O2 and MI.

[Dwindlin]

So I like to frequent the case studies at ems12lead.com. I was reading through one the other day and a comment peaked my interest. It was a comment about O2 therapy in AMI. Now in my area we follow "MONA" pretty religiously, and from most of the comments I see on that blog seem to be similar in that AMI gets MONA.

So anyways that comment peaked my interest and I discovered a couple reviews and a statement from the BMJ

Review 1
Review 2

BMJ Statement Quote:

The British Thoracic Society (BTS) guideline for emergency oxygen use recommends that oxygen should be given to patients with heart attack (and patients with angina) only if they are hypoxaemic to aim for a near normal saturation range of 94-98%.4 This guideline was endorsed by the British Cardiovascular Society, 21 other societies, and the National Institute for Health and Clinical Excellence (NICE).5

I realize both studies are non-significant, however I am still surprised by the results, I would have expected O2 to be firmly beneficial. So is this already common knowledge that "prophylactic" O2 may be harmful? Am I that far behind or is this surprising to anyone else?

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[Paseo Del Norte]

The current concensus regarding AHA:

http://circ.ahajournals.org/cgi/content/full/122/18_suppl_3/S787

 

[turkeyjerky]

Why exactly would you think that giving supplemental O2 would be beneficial?

I'm no expert in the subject, but it makes sense to me that exposing a bunch of ischemic/soon-to-be-infarcted cells to toxic concentrations of free radicals would be damaging. Not to mention that supraphysiologic O2 tension has been shown to cause coronary vasoconstriction in animal models. More importantly though, is there any actual reason to give a therapy that you know isn't going to accomplish anything? I think it's a reasonable assumption that every intervention we employ will have some incidence of adverse effects; given that, should we employ therapies that have neither evidence of benefit nor underlying scientific principles?

 

[Dwindlin]

Why exactly would you think that giving supplemental O2 would be beneficial?

I'm no expert in the subject, but it makes sense to me that exposing a bunch of ischemic/soon-to-be-infarcted cells to toxic concentrations of free radicals would be damaging. Not to mention that supraphysiologic O2 tension has been shown to cause coronary vasoconstriction in animal models. More importantly though, is there any actual reason to give a therapy that you know isn't going to accomplish anything? I think it's a reasonable assumption that every intervention we employ will have some incidence of adverse effects; given that, should we employ therapies that have neither evidence of benefit nor underlying scientific principles?

I guess I never really thought supplemental O2 (at least the amount coming from a cannula) would create enough of a tension to cause further harm, but I do understand what you are saying. I think the more distressing part for me though is that I still get ripped for not putting O2 on all my MI/ACS patients even with normal SpO2 readings, when it sounds as if this has very much become the standard. I guess now at least I have some ammunition to toss back at my chief.

 

[csmmedic]

I give my suspected ACS patients a nasal cannula, flow titrated to keep SpO2 > 92-94%

The latest science supports this, check the AHA consensus. I have never understood why EMS believes that high flow O2 via NRB is the greatest thing since sliced bread for everyone that calls 911. As for dealing with pushback, my protocols do not say that I *have* to place patients on 15L, they just state that chest pain patients should receive oxygen. I interpret this to mean I can use my clinical judgement.

 

[Dwindlin]

I give my suspected ACS patients a nasal cannula, flow titrated to keep SpO2 > 92-94%

The latest science supports this, check the AHA consensus. I have never understood why EMS believes that high flow O2 via NRB is the greatest thing since sliced bread for everyone that calls 911. As for dealing with pushback, my protocols do not say that I *have* to place patients on 15L, they just state that chest pain patients should receive oxygen. I interpret this to mean I can use my clinical judgement.

I'm not talking about high flow. I'm talking about getting ripped for not putting at least a cannula on someone who's SpO2 is >95%. When again if I am reading those articles right (and from some of the comments above) may not be good for the patient.

 

[csmmedic]

I'm not talking about high flow. I'm talking about getting ripped for not putting at least a cannula on someone who's SpO2 is >95%. When again if I am reading those articles right (and from some of the comments above) may not be good for the patient.

I downloaded a powerpoint lecture from Bryan Bledsoe recently about the science behind reprofusion injury, free radicals, etc. I think that this stuff is in its infancy, as far as the research goes. I am willing to say that placing ACS/MI patients on a few liters is probably not gonna do much harm. Plus it keeps you out of trouble when the run ticket gets to QI.

