If you take a COPD patient off O2 suddenly, why do they become hypoxemic?

[bomgd3]

Pulmonary Pathophysiology by West offers this explanation:

