# Why can't COPD pts be on a non rebreather mask?



## ThatEMTGuy (Mar 14, 2015)

I literally forget how that works out.


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## STXmedic (Mar 14, 2015)

They can.


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## Chewy20 (Mar 14, 2015)

ThatEMTGuy said:


> I literally forget how that works out.


 
Who told you they can't be? If someone has low o2 sats you give them oxygen. It may or may not help, if it doesn't then throw them on CPAP with the PEEP set at 5, or 10 if they have fluid in their lungs.

You are not going to shut someone's respiratory drive down by putting on an NRB.


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## COmedic17 (Mar 14, 2015)

That idea stems from oxygen toxicity. If a pt receives too much oxygen (ex- NRB) theres a risk that you might knock out the patients respiratory drive ( remember people with COPD run off of hypoxic drive as opposed to high co2 levels) , and there's risks of vasoconstriction.

But if a pt needs oxygen-give them oxygen. The goal is an spo2 reading between 94-99% (According to the books)..

However, the studies show with COPD exacterbation you should titrate oxygen since it reduces the likelihood of hypercapnia and respiratory acidosis as opposed to starting right off the bat with high flow O2. Since NRBs have a oxygen resovior bag, they are harder to titrate then say a Venturi mask or nasal cannula or bipap/Cpap.


That's the theory behind it. But I have never had a pt on a NRB exhibit any negative side effects.


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## medicaltransient (Mar 14, 2015)

They can. Your thinking of obsorbative atalectasis, it's when you wash out all the nitrogen and they stop making surfactant. Nitrogen is what triggers surfactant to be made. Something like that, look it up on google scholar.


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## Av8or007 (Mar 14, 2015)

http://www.bmj.com/content/341/bmj.c5462


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## Burritomedic1127 (Mar 14, 2015)

medicaltransient said:


> They can. Your thinking of obsorbative atalectasis, it's when you wash out all the nitrogen and they stop making surfactant. Nitrogen is what triggers surfactant to be made. Something like that, look it up on google scholar.


Surfactant is produced in the Type II alveolar cells, most of it is continuously recycled


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## NomadicMedic (Mar 14, 2015)

You're actually thinking of the old EMS instructor adage, "if you put oxygen on a COPD patient, it'll kill them because they rely on hypoxic drive."

Untrue. EMS instructors also like to tell tales such as, "if you don't put everyone in a motor vehicle accident on a backboard with a c-collar, they could turn their neck and die."

Or this gem, "if they have a radial pulse, they have a blood pressure of at least 90"

If an EMS instructor ever presents something that results in devastating consequences as an absolute, it's usually BS. Look it up and do some research.


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## DesertMedic66 (Mar 14, 2015)

DEmedic said:


> You're actually thinking of the old EMS instructor adage, "if you put oxygen on a COPD patient, it'll kill them because they rely on hypoxic drive."
> 
> Untrue. EMS instructors also like to tell tales such as, "if you don't put everyone in a motor vehicle accident on a backboard with a c-collar, they could turn their neck and die."
> 
> ...



The one that I made bold I hear all the time from nurses, medics, and EMTs. I hate when providers say it. I'm surprised with how many medics actually use that as a scale to give meds "they have a radial pulse so we can give nitro"


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## MackTheKnife (Mar 14, 2015)

COmedic17 said:


> That idea stems from oxygen toxicity. If a pt receives too much oxygen (ex- NRB) theres a risk that you might knock out the patients respiratory drive ( remember people with COPD run off of hypoxic drive as opposed to high co2 levels) , and there's risks of vasoconstriction.
> 
> But if a pt needs oxygen-give them oxygen. The goal is an spo2 reading between 94-99% (According to the books)..
> 
> ...


Great point about hypoxic drive. Many forget that.


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## captaindepth (Mar 14, 2015)

COmedic17 said:


> That idea stems from oxygen toxicity. If a pt receives too much oxygen (ex- NRB) theres a risk that you might knock out the patients respiratory drive ( remember people with COPD run off of hypoxic drive as opposed to high co2 levels) , and there's risks of vasoconstriction.
> 
> But if a pt needs oxygen-give them oxygen. The goal is an spo2 reading between 94-99% (According to the books)..
> 
> ...