 

[pseudoknot]

I downloaded a powerpoint lecture from Bryan Bledsoe recently about the science behind reprofusion injury, free radicals, etc. I think that this stuff is in its infancy, as far as the research goes. I am willing to say that placing ACS/MI patients on a few liters is probably not gonna do much harm. Plus it keeps you out of trouble when the run ticket gets to QI.

There is observational data showing that this is associated with increased mortality in MI patients, which is partly why this was removed from the AHA ACLS guidelines in 2010. If you are getting problems in QI for not giving O2 when it isn't needed then your protocols are out of date.

 

[Dwindlin]

There is observational data showing that this is associated with increased mortality in MI patients, which is partly why this was removed from the AHA ACLS guidelines in 2010. If you are getting problems in QI for not giving O2 when it isn't needed then your protocols are out of date.

Our protocols are vague enough that I shouldn't have to be putting O2 on a person with normal sats. It's a departmental issue. My Bat. Chief who does QI is a dinosaur who is set in his ways. Our protocol has spinal clearance written in it, but when I first got to the department we weren't allowed to do it. Took me the better part of a year to convince him with all the literature that in fact medics can successfully do spinal clearance and not kill people (even though the entire immobilization thing is voodoo).

 

[turkeyjerky]

I am willing to say that placing ACS/MI patients on a few liters is probably not gonna do much harm. Plus it keeps you out of trouble when the run ticket gets to QI.

Yes, but are you an expert on the matter? Maybe you are, maybe you've reviewed the literature extensively and have personally conducted studies in the matter. Or maybe you're just some guy who's saying "probably won't hurt". Medicine is littered w/ examples of things that "probably won't hurt" that actually ended up killing people.

Consider again whether there is any reason whatsoever to give supplemental O2 to a normoxic patient. I can't think of any, and I'm not aware of any evidence that there is. I do think it is biologically plausible that O2, a toxic molecule, can cause harm when it leads to superoxia. There is some evidence to support this, although it's not conclusive. The question remains, why do something if you know it won't help and it might hurt?

 

[leviathan]

There's still debate about how much injury occurs from free radicals. On the flip side, there's no debate about the effects of hypoxemia. That's why I personally put ACS patients on a nasal cannula at 2-3 LPM, because I don't necessarily trust those pulse oximeters to be accurate, especially if the patient is feeling short of breath or I hear rales and see a normal sat. 2-3 LPM will not raise the PaO2 to any significant degree, but it will raise the SaO2 easily if it started off lower. I do agree that non-rebreathers are dangerous.

 

[turkeyjerky]

Saying the O2 will raise the SpO2 but won't affect the PaO2 doesn't make any sense. If you have a good waveform and a saturation in the mid 90s then it's reliable, pulse oximetry is more accurate with higher sats, it's more likely that the reading in the low80s is erroneous than the normal Reading. I agree with empiric O2 prior to Having the pulse ox in place, but it's silly to give supplemental oxygen in the face of normoxia. If you're worried you can keep the NC in place and let the patient believe he's getting the good stuff.

 

[turkeyjerky]

Here's a recently published letter that argues, about time, to get rid of the truly awful MONA acronynm. We really need to stop teaching this to students. Courtesy of Emergency Medicine Literature of Note

 

[MedicFL]

Here's a recently published letter that argues, about time, to get rid of the truly awful MONA acronynm. We really need to stop teaching this to students. Courtesy of Emergency Medicine Literature of Note

Arent you a medical student yourself? Your opinion carries about much weight as does mine. I have been a medic for 10 years and an EMS instructor for 5 years. And one thing I can say as with any government change is slow. MONA is still taught and ASA, Nitro, O2, MSo4 is still the pretty much golden standard for an MI call. Right wrong or otherwise, change takes time. I think as more definitive studies emerge you will start to see a shift in thinking. But I agree with Leviathan, pulse ox are known to not be super accurate. Without a blood gas in my humble opinion putting a pt who is having a possible MI on 2-3L NC isn't probally going to harm them. This pt is probally worked up and huffing and puffing away in a pain, that 2-3L in the short run probally isn't going to shift there PA02 very much at all.

