The Role of Oxygen in Acute MI Questioned Again

September 23, 2010

September 23, 2010 (Hershey, Pennsylvania) — The practice of routinely giving oxygen to patients with acute MI has again been questioned, this time in a "Viewpoint" article in the September 21, 2010 issue of the Journal of the American College of Cardiology [1].

In the article, Drs Raman Moradkhan and Lawrence Sinoway (Pennsylvania State University College of Medicine, Hershey, PA) point out that studies of oxygen therapy in normoxic cardiac patients have shown conflicting results, and no randomized, blinded, controlled studies have shown a benefit of such treatment, yet the use of supplemental oxygen is widespread in cardiac patients. They say this is raising the occurrence of inadvertent hyperoxia, which can actually be harmful.

They note that current ACC/AHA guidelines give a class I recommendation for oxygen use to correct arterial oxygen desaturation and a class IIa recommendation for all patients with unstable angina/non-STEMI and uncomplicated STEMI within the first six hours after presentation, the rationale being that this will reduce the acute ischemic injury and the eventual infarct area and because some patients with uncomplicated MI have arterial hypoxemia due to fluid retention in the lungs and a ventilation-perfusion mismatch.

Oxygen May Be Causing Vasoconstriction

But they say there is no evidence that normoxic subjects undergoing PCI for MI derive any benefit from supplemental oxygen or to support the common practice of oxygen therapy after successful PCI. They report that the first randomized trial of oxygen therapy in MI patients showed no benefit, and oxygen was associated with an increased aspartate-aminotransferase level, suggesting infarct expansion and an increased mortality rate compared with control, although this was not significant because of low patient numbers in the study. And they cite mechanistic studies suggesting that hyperoxia actually causes vasoconstriction, which would be detrimental in the setting of an acute cardiac event.

Moradkhan and Sinoway conclude: "Although the use of oxygen is clearly appropriate and advisable to treat hypoxia, we hypothesize that excessive use of supplemental oxygen in normoxic cardiac patients could potentially lead to worse outcomes in a number of patients. The current guidelines of oxygen therapy are not based on randomized, double-blinded, controlled studies. We propose that such studies are imperative to delineate the precise role of oxygen therapy in these conditions. In the interim, the potential physiologic ramifications of such therapy should be considered."

The concerns raised over oxygen therapy in this Viewpoint echo opinions put forward in a recent Cochrane review on the subject [2]. In the Cochrane meta-analysis of the three randomized trials conducted of oxygen in MI, there were almost three times as many deaths in patients who had been randomized to oxygen therapy as in those who had been given air and there were no benefits in terms of pain relief. But the authors noted that because the trials included involved only a small number of patients, their results need confirmation in a large trial.

Avoid Oxygen Unless Patients Are Hypoxic

The European Society of Cardiology (ESC) issued a statement saying it welcomed the current papers questioning the role of oxygen in MI and that this area will be addressed in the new ESC Clinical Practice Guidelines for the management of STEMI, to be published in 2012.

Dr Stefan James (Uppsala Clinical Research Center, Sweden), who is cochair of the ESC AMI-STEMI task force, reported that supplemental oxygen therapy is currently recommended in European guidelines for patients with desaturation hypoxia but that there is no clear guidance about what to do for normoxic MI patients. "The reality is that supplemental oxygen is given to virtually all patients in the early phase of an MI, whether in the ambulance, emergency department, or while undergoing PCI in the cath lab. But following the publication of these two papers, we need to consider whether it should be clearly stated that oxygen therapy is appropriate only for hypoxic patients," he said. He added: "It’s widely known that an MI causes oxygen deficits in the heart muscle, so it seems logical to provide additional oxygen. However, the reality is that it doesn't follow that if you increase inhaled oxygen you will automatically transfer oxygen to the heart. In fact, there are data to show that oxygen is a vasoconstrictor and may therefore act to increase the damage caused by an MI." James reiterated the need for large-scale randomized trials on this issue, and in the meantime, until new guidelines are published, he advises that oxygen should be avoided in acute MI patients, unless they have demonstrably low oxygen levels.