Air Versus Oxygen in ST-Segment-Elevation Myocardial Infarction

Dion Stub, Karen Smith, Stephen Bernard, Ziad Nehme, Michael Stephenson, Janet E Bray, Peter Cameron, Bill Barger, Andris H Ellims, Andrew J Taylor, Ian T Meredith, David M Kaye
Circulation 2015 June 16, 131 (24): 2143-50

BACKGROUND: Oxygen is commonly administered to patients with ST-elevation-myocardial infarction despite previous studies suggesting a possible increase in myocardial injury as a result of coronary vasoconstriction and heightened oxidative stress.

METHODS AND RESULTS: We conducted a multicenter, prospective, randomized, controlled trial comparing oxygen (8 L/min) with no supplemental oxygen in patients with ST-elevation-myocardial infarction diagnosed on paramedic 12-lead ECG. Of 638 patients randomized, 441 patients had confirmed ST-elevation-myocardial infarction and underwent primary end-point analysis. The primary end point was myocardial infarct size as assessed by cardiac enzymes, troponin I, and creatine kinase. Secondary end points included recurrent myocardial infarction, cardiac arrhythmia, and myocardial infarct size assessed by cardiac magnetic resonance imaging at 6 months. Mean peak troponin was similar in the oxygen and no oxygen groups (57.4 versus 48.0 μg/L; ratio, 1.20; 95% confidence interval, 0.92-1.56; P=0.18). There was a significant increase in mean peak creatine kinase in the oxygen group compared with the no oxygen group (1948 versus 1543 U/L; means ratio, 1.27; 95% confidence interval, 1.04-1.52; P=0.01). There was an increase in the rate of recurrent myocardial infarction in the oxygen group compared with the no oxygen group (5.5% versus 0.9%; P=0.006) and an increase in frequency of cardiac arrhythmia (40.4% versus 31.4%; P=0.05). At 6 months, the oxygen group had an increase in myocardial infarct size on cardiac magnetic resonance (n=139; 20.3 versus 13.1 g; P=0.04).

CONCLUSION: Supplemental oxygen therapy in patients with ST-elevation-myocardial infarction but without hypoxia may increase early myocardial injury and was associated with larger myocardial infarct size assessed at 6 months.

CLINICAL TRIAL REGISTRATION: URL: Unique identifier: NCT01272713.

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Derek Brown

All enrolled patients were STEMI by EMS EKG prior to arrival and O2 sats >94%, so normoxic. Pt were excluded if upon hospital arrival were determined to have alternative diagnosis other than STEMI, with matched demographics in each arm.

Oxygen arm was started on 8L/min by face mask. If NonOxygen arm got oxygen for hypoxia (10pts total) they were started on 4L NC or 8L face mask.

I thought this study was well designed. 8L/min by face mask is not excessive, in fact applying O2 by NRB I generally start at 15L (in hypoxic pts).

My biggest concern is that the primary endpoints are not patient centered.

When you look at the paper, there is a trend toward increased mortality in the nonoxygen group at 30 days and 6months that does not reach statistical significance. Interestingly, the only patients intubated were also in the nonoxygen group.

The clinically and patient centered outcomes of increased infarct size on CMR, recurrent MI, and arrhythmia I think is most interesting. It looks to favor no oxygen therapy in patients who are not hypoxic.

My training and practice has been to place O2 to maintain sats 98-100% but titrate down to least O2 required to avoid hyperoxia. Any O2 therapy will create hyperoxia in the lung, which has known deleterious effects over time. However, in STEMI the goal is to maximize cardiac oxygenation during the acute ischemic event while limiting free radical damage in already stressed cells.

Interesting study. I think I will continue to oxygen optimization approach, smallest dose to maintain normoxia.


Jamie Gross

Based on this paper, why would you give 2L/min oxygen if the patient is normoxaemic? This is a well designed trial in my opinion. We just need to wait for a further study with more clinically relevant end-points as the primary outcome.


Israel León Pedroza

I was just wondering the same. Why did the authors decide use 8 L/min? Is it even ethical? Oxygen has toxicity. Why didn't they try an intermediate dose at least?


Michael Klevens

Nobody uses 8L/min. That's a key error. Most use 2L/min. The study is flawed but worth reading.


Joe Weatherly

The fact that the standard of care didn't win in overwhelming fashion is what is most interesting to me. The harm may not be found in future studies, who knows. I am leaning away from O2 in any normOxic patients. No proof that it helps for sure!


tiago gil

the abstract didn't say which kind of oxygen delivery system was used, nasal canula, face mask, venturi.
The toxicity of oxygen is valid in preterm infants, long term ventilated patients because of atelectasias, not for awake, facemask, breathing patients.
it´s too early to adopt the strategy?
I can only do when ACLS adopt...


Daniel Crook

Agree with Michael Klevens. There is clearly a level where oxygen causes harm but low flow exerts different physics and physiology entirely so may be beneficial. Can't extrapolate.


Tan T

Unfortunately 8l/min si a too High dose to use in this setting of patients! I don't know if somebody use such a high dose of oxygen in his daily practice....


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