 

[pseudoknot]

change is slow. MONA is still taught and ASA, Nitro, O2, MSo4 is still the pretty much golden standard for an MI call.

Well, you have the AHA and all of its sister organizations around the world saying that oxygen is not indicated for ACS patients who aren't hypoxic, in the nearly two-year-old ACLS guidelines. We're not talking about changing practice based on a paper or two in some fringe journal. This is the the recommendation of an internationally accepted set of guidelines, put out by the leaders in the field. I think in medicine when your professional society says you should do something, you need to have a better reason for doing it some other way than "this is what I was taught 10 years ago by someone with a high school education."

 

[Lawsonc]

If medics (in your system) are strictly following MONA/FONA to the letter, oxygen is the least of your worries.

 

[MedicFL]

Well, you have the AHA and all of its sister organizations around the world saying that oxygen is not indicated for ACS patients who aren't hypoxic, in the nearly two-year-old ACLS guidelines. We're not talking about changing practice based on a paper or two in some fringe journal. This is the the recommendation of an internationally accepted set of guidelines, put out by the leaders in the field. I think in medicine when your professional society says you should do something, you need to have a better reason for doing it some other way than "this is what I was taught 10 years ago by someone with a high school education."

I'm not disagreeing with the recommendations my point is that this is still a common practice. I still do some EMS based research, however am not a active medic currently. But as others have put it in this thread Oxygen is still a common requirement for the QI process. And I find your comment about the high school education a low blow. I have worked with several EMS Admins that have PHD's and Masters.

My point is that, this is not just isolated to the undereducated EMS types. A teaching hospital that I run reasearch out of, I often see the high and mighty Residents want Oxygen on nonhypoxic pt's. So my point is that while the recommendations are out there, change is slow.

 

[wook]

I'm not disagreeing with the recommendations my point is that this is still a common practice.

As several others (including yourself) have stated, we in medicine are slow to change. The AHA guidelines based on several studies have started our slow change away from oxygen. I've encouraged my medics not to use the oxygen unless the O2 sat is low or they clinically suspect it.

But as other had put it in this thread Oxygen is still a common require for the QI process.

I share your frustration with this the slow change, but QI should change more quickly and be more up-to-date to help encourage the change.

My point is that, this is not just isolated to the undereducated EMS types. A teaching hospital that I run reasearch out of, I often see the high and mighty Residents want Oxygen on nonhypoxic pt's. So my point is that while the recommendations are out there, change is slow.

I can easily see this. We do alot of things in medicine because this is the way we've always done it. At my previous place of employment, I would discourage the residents from intubating during a code. I preferred that the King LT was left in place, as we could always intubate after we got a ROSC. The focus should be on good compressions. Eventually, most of us will follow the literature. However, most don't want to be the first to do the new stuff.

Thanks.


Wook

 

[wook]

This is the the recommendation of an internationally accepted set of guidelines, put out by the leaders in the field.

Dr. R O'connor was in town a month ago talking about the resuscitation consortium. Next time he or someone else is in town, I'll have to drop you a line so you can attend if interested.

Thanks.


Wook

 

[pseudoknot]

Dr. R O'connor was in town a month ago talking about the resuscitation consortium. Next time he or someone else is in town, I'll have to drop you a line so you can attend if interested.

Absolutely. I had the good fortune to hear him speak about the 2010 guidelines at VaCEP last year. He has quite a presence.

Eventually, most of us will follow the literature. However, most don't want to be the first to do the new stuff.

My problem is that I'm one of those who DOES want to be a pioneer!

I will say that if it took us this long to see the negative effect of oxygen in population studies, it's probably not going to be a huge effect. I don't think O2 is deadly poison or anything. I'm just in favor of minimizing our interventions whenever possible.

 

[wook]

My problem is that I'm one of those who DOES want to be a pioneer!

If you have some pre-hospital research ideas, let's do it!


Thanks.


Wook

 

[leviathan]

Saying the O2 will raise the SpO2 but won't affect the PaO2 doesn't make any sense.

I said it would negligibly affect the PaO2. You should go review the oxygen-hemoglobin dissociation curve if you don't understand why.

If you have a good waveform and a saturation in the mid 90s then it's reliable, pulse oximetry is more accurate with higher sats, it's more likely that the reading in the low80s is erroneous than the normal Reading.

