practice.

In 1968, Brown and Hugget published this great nugget: “Oxygen at elevated pressures is known to be toxic for many forms of life. The toxicity is clearly related to both partial pressure of oxygen and the duration of exposure.”³ Although they were trying to kill bacteria with hyperoxia, they still recognized the concept that hyperoxia can be toxic.

In 1988, the effects of hyperoxia on cerebral blood flow (velocity) were actually studied. The authors reported that, “Hyperoxia has a consistent and predictable effect on cerebral blood flow in healthy adult brains.”⁴ Studying 15 term and 17 premature infants exposed to three times normal oxygen tension, they concluded, “The cerebral blood flow velocity fell in all 15 infants born at full term during hyperoxia, but there was a simultaneous and significant reduction in PCO2 at the same time as the hyperoxia. Analysis of variance suggested that in the infants born at full term, the change in carbon dioxide had most effect in the reduction of cerebral blood flow velocity, rather than the hyperoxia itself. We conclude that in premature infants, cerebral vascular resistance may be altered by a fall in cerebral blood flow velocity in the presence of hyperoxia.”

In 2005, coronary blood flow during left heart catheterization was studied.⁵ Compared to patients who received room air, patients who received 100 percent FiO2 experienced a 40 percent increase in coronary artery vascular resistance, which was accompanied by a 30 percent reduction in coronary blood flow.

A Cochrane database systematic review was performed in 2010.⁶ The authors identified three articles (one dating back to 1976), which encompassed 387 patients and 14 associated deaths. The relative risk for death in patients with confirmed acute myocardial infarction (AMI) who were receiving supplemental oxygen was 3.03. However, the authors admitted that the low number of reported deaths could also be attributed to chance. They noted the suggestion of harm and that no conclusive evidence exists to support the routine use of supplemental oxygen therapy in these patients. This review was updated in 2013. One additional trial was identified, increasing the total patient count to 430, with 17 deaths. The conclusions were unchanged, including a call to action for a more definitive study.