pao2 vs pulse ox discrepancy

[iaskdumbquestions]

I've seen a few ABG recently where a patient would have saturation by pulse ox of 90s, but pao2 would be unexpectedly low, say O2 saturation of 92% with pao2 of 55 on 2L nasal cannula. I've been seeing this somewhat frequently and nobody has a solid reason why it happens, or which to go by.

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[jdh71]

I've seen a few ABG recently where a patient would have saturation by pulse ox of 90s, but pao2 would be unexpectedly low, say O2 saturation of 92% with pao2 of 55 on 2L nasal cannula. I've been seeing this somewhat frequently and nobody has a solid reason why it happens, or which to go by.

it matter only a little how much is actually dissolved in the blood - we often use this number to make assessments about the amount of oxygen to use on vent and have this “arbitrary” cut off of 65-70.

what is really important is oxygen DELIVERY and so if your oxygen “box cars” are full of oxygen that is what is going to the tissues. The dissolved o2 contributes so little to delivery it doesn’t matter that much. So if you think you can believe your oxygen sat (there isn’t a case of CO poisoning) then run with that.

 

[bigtuna]

Look up “oxyhemoglobin disassociation curve”

 

[gro2001]

I've seen a few ABG recently where a patient would have saturation by pulse ox of 90s, but pao2 would be unexpectedly low, say O2 saturation of 92% with pao2 of 55 on 2L nasal cannula. I've been seeing this somewhat frequently and nobody has a solid reason why it happens, or which to go by.

What you describe is not inconsistent with normal physiology.

As others have said, the vast majority of the oxygen is bound to hemoglobin (SpO2), and only a relatively tiny portion is dissolved in the blood (PaO2). In fact, you begin to wonder why we even care and report a PaO2 at all? Well, most of the time we don't really. Outside a few specific situations (P/F ratio for ARDS) the PaO2 is a historical artifact from the days before pulse oximeters were invented. We would measure the PaO2, look up a table like this and calculate that the minimum SpO2 that the patient must have with the PaO2 is X. So using your example, we'd find out that a 55 mmHg would mean the patient is at least at 88%.

That is assuming we are at sea level. You aren't on a mountain are you? There are different tables for that.

 

[Radetzky]

Your oxyhemoglobin curve is left shifted. This is a pretty common thing. Delivery of O2 (sats) is what matters.

 

[iaskdumbquestions]

I appreciate the replies and have a follow up question. Often these ABG will, below the pao2 somewhere, report the Hgb saturation and it will invariably be in the 70s-80s. Is this a measured saturation or one that is somehow calculated / estimated? And why is it sometimes so far off from the O2 saturation via probe (assuming good waveform / location etc)?

 

[deleted171991]

I've seen a few ABG recently where a patient would have saturation by pulse ox of 90s, but pao2 would be unexpectedly low, say O2 saturation of 92% with pao2 of 55 on 2L nasal cannula. I've been seeing this somewhat frequently and nobody has a solid reason why it happens, or which to go by.

Respiratory alkalosis. PaO2 is real.

And while people may throw the O2 content equation at me, which shows the importance of O2 sats over PaO2:
Arterial blood O2 content = 1.34 x Hgb x O2 sat + 0.003 x PaO2 = 1.34 x 12 x 1 + 0.003 x 100 = 17.42 + 0.3 (in ml O2/dL of blood)

... I want to remind everybody that, in respiratory alkalosis, there is decreased dissociation of O2 from oxyHgb, hence it's wise to go by PaO2 (which should be over 60, right?), and target higher sats than one usually would. My cut off is around 94-96% in that situation (so my PaO2 will be over 60 mmHg). Especially if the patient has pre-existing CAD or signs of hypoxemia-related organ dysfunction.

It's not by chance that we define respiratory failure based on PaO2, and not on the O2 sat.

You can find a better explanation in Judd Landsberg's "Clinical Practice Manual for Pulmonary and Critical Care Medicine" (worth every penny).

 

[Radetzky]

I appreciate the replies and have a follow up question. Often these ABG will, below the pao2 somewhere, report the Hgb saturation and it will invariably be in the 70s-80s. Is this a measured saturation or one that is somehow calculated / estimated? And why is it sometimes so far off from the O2 saturation via probe (assuming good waveform / location etc)?

It depends if your gas machine estimates the Hb Sat (based off the PaO2) or if it actually directly measures it using spectrophotometry.

