Respiratory alkalosis. PaO2 is real.
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!
Lower pO2 shouldn't mean respiratory failure-level pO2 (i.e. under 60 mmHg)..
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.
, 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.)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
This is the book (get the printed version and download the free ebook to your phone):
Amazon product ASIN 0323399525
And this is a quote from it:
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).
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).
(Sorry if it comes across as anything less than.)
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.
I edited a bit my previous post. It was a bit too aggressive, sorry.
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.
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.
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.
www.ncbi.nlm.nih.gov
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.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.
Grade A rec (bullet A3) by ATS for 88-92 target for sats in COPDers
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
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.
