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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Dr. Nikolas Nikolaou
Prof. Dan Atar,
Should oxygen be routinely administered to all patients with ACS for the first six hours from onset?Yes 42%No 58%
Competing interests: None In the current ACCA-poll, the majority of voters favor a strategy of no routine administration of oxygen in ACS patients in their initial phase. This is a very interesting finding, given the fact that establishing oxygen supplementation is practiced very ubiquitously in most ambulances and hospitals. So why has our reasoning evolved from an obvious “yes” just a few years ago, to a scepticism regarding the well-doings of oxygen? The reasons are many:
One of the reasons for what we might call a “reflex” to supply oxygen in ACS is the pathophysiological insight into the undisputed fact that myocardial ischemia is caused by a lack of oxygen supply to the myocardium. We do have knowlegde of the dynamic – often “on-and-off” - changes of a ruptured plaque triggering thrombus formation in a coronary artery, and the only partial occlusion that is frequently encountered (i.e., with TIMI flow > 1 in culprit leasons). Henceforth, it appears not unreasonable to anticipate an increase in oxygen supply to an ischemic part of the myocardium when giving oxygen to an ACS patient. The assumption is simply that this might lead to a certain salvage effect in acutely jeopardized cardiomyocytes. Taken together, until we learn more about this topic, one can argue that:
Competing interests: none
The outcome of this ACCA-pole indicates the end of a long-standing tradition. For over 100 years, O2 has been routinely administered during initial treatment of ACS with the expectation for increased O2 delivery to the ischaemic myocardium and subsequent benefit on patient symptoms, size of MI and patient outcomes. Evidence in support of this approach was derived primarily from animal models, uncontrolled human data and studies indicating that O2 administration may reduce the incidence of unsuspected hypoxaemia in patients with ACS.This line of reasoning, however, has been greatly challenged by studies showing possible untoward effects of hyperoxaemia on both the systemic and the coronary circulation. In healthy volunteers and patients with stable CAD, inhalation of 100% O2 is associated with a decrease in coronary blood flow through constriction of the microvascular resistance vessels (A). Hyperoxia may induce coronary vasoconstriction by inhibition of local vasorelaxation and also increasing levels of potent vasoconstrictors.Also hyperoxia may exacerbate reperfusion injury to the heart, through increased production of oxygen free radicals.Recent overviews of the existing literature underline the risk for harm with routine O2 use and advocate an urgent need for randomised controlled trials that would be sufficiently powered to evaluate the effect of O2 therapy on the risk of mortality in patients with MI.To allow for these concerns, current guidelines suggest that O2 should be administered only to hypoxaemic patients under guidance by pulse oximetry so that O2 flow may be targeted to achieve a certain O2 saturation range (B).
1. Bodetoft S, Carlsson M, Arheden H, et al.: Effects of oxygen inhalation on cardiac output, coronary blood flow and oxygen delivery in healthy individuals, assessed with MRI. Eur J Emerg Med. 2010 May 12. PMID:20467322.
2. Cabello JB, Burls A, Emparanza JI, et al.: Oxygen therapy for acute myocardial infarction. Cochrane Database of Systematic Reviews 2010, Issue 6. Art. No.: CD007160. DOI: 10.1002/14651858.CD007160.pub2
A. McNulty PH, Robertson BJ, Tulli MA et al. Effect of hyperoxia and vitamin C on coronary blood flow in patients with ischemic heart disease. J Appl Physiol 2007; 102: 2040 –2045
B. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Steg PG, James SK, Atar D, et al. Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC) Eur Heart J. 2012 ;33: 2569-619.
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