You're probably right that it is accurate, although I'd like to see some research correlating sats with blood gases. There might be lots out there but I haven't had a chance to look. Again, the consequences of having hypoxemia are much more serious than having a PaO2 in the 160s because of a low flow nasal cannula.

 

[turkeyjerky]

Arent you a medical student yourself? Your opinion carries about much weight as does mine. I have been a medic for 10 years and an EMS instructor for 5 years. And one thing I can say as with any government change is slow. MONA is still taught and ASA, Nitro, O2, MSo4 is still the pretty much golden standard for an MI call. Right wrong or otherwise, change takes time. I think as more definitive studies emerge you will start to see a shift in thinking. But I agree with Leviathan, pulse ox are known to not be super accurate. Without a blood gas in my humble opinion putting a pt who is having a possible MI on 2-3L NC isn't probally going to harm them. This pt is probally worked up and huffing and puffing away in a pain, that 2-3L in the short run probally isn't going to shift there PA02 very much at all.

So because of my training level nothing I say matters, despite the fact that it's backed up by basic science, clinical research and authoritative guidelines? Thats interesting. So I guess if I come back in 9 months when I'm a resident and say the same thing you'll believe me?

The fact that "change takes time" is a bs argument. You're aware of the research and the guidelines, so make the f'ing change already. You're an instructor, so stop teaching MONA!


I don't know why you keep saying pulse ox is "known" to be unreliable. In fact it's known to be quite reliable, especially when values are greater than 90 (it's less accurate at lower values). Read about it in any textbook that covers monitoring. Pulse oximetry is used everyday to make decisions important decisions; these guys aren't all getting ABGsdone when they roll in the door you know.





My point is that, this is not just isolated to the undereducated EMS types. A teaching hospital that I run reasearch out of, I often see the high and mighty Residents want Oxygen on nonhypoxic pt's. So my point is that while the recommendations are out there, change is slow.

you're right, all residents aren't perfect either--prolly cause they were taught Mona at one point as well.

 

[turkeyjerky]

I said it would negligibly affect the PaO2. You should go review the oxygen-hemoglobin dissociation curve if you don't understand why.

You're right--that was sorta an ******* thing for me to say, I knew what you meant.


Look, the thing is lots of these guys come in on 15 L, and then get left on it cause nurses and doctors also believe in using O2. I do believe that has the potential for harm. I not sure what dose of O2 was studied, I'll have to look into that.

 

[pseudoknot]

Look, the thing is lots of these guys come in on 15 L, and then get left on it cause nurses and doctors also believe in using O2. I do believe that has the potential for harm. I not sure what dose of O2 was studied, I'll have to look into that.

The big JAMA study on this defined hyperoxia as over 300mmHg PaO2:
JAMA. 2010;303(21):2165-2171
http://jama.ama-assn.org/cgi/content/short/303/21/2165

According to one paper I found, PaO2 increases by 12mmHg for each liter of 97% O2 per minute by nasal cannula:
http://www.rcjournal.com/contents/04.10/04.10.0453.pdf

So absent lung disease, a 2L cannula would only bring you to a PaO2 of about 125. So you probably have to be on a nonrebreather to have a significant effect. But I don't think there's enough data to really know.

 

[turkeyjerky]

Just looked it up. The three studies included in the cochrane review on this studied administration of 4-6 L O2 by either face mask or NC.

 

[leviathan]

You're right--that was sorta an ******* thing for me to say, I knew what you meant.


Look, the thing is lots of these guys come in on 15 L, and then get left on it cause nurses and doctors also believe in using O2. I do believe that has the potential for harm. I not sure what dose of O2 was studied, I'll have to look into that.

I absolutely agree that a non-rebreather mask on a person who is satting at 99% on a pulse ox is absurd, and even if I don't trust pulse oximeters, I know they aren't THAT inaccurate that someone needs to have that much extra o2. Bare in mind that I haven't worked as a paramedic since the days before the AHA had updated their recs and when every paramedic was using a NRB. The nurses would have looked at me like I was a nutbar if I brought a patient in without any supplemental oxygen. I used to compromise with a nasal cannula when they were satting well and not short of breath. I guess if those pulse oxes are as reliable as they claim, I would feel comfortable withholding it from patients whenever I'm taking care of ACS patients again on my own as an MD.

