COPD w/ high flow O2

Sizz

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Hey all

Picked up a 84 y/o m with COPD last night who was having trouble breathing pretty badly last night I believe his O2 sat was 80% he was on home oxygen 3lpm NC...so as I was taught by some medics we bust out the NRB 10-15 lpm which brings up his 02 sat and he feels much better for the time being. We have a 2 min trip to local hospital in which the nurse immediately switches back to 4-6L via NC.

We ended up showing up a few hours later to transfer him to the heli pad to a larger faciliaty when we arrived he was back on the NRB at 10lpm and so forth.

Now I'm thinking about the whole hypoxia drive and such for the COPD pt is different and O2 can (make it worse) but for the time being my pt was having trouble breathing so we put high flow on which helped for the short time. It seems the nurses can have strokes and go nuts when they see a COPD pt come in with NRB running. Then again he left their care with it as well.

Anyone able to clear this up or relate or was it just the worse thing in the world to have him on high flow O2 for 5-10 mins until he was out of our care?

Hopefully I'll learn more about this.
 

medicdan

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I will let others comment on, or discuss hypoxic drive...but my guess was that the triage nurse was getting baseline vitals... on the flow of oxygen the patient takes at home...
 
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Sizz

Sizz

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That could be the reason she dropped it but I'm guessing not since she was rambling "O he's a COPD pt lets drop his O2 back to this NC etc" and I'm thinking since his O2 did not come back up or his condition was not improving they transferred him to a larger hospital.

I do see why they would want his "at home vitals" for comparison since he usually runs 3lpm.
 

Shishkabob

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The hypoxic drive only exist in a small portion of COPD patients as a whole.


As you know, the typical COPD patient is usually in the high 80/ low 90 sat range. Our (your) goal is to bring your patient back up to their usual baseline and NOT to as close to 100% as possible. But if 3lpm via NC is not cutting it, there is no way in hell 6 will, and as such you need to do a mask. Maybe not an NRB, but something with a higher concentration. He was obviously in failure and needed to be corrected.

The nurse is probably stuck in the olden times where "OH NO HIGH FLOW O2 IS BAD!"
 

MSDeltaFlt

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Hey all

Picked up a 84 y/o m with COPD last night who was having trouble breathing pretty badly last night I believe his O2 sat was 80% he was on home oxygen 3lpm NC...so as I was taught by some medics we bust out the NRB 10-15 lpm which brings up his 02 sat and he feels much better for the time being. We have a 2 min trip to local hospital in which the nurse immediately switches back to 4-6L via NC.

We ended up showing up a few hours later to transfer him to the heli pad to a larger faciliaty when we arrived he was back on the NRB at 10lpm and so forth.

Now I'm thinking about the whole hypoxia drive and such for the COPD pt is different and O2 can (make it worse) but for the time being my pt was having trouble breathing so we put high flow on which helped for the short time. It seems the nurses can have strokes and go nuts when they see a COPD pt come in with NRB running. Then again he left their care with it as well.

Anyone able to clear this up or relate or was it just the worse thing in the world to have him on high flow O2 for 5-10 mins until he was out of our care?

Hopefully I'll learn more about this.

Just because they are diagnosed with COPD does not uniformly mean they are CO2 retainers with a hypoxic drive even if they are on home O2. That requires documentation. They probably have other co-morbid fastors as well (cardiomegally, dyspnea on exertion, etc). Your crew did just fine and the correct thing by putting him on the low-flow system of 10-15 L/min NRM.

The nurse dropping his O2 when you showed up probably wasn't that bad of a decision to try to get an accurate baseline VS. However, screaming "He's got COPD" was ill-placed. If they're hypoxic, give them O2. If they stop breathing, tube 'em. It makes absolutely no difference what they're chronic diagnosis is.

Your short transport will not be the "game ender" for your pt's hypoxic drive. It's been my experience that there are very few pts who will stop breathing with 15 L/min NRB: End-Stage COPD pts (to the point that they are currently dying from it) and those with Pickwickian Syndrome.

http://www.medterms.com/script/main/art.asp?articlekey=4896

The latter are REAL sensitive. These are the ones walking through the grocery store with RA SpO2's = 78% and doing just fine.