I don't believe oxygen toxicity is involved in COPD pts and their dependance on a hypoxic drive. Oxygen toxicity occurs at high partial pressures and can lead to seizures as well as other complications. This is usually experienced in hyperbaric chambers when breathing oxygen enriched air or regular air at deep depths. 

Pts with COPD become desensitized high CO2 levels in their blood and there for they may not rely on increased CO2 levels to stimulate increased respirations. They begin to rely on their hypoxic drive to stimulate increased respirations, but I would never with hold O2 from a pt who needs it with the worry that they would all of a sudden stop breathing.


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## COmedic17 (Mar 14, 2015)

captaindepth said:


> Pts with COPD become desensitized high CO2 levels in their blood and there for they may not rely on increased CO2 levels to stimulate increased respirations. They begin to rely on their hypoxic drive to stimulate increased respirations, but I would never with hold O2 from a pt who needs it with the worry that they would all of a sudden stop breathing.




You do realize you said exactly what I said, right?


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## luke_31 (Mar 14, 2015)

Easiest thing is to give oxygen to any patient who needs it. If the patient stops breathing then use a bvm until they start breathing again.


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## captaindepth (Mar 14, 2015)

COmedic17 said:


> You do realize you said exactly what I said, right?


 yes I do realize we said similar things but I was mostly commenting on oxygen toxicity and that its not involved in this particular discussion.


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## RedAirplane (Mar 15, 2015)

DesertEMT66 said:


> The one that I made bold I hear all the time from nurses, medics, and EMTs. I hate when providers say it. I'm surprised with how many medics actually use that as a scale to give meds "they have a radial pulse so we can give nitro"



It is true that the carotid pulse will be the last to vanish with decreasing blood pressure, right? So, even if not 90mmHg, wouldn't a radial pulse mean that the blood pressure is above some threshold?


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## Akulahawk (Mar 15, 2015)

Ishan said:


> It is true that the carotid pulse will be the last to vanish with decreasing blood pressure, right? So, even if not 90mmHg, *wouldn't a radial pulse mean that the blood pressure is above some threshold?*


Having a radial pulse means that you have a radial pulse. That's all it really means. It doesn't mean that someone has an SBP over some specific number. Yesterday I (while doing an EMS ride along) had a patient that had a BP of 82/58. I'd call his radial pulse a 2+ in terms of quality... because it was. He probably could have gone as low as having an SBP of 70 or so before losing the radial pulse. Everyone is different so while the SBP may be low, if there's a radial pulse, chances are the patient is still perfusing most organs.


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## jrm818 (Mar 15, 2015)

Akulahawk said:


> Having a radial pulse means that you have a radial pulse. That's all it really means. It doesn't mean that someone has an SBP over some specific number. Yesterday I (while doing an EMS ride along) had a patient that had a BP of 82/58. I'd call his radial pulse a 2+ in terms of quality... because it was. He probably could have gone as low as having an SBP of 70 or so before losing the radial pulse. Everyone is different so while the SBP may be low, if there's a radial pulse, chances are the patient is still perfusing most organs.



And really, the most important organ (or at least the most intolerant of ischemia, even for very short periods) is the one inside your skull.  If they're awake, they're definitely perfusing their brain.


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## Brandon O (Mar 15, 2015)

Ishan said:


> It is true that the carotid pulse will be the last to vanish with decreasing blood pressure, right? So, even if not 90mmHg, wouldn't a radial pulse mean that the blood pressure is above some threshold?



Yes. It has some use as a qualitative measure. The military (last I heard anyway) uses it as a marker for fluid resuscitation, along with mental status. Just don't try to put a number on it.


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## Carlos Danger (Mar 15, 2015)

Hypoxic drive inhibition and oxygen toxicity are completely separate concepts.

Also, absorption atelectasis has nothing to do with surfactant production.


