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shr7 · 04-10-2009, 23:47

If I may add a little for now. Maybe when the computer is not behaving badly I can elaborate.

The ACC/AHA guidelines in patients with STEMI is linked below:

http://circ.ahajournals.org/cgi/reprint/110/9/e82

These are the 2004 guidelines. There was a 2007 focus update performed, but it added nothing to the debate about oxygen use. These are the full guidelines, so they are quite in depth. Section 6.3.1.1. on page e116 devotes a few paragraphs to oxygen use as routine management.

To me, it is all about using therapies with proven mortality benefit. Some would be surprised that many (most) of the initial therapies we use in our patients in these situations have no proven mortality benefit. However, this does not override good clinical judgment. Just because morphine has not been proven conclusively to have a mortality benefit in acute MI does not mean we let the patient suffer in agony and potentially exacerbate the problem.

The use of oxygen has not been proven to limit myocardial damage or to reduce morbidity or mortality in this population. This, of course, does not mean we do not use oxygen at all. The suggestions from the ACC/AHA:

Class I
Supplemental oxygen should be administered to
patients with arterial oxygen desaturation (SaO2 less
than 90%). (Level of Evidence: B)

Class IIa
It is reasonable to administer supplemental oxygen to
all patients with uncomplicated STEMI during the
first 6 hours. (Level of Evidence: C)

Notice the low level of evidence and the "soft" suggestion about administering to all patients with uncomplicated STEMI.

To (attempt to) answer your question, I would imagine "these MDs do this" because in their clinical judgment, the use of supplemental O2 greater than 2L NC is not called for. The low level of evidence does not indicate the more the better when it comes to O2 delivery during acute MI. In fact, some more recent literature calls into question the use of high-flow O2 in the management of uncomplicated MI at all. Link below:

http://heart.bmj.com/cgi/reprint/95/3/198

This systematic review was very inconclusive, and relied on very limited evidence, and in no way does it prove that high flow O2 therapy will increase infarction size and increase mortality, but it certainly calls into question the recommendations of the ACC/AHA as shown above. In other words, yeah this study was crappy, but the ACC/AHA guidelines were based on a very low level of evidence to begin with, so next to them, this study doesn't look so bad.

The suggested mechanism in this study is that high concentration O2 therapy can in fact decrease coronary blood flow. The major determinant of the size and degree of infarcted heart tissue is amount of coronary blood flow, not O2 sats (especially in the mid 90's).

Also mentioned in the ACC/AHA guidelines is the risk of using O2 therapy in the patient with COPD. This is still under very much debate at the times, but in this case, if we don't really see any benefit, do we take a chance on the risk? One study that I could find for free discussed the ongoing debate. Link below:
http://www.jephc.com/uploads/LP990280.pdf

OK, back on target. To conclude, unless I am missing something, CP is no indication for high flow O2 use, and increasing CP does not mean to me that I should be using increasing amounts of O2. According to current guidelines, there is no evidence that O2 use improves morbidity and mortality, and it may even worsen outcomes. If I'm having a routine MI without serious desaturation <90%, until something new comes along, I'll take the NC.

SR

Edited to add: I realize I forgot to mention that I do realize that many therapies we use, especially in the emergent or intensive care setting have a paucity of evidence to support them, and we use them anyway because they make sense. Take the morphine for example, it makes sense to use it to limit increased myocardial demand due to anxiety and pain and also from a hemodynamic standpoint. But still, there is no evidence to support its use in decreasing mortality from acute MI. Even so, it is still present in consensus guidelines from 2 large professional organizations. In the case of O2, I would suggest that use of such high-flow oxygen in the situations outlined above are not covered by these consensus guidelines, have no evidence to suggest they improve morbidity and mortality, and may possibly harm the patient.

04-10-2009, 23:47	#3
shr7 Asset Join Date: Dec 2007 Location: Pittsburgh PA Posts: 50	If I may add a little for now. Maybe when the computer is not behaving badly I can elaborate. The ACC/AHA guidelines in patients with STEMI is linked below: http://circ.ahajournals.org/cgi/reprint/110/9/e82 These are the 2004 guidelines. There was a 2007 focus update performed, but it added nothing to the debate about oxygen use. These are the full guidelines, so they are quite in depth. Section 6.3.1.1. on page e116 devotes a few paragraphs to oxygen use as routine management. To me, it is all about using therapies with proven mortality benefit. Some would be surprised that many (most) of the initial therapies we use in our patients in these situations have no proven mortality benefit. However, this does not override good clinical judgment. Just because morphine has not been proven conclusively to have a mortality benefit in acute MI does not mean we let the patient suffer in agony and potentially exacerbate the problem. The use of oxygen has not been proven to limit myocardial damage or to reduce morbidity or mortality in this population. This, of course, does not mean we do not use oxygen at all. The suggestions from the ACC/AHA: Class I Supplemental oxygen should be administered to patients with arterial oxygen desaturation (SaO2 less than 90%). (Level of Evidence: B) Class IIa It is reasonable to administer supplemental oxygen to all patients with uncomplicated STEMI during the first 6 hours. (Level of Evidence: C) Notice the low level of evidence and the "soft" suggestion about administering to all patients with uncomplicated STEMI. To (attempt to) answer your question, I would imagine "these MDs do this" because in their clinical judgment, the use of supplemental O2 greater than 2L NC is not called for. The low level of evidence does not indicate the more the better when it comes to O2 delivery during acute MI. In fact, some more recent literature calls into question the use of high-flow O2 in the management of uncomplicated MI at all. Link below: http://heart.bmj.com/cgi/reprint/95/3/198 This systematic review was very inconclusive, and relied on very limited evidence, and in no way does it prove that high flow O2 therapy will increase infarction size and increase mortality, but it certainly calls into question the recommendations of the ACC/AHA as shown above. In other words, yeah this study was crappy, but the ACC/AHA guidelines were based on a very low level of evidence to begin with, so next to them, this study doesn't look so bad. The suggested mechanism in this study is that high concentration O2 therapy can in fact decrease coronary blood flow. The major determinant of the size and degree of infarcted heart tissue is amount of coronary blood flow, not O2 sats (especially in the mid 90's). Also mentioned in the ACC/AHA guidelines is the risk of using O2 therapy in the patient with COPD. This is still under very much debate at the times, but in this case, if we don't really see any benefit, do we take a chance on the risk? One study that I could find for free discussed the ongoing debate. Link below: http://www.jephc.com/uploads/LP990280.pdf OK, back on target. To conclude, unless I am missing something, CP is no indication for high flow O2 use, and increasing CP does not mean to me that I should be using increasing amounts of O2. According to current guidelines, there is no evidence that O2 use improves morbidity and mortality, and it may even worsen outcomes. If I'm having a routine MI without serious desaturation <90%, until something new comes along, I'll take the NC. SR Edited to add: I realize I forgot to mention that I do realize that many therapies we use, especially in the emergent or intensive care setting have a paucity of evidence to support them, and we use them anyway because they make sense. Take the morphine for example, it makes sense to use it to limit increased myocardial demand due to anxiety and pain and also from a hemodynamic standpoint. But still, there is no evidence to support its use in decreasing mortality from acute MI. Even so, it is still present in consensus guidelines from 2 large professional organizations. In the case of O2, I would suggest that use of such high-flow oxygen in the situations outlined above are not covered by these consensus guidelines, have no evidence to suggest they improve morbidity and mortality, and may possibly harm the patient. Last edited by shr7; 04-11-2009 at 11:51.
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