If it measures the Hb Sat and the pulse ox is over-reading causes for this are the presence of carboxyhemoglobin, or just the fact that pulse oxs are not well calibrated for saturations less than 80%.

 

[MoMoGesiologist]

You think we should lower our O2 targets? ARDSNET showed us less extreme vent settings lead to less death rather than doing everything we can to get a good PaO2. In the age of COVID, maybe a sat if 86-88 is fine to tolerate, no need to blast the vent to get higher pressures/TVs. Just lower the PO2 goal

 

[deleted171991]

You think we should lower our O2 targets? ARDSNET showed us less extreme vent settings lead to less death rather than doing everything we can to get a good PaO2. In the age of COVID, maybe a sat if 86-88 is fine to tolerate, no need to blast the vent to get higher pressures/TVs. Just lower the PO2 goal

Except in patients with atherosclerosis and decreased functional capacity, which won't do so great with decreased oxygen delivery to vital organs (think heart, kidneys).

 

[MoMoGesiologist]

Except in patients with atherosclerosis and decreased functional capacity, which won't do so great with decreased oxygen delivery to vital organs (think heart, kidneys).

If we tolerate 88% as a baseline sat in COPD, then a little lower goals for other doesn’t seem so extreme as long as we maintain delivery O2 (maintain CO and Hgb if tolerating low PO2). We alrdy have good data lower PO2s have better outcomes in MI and stroke. We need a trial comparing even lower PO2 goals!

 

[deleted171991]

If we tolerate 88% as a baseline sat in COPD, then a little lower goals for other doesn’t seem so extreme as long as we maintain delivery O2 (maintain CO and Hgb if tolerating low PO2). We alrdy have good data lower PO2s have better outcomes in MI and stroke. We need a trial comparing even lower PO2 goals!

Lower pO2 shouldn't mean respiratory failure-level pO2 (i.e. under 60 mmHg)..

The body only uses like 20% of the delivered O2, so there is a reserve there, I get it. Still, most major organs don't do well with hypoxemia (think heart, think CAD, think diastolic dysfunction, think kidney, think AKI, think brain, think AMS).

And only idiots tolerate 88% in COPD, when there is oxygen on the wall. My goals are 92-94% in COPD patients. Landsberg is right.

 

[MoMoGesiologist]

Lower pO2 shouldn't mean respiratory failure-level pO2.

The body only uses like 20% of the delivered O2, so there is a reserve there, I get it. Still, most major organs don't do well with hypoxemia (think heart, think CAD, think diastolic dysfunction, think kidney, think AKI, think brain, think AMS).

And only idiots tolerate 88% in COPD, when there is oxygen on the wall. My goals are 92-94% in COPD patients. Landsberg is right.

I’ll have to check out this book. Gonna search for a PDF copy now!

Also, I thought it was pulm docs recommending PO2 88 in COPD. Did that change?

 

[deleted171991]

I’ll have to check out this book. Gonna search for a PDF copy now!

Also, I thought it was pulm docs recommending PO2 88 in COPD. Did that change?

BUY IT! You'll thank me later. Best medical critical care read since Marik's Evidence-Based Critical Care (just different). It comes with a free Inkling e-book version.

Pulm docs are like surgical intensivists: some of them are great, some suck. Most of us suck more than we think at modern (patho)physiology, and some just follow/perpetuate dogma (such as O2-induced apnea and hypercarbia in COPD). Keeping up takes a lot of time, and most intensivists are overworked as it is. Also, most teaching intensivists don't spend enough time with their patients to see the results of their therapies; they just assume the patient got worse because of the disease. Then they teach the same sh-t to the next generation.

Be skeptical about what you read (unless you see your patients getting better, which I have). I learned that from @bigdan , as a fellow, back when I first became a cultist in the church of Marik. (Now that I am an attending, I am a cultist in multiple churches.)

This is the book (get the printed version and download the free ebook to your phone):
Amazon product

And this is a quote from it:

Shouldn’t I target O2 sats 88–92% in my hospitalized patients with severe COPD?

No. Oxygen does not significantly inhibit respiratory drive. More importantly, in the setting of acute illness, hypoxemia (PaO2 < 60 mm Hg) will complicate and worsen any disease presentation. In contrast, a lower than normal O2 sat (88–92%) is tolerated in outpatients with severe chronic lung disease, pragmatically because it is not feasible to deliver oxygen at more than 6 L/min in the home setting. Therefore, when hospitalized, patients with chronic lung disease should have the same oxygenation goal as everybody else.

