One of my pet peeves is how every time oxygen therapy comes up in class the prof will drone on and on about COPD'ers and their hypoxic drive and not overloading them with oxygen because it will "cut out their respiratory drive and they'll stop breathing".
ARgghhhhhhhh.
I get the theory behind this but I can say (with a hand on my heart) that in 10 years of nursing school/working in emergency departments and dealing with countless and I mean countless respiratory distressed patients (and *most* of them COPD'ers) I have never, evah, seen one of them lose their drive and stop breathing from being overly oxygentated.
Not one.
Now I am sure there will be some readers out there that will disagree or have a case example of when it has happened (which is fine) but teaching an academic theory that is very very very very unlikely clinically seems odd to me since most of my classmates now believe that you can't give more than 2L of O2 to someone with COPD.
I flash to the last severe respiratory distress patient I had with severe COPD (I was actually positive the guy was going to code but thank heavens he didn't). The man was a very unnatural shade of blue, very tachypnic, tachycardic, frightened out of his mind, and sucking so hard on that non-rebreather. Ummm I don't think the oxygen was coming close to knocking out his drive to breathe, the oxygen was keeping him alive.
ANYWAY.
Today we had a lecture from a visiting respirologist who stated in his lecture (and I quote):
...there is all this talk about C02 retainers and patients with COPD, about how you need to be very judicious with oxygen therapy because they will lose their respiratory drive...in my experience this is purely an academic concept and I can say that I have never, ever seen it demonstrated in the clinical setting, it's not really a concern...
I swear I almost jumped up and yelled "THANK YOU!!!"
But I didn't.
Yay! Now I have a respiratory specialist *ON TAPE* making that statement. I can sit back and feel vindicated. Even my study buddy looked over at me when he said it and gave me the thumbs up.
Huzzah!
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17 comments:
And who cares if you happen to get that one patient in a million that does have his respiratory drive knocked out. His body still needs the oxygen, If he stops breathing, bag 'em with oxygen!
EXACTLY!!! aggghhhhhh So. Right.
Dude, thanks for this. We often keep our COPD-ers' on *only* 2L and their SpO2 in the 90-92% range and everyone acts like if we were to bump them up to say *gasp* 3 or 4L they'd up and die on the spot. It has always simultaneously scared the crap out of me and sounded a little suspicious.
I remember the same thing getting so drilled into me in nursing school that I was sure the phenomenon happened every day in ED's around the world.
Our lecturer today did remind us that for non-chronic patients ideal levels would be >96% and in patients with COPD the 90-92% mark is acceptable because that is their baseline. Still, if they are breathless at that level then bring them up.
It is good to be vigilant (after all oxygen *is* a drug) but really lets be honest about the true risks.
Glad I could be of service! :)
I think this is one of those things where interpret what we see to see what we expected.
I'm pretty sure I've seen at least 3 COPD patients crash after too much O2. These were all really advanced "facultative anaerobe" patients. They'd been living with sats in the 80's for years but seemed stable. The nurse cranks up the O2 shooting for a sat >90% and all of a sudden they start guppy-breathing and need intubation. Not every end-stage COPDer does this but I've seen it happen.
What happened?
Depends on what you believe: Maybe the O2 pushed them over the edge? Or maybe they were about go into respiratory failure anyway and the O2 was incidental?
You don't have the option of going back in time and leaving them on a nasal canula to see what would have happened. The bias in the two camps is so strong that to establish any believable proof you would need a double-blinded trial, and I have no idea how you could possibly design such a trial.
So it is left to a matter of faith.
I believe in 100% O2 suppressing respiratory drive and nothing Albino Black Bear can say will convince me otherwise! God is on my side!
Also remember there are two purposes of breathing -- 1) get O2, 2) get rid of CO2. If you don't breathe as often, you will fail to get rid of all the CO2 you are producing.
I should add that of course your kidneys will compensate somewhat... but not entirely.
DocD--Hahah, are you suggesting that I have the *opposite* of God on my side because of my views?? :)
Fair enough regarding your experiences and your interpretation. I suppose that once you've seen one case where you believe the two factors were linked then naturally you'd be wanting to err on the caution side. Girl can't argue with that!
The lecturer today commented on exactly your point about inability to perform ethical studies in these situations (he was citing the use of certain meds like lidocaine, magnesium, inhaled anesthetics, etc in status asthmaticus--as in you aren't going to give a placebo if nothing else is working and the patient is crumping).
OMDG--Yep, that is a good point, it is not just a one way street.
One thing which I found interesting with regard to that is, in people with obstructive diseases their FEV rate is greatly reduced. Since long expirations times are required for them to blow off-- when they become tachypnic their expiration time is greatly reduced. This actually makes them hypercapnic. Sometimes the method needed to treat this is hypoventilation. (Sounds paradoxical and it definitely took me a minute to wrap my head around it in the lecture).
Anyway, yeah..I thought it was really fascinating. Especially when he was talking about taking paralyzed/sedated pts OFF THE VENT for long periods of time in order to facilitate this (maybe this is all old news to you but I was totally slack jawed).
Crazy interesting critical care stuff.
Working at the VA, we had a couple chronic anerobic COPD'ers who would happily forget to breathe if their sats went much over 90%...IF your patient lives long enough at low enough sats, they will most annoyingly become massively hypercarbic if you up their sats enough---which is why there is BiPap with a backup rate......at least at that point they're too obtunded to yank at the mask.....
