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

Brandon O

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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.
 

medicaltransient

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

Akulahawk

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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.
 

Av8or007

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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.
 

Brandon O

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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.

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.
 

Carlos Danger

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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?

Hyperoxia kills people. Period.

Not nearly the threat that hypoxemia is, though.
 

Brandon O

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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 :)
 

Carlos Danger

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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.
 

Av8or007

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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.
 

Brandon O

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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.
 

voodoomedic90

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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.
 

ThadeusJ

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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.
 

PA12345

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The primary reason for this has to do with pathophysiology which is not extensively well discussed in EMT school, but it all stems from the chemoreceptors in a patient lungs. The chemoreceptors in healthy people rely on CO2 levels to moderate the respiratory rate. Ex. high CO2 = increased respiration. However, in patients with COPD they have chronically high levels of CO2 since they have an obstructive illness that prevents appropriate expiration. For this reason, their chemoreceptors rely on their O2 levels to moderate their breathing known as a "hypoxic drive". CO2 is an acidic gas and will cause acidosis of the blood in high concentrations but COPD patients have normal blood PH levels as their bodies will compensate.

It is not bad to put them on a cannula or a high flow O2 via a facemask as some of them are even on long-term O2 therapy but an NRB mask is capable of delivering an Fi02 content of >50%. What can happen is the risk that respiratory depression will begin in a COPD patient since their hypoxic drive will cause them to lower their respiratory rate in response to high concentration of O2. But respiratory depression is not really the primary concern. The real concern is that since their CO2 levels are chronically high, respiratory depression will further exacerbate their blood gas issue. It is only the beginning of a cascade that will further elevate their CO2 levels due to hypoventilation and create an acute bout of acidosis.
 

akflightmedic

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The primary reason for this has to do with pathophysiology which is not extensively well discussed in EMT school, but it all stems from the chemoreceptors in a patient lungs. The chemoreceptors in healthy people rely on CO2 levels to moderate the respiratory rate. Ex. high CO2 = increased respiration. However, in patients with COPD they have chronically high levels of CO2 since they have an obstructive illness that prevents appropriate expiration. For this reason, their chemoreceptors rely on their O2 levels to moderate their breathing known as a "hypoxic drive". CO2 is an acidic gas and will cause acidosis of the blood in high concentrations but COPD patients have normal blood PH levels as their bodies will compensate.

It is not bad to put them on a cannula or a high flow O2 via a facemask as some of them are even on long-term O2 therapy but an NRB mask is capable of delivering an Fi02 content of >50%. What can happen is the risk that respiratory depression will begin in a COPD patient since their hypoxic drive will cause them to lower their respiratory rate in response to high concentration of O2. But respiratory depression is not really the primary concern. The real concern is that since their CO2 levels are chronically high, respiratory depression will further exacerbate their blood gas issue. It is only the beginning of a cascade that will further elevate their CO2 levels due to hypoventilation and create an acute bout of acidosis.

WOW!! Almost an 8 YEAR revival....not the record here, but outstanding effort for a first time poster. 8 years....oofah.
 

johnrsemt

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I love the old EMS tale about pulse locations and BP. I have been as low as 62/24 and had strong radial pulses.
Just 3 weeks ago as a ED patient (getting staples in my head) I was 78/30 and the ED nurse said that the monitor was wrong because I had a radial pulse. Doctor wanted to push Dopamine..... I told her to go get the Attending and look at my previous admit VS
 

DrParasite

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I have questions...
I love the old EMS tale about pulse locations and BP. I have been as low as 62/24 and had strong radial pulses.
that's impressive.... isn't checking for radial pulses still used in the START triage algorithm to differenciate red vs yellow?
Just 3 weeks ago as a ED patient (getting staples in my head) I was 78/30 and the ED nurse said that the monitor was wrong because I had a radial pulse.
ok, got to ask... what did you go to end up going to the ER to get staples?

Also, aren't nurses taught to treat the patient not the monitor?
Doctor wanted to push Dopamine..... I told her to go get the Attending and look at my previous admit VS
Dopamine is the first line treatment for hypotension? isn't a fluid challenge the first response, as it has less side effects than a vasopressor?

Not that you needed it anyway, but just as a general practice
 
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