 

[Radetzky]

BUY IT! You'll thank me later. Best medical critical care read since Marik's Evidence-Based Critical Care (just different). It comes with a free Inkling e-book version.

Pulm docs are like surgical intensivists: some of them are great, some suck. Most of us suck more than we think at modern (patho)physiology, and some just follow/perpetuate dogma (such as O2-induced apnea and hypercarbia in COPD). Keeping up takes a lot of time, and most intensivists are overworked as it is. Also, most teaching intensivists don't spend enough time with their patients to see the results of their therapies; they just assume the patient got worse because of the disease. Then they teach the same sh-t to the next generation.

Be skeptical about what you read (unless you see your patients getting better, which I have). I learned that from @bigdan , as a fellow, back when I first became a cultist in the church of Marik. (Now that I am an attending, I am a cultist in multiple churches.)

This is the book (get the printed version and download the free ebook to your phone):
Amazon product

And this is a quote from it:

Id like to see evidence for the statement that hypoxemia worsens any acute illness. As you said, there is a tremendous reserve of oxygen extraction. Measure most of these patients SVO2 and it’s normal. Their organs are getting oxygen just fine. Why would you aim higher with someone than they’ve had for years at home?

 

[deleted171991]

Id like to see evidence for the statement that hypoxemia worsens any acute illness. As you said, there is a tremendous reserve of oxygen extraction. Measure most of these patients SVO2 and it’s normal. Their organs are getting oxygen just fine. Why would you aim higher with someone than they’ve had for years at home?

I should point out that I am talking about ICU-level patients, or patients with acute cardiorespiratory issues. I am not trying to fix them or make them perfect. Also, we could debate about the patient with a sat of 88% who's so well-adapted he has a pO2 over 60 mmHg (i.e. not technically in respiratory failure).

At home, these sick patients with cardiorespiratory comorbidities are "compensated" (and many times told that "it's the new normal", instead of being optimized). Once they decompensate and come to the hospital, everything becomes more apparent, including the limits of their functional capacities (like a "stress test"). For example, their nice diastolic dysfunction from hypoxia and/or fluid overload (they don't have "cor pulmonale" and type 3 PHTN as much as undiagnosed type 2 - smokers who get COPD may also have CAD and stiff hearts). Then they also get fluids, to fix their (ischemia-/stress-induced) hypotension, making things even worse.

We don't withhold oxygen from a cardiac patient having angina and satting 88%. Then why would we from a COPD-er? I doubt we do more good than harm; 88% is simply not normal, especially when the O2 comes from the wall.

 

[MoMoGesiologist]

I'll try to breathe... and count...

At home, these sick patients with cardiorespiratory comorbidities are "compensated". Once they decompensate and come to the hospital, everything becomes more apparent, including the limits of their functional capacities (like a "stress test"). For example, their nice diastolic dysfunction from hypoxia (no, not all of them have "cor pulmonale" and type 3 PHTN, most of them are undiagnosed type 2) - missed by 90% of intensivists.

Would you withhold oxygen from a cardiac patient having angina and satting 88%? Then why would you from a COPD exacerbation?

What you say makes sense physiologically, but do you have a trial showing targeting higher O2 sats improves outcomes? We do have some evidence trying to target sats of 100% worsen MI outcomes. Not doubting what you’re saying, but many things that seem to make sense turn out to be to be useless or harmful when actually studied.

 

[deleted171991]

What you say makes sense physiologically, but do you have a trial showing targeting higher O2 sats improves outcomes? We do have some evidence trying to target sats of 100% worsen MI outcomes. Not doubting what you’re saying, but many things that seem to make sense turn out to be to be useless or harmful when actually studied.

There is no evidence saying that O2 sats of 92-96% are hyperoxic (and I doubt there will be, given healthy people's usual sats on room air). We define respiratory failure as a pO2 of 60 mmHg (that's a sat of 91-92% at normal pH and temperature). I don't see any reason to keep somebody at low O2 sats, unless I don't have a choice (e.g. severe ARDS).

I too care about doing no harm. Chronic O2 sats in the 80s are harmful; they induce pulmonary vasoconstriction and PHTN (see OSA). I don't keep my patients at 100% either; I am not preaching hyperoxia, just normoxia. I do realize that O2 is toxic, especially in an inflamed lung.
tw, lots of respect for you. (Sorry if it comes across as anything less than.)

