Goodbye MONA? Oxygen in AMI

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Goodbye MONA?

From: Best Mona Lisa Parodies @

Dr. Mayuri Patel PGY3

CC: Chest pain and Shortness of breath

HPI: 72F w/ PMHx of Rheumatic fever (s/p AVR repair 9 years prior), pHTN, hFrEF (EF 30%), HLD, DVT (on coumadin) s/p IVC filter BIBEMS for progressive DOE over 1 month. Prior to arrival to ED, pt developed substernal chest pain radiating to jaw associated with diaphoresis and nausea. EMS placed patient on NRB.

Triage VS afebrile BP 129/85 HR 74 RR 24 02 96%RA

General: awake, mild distress, oriented to person, place and time


Pulm: CTA – b/l

Abd: +bs, soft, nt/nd

Ext: 2+ pulses, no cyanosis or edema

EKG – Sinus rhythm, HR 74, STE II, III, aVF with reciprocal changes

Troponin – 12; CPK – 377


MEHEART was activated, patient transferred to Weiler for cardiac catheterization.

Patient given Heparin 5000 Units, NTG Sl, Plavix 600mg, ASA 162mg. En route to Weiler hospital, pt placed on 2L NC.

Hospital course:

Cardiac cath showed mild coronary artery disease for the left ventricle. The 1st acute marginal artery to the right ventricle occluded (possibly culprit). Intervention – medical management.

Patient was admitted to telemetry s/p cardiac cath. ECHO showed dilated left ventricle, EF 20-25%. Patient was elevated by heart failure team for ICD placement, because patient met NYS Class IIa criteria. Patient opted for medical management instead of ICD placement. Patient was evaluated for LifeVest and discharged after medical management.


Traditionally, we are taught that administration of high flow oxygen is the standard of care for patients presenting with cardiac emergencies. However, where does this dogma come from? The earliest evidence comes from 1900, when Steele observed that oxygen relieved pain during episodes of angina pectoris(1). The evidence for this observation came in 1928, when the cause of angina was attributed to hypoxia of the myocardium (2).

It is indeed a strange phenomena that our current day practices are based on studies in early 1900s. There have been multiple subsequent studies showing the harmful effects of oxygen. In 1950, Russek et al. showed that administration of 100% oxygen prolonged EKG changes during exercise tolerance testing and had no effect on anginal pain (3). A 1964 study reported that breathing high concentrations of oxygen (85% to 90%) for at least 30 minutes in the first 24 hours after MI resulted in decreased heart rate, reduced cardiac output, and increased systemic vascular resistance (4). In the following year, a study by Thomas et al. showed that giving 40% oxygen for 20 minutes to patients following MI resulted in a 17% decrease in cardiac output and a 5% rise in arterial blood pressure (5). Certainly not an ideal situation after an AMI. In 1969, a study by Neill showed that in “normal subjects” the availability of oxygen for myocardial metabolism was not affected until arterial oxygen saturation falls as low as 50% (6). However, in patients with CAD, myocardial ischemia was observed in some patients when oxygen saturation fell below 85%. In a subset of patients with triple-vessel disease, 6 minutes of high-flow oxygen reduced coronary blood flow sufficiently to induce myocardial ischemia (7).


The first randomized, double blinded controlled trial of oxygen therapy was conducted in 1976. The study randomized 200 consecutive patients thought to have MI to treatment with oxygen (given via medium concentration mask at 6L/min) or air for the first 24 hours. Patients with CHF, chronic pulmonary disease, or breathlessness from any cause other than AMI were excluded. The group receiving oxygen therapy had a higher level of serum aspartate aminotransferase level than the group receiving room air, indicating greater myocardial damage. Forty-three patients were excluded post-hoc when the diagnosis of MI was revoked. There was a mortality rate of 11% (9/80) in the oxygen group vs. 4% (3/77) in the air group, but this did not achieve statistical significance. The relative risk of mortality in oxygen group 2.9 (95% CI 0.81-10.3; P=0.08). The authors concluded that the results are suggestive of “deleterious effect” of oxygen and that administration of it in patients with uncomplicated MI is not beneficial (8).


What causes the deleterious effects of oxygen therapy? It is theorized that reactive oxygen species are responsible for vasoconstriction. This was shown by McNulty et al. in 2007 in patients with AMI. The study showed that breathing 100% oxygen for 10 minutes increased vascular resistance in the LAD by 23% (9). Interestingly, this increase could be prevented by co-administration of the antioxidant ascorbic acid. The diameter of the large conduit coronary arteries was not appreciably affected, suggesting that vasoconstriction occurs at the level of the myocardial microcirculation.

A Cochrane review in 2013 meta-analyzed available studies on oxygen therapy in patients with AMI. Combing the 4 randomized controlled trials (430 patients with 17 deaths) generated a relative risk of mortality of 2.11 (95% CI 0.78 to 5.68) in participants with confirmed AMI. The authors concluded that due to the small number of deaths, it could be a chance occurrence (10).