Don't sweat it. You did a good job. The ER did fine as well, because they flew dude out and put him back on the NRM.
 

dudemanguy

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I've asked the same question. I had two emergency room doctors, both medical directors, tell me unequivacably to go with the high flow 02 by NRB. They both said for the relatively short amount of time you are with the patient, it wont do any harm.
 

rescue99

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Hey all

Picked up a 84 y/o m with COPD last night who was having trouble breathing pretty badly last night I believe his O2 sat was 80% he was on home oxygen 3lpm NC...so as I was taught by some medics we bust out the NRB 10-15 lpm which brings up his 02 sat and he feels much better for the time being. We have a 2 min trip to local hospital in which the nurse immediately switches back to 4-6L via NC.

We ended up showing up a few hours later to transfer him to the heli pad to a larger faciliaty when we arrived he was back on the NRB at 10lpm and so forth.

Now I'm thinking about the whole hypoxia drive and such for the COPD pt is different and O2 can (make it worse) but for the time being my pt was having trouble breathing so we put high flow on which helped for the short time. It seems the nurses can have strokes and go nuts when they see a COPD pt come in with NRB running. Then again he left their care with it as well.

Anyone able to clear this up or relate or was it just the worse thing in the world to have him on high flow O2 for 5-10 mins until he was out of our care?

Hopefully I'll learn more about this.

It seems to be a common method of realizing whether the patient actually "needed" the higher flow 02. ER will reduce the % only to increase it once they figure out it was there for a reason. In reality, it isn't a bad idea and pretty non invasive. Wonder what they charge for this highly sophisticated test??
 

Lifeguards For Life

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The hypoxic drive only exist in a small portion of COPD patients as a whole.




The nurse is probably stuck in the olden times where "OH NO HIGH FLOW O2 IS BAD!"

I've heard our medical director refer to the hypoxic drive theory as "the dracula of modern medicine, because non on can drive a stake through the damn things heart."

http://www.learnmoresavelives.com/b...c-drive-mediated-sudden-hyperoxic-death-oh-my

http://home.pacbell.net/whitnack/The_Death_of_the_Hypoxic_Drive_Theory.htm
 

Veneficus

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I've heard our medical director refer to the hypoxic drive theory as "the dracula of modern medicine, because non on can drive a stake through the damn things heart."

http://www.learnmoresavelives.com/b...c-drive-mediated-sudden-hyperoxic-death-oh-my

http://home.pacbell.net/whitnack/The_Death_of_the_Hypoxic_Drive_Theory.htm

That is a great way to say it.

I think it is another one of those n=1 experiences that somehow get out of control. You know...

My uncles,cousins, brothers, nephews, second removed cousin saw it and then suddenly a rather rare or obscure case gets elevated to the status of being a majority of presentations, or one with such rumored world ending consequences that it really does become "like dracula."
 
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Sizz

Sizz

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Great feedback everyone thank you!
 

MonkeySquasher

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Sizz -

As others stated, COPD is a chronic condition, for which he was on home O2. But clearly, something is not right, and the home O2 isn't working, hence the reason you were called.. ;) While, yes, an O2 sat of mid-80s may be normal for him, it may not be, either. You were right to put him on the NRB, and this is shown by the patient himself stating relief.

In order to really screw up the average person/COPD'ers O2/CO2 drive, you'd need to have them on a NRB for quite a length of time (Not counting Pickwickian's, obviously). Newborns/neonates are also a population to be careful with, but only over prolonged periods of time.

If I had to guess, I would think (hope?) the nurse was putting him back on the NC for one of two reasons..
1) To see how he is post-O2 treatment by EMS. Did he recover and his saturations stay up? What do they drop to post-treatment? Does the dyspnea return when he's returned to baseline home O2 use? Maybe he just needs a slight medication adjustment, or a different method of home O2.
2) Because he's going to be there for awhile, and all of that high-flow over hours WOULD screw up his drive. Basically a mindset of "save it til you need it".