 

[Radetzky]

I should point out that I am talking about ICU-level patients, or patients with acute cardiorespiratory issues. I am not trying to fix them or make them perfect.

At home, these sick patients with cardiorespiratory comorbidities are "compensated" (and many times told that "it's the new normal", instead of being optimized). Once they decompensate and come to the hospital, everything becomes more apparent, including the limits of their functional capacities (like a "stress test"). For example, their nice diastolic dysfunction from hypoxia and/or fluid overload (they don't have "cor pulmonale" and type 3 PHTN as much as undiagnosed type 2). Then they also get fluids, to fix their (ischemia/stress-induced) hypotension, making things even worse.

We don't withhold oxygen from a cardiac patient having angina and satting 88%. Then why would we from a COPD-er? I doubt we do more good than harm; 88% is simply not normal, especially when the O2 comes from the wall.

Interesting points.

Yes we are talking about an icu population.

I guess what we forget about is that it’s PO2 not SO2 that provides the driving pressure for cellular uptake.

What other things like this do you think we get wrong? I’m sure you have a list of em..

 

[MoMoGesiologist]

There is no evidence saying that O2 sats of 92-96% are hyperoxic (and I doubt there will be, given healthy people's usual sats on room air). We define respiratory failure as a pO2 of 60 mmHg (that's a sat of 91-92% at normal pH and temperature). I don't see any reason to keep somebody at low O2 sats, unless I don't have a choice (e.g. severe ARDS).

I too care about doing no harm. Chronic O2 sats in the 80s are harmful; they induce pulmonary vasoconstriction and PHTN (see OSA). I don't keep my patients at 100% either; I am not preaching hyperoxia, just normoxia. I do realize that O2 is toxic, especially in an inflamed lung.
Btw, lots of respect for you. (Sorry if it comes across as anything less than.)

Definite respect for you as well. I look for your response on crit care and anesthesia questions all the time and appreciate the pearls.

I like normoxia also. I guess my commentary re tolerating or even encouraging lower O2 is in regards to resp failure pts. I have seen colleagues set vents with plateau pressures in 30-40s to force a higher PO2, sacrifice PEEP to maintain TVs because want to avoid hypercarbia. Yes that sat >90% looks awesome and the nurses and residents love it and think it’s great medical care, then I come on and people think I’m a fool for changing vent settings and suddenly sats drop and numbers don’t look as good. I would rather have lower plateaus and TVs and tolerate sat 88%, PaO2 >55 than get perfect ABG numbers because that’s what I feel ARDSNET emphasized and taught us will save patients lives and that’s what I learned training at an ECMO center that got our regional VV ECMO evals for ARDS. How many patients do we see come to preop with low sats mentating and feeling perfectly fine? However, definitely if they r having multi organ failure and not just respiratory issues, got to rethink whether to tolerate low O2.

This reminds me of your commentary re starting inotropes in septic cardiomyopathy. To many of us, it makes sense. The BPs will get better, echo will look better. But you argued it doesn’t change outcome or may even make things worse. Without a good trial, we simply don’t know how our “common sense” interventions help or harm pts. Its what makes crit care so interesting and also very frustrating

 

[deleted171991]

Interesting points.

Yes we are talking about an icu population.

I guess what we forget about is that it’s PO2 not SO2 that provides the driving pressure for cellular uptake.

What other things like this do you think we get wrong? I’m sure you have a list of em..

I edited a bit my previous post. It was a bit too aggressive, sorry.

One point I added was that we could debate whether it's worth giving O2 to the stable chronic COPD-er who has a sat of 88%, but a pO2 over 60 (being so well-adapted). I don't really have an answer for that.

I am just a grasshopper, trying to learn from the real masters of the trade. I do have a number of pet peeves, but, if I list them, my fellows will recognize me.

 

[deleted171991]

Definite respect for you as well. I look for your response on crit care and anesthesia questions all the time and appreciate the pearls.

I like normoxia also. I guess my commentary re tolerating or even encouraging lower O2 is in regards to resp failure pts. I have seen colleagues set vents with plateau pressures in 30-40s to force a higher PO2, sacrifice PEEP to maintain TVs because want to avoid hypercarbia. Yes that sat >90% looks awesome and the nurses and residents love it and think it’s great medical care, then I come on and people think I’m a fool for changing vent settings and suddenly sats drop and numbers don’t look as good. I would rather have lower plateaus and TVs and tolerate sat 88%, PaO2 >55 than get perfect ABG numbers because that’s what I feel ARDSNET emphasized and taught us will save patients lives and that’s what I learned training at an ECMO center that got our regional VV ECMO evals for ARDS. How many patients do we see come to preop with low sats mentating and feeling perfectly fine? However, definitely if they r having multi organ failure and not just respiratory issues, got to rethink whether to tolerate low O2.