Dr. D:
So would you say it's the O2 suppressing the respiratory drive, as in 02 toxicity, or would you say that moving them so quickly out of their "normal" parameters upsets their homeostasis and they freak out?
A similar reaction can be seen in someone who's had chronic high blood sugars and we bring them down quickly with an insulin drip because they've finally hit DKA. Drop their sugar outside their normal, and all kinds of funky stuff starts happening.
Nurse XY:
Oxygen Toxicity is actually a different phenomenon. It is the damage done to lung tissues with high O2 over a long period of time. It happens when you leave somebody on a vent for a week with 100% FiO2.
I'm not sure that a "freak out" similar to a bad diabetic at a normal sugar is a good analogy. People breath harder when they're freaking out.
The situations I'm talking about the patients actually calmed down right before stopping breathing.
Air hunger is a fact of life for bad COPDers and I imagine it can be scary. It may very well be a "freak out" that causes a healthcare worker to check a sat on a facultative anaerobe and start turning up the O2 in response to our own freak out that this person has a sat of 80%. (Which is probably where this person lives anyway.)
The calm of loosing the respiratory drive and thus the air hunger might be quite relaxing. Throw in some C02 retention and it probably is one of the mellowest ways to go.
Of course, this is actually a leap of faith on my part. It could be the air hunger isn't a freak out, but an acute worsening of the underlying condition which would eventually cause the respiratory arrest with or without the extra O2.
Who knows. You just pick a side and accuse the other side of non-scientific heresy.
But thanks to this enlightening post by ABB I now consider myself an O2-Respiratory-Drive Agnostic!
OK ok ok...maybe I need to clarify what I mean by "respiratory distress".
I am not saying that I go around putting NRB's @100% on grandpa while he's eating a pork chop if his sats get below 90% (and he's usually sitting at 85% anyway)!
I am talking about respiratory distress in emergency situations, like when people call 911 for not being able to breathe at ALL. When people get all freaky about not turning up the O2 while the patient is symptomatically hypoxic, tachypnic, and DISTRESSED.
Just don't want ye all thinking I am on some weird oxygen crusade to bring the world to 98% or something...
I've always been told, if they're COPD, aim for around 92%, and if they're COPD and trying to die on you, go for 15L on a non-rebreather, hypoxic drive be damned.
The logic behind this was, the hypoxic drive is not likely to change quickly and if a person is about to arrest, you want to focus on the imminent problem, not the one that might arise 15-20 minutes down the line.
Yes, yes and yes.
I reiterate that I was referring to BIG sick people, not little sick people. Glad I am not losing my mind (or demonstrating bad practice!)
The lecturer today commented on exactly your point about inability to perform ethical studies in these situations (he was citing the use of certain meds like lidocaine, magnesium, inhaled anesthetics, etc in status asthmaticus--as in you aren't going to give a placebo if nothing else is working and the patient is crumping).
In other words, when the patient looks bad, we need to use whatever is traditional, rather than come up with a study to find out if the traditional treatment is efficacious, ineffective, or harmful.
How is this ethical?
One old example of this is Internal mammary artery ligation. There were people claiming that this was unethical research.
"We cannot ethically deprive patients of this life-saving treatment!!!11!!!"
An evaluation of internal-mammary-artery ligation by a double-blind technic.
COBB LA, THOMAS GI, DILLARD DH, MERENDINO KA, BRUCE RA.
N Engl J Med. 1959 May 28;260(22):1115-8.
PMID: 13657350 [PubMed - indexed for MEDLINE]
No abstract available.
The result was that the patients with the sham surgery did significantly better than the patients with the real surgery.
One patient had flipped T-waves after 4 minutes of an exercise stress test before the procedure, but was able to continue for 10 minutes of the same exercise stress test without any ECG changes after the procedure. However, he was in the sham surgery group.
I regularly rant about the ACLS drugs and the complete absence of evidence of improved survival to discharge (as if any other outcome matters). I continued yesterday with Ethics, Research, and IRBs – Part I
We need to demand an expiration date on all expert opinions that are not followed up with well done research.
COPD retainers do not have the normal CO2 drive to breathe, so they depend on low oxygen levels to encourage breathing. I don't know what that feels like, but for the rest of us, if we hold our breath, what makes it uncomfortable/intolerable is the increased CO2 levels.
This is why you see some people hyperventilate before swimming underwater. They are blowing off as much CO2 as possible, so they do not feel as much need to breathe. Some of them may pass out under water.
COPD patients do not have just hypoxia to deal with, but if they are experiencing hypoxia and small amounts of oxygen and large amounts of other medications are not turning things around, then large amounts of oxygen would be appropriate.
I have knocked out the hypoxic drive on 2 patients. both responded by hyperventilating, rather than hypoventilating.
I try to avoid too much oxygen, not because I worry about knocking out their hypoxic drive, but because it is not going to be easy to wean them back to their normal oxygen levels. If they end up intubated, that may be much worse for the patient than the hypoxia. COPD patients do not respond well to invasive ventilation.
For oriented patients, I am much more interested in what the patient tells me they think they need than what the pulse oximeter tells me. They have been living with this for years and often know what feels right.
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