View Full Version : Question for the Doctors on the Board

04-10-2009, 22:12
This is a question I have for the MD's on the board, not so much the Deltas here, but if an 18D can answer this question, I'm all ears.

Is there a medical reason why MDs (or RNs for that matter) don't increase O2 on pts c/o CP?

As some of you may know, I work for AMR here in Denver and we have the contracts for various medical/insurance companies. These companies have various clinics around the Denver metro area, and many is the time we are called to these clinics for pts c/o CP, and we walk in and the pts are only on Nasal Cannulas at 2L. Is there a medical reason, or Even a "fear" of putting a pt with CP on a NRB?

Sure, the pt may have good O2 sats, but still c/o CP.

These clinics may have started CP procedure, O2, 324 ASA, Nitro, even MS, PTA, but these pts are still on NCs when we get there.

I'm going to give a couple of examples of 2 calls my Medic and I ran yesterday and then again today.

1st call:
Dispatched to a clinic for a 52 y/o male c/o CP. Arrive on scene to find pt c/o 6 out of 10 CP, radiating to L shoulder and in between shoulder blades. Pt AAO x3. Diaforetic with slight nausea. Pt has Hx of MI. One in 2002 and another in 2004. Stents placed both times. States the pain he is experiencing is the same as before.

PTA.....Line established, 18g L AC. Pt started on 2L O2 NC, 324 ASA 0.4mg Nitro X3, Nitropaste L Pectoral and 4mg MS. 12 lead shows 2mm elevation in Leads 2 and 3, as well as in aVF and aVR.

Pt transferred to our cot, and the 1st thing I do is put Pt on NRB at 15L.

We wheel Pt out to ambulance and load. Code 3. Cardiac Alert.

Time taken since I put Pt on NRB at 15L to when we get him in the back of the rig, aprox 6 minutes. Pt now states pain at 5 out of 10.

My Medic gives Pt another 10mg of MS while in route.

Transport time....aprox 12 minutes to Hsp. While in ED, Cardiologist confirms Cardiac alert and sends Pt to Cath Lab.

Door to balloon........9 minutes.

2nd call:
Called to a clinic for a 68 y/o female c/o CP. Arrive on scene to find Pt c/o 5 out of 10 R sided CP, non radiating. Pt also confirm to have pneumonia. States she's had breathing problems for past 6 days. R base crackles upon exhalation.

Vitals PTA.....BP 148/84, Rate 88, Resps 20, O2 stats 94 on 2L NC. Pt given 324 ASA.
NO LINE ESTABLISHED. Multiple attempts by clinic. So they were unable to give Nitro.

Transferred to cot. Got Pt on monitor. EKG show SR with occasional PACs.

I put Pt on 15L NRB. 5 minutes later, ectopy is gone. But 12 lead shows inverted T waves in leads 2, 3, V1, V2, aVF, and aVR. There is no ST elevation, so no Cardiac Alert called.

Get Pt out to ambulance. Start IV. 22g L forearm. (Only spot available to me after clinics multiple attempts). Pt given 0.4 Nitro SubQ.

Begin Transport. Non-emergent to HSP.

Medic gives 0.4 Nitro x2 SubQ. Pt claims pain increasing after each Nitro given. After 1st Nitro, pain at 7 out of 10.
2nd Nitro......8 out of 10
3rd Nitro.....9 out of 10

No EKG ectopy noted.

Stepped up to Code 3. Diverted to closest Hsp. Medic gives 10mg MS by the time we pull into ED.

*Pt sat in clinic for aprox 30 minutes before being seen. Sat another 25 minutes while staff attempted to start line before we were called. Our response time was 24 minutes to clinic. Called in non-emergent. Pt sat for aporx 49 minutes on 2L O2. With 6 out of 10 CP.

The question I have again is, why don't these clinics increase the O2. They put these Pts on NCs and get sats in the mid to upper 90s and just say, they're sating fine.

We don't care how much O2 is in a Pts finger, the HEART NEEDS O2 !!!!!!!

Time and time again, call after call, we go to these clinics, these "Docs in a Box", for people having CP and all they do is put them on a NC at 2L.

I always carry in a NRB with me, when we get dispatched to these clinics, and 98% of the time, I end up putting them on the Pts.

Is there a Medical reason why these MDs do this?

04-10-2009, 23:27
I am only an M1 in medical school, but in I will take a shot and hopefully be somewhat on track or be corrected and learn if wrong.

I am not sure what would be causing the decreased O2 sat to 90 in an MI, but could it possibly be from hyperventilation and shallow breathing due to severe pain causing a low V/Q ratio breathing or hypoventilation due to the pain and not breathing enough?

First, I do not think it would hurt to give O2, but remembering the Oxygen-Hemoglobin dissociation curve from respiratory physiology: 90% sat to 100% is on the plateau of the curve where increasing PO2 at that point really does not let you bind any significant amount more of O2 as the far majority of your hemoglobins O2 sites are occupied.

This is assuming the patients have a normal amount of hemoglobin (as if they had a lower hemoglobin count they could not carry much O2 even if they were 100% sat) Also, dissolved O2 accounts for hardly any O2 in the body.