This reminds me of your commentary re starting inotropes in septic cardiomyopathy. To many of us, it makes sense. The BPs will get better, echo will look better. But you argued it doesn’t change outcome or may even make things worse. Without a good trial, we simply don’t know how our “common sense” interventions help or harm pts. Its what makes crit care so interesting and also very frustrating

We are on the same page here. I really do believe in first do no harm. So I protect the lung first, including permissive hypercarbia (unless increased ICP, for example). I don't chase or treat numbers; I try to see the big picture. That's something OR anesthesiologists and I tend to disagree on (e.g. I rarely give bicarb in the OR). As an intensivist, I was trained mostly by internists (I include the book authors here) and I tend to believe in most of their dogmas.

What I (hopefully) said about inotropes in sepsis is that they are not my first-line medications. I usually prop the blood pressure up with norepi first (because it's a pretty benign medication in low doses), then add some epi (if still needed). And yes, I have seen some bad outcomes from people who use inodilators first, without a pressor, hence increasing cardiac output at the cost of the HR and oxygen consumption. I have seen people die from prolonged tachycardia while on dobutamine (not on my watch).

People tend to overlook the signs of diastolic dysfunction on echo, and think that a good baseline EF means a good heart. Many more people have diastolic dysfunction than systolic, with all its consequences. Hence there is a point where inotropes do more harm than good (especially O2-wise). That's the line I try not to cross. Also, inotropes can be arrhythmogenic, which is never good in a sick patient. I am not a cardiac anesthesiologist, so I don't treat patients as if they were in the cardiac room. I don't treat the EF; I treat the peripheral perfusion (and I do realize an inodilator can be sometimes better, so then I use it). E.g. I will not chase like crazy a MAP of 65 if the patient is doing really well at 55-60, by all measures. Better is the enemy of good.

Whatever works for my patients; I am just the shaman, trying all kinds of herbs.

P.S. Now I remember why I don't give inotropes first in acute cardiomyopathies. Because they worsen outcomes in acute decompensated heart failure. There is evidence about that, referenced by Marik (don't have his book nearby).

 

[DrDrummer]

P.S. Now I remember why I don't give inotropes first in acute cardiomyopathies. Because they worsen outcomes in acute decompensated heart failure. There is evidence about that, referenced by Marik (don't have his book nearby).

This section?

Inotropic Agents
Dobutamine may have a role in patients with acute left ventricular failure due to myocardial ischemia. In this setting dobutamine may recruit hibernating myocardium and improve cardiac function. Furthermore, dobutamine should be considered in patients with sepsis induced acute systolic dysfunction. The role of dobutamine in patients with chronic heart failure is unclear. Chronic heart failure is characterized by sympathetic hyper-activation and β-receptor downregulation. Short term infusions or continuous β-stimulant therapies have not been demonstrated to be beneficial in these patients [ 54 ]. Tacon et al. performed a meta-analysis of RCT that evaluated the role of dobutamine in patients with ADHF [ 55 ]. In this study the odds ratio for mortality for patients treated with dobutamine compared with standard care or placebo was 1.47 (CI 0.98–2.21, p = 0.06). This meta-analysis demonstrated that dobutamine is not associated with improved outcome in patients with heart failure, but was associated with a strong trend towards increased mortality. β-blockers have been demonstrated to improve outcome in patients with compensated heart failure and it therefore appears counterintuitive that β-stimulant therapy would have a role in ADHF. Milrinone acts by inhibiting the phosphodiesterase III isoenzyme, which leads to increased cyclic adenosine monophosphate (cAMP) and enhanced inotropy. It differs from dobutamine, because it elevates cAMP by preventing its degradation as opposed to dobutamine, which increases cAMP production. In the OPTIME-CHF study the use of milrinone in patients with an ischemic cardiomyopathy was associated with an increase in the composite of death or rehospitalization (42 vs. 36 % for placebo, p = 0.01) [ 56 ]. Furthermore, in the ESCAPE heart failure trial, the use of an inotrope was associated with an increased risk of death; RR of 2.14, (95 % CI 1.10– 4.15) [ 57 ]. This data suggests that both dobutamine and milrinone have a limited role in the management of patients with ADHF.