MrBrown-

Those are nice! I haven't seen anything like that in my area, but it sure would be nice.
 
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8jimi8

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I've heard our medical director refer to the hypoxic drive theory as "the dracula of modern medicine, because non on can drive a stake through the damn things heart."

http://www.learnmoresavelives.com/b...c-drive-mediated-sudden-hyperoxic-death-oh-my

http://home.pacbell.net/whitnack/The_Death_of_the_Hypoxic_Drive_Theory.htm

Could it be that 15l/min NRB is also the dracula of modern medicine? I remember a thread where everyone was chiming in about how it wasn't necessary to put all patients on an NRB w/ 100%.

The point being, if the patient is having trouble oxygenating, give o2 until you get to definitive care, at which a decision will be made as to what treatment modality will best benefit the patient.

I don't think its a bad thing to consider that the patient has COPD and MAY decompensate with high flow O2 after a period of time.

Do i think it will ever only take a few minutes? No.
 

MrBrown

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The point being, if the patient is having trouble oxygenating, give o2 until you get to definitive care, at which a decision will be made as to what treatment modality will best benefit the patient.

What is preventing you from making such a decision? What type of oxygen treatment are you going to give? (flow rate and device)

And yes, there is nothing magic about 15 litres via NRBM; oxygen is often given to patients who do not require it and/or in concentrations above what is required.
 

MonkeySquasher

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And yes, there is nothing magic about 15 litres via NRBM; oxygen is often given to patients who do not require it and/or in concentrations above what is required.

Agreed. My protocols may say 15LPM, but unless it's a large man huffing a lot, it's overkill. I don't want to blow Granny's eyelashes out... I usually make sure there's a good mask seal and set it around 10LPM.

Doing the right thing isn't doing the right thing, etc.
 

Shishkabob

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I don't think its a bad thing to consider that the patient has COPD and MAY decompensate with high flow O2 after a period of time.

Do i think it will ever only take a few minutes? No.

Meh. If they somehow end up going in to respiratory failure due to the high FiO2, we can fix that.

Can't fix the hypoxia/hypoxemia caused damage if we don't give them O2. Honestly, lesser of 2 evils.



But also that's why we get a good patient history when possible.
 

medic417

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With most of you having short transports odds are you will not trigger any COPD to stop breathing. If you do no big deal just remove the O2 and bag a couple of times and most resume breathing on their own. If not you just keep breathing to the hospital for them.

We need Vent to come give some more information. She really is best on here in providing good reference material to help those that want to improve do so.
 

Lifeguards For Life

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With most of you having short transports odds are you will not trigger any COPD to stop breathing. If you do no big deal just remove the O2 and bag a couple of times and most resume breathing on their own. If not you just keep breathing to the hospital for them.

We need Vent to come give some more information. She really is best on here in providing good reference material to help those that want to improve do so.

You've seen a patient with COPD deteriorate, from high flow oxygen administration?
 

MonkeySquasher

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Meh. If they somehow end up going in to respiratory failure due to the high FiO2, we can fix that.

Yeah, but that'll take time. Screw it, let's just pump them full of fluid, lay them back, and tube them when they go into failure! :beerchug:
 
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Lifeguards For Life

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To quote Dr. Hoyt,

"There are examples of mythology that float about in the atmosphere of medical information that desperately need to be debunked because they influence the care of patients. One sample of medical mythology is the commonly told story that the administration of oxygen to a patient with chronic obstructive lung disease will shut down the patient's hypoxic respiratory drive and lead to apnea, cardiorespiratory arrest, and the subsequent death of the patient.

It is not clear where this fallacious information comes from, but it seems to enter the medical information database at an early age, at the medical student or resident level, almost like a computer virus corrupting the appropriate function of the equipment. In addition, this myth becomes very difficult to extinguish during the career of the physician, even with clear factual information of long standing. The danger here is that this medical mythology will inappropriately influence treatment decisions in patients.

