Review
Oxygen Therapy for Acute Myocardial Infarction—Then and Now. A Century of Uncertainty

https://doi.org/10.1016/j.amjmed.2011.04.034Get rights and content

Abstract

For about 100 years, inhaled oxygen has been administered to all patients suspected of having an acute myocardial infarction. The basis for this practice was the belief that oxygen supplementation raised often-deficient arterial oxygen content to improve myocardial oxygenation, thereby reducing infarct size. This assumption is conditional and not evidence-based. While such physiological changes may pertain in some patients who are hypoxemic, considerable data suggest that oxygen therapy may be detrimental in others. Acute oxygen therapy may raise blood pressure and lower cardiac index, heart rate, cardiac oxygen consumption, and blood flow in the cerebral and renal beds. Oxygen also may lower capillary density and redistribute blood in the microcirculation. Several reports now confirm that these changes occur in humans. In patients with both acute coronary syndromes and stable coronary disease, oxygen administration may constrict the coronary vessels, lower myocardial oxygen delivery, and may actually worsen ischemia. There are no large, contemporary, randomized studies that examine clinical outcomes after this intervention. Hence, this long-accepted but potentially harmful tradition urgently needs reevaluation. Clinical guidelines appear to be changing, favoring use of oxygen only in hypoxemic patients, and then cautiously titrating to individual oxygen tensions.

Section snippets

Early Laboratory and Clinical Trials

After Steele successfully used inhaled oxygen to relieve angina in 1900,4 the practice endured, based upon the popular notion that administered oxygen increased oxygen delivery to the myocardium and reduced infarct size.5, 6 Fifty years later Russek et al7 found that 100% oxygen given by mask not only failed to relieve or modify angina, but accentuated and prolonged some electrocardiographic changes of ischemia. They postulated that hyperoxic blood prevented reactive hyperemia in ischemic

Hemodynamic Effects of Oxygen and Myocardial Oxygen Availability

Oxygen is a vasoactive substance, and the hemodynamic effects upon healthy subjects and patients with AMI are fairly well known. Acute oxygen administration may raise blood pressure13 and lower cardiac index, heart rate, and cardiac oxygen consumption.14, 15 Coronary blood flow falls in response to hyperoxia-induced vasoconstriction regardless of initial saturation.16 Oxygen-induced vasoconstriction may similarly lower cerebral17 and renal blood flow.18 Thomas et al19 found that 40% oxygen

Systematic Reviews

Several systematic reviews of the effects of oxygen in patients with CHD are available. In 2004, a review of 9 trials failed to demonstrate effectiveness because of insufficient evidence.30 In 2008, Wijesinghe et al31 identified 51 studies, but only 2 met inclusion criteria of substantive clinical outcomes. It was concluded that evidence was limited, but primarily using the trial results of Rawles and Kenmure,11 support for oxygen therapy in all patients with uncomplicated AMI was lacking, and

What the Guidelines Say

Of guidelines that no longer recommend oxygen for all AMI patients, one of the first was the British Thoracic Society Guideline for Emergency Oxygen use, in which oxygen was recommended only for hypoxemic patients.39 The National Institute for Health and Clinical Excellence (NICE) Guideline on the management of chest pain of suspected cardiac origin, the UK Ambulance Service oxygen guideline, and a number of other societies subsequently adopted similar advice.40, 41, 42 The NICE guideline

Conclusion

Oxygen is a vasoactive drug and should be prescribed only when indicated. The burden of proof properly falls on the intervention, and there is no large, contemporary, randomized study available. Evidence supporting use of oxygen in patients suspected of having an AMI who are normoxemic is of poor quality and now old, predating modern trial methods, reperfusion, and other advances in management. Recent data suggest that physiological evidence of harm is strong, clinical evidence of harm is weak,

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  • Cited by (34)

    • DETermination of the role of OXygen in suspected Acute Myocardial Infarction trial

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      Citation Excerpt :

      Furthermore, acceptance from the medical community to challenge a “common knowledge” has been questioned,28 and the study has therefore been difficult to undertake. However, the issue is nowadays frequently discussed in various articles, blogs, and reviews, which could indicate a changing attitude.28-34 Since 2012, 2 RCTs have been started investigating oxygen therapy in STEMI patients; the Australian AVOID study35 is aiming to include 490 patients looking at infarct size by cardiac biomarkers as primary end point, whereas the Swedish SOCCER trial assesses myocardial salvage index by cardiac magnetic resonance imaging in 100 patients.36

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    Funding: None.

    Conflict of Interest: None.

    Authorship: The author is solely responsible for the entire content of this review.

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