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## hogwiley (Mar 15, 2015)

The reasons people used to say not to put a NRB on someone with COPD is a different issue from oxygen toxicity. Oxygen toxicity is why you should generally use o2 sparingly in any situation unless its to reverse suspected hypoxia, and not just throw people on o2 for the hell of it. I dont know the exact pathophysiology of it but if I remember it has to do with oxygen free radicals causing cellular damage along with other unwanted effects. With COPD the issue is relatively high blood oxygen saturation levels wiping out a COPD patient's hypoxic drive, which is driven by low o2 levels rather than co2 levels.

As most people have said the whole hypoxic drive thing is no longer considered a reason to withhold o2 if a patient is truly hypoxic, but my understanding is that hypoxic drive is still real, its not some urban legend. It just is not something your likely to wipe out giving high flow o2 for a short time, and if by some chance they did stop breathing you can still bag them and if needed go with an advanced airway.


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## Brandon O (Mar 15, 2015)

It should make sense that oxygen toxicity is not relevant in a COPD exacerbation, because they're presumably hypoxemic and you're trying to overcome their shunt to make them normoxemic. If you're even capable of making them hyperoxic, uh... they're probably doing okay.


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## medicaltransient (Mar 15, 2015)

Hyperoxemia in copd is bad, thats what I hear


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## medicaltransient (Mar 15, 2015)

You just don't want hyperoxic oxemia or absorbativeisis atalecasisemia.


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## Akulahawk (Mar 16, 2015)

Oxygen toxicity is more of an issue in hyperbaric conditions... like diving or hyperbaric chambers where the partial pressure of oxygen exceeds 1 atmosphere. Hyperoxia is certainly possible even under normal atmospheric conditions. However, in the short run, it's only a problem in the very few patients that truly are on hypoxic drive. Most COPD patients aren't actually doing hypoxic drive, their respiratory drive is still triggered by CO2... just a higher amount of it than the rest of us require. 

In short, if  your COPD patient needs a higher percentage of oxygen to bring their SpO2 to their normal level, give it to them.


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## Av8or007 (Mar 16, 2015)

Brandon O said:


> It should make sense that oxygen toxicity is not relevant in a COPD exacerbation, because they're presumably hypoxemic and you're trying to overcome their shunt to make them normoxemic. If you're even capable of making them hyperoxic, uh... they're probably doing okay.




Shunt is oxygen unresponsive.

Oxygenation ≠ ventilation. COPD exacerbation induced resp failure s nearly always a Type II resp failure.

Hyperoxia also is extremely relevant, as several studies and trials have demonstrated.

Hyperoxia kills people. Period.

Use the minimum required FiO2 to maintain saturation in the target range. For COPD pts this is usually 88-92% or the goal SpO2 set by their doc.


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## Brandon O (Mar 16, 2015)

Av8or007 said:


> Shunt is oxygen unresponsive.
> 
> Oxygenation ≠ ventilation. COPD exacerbation induced resp failure s nearly always a Type II resp failure.
> 
> ...



I admit I'm puzzled that you'd say hypoxemia secondary to pulmonary shunting is completely unresponsive to increased FiO2. While non-ventilated portions of the respiratory tree are obviously unavailable regardless of what type of gas we blow at them, increased oxygen to the functioning portions can still be compensatory. Do you mean to say that you don't provide supplemental oxygen to (for instance) your pneumonia patients?

Otherwise I think we agree. My point was just that giving oxygen doesn't have to mean hyperoxygenating so long as you titrate to SpO2, and indeed for a patient with seriously compromised lung function you may wish you had that problem. It's clear that blind "high flow O2" is not a sound practice.


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## Carlos Danger (Mar 16, 2015)

Av8or007 said:


> Shunt is oxygen unresponsive.



This is a misleading statement.

A pulmonary segment without blood flow will not participate in gas exchange, but do you not think the fraction of perfused lung tissue can still benefit from an increased fio2?



Av8or007 said:


> Hyperoxia kills people. Period.



Not nearly the threat that hypoxemia is, though.


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## Brandon O (Mar 16, 2015)

Remi said:


> A pulmonary segment without blood flow will not participate in gas exchange, but do you not think the fraction of perfused lung tissue can still benefit from an increased fio2?