 

[lymphocyte]

If we tolerate 88% as a baseline sat in COPD, then a little lower goals for other doesn’t seem so extreme as long as we maintain delivery O2 (maintain CO and Hgb if tolerating low PO2). We alrdy have good data lower PO2s have better outcomes in MI and stroke. We need a trial comparing even lower PO2 goals!

Conservative oxygenation kills in ARDS as per the just published LOCO2 trial. They stopped the trial early as a result. Aim PaO2 90-105, SpO2 > 96%. I thought it was a well-done trial.

https://www.nejm.org/doi/full/10.1056/NEJMoa1916431

 

[vector2]

Conservative oxygenation kills in ARDS as per the just published LOCO2 trial. They stopped the trial early as a result. Aim PaO2 90-105, SpO2 > 96%. I thought it was a well-done trial.

https://www.nejm.org/doi/full/10.1056/NEJMoa1916431

Not ARDS specific but ICU-ROX with 1000 pts shows no difference

https://www.nejm.org/doi/full/10.1056/NEJMoa1903297?query=recirc_curatedRelated_article

 

[lymphocyte]

Not ARDS specific but ICU-ROX with 1000 pts shows no difference

https://www.nejm.org/doi/full/10.1056/NEJMoa1903297?query=recirc_curatedRelated_article

The upper limit of the conservative oxygen group was 97%, which is a completely different treatment paradigm. And as you mention, ICU-ROX was not ARDS specific.

 

[Radetzky]

Conservative oxygenation kills in ARDS as per the just published LOCO2 trial. They stopped the trial early as a result. Aim PaO2 90-105, SpO2 > 96%. I thought it was a well-done trial.

https://www.nejm.org/doi/full/10.1056/NEJMoa1916431

I wonder if 92-96 would have been better than either 88-92 or >96.

 

[WheezyBaby]

FFP, I'd be interested in if you have good data to the contrary, but I'd done a chart dive on oxygen induced hypercapnea several months ago and recall the data being pretty convincingly supportive, with most of the debate around mechanisms. Can try to dig up some cites

 

[Radetzky]

FFP, I'd be interested in if you have good data to the contrary, but I'd done a chart dive on oxygen induced hypercapnea several months ago and recall the data being pretty convincingly supportive, with most of the debate around mechanisms. Can try to dig up some cites

oxygen induced hypercapnia is definitely real but the mechanism is displacement of co2 off Hemoglobin rather than loss of respiratory drive ie you won’t make someone apneic with oxygen

Oxygen-induced hypercapnia in COPD: myths and facts

 

[deleted171991]

FFP, I'd be interested in if you have good data to the contrary, but I'd done a chart dive on oxygen induced hypercapnea several months ago and recall the data being pretty convincingly supportive, with most of the debate around mechanisms. Can try to dig up some cites

I must admit I haven't treated severe COPD exacerbation for a few years now, but all of my COPD patients are kept at 92-94%, at least. I am way more afraid of hypoxemic organ failure than hypercarbia, in an ICU patient. And I have never ever seen any of them go apneic.

 

[turkeyjerky]

I must admit I haven't treated severe COPD exacerbation for a few years now, but all of my COPD patients are kept at 92-94%, at least. I am way more afraid of hypoxemic organ failure than hypercarbia, in an ICU patient. And I have never ever seen any of them go apneic.

Yeah, I think the bigger issue is they get encepahlopathic, a RRT gets called in the middle of the night and they end up unnecessarily intubated

 

[deleted171991]

Yeah, I think the bigger issue is they get encepahlopathic, a RRT gets called in the middle of the night and they end up unnecessarily intubated

If a patient gets intubated for hypercarbia in the middle of the night, that speaks volumes about the quality of the ICU and the hospital, no offense.

I haven't even stopped to think about reducing FiO2 for a COPD-er in the SICU, not for a second, in years. It's mostly just MICU dogma (to me). I don't remember encountering the problem even when I worked in the MICU during my fellowship, but that was years ago.

To me, there is simply no practical benefit of not keeping a patient at minimum 92-96% in the ICU. I just HATE when people use the excuse that the patient's baseline is in the 80s, so they should be fine. That's like when they claim that the patient has chronic peripheral edema at home, "at baseline", i.e. we shouldn't bother to get him better. And I have never had a COPD patient complain that he's feeling worse when I correct their O2.