The AVOID trial from Australia might be the last straw in the age-old dogma of oxygen for AMI. It is a prospective, multicenter trial with both pre-hospital and in-hospital treatment comparing oxygen (8L/min) with air. It included patients that met STEMI criteria, had symptoms for less than 12 hours and initial 02 saturation >94%. Exclusion criteria included 02 saturations <94%, AMS, and oxygen administration prior to randomization. Primary end points for the study were infarct size measured by Troponin T (TnT) and CK-MB. Secondary endpoints were recurrent myocardial infarction, cardiac arrhythmia and myocardial infarct size assessed by cardiac magnetic resonance (CMR) imaging at 6 months. There were 638 patients randomized, of which 441 were confirmed STEMI who underwent primary endpoint analysis (218 in oxygen group vs. 223 in no oxygen group). The baseline characteristics were similar except for 38% in the oxygen group had anterior infract vs. 33 % in no oxygen group. There was a statistically significant increase in mean CK-MB, however mean TnT was similar. There was an increase in the rate of recurrent myocardial infarction in the oxygen group compared to the no oxygen group (5.5% vs. 0.9%, P=0.006) along with increase in frequency of cardiac arrhythmia (40.4% vs. 31.4%; P=0.05). At 6 months, the oxygen group (139 patients) had an increase in myocardial infarct size on CMR (20.3grams vs. 13.1grams; P=0.04) (11).

The AVOID trail concludes that supplemental oxygen in normoxic STEMI patients increased myocardial injury along with cardiac arrhythmia, and recurrent MI. It was also associated with larger myocardial infarct size. However, the study is not without its flaws. The use of 02 at 8L/min seems excessive and could account for the differences. Also, patients in no oxygen group were given oxygen either during catheterization or in the hospital stay (if 02 saturation dropped below 94%).

Where do we go from here? It seems that every patient who arrives via EMS with complaint of chest pain is placed on a NRB. The literature does not support this notion, and we may in fact be doing disservice to our patients. If there is to be a change in practice, it has to come from both pre-hospital setting as well as ED. There is no denying the importance of oxygen in patients who are hypoxic and having AMI. However, for normoxic patients it might be prudent to stay away from oxygen.


  1. Steele C. Severe angina pectoris relieved by oxygen inhalations. BMJ1900, 2:1568.
  2. Keefer CS, Resnik WH. Angina pectoris: a syndrome caused by anoxemia of the myocardium. Arch Intern Med 1928, 41:769-807.
  3. Russek HI, Regan FD, Naegele CF. One hundred percent oxygen in the treatment of acute myocardial infarction and severe angina pectoris. JAMA 1950, 144:373-375.
  4. MacKenzie GJ, Flenley DC, Taylor SH, McDonald AH, Stanton HP, Donald KW. Circulatory and respiratory studies in myocardial infarction and cardiogenic shock. Lancet 1964, 2:825-832.
  5. Thomas M, Malmcroma R, Shillingford J. Haemodynamic effects of oxygen in myocardial infarction. Brit Heart J 1965,27:401-407.
  6. Neill WA. Effects of arterial hypoxemia and hyperoxia on oxygen availability for myocardial metabolism: patients with and without coronary artery disease. Am J Cardiol 1969, 24:166-171.
  7. Bourassa MG, Campeau L, Bois MA, Rico O. The effects of inhalation of 100 percent oxygen on myocardial lactate metabolism in coronary heart disease. Am J Cardiol 1969, 24:172-177.
  8. Rawles JM, Kenmure AC:Controlled trial of oxygen in uncomplicated myocardial infarction. Br Med J 1976, 1:1121-1123.
  9. McNulty PH, Robertson BJ, Tulli MA, Hess J, Harach LA, Scott S, Sinoway LI. Effect of hyperoxemia and vitamin C on coronary blood flow in patients with ischemic heart disease. J Appl Physiol 2007, 102:2040-2045.
  10. Cabello JB, Burls A, Emparanza JI, Bayliss S, Quinn T:Oxygen therapy for acute myocardial infarction. Cochrane Database Syst Rev2013, 8:
  11. Stub D, Smith K, Bernard S, Bray JE, Stephenson M, Cameron P, Meredith I, Kaye DM: A randomized controlled trial of oxygen therapy in acute myocardial infarction Air Verses Oxygen In myocarDial infarction study (AVOID Study). American Heart Journal 2012, Volume 163, Issue 3, 339 – 345.e1.





One Comment

  • Great job looking through literature with decades of dust on it.
    I think it’s safe to say that oxygen isn’t helping an ACS patient with a normal pulse ox, and the risk of harm is uncertain in the absence of an RCT. I take my ROMIs off oxygen when they arrive by EMS or whether the ED nurse puts them on it.

    A thoughtful PGY3 EMS rotation required presentation to FDNY would be about this, and the fellows will be interested in talking about pre-hospital oxygenation for ACS.


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