Remember that shunt is perfusion without ventilation, not the reverse; you're describing dead space. Just a mistype, I imagine, since you're otherwise speaking truths


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## Carlos Danger (Mar 16, 2015)

Brandon O said:


> Remember that shunt is perfusion without ventilation, not the reverse; you're describing dead space. Just a mistype, I imagine, since you're otherwise speaking truths



You are right. I'm on vacation and have been imbibing more than a little today. 

Point is that whatever area does not have a mismatch will benefit from a higher fio2.


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## Av8or007 (Mar 16, 2015)

> I admit I'm puzzled that you'd say hypoxemia secondary to pulmonary shunting is completely unresponsive to increased FiO2. While non-ventilated portions of the respiratory tree are obviously unavailable regardless of what type of gas we blow at them, increased oxygen to the functioning portions can still be compensatory. Do you mean to say that you don't provide supplemental oxygen to (for instance) your pneumonia patients?
> 
> Otherwise I think we agree. My point was just that giving oxygen doesn't have to mean hyperoxygenating so long as you titrate to SpO2, and indeed for a patient with seriously compromised lung function you may wish you had that problem. It's clear that blind "high flow O2" is not a sound practice.



Agree and very true, as long as SpO2 (or PaO2) are hypoxic. As soon as you get the SpO2 into the target range, then more oxygen will NOT help the PT and WILL cause significant harm. Give the oxygen, but titrate it. DO NOT GIVE NON TITRATED O2 to these patients - it kills them. 

But if you are not reaching the SpO2 target on >50-60 FiO2, then yes, this shunt is likely OXYGEN UNRESPONSIVE. Time for a strategy that addresses the cause of the problem or at least works on the ventilation side of things. E.g. BiPAP or CPAP, or in extreme cases, BVM with PEEP (titrated PRN).



> Not nearly the threat that hypoxemia is, though.



This is debatable. Absolutely use oxygen when indicated -> i.e. hypoxemia. BUT if the PT is normoxic, then more oxygen does not help and does harm - significantly. Titrate the oxygen.


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## Brandon O (Mar 16, 2015)

I think we agree. Especially on the point that if you're hitting high FiO2s and are not seeing a good response in saturation (everyone will probably have SOME response, but in some folks it's like turning on a table fan...), that is prima facie evidence of V/Q mismatch -- usually shunt.

Some people seem to have the idea that just ventilating harder, better, faster, stronger is the answer, which is deeply flawed. Normal lungs should be able to oxygenate at high FiO2 with hardly any minute volume. Crank it up, of course, but think about PEEP and think about other avenues.


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## voodoomedic90 (Mar 18, 2015)

In a EMS setting this issue is irrelevant, as what you are referring to is something that contraindicated for long term care - 3-4 days and more. You are asking about the chemoreceptors. A person with a healthy respiratory drive breath in O2 when the chemoreceptors detect too much CO2 in the blood. This triggers to body to breath in Oxygen, facilitate diffusion of O2 onto the blood and CO2 being exhaled. With someone where the chemoreceptors are not working as they are suppose to, they default to a "back up system." This is called hypoxic drive. Instead of the chemoreceptors detecting level of CO2 to trigger breathing, but the level of O2. If you have a pt that has COPD and they are constantly on high flow O2 the body may detect this Oxygen rich environment and may not breath. I think that is how the etiology works.


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## ThadeusJ (Mar 19, 2015)

Voodoo...that's the theory but it has been disproven for so long the argument is tedious.  Patients don't just "stop breathing" like they're sitting there with no chest movement.  The persistence of this myth (as described above) has led to people with chronic respiratory diseases to remain hypoxic unnecessarily and to their detriment. One _can_ treat a COPD'er with very high levels of oxygen and not have any issues whatsoever.  If the concern is high blood oxygen levels, you titrate the delivered oxygen level to your desired outcome.  

It very relevant because of the long standing belief has led to very poorly written protocols that are a disservice to the patient.  These protocols are perpetuated (if not derived) within the hospital system, so the mistreatment continues along the patient care continuum.  I call it the "Flat Earth" method of medicine.


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