Recently a new graduate questioned why oxygen was not immediately administered to a patient suspected of having an acute myocardial infarction (AMI). I know the practice of routinely giving oxygen to treat AMI has been discredited, but I could not cite the evidence. Can you help?-D.R., FLA.
Leon L. Chen, DNP, AGACNP-BC, CCRN, CEN, FCCP, and Fidel Lim, DNP, RN, CCRN, reply: One of the most persistent traditional practices still taught in many nursing schools is the routine administration of morphine, oxygen, nitroglycerin, and aspirin (MONA) during AMI. The MONA mnemonic has been hammered into generations of nursing and medical students based in part on the unquestioned assumption that oxygen therapy is beneficial to all patients experiencing an AMI, with or without hypoxemia. One study surveying physicians revealed that 96% of them administered supplemental oxygen to their patients with AMI and 50% of them believed that it provided mortality benefit.1 But does the evidence support this belief?
Theoretically, one can rationalize that in the setting of AMI, when the myocardium is deprived of oxygen because of coronary artery stenosis or occlusion, giving supplemental oxygen may reduce further damage. This rationale, however, does not account for the negative effect of hyperoxemia on coronary artery blood flow and vascular resistance. Moreover, hyperoxemia appears to produce cellular injury through increased production of reactive oxygen intermediates, such as the superoxide anion, the hydroxyl radical, and hydrogen peroxide.2 Evidence from as far back as 2004 has shown that supplemental oxygen provides no discernible benefit to patients with AMI who did not have hypoxemia, and multiple Cochrane Database Reviews support this conclusion.1,3-5
In 2017, The New England Journal of Medicine published results of a large trial named Oxygen Therapy in Suspected Acute Myocardial Infarction.6 In this multicenter, registry-based randomized clinical trial, 6,629 patients with an oxygen saturation of 90% or above who were suspected of having an AMI were randomly assigned to receive either oxygen therapy (at 6 L/minute for 6 to 12 hours delivered through an open face mask) or ambient air. The primary endpoint was all-cause mortality within 1 year after randomization. The authors found no statistically significant difference between the groups or in median troponin level and repeat hospitalization rate for AMI within 1 year.
Some may argue that supplemental oxygen in patients without hypoxemia during AMI may not provide any discernible benefit, but at least it is not causing harm. Yet this is also questionable. In 2015, a multicenter prospective randomized, controlled trial demonstrated that for nonhypoxic patients with AMI, supplemental oxygen was associated with increased myocardial infarction size demonstrated by increased serum creatine kinase levels, increased recurrence of AMI, and increased cardiac dysrhythmias.7 In 2017, the European Society of Cardiology cited the lack of clear evidence for benefit and evidence for potential harm in their recommendation against the routine use of supplemental oxygen for patients who are not hypoxic (SaO2 of 90% or greater).8
Every clinician is inevitably a teacher, whether we practice in hospitals or academia. We need to change not only the way we practice, but also the way we educate future clinicians. Nursing cannot progress fully to evidence-based practice if myths and dogmas that have strong contradictory evidence are still being taught.
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