SHOULD WE STILL FOLLOW "MONA"?

We use to advocate that the ER ( Emergency Room ) or pre-hospital phase on management of Acute Myocardial Infarction should begin with MONA, an acronym which allows junior doctors to quickly remember what should be done. MONA stands for Morphine, Oxygen, Nitrates and aspirin. Well over the course of the last 10 years, we have seen the use of "nitrates" being challenged. Some say that nitrates may help, white others say that nitrates may harm, because nitrates may divert much needed blood from the vital infarcted segments to the more normal segments because of its unequal dilating properties for normal vessels and atherosclerotic vessels.
Well the "O" in MONA is also under attack now. A paper presented by Dr Dion Stub, formally of Monash Australia, presently of the St. Paul's Hospital ( Vancouver ), at the just concluded American Heart Association Annual Scientific Meeting, Chicago, seemed to show that giving O2 to people with normal O2 saturation post chest pains, may do more harm then good.
Dr Stephen Bernard ( lead investigator ) and group ( 9 hospitals in the Melbourne area ), studied 441 patients with STEMI. He divided these patients into the O2 group and the no O2 group. All of them ( inclusion criteria ), had suspected STEMI with chest pains of not more than 12 hours duration, and relevant ECG and enzyme changes. They all had O2 saturation ( by pulse oximeter ) of >94%. This was deemed as the normal. 218 of these patients received O2 at 8 L/min and the other group of 223 patients received room air ( avoid O2 ). This study was called AVOID ( Air Vs Oxygen in STEMI ). The primary end point was infarct size as measured by cardiac enzyme, and secondary endpoint was infarct size estimation by cardiac MRI. All of them upon admission received primary angiopasty.
At the end of hospital stay, those receiving room air ( avoid oxygen group ) has lesser CPK enzyme rise when compared with those receiving O2. There was no difference in mortality and morbidity endpoints, as the study was under powered for that. The 6 months cardiac MRI also showed that those receiving O2 had larger infarct size when compared to those who received room air.
What could be a possible explanation?
The theory is that after 15 mins of O2 at 8L/Min, the blood becomes hyperoxic. These will cause changes in the coronary microvasculature which may become vasoconstricted because of the instant hyperoxia.  This will increase free radicals in the infarcted zone, and the bottomline is that infarct size may increase.
Caution is required here as this study is small and there are studies showing that administering O2 cause no difference.
For the moment, the jury is still out on routine oxygen therapy post STEMI. Most of us will reflexly give it. Those who forgot to, now have some evidence to back them.
As for MONA, well we may end up with MOA or even MA.