Supplementary O2 could possibly help a little bit, but in this case there is a much bigger fish to fry:

If my heart is beating out of my chest and hurts like hell hopefully taking care of that will alleviate my breathing issues. You can give me as much 02 as you want, but as long as I'm not hypoxemic, it is not really helping me out.... you are just dealing with a
symptom caused by the main problem...and that symptom really hasn't become an issue yet....deal with the problem causing the symptom and you are set.....90% hemoglobin sat...you could be better...but....as long as patient not going cyanotic.....or showing signs of hypoxemia...give supplementary 02 if it makes 'em feel better, but you are not really dealing with the big fish....fix the chest pain...all goes back in line. Deal with symptoms if they start causing major issues.....02 saturatino of 90%, not a huge issue...but you can fix it if you really want to.

Maybe another correlation to this could be someone with an pneumonia, which could cause issues with inflammation and fluid in the lungs causing a small decrease in O2 sat, another could be, something like fibrosis causing an increase in the thickness of the lung wall and a decrease in O2s ability to diffuse and saturate the blood, causing a diffusion limited problem. delta x in some equation I remember.
again, unless patient is severe and is in respiratory distress a minor decrase in O2 sat is not hurting your abiltiy to deliver O2.

Bottom line is that an O2 sat like the ones you present is not low enough to be a major worry and is not the underying issue - I think?

An example of a case where supplemental O2 treatment would be very beneficial would be if a patient does have seriously depressed O2 sats and the cause is hypoventilation with a lack of a v/q defect, administering 02 will help.

04-11-2009, 00:47
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:


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 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:


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:

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.


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.

04-11-2009, 12:34
One thing I didn't really talk about is that patients experiencing acute coronary syndrome suffer from an imbalance between supply of oxygenated blood to the heart, and myocardial demand. Our therapies are directed at reducing demand or increasing supply. O2 supplementation can increase supply in the hypoxemic patient, but the difference between a patient satting in the mid 90's is not that different than one at 100%. The major factor here is a reduction in supply due to occlusion of a coronary artery.

The heart is not getting enough oxygen, but it is due to lack of blood flow vs. blood oxygenation. The best way to get more oxygen to the tissue is to open up that artery or bust the clot. This is why O2 therapy is supplementary in acute MI while medical and surgical interventions to provide more blood flow to the heart are the primary therapies.


04-13-2009, 06:26
As far as a "fear" of high flow O2 goes, the only rational argument against it is free radical oxygen damage to lung tissues. Some fear the COPD patient with high flow, but most know that the hypoxic drive is insufficient to rapidly cause hypoventilation in the short term setting.

In the presence of functioning hemoglobin, the increased PO2 dissolved in the blood by high flow via NRB makes a negligible contribution to oxygen delivery to tissues. There are settings in which it is more appropriate, such as where Hgb oxygen-carrying capacity is impaired (such as CO poisoning, where the Hgb has trouble carrying the oxygen, and high flow O2 also significantly decreases the time to dissociation of the CO from the Hgb, and high PO2 is the only good way to deliver oxygen to tissues. Methemoglobinemia is another example). This also will be helpful in severe anemia, where Hgb is so low that it is not carrying oxygen to the tissues. Here, the added O2 delivery from O2 dissolved in the blood will help.

So the short answer is, high flow O2 will not hurt, but will help in a minority of cases of cardiac related chest pain.

The second case that you describe sounds more like a pulmonary issue: pneumonia with CP. The t-wave inversions you mention are nonspecific. T-wave inversion in aVR is not uncommon and generally ignored for the acute setting. T-wave inversions in V1 and V2 are frequently normal findings, as they often are in lead III. Without seeing the EKG there's not much else I can say. High flow O2 may or may not be indicated here based on what else you think might be going on, but I wouldn't disagree with its application. Pneumonia, PE, dissection, etc. are diagnoses to be considered. Accelerating chest pain is not necessarily reason to increase the O2, but increasing shortness of breath or respiratory effort would be.


04-14-2009, 16:47
Firstly, I apologize a bit for the tone of my first posts. Just trying to play the Devil's advocate and I probably got a little carried away. I do want to make it clear that I was not trying to advocate any medical treatment, just presenting an opposing point of view stating that the Dr.s at these clinics are not out of line for running 2L NC.

Dr. 'zilla,

I do have a couple questions.

Firstly, about the COPD patient. I understand the myth of suppression of hypoxic ventilatory drive with O2 administration to the chronically hypercapnic patient, and that this interpretation is largely incorrect. However, it was my impression that it was only the above mechanism that was debunked, but not the presence of the possibility of exacerbating hypercapnia in these patients through multiple mechanisms, including an increase in dead space ventilation (due to loss of compensatory pulmonary vasoconstriction), the Haldane effect, as well as a small decrease in minute ventilation. All of these can take effect within the first hour, which is within the time frame offered in the cases above.

I also understand that most of these patients are at greater risk for hypoxemia than hypercapnia and previously many patients who needed O2 were not getting it due to the traditional teaching that they would stop breathing. However, I interpreted the question as one in which the patient was having increasing chest pain in an acute MI setting, was satting well to begin with, and was not having trouble breathing.

My second question related to the possibility of a deleterious effect of high-flow O2 on cardiovascular function. I know it has been looked at in a few human and animal studies, that high flow O2 can cause coronary vasoconstriction, potentially worsening infarction. Not any real solid evidence that links mechanism with poor outcomes. Just wondering on your opinion?

Thank you