 

[WheezyBaby]

Had a chance to look back through some of the citations I'd saved

oxygen induced hypercapnia is definitely real but the mechanism is displacement of co2 off Hemoglobin rather than loss of respiratory drive ie you won’t make someone apneic with oxygen

Oxygen-induced hypercapnia in COPD: myths and facts

I don't believe it's exclusively haldane effect

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3682248/pdf/cc11475.pdf

If a patient gets intubated for hypercarbia in the middle of the night, that speaks volumes about the quality of the ICU and the hospital, no offense.

I haven't even stopped to think about reducing FiO2 for a COPD-er in the SICU, not for a second, in years. It's mostly just MICU dogma (to me). I don't remember encountering the problem even when I worked in the MICU during my fellowship, but that was years ago.

To me, there is simply no practical benefit of not keeping a patient at minimum 92-96% in the ICU. I just HATE when people use the excuse that the patient's baseline is in the 80s, so they should be fine. That's like when they claim that the patient also has peripheral edema at home, "at baseline".

Mortality reduction for titrated oxygen therapy in COPD

Using titrated oxygen instead of high flow oxygen during an acute exacerbation of chronic obstructive pulmonary disease (COPD) saves lives - PubMed

In patients with a suspected acute exacerbation of COPD, using titrated oxygen to maintain SpO(2) between 88% and 92% reduced the risk of mortality by 58%. Physiotherapists working in acute care should strive to ensure that these patients are not treated with high-flow oxygen.

www.ncbi.nlm.nih.gov

Grade A rec (bullet A3) by ATS for 88-92 target for sats in COPDers

https://thorax.bmj.com/content/thoraxjnl/72/Suppl_1/ii1.full.pdf

IOTA meta-analysis on mortality and oxygen targets (beyond COPD)

Mortality and morbidity in acutely ill adults treated with liberal versus conservative oxygen therapy (IOTA): a systematic review and meta-analysis

Supplemental oxygen is often administered liberally to acutely ill adults, but the credibility of the evidence for this practice is unclear. We system…

www.sciencedirect.com

 

[deleted171991]

Mortality reduction for titrated oxygen therapy in COPD

Using titrated oxygen instead of high flow oxygen during an acute exacerbation of chronic obstructive pulmonary disease (COPD) saves lives - PubMed

In patients with a suspected acute exacerbation of COPD, using titrated oxygen to maintain SpO(2) between 88% and 92% reduced the risk of mortality by 58%. Physiotherapists working in acute care should strive to ensure that these patients are not treated with high-flow oxygen.

www.ncbi.nlm.nih.gov

Grade A rec (bullet A3) by ATS for 88-92 target for sats in COPDers

https://thorax.bmj.com/content/thoraxjnl/72/Suppl_1/ii1.full.pdf

IOTA meta-analysis on mortality and oxygen targets (beyond COPD)

Mortality and morbidity in acutely ill adults treated with liberal versus conservative oxygen therapy (IOTA): a systematic review and meta-analysis

Supplemental oxygen is often administered liberally to acutely ill adults, but the credibility of the evidence for this practice is unclear. We system…

www.sciencedirect.com

You really don't want to convince me to base my treatment on a poor study done in pre-hospital treatment of COPD exacerbation by paramedics,, where they compared 88-92% saturation with basically 100% (as in no target, just NRB and a ton of O2). That's like telling me that I should only use 6 ml/kg of VT, because the ARDSnet study was 6 ml/kg versus 12 ml/kg, even if 8 ml/kg has never been proven to hurt anybody. The only thing that study proved is that less is more, that 88-92% is better than 100. Not 92-96, because they never bothered to titrate the control group! Also, these were patients with acute COPD exacerbation, not just any COPD-ers. And they weren't ICU-level patients, just picked up by an ambulance.

I've been preaching against targeting really high O2 sats for like 5 years, because O2 is pro-inflammatory. But 88% and 94% are two different animals for anybody who knows a hint of physiology. And I don't treat patients based on (BTS) guidelines, but on the individual pathophysiology, and what the best minds I know do; I am not a nurse practitioner, I am not a cook, I don't follow recipes or weak evidence.