The basic issue in this story is oxygen. The human body, particularly key organs such as the heart and brain, are not at all forgiving of insufficient supplies of oxygen. Thus, medical decision-making-based on the mythology that oxygen causes apnea and cardiorespiratory arrest in patients with chronic obstructive lung disease by turning off the oxygen respiratory drive-might take the path of withholding or delivering inadequate doses of oxygen to meet the metabolic needs of the patient in respiratory failure. This mistake is generally fatal for the patient, and a treatment tragedy for the misinformed physician.

The article by Dr. Crossley and colleagues [1] in this issue of Critical Care Medicine is an elegant project capable of debunking the mythological relationship between oxygen and apnea in patients with chronic obstructive lung disease. The authors [1] nicely demonstrate that a substantial dose of oxygen in intubated but spontaneously breathing patients with chronic obstructive lung disease has no effect on PaCO2, deadspace, and respiratory drive. The discussion section of the article [1] is superb. The authors [1] assembled facts from the respiratory physiology literature to demonstrate that oxygen releases hypoxic pulmonary vasoconstriction in chronic obstructive lung disease patients. This release of hypoxic pulmonary vasoconstriction leads to a further mismatch of ventilation and perfusion in chronic obstructive lung disease patients, with a subsequent increase in deadspace. In this situation, minute volume largely stays the same or may increase slightly to eliminate CO2, but the elimination of CO2 has by now become more difficult, as the deadspace has increased.

Most mythological stories are based on some observation, which may be a correct observation but an incorrect interpretation of the events. It is true that the administration of oxygen to a patient with exacerbated chronic obstructive lung disease and acute respiratory failure may lead to an increased CO2. It is true that the hypercarbia may become severe and be associated with cardiorespiratory arrest. The problem is with interpreting the cause of this event. As Dr. Crossley and colleagues [1] indicate, the hypercarbia is caused by release of hypoxic pulmonary vasoconstriction with increased deadspace, and not by down-regulating the hypoxic drive. Thus, one should not fear apnea and cardiorespiratory arrest when giving oxygen to a patient with an exacerbated chronic obstructive lung disease and respiratory failure. Instead, one should be prepared to help the patient eliminate CO2 when deadspace increases. Providing assistance with the elimination of CO2 has been around since the beginning of critical care medicine. It is called mechanical ventilation.

A clear and scientific interpretation of the response to oxygen in a patient with exacerbated chronic obstructive lung disease and acute respiratory failure has always been important, but currently, such an interpretation is essential. As health care transforms itself, a variety of individuals, organizations, and healthcare facilities are attempting to translate medical information into critical pathways. These critical pathways are being used by a wide range of professionals to guide the treatment of patients. The critical pathways must be accurate, and based on the best medical science to protect the life of the patient. A critical pathway for a patient with exacerbated chronic obstructive lung disease and acute respiratory failure based on a down-regulation of hypoxic drive might be constructed to minimize the dose of oxygen to keep the patient breathing spontaneously. However, a critical pathway based on an increase in deadspace and difficulty eliminating CO2 should be constructed to help the patient eliminate CO2 with mechanical ventilation, while meeting the patient's uncompromising physiologic needs for oxygen.

Dr. Crossley and colleagues [1] cite a textbook on respiratory physiology by the British author J. F. Nunn [2]. This book [2], along with the monographs edited by John West on respiratory function and pathophysiology [3,4], has been required reading for anesthesia residents for many years. The books should be read by all physicians caring for critically ill patients. These textbooks create a clear picture of the physiologic changes in lung function that are associated with chronic obstructive lung disease. They allow for the debunking of medical mythology and the appropriate creation of treatment protocols for the management of respiratory failure."

The Control of Breathing in Clinical Practice, Caruana-Montaldo, et al, Chest 117/1 Jan., 2000, pages 205-225

Critical Care Medicine September 1997 Editorial “Debunking Myths of Chronic Obstructive Lung Disease”, by Dr. John Hoyt
 
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