Oxygen and ACS

MedicIntern305

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alrighty, so I just took a test and one of the questions is in regards to ACS and oxygen. It in shortened form states "you have a 72 yo male blah blah blah with chest pain, spo2 reads 95%, of which of the following is correct, out of the 4 these two made more sense

1) there is no need for oxygen with spo2 greater or equal to 94%
2) everyone presenting with ACS gets oxygen


I've seen it go both ways, what do y'all think?


Ps I'll probably through in a few other questions about other questions on the test in this feed eventually
 
#1 is correct. We don't give oxygen anymore "just because"- including ACS and CVAs.
 
Unless the test was dated 1990, I'd go with #1.

Not gonna lie, I laughed out loud - that is too true.
"you have a 72 yo male blah blah blah with chest pain, spo2 reads 95%, of which of the following is correct, out of the 4 these two made more sense

1) there is no need for oxygen with spo2 greater or equal to 94%
2) everyone presenting with ACS gets oxygen

Short answer, #1 is correct. We don't administer prophylactic oxygen for ACS. Indeed, there's evidence that "hyperoxia" can be harmful in ACS. Indeed, there was knowledge of the harm of this practice as early as the 1940s. I love this history, it really demonstrates how slow we are to adopt evidence-based practice.

I think the longer answer is, given that we've had RCTs, say, this one for STEMI, we have a high degree of confidence that oxygen administration is not entirely harmless for ACS.

This is actually not a bad EMSWorld review (I know, I know) on the subject.
 
It depends who is asking the question.
NREMT wants #2, but the latest est evidence says #1 is right. Base you answer on how up to date the text, material, test, protocols, etc is.
 
I have some major issues with trying to apply evidence broadly in the critically ill population. However, early supplemental oxygen administration in MI is becoming more well-established as a harmful intervention, at least in my own mind. There were several relatively well done prospective, controlled RCTs published quite recently that add even further to credence to this theory.


https://www.ncbi.nlm.nih.gov/m/pubmed/26740484/?i=3&from=supplemental oxygen myocardial infarction
450 patients trending cardiac enzymes based on supplemental oxygen exposure in the first 12 hours

https://www.ncbi.nlm.nih.gov/m/pubmed/26002889/?i=6&from=supplemental oxygen myocardial infarction
This one also had 450 patients. The supplemental oxygen arm of this study actually had a demonstrable increase in infarcts size at 6-months on follow-up cardiac MRI.

These are both prospective and randomized trials. Assuming that the reported data is accurate, these types of results are pretty meaningful. Certainly more so than retrospective studies or meta analysis.

Thus far, I buy it. Supplementing O2 in the absence of hypoxemia during acute STEMI seems to actually be relatively bad for your ticker.
 
O2 is supposedly a vasoconstrictor, so in ACLS that'll decrease perfusion.

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alrighty, so I just took a test and one of the questions is in regards to ACS and oxygen. It in shortened form states "you have a 72 yo male blah blah blah with chest pain, spo2 reads 95%, of which of the following is correct, out of the 4 these two made more sense

1) there is no need for oxygen with spo2 greater or equal to 94%
2) everyone presenting with ACS gets oxygen


I've seen it go both ways, what do y'all think?


Ps I'll probably through in a few other questions about other questions on the test in this feed eventually

Per ACLS guidelines, in general...
Supplemental oxygen should be avoided if the SpO2 is normal and they have no respiratory distress. This includes ACS, STEMI, ROSC, etc.
 
Per ACLS guidelines, in general...
Supplemental oxygen should be avoided if the SpO2 is normal and they have no respiratory distress. This includes ACS, STEMI, ROSC, etc.
Key words: grain of salt. I get the CVA/ TIA/ AMI/ ACS patients, particularly with a RA SPO2 (>) 94% on an NRB, however the flip side of the coin being hypoxia is still very much a killer.

Take for example, the ICH, and/ TBI patient, adequate oxygenation, and an adequate MAP (>) 65 are target end goals to their road to recovery.

I just don't want us to get into the habit of painting a broad brush, especially for those on this forum that may be newer, less experienced, or have trouble reading beyond the lines.

In summary, every patient is different.
 
Any thoughts on routine EtCO2 for suspected CVA? I would expect that we'd want EtCO2 monitoring in addition to SPO2?
 
Any thoughts on routine EtCO2 for suspected CVA? I would expect that we'd want EtCO2 monitoring in addition to SPO2?
Good question. I don't think it's a terrible idea. For the clear cut CVA patients, and/ or even TIA folks not requiring ETI, I don't know that it would provide a significant enough advantage overall in-field to be adopte quite yet, though I am sure there are studies being done now.

I would equate it to clear cut AMI folks, the ultimate/ definitive care still being early recognition and efficient transport to the proper treatment centers, being able to monitor their ETCO2 would perhaps have some degree of significance, I just don't know how inclined neurologists are to ask what the numbers have been like in the field.
 
In summary, every patient is different.

Very much so. It's kinda hypocritical of me to quote "ACLS Guidelines", especially if you're a thinking medic who follows your brain and not some protocol.

I will say that SpO2 can be misleading, even with a great pleth waveform. Think about the on-loading and off-loading of oxygen to/from the hemoglobin in cases of acidosis or alkalosis; SpO2 may read great, but that doesn't mean that the oxygen is actually getting delivered. (If you really want to get complicated, take a gander at oxygen content, A-V gradient, oxygen delivery, and oxygen consumption equations).

To keep it simple and to avoid hypoxia, if your patient is unstable, give them a cannula. If they need a NRB for saturation, they probably need High Flow Cannula or Non Invasive Support.

A good example of me going against my SpO2 >94% rule is sepsis. Why are these patients acidotic? Because they have poor perfusion. Poor perfusion leads to poor oxygenation, and poor oxygenation leads to anaerobic metabolism, and anaerobic metabolism leads to lactate buildup. Sooo... I usually put my "Sepsis Alert" patients on 2 Lpm NC for good measure. Does it change anything? Probably not. Is it harmful? Probably not. But does it optimize oxygenation? Maybe.

That's why we practice. Everyday. Medicine is as much an art as it is a science.
 
Any thoughts on routine EtCO2 for suspected CVA? I would expect that we'd want EtCO2 monitoring in addition to SPO2?

Although I don't have any thoughts specifically about ETCO2 and CVA (unless there is LOC changes; use to monitor ventilation), ETCO2 is a great tool for Sepsis! I know JEMS put out an article talking about ETCO2 levels less than 27 mmHg usually means lactate levels >4.0.
 
Very much so. It's kinda hypocritical of me to quote "ACLS Guidelines", especially if you're a thinking medic who follows your brain and not some protocol.

I go back and forth on this every day.
Our protocols currently require oxygen in nearly all ALS patients except under Tachycardia and AMS protocol where it says only if spo2 is <94%.

Thing is, I know our medical director prefers oxygen administration titrated as needed, not a blanket approach.

Classic spirit of the law vs letter of the law.

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I go back and forth on this every day.
Our protocols currently require oxygen in nearly all ALS patients except under Tachycardia and AMS protocol where it says only if spo2 is <94%.
Re-read your CVA protocols;).
 
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