 

[proman]

I absolutely agree that a non-rebreather mask on a person who is satting at 99% on a pulse ox is absurd, and even if I don't trust pulse oximeters, I know they aren't THAT inaccurate that someone needs to have that much extra o2. Bare in mind that I haven't worked as a paramedic since the days before the AHA had updated their recs and when every paramedic was using a NRB. The nurses would have looked at me like I was a nutbar if I brought a patient in without any supplemental oxygen. I used to compromise with a nasal cannula when they were satting well and not short of breath. I guess if those pulse oxes are as reliable as they claim, I would feel comfortable withholding it from patients whenever I'm taking care of ACS patients again on my own as an MD.

Why don't you trust pulse oximeters? Hyperoxia is a well recognized danger. From neonatal and adult resuscitation, to spinal cord injury, to post radiation lung injury, to mechanical ventilation, the principle is the same: give enough oxygen but not too much.

 

[pseudoknot]

A blog post about another study showing some possible harm from oxygen, this time in asthma patients. Again, it has its place, but maybe it's not totally benign and maybe we need to think a little harder about indications.

http://resusme.em.extrememember.com/?p=5447

 

[turkeyjerky]

A blog post about another study showing some possible harm from oxygen, this time in asthma patients. Again, it has its place, but maybe it's not totally benign and maybe we need to think a little harder about indications.

http://resusme.em.extrememember.com/?p=5447

I think I'm gonna hold on to that one for the next time someone tries to "educate" me on how giving O2 to a COPDer suppresses their drive to breath.

 

[Lawsonc]

Why don't you trust pulse oximeters? Hyperoxia is a well recognized danger. From neonatal and adult resuscitation, to spinal cord injury, to post radiation lung injury, to mechanical ventilation, the principle is the same: give enough oxygen but not too much.

Pulse Ox- where to begin! My post is not necessarily in context to the previous post.

However, the Pulse Ox is an over glorified tool! Especially for field usage. Firstly, lets talk about its inherent inaccuracies due to it non invasive properties. Temperature has an effect, visual(direct line of sight/cleanliness of extremity) HX of poor peripheral circulation.

That is not taking into consideration the fact that it measures hemoglobin, which might be lacking (anemia) and or saturated with another gas (carbon monoxide)

Its a great tool, but it has its limitations.

The best way to assess adequate respiratory function is with multiple tools. Firstly treating the patient and not the monitor- how does the patient look? Secondly is wave form capnography- do we have nice plateaus? good rate? What is the values? And lastly pulse ox.

EDIT- not trying to "teach" anyone anything, this was more an informal post into my thought process, and rational.

 

[pseudoknot]

Pulse Ox- where to begin! My post is not necessarily in context to the previous post.

However, the Pulse Ox is an over glorified tool! Especially for field usage. Firstly, lets talk about its inherent inaccuracies due to it non invasive properties. Temperature has an effect, visual(direct line of sight/cleanliness of extremity) HX of poor peripheral circulation.

That is not taking into consideration the fact that it measures hemoglobin, which might be lacking (anemia) and or saturated with another gas (carbon monoxide)

Its a great tool, but it has its limitations.

The best way to assess adequate respiratory function is with multiple tools. Firstly treating the patient and not the monitor- how does the patient look? Secondly is wave form capnography- do we have nice plateaus? good rate? What is the values? And lastly pulse ox.

EDIT- not trying to "teach" anyone anything, this was more an informal post into my thought process, and rational.

I think prehospital providers tend to be overly dismissive of the pulse oximeter. Although it is not perfect, it has a pretty high negative predictive value. That is to say, if it is reading above 92%, then your patient is very unlikely to be hypoxic. Yes, there are situations where it may read falsely high. The anemic patient is not going to benefit much from supplemental oxygen, because there are still only four binding sites on that patient's scarce hemoglobin complexes, right? And the amount of oxygen that can be dissolved into solution is pretty minimal. As for the CO-poisoned patient, those are fairly rare and you ought to be able to find them by your history and scene assessment.

On the other hand, the positive predictive value of an SpO2 less than 92% or whatever is not great, because of reasons you mentioned above. It is still pretty reliable if you have a good waveform, and on many monitors in use in the field you can see this in certain modes.