And the meta-"analysis" you quoted, which is usually among the the "garbagest" of research studies in my book (because most studies are so different statistically that it's very hard to grab a statistically-solid conclusion, that's just clear to anybody who knows math), dumped together all studies with a sat between 94 and 99%. Since 94 and 99% are VERY different physiologically (99% is well within the measuring error of a 100% saturation by a pulse ox or ABG), its conclusions are simply worthless to me, even if the conclusions support my own therapeutic philosophy (isn't it ironic, don't you think?):

In acutely ill adults, high-quality evidence shows that liberal oxygen therapy increases mortality without improving other patient-important outcomes. Supplemental oxygen might become unfavourable above an SpO2 range of 94–96%.

Now maybe that's because I have seen more studies that were proven wrong (and bad medicine based on them) than those that stood the test of time, and were proven true again and again. Or maybe it's my contrarian streak. I also admit that I looked for the major disqualifiers, and did not try to see what they actually did right. Hope I wasn't too nasty (it's hard to filter that mouth out when writing), my apologies. Let's not mention that this post is too long!

 

[WheezyBaby]

You really don't want to convince me to base my treatment on a poor study done in pre-hospital treatment of COPD exacerbation by paramedics,, where they compared 88-92% saturation with basically 100%. That's like telling me that I should only use 6 ml/kg of VT, because the ARDSnet study was 6 ml/kg versus 12 ml/kg, even if 8 ml/kg has never been proven to hurt anybody. The only thing that study proved is that less is more, that 88-92% is better than 100. Not 92-96, just 100!

I've been preaching against targeting really high O2 sats for like 5 years, because O2 is pro-inflammatory. But 88% and 94% are two different animals for anybody who knows a hint of physiology. And I don't treat patients based on (BTS) guidelines, but on the individual pathophysiology, and what the best minds I know do; I am not a nurse practitioner, I am not a cook, I don't follow recipes or weak evidence.

And the meta-"analysis" you quoted, which is usually among the the "garbagest" of research studies in my book (because most studies are so different statistically that it's very hard to grab a statistically-solid conclusion, that's just clear to anybody who knows math), dumped together all studies with a sat between 94 and 99%. Since 94 and 99% are VERY different physiologically (99% is well within the measuring error of a 100% saturation by a pulse ox or ABG), its conclusions are simply worthless to me. Even if its conclusion supports my own therapeutic philosophy (isn't it ironic, don't you think?):


Now maybe that's because I have seen more studies that were proven wrong (and bad medicine based on them) than those that stood the test of time. Or maybe it's my contrarian streak. I also admit that I looked for the major disqualifiers, and did not try to see what they actually did right. Hope I wasn't too nasty, my apologies.

Not nasty at all, happy to have a discussion. I know the data is not ideal, but it's what exists. What's the data driven basis for driving the sat to "at minimum 92-96" in chronic co2 retainers? It's discordant with how the intensivists I know practice

 

[deleted171991]

Not nasty at all, happy to have a discussion. I know the data is not ideal, but it's what exists. What's the data driven basis for driving the sat to "at minimum 92-96" in chronic co2 retainers?

I don't know. All I know that there is data against 100, and that the lower limit of "normal" (i.e. mean - 2 SD in healthy people) is probably not 88-90%, even in healthy functional elderly. And that there is no proof that 92-96(-?98)% harms anyone. To me, weak evidence is no evidence. So is "expert opinion" based on it, unless it comes from experts I know and respect. I think we have a lot of dogma in medicine, and this may be one example.

I understand that some lung patients are conditioned to function even at a lower tissue O2 (somewhat like athletes), and can tolerate O2 sats of 88% without issues. I am not trying to fix their PaO2 when they are doing well, but when it may be contributing to badness. Also, it's a big difference between a patient watching TV at 88-92%, and a tachypneic 88-92%. An alkalotic patient will shift the dissociation curve to the left, so it's not their "baseline" physiology anymore.

In the end, everything is a matter of risks vs benefits and alternatives for a particular patient and situation.

Disclaimer:
I tend to deal not with COPD exacerbations, but with other ICU/stepdown problems in surgical patients who also happen to have COPD. I would probably treat a COPD exacerbation more conservatively, especially if "blue bloater", to avoid risk of further hypercapnia (although a COPD exacerbation may end up on some BiPAP anyway, which will also fix the O2 sats).

I'll leave you with some food for thought from smarter people than I am: Is Too Much Supplemental O2 Harmful in COPD Exacerbations? - REBEL EM - Emergency Medicine Blog

 

[turkeyjerky]

If a patient gets intubated for hypercarbia in the middle of the night, that speaks volumes about the quality of the ICU and the hospital, no offense.

Yeah, agreed. I was more thinking about medical residents or nurses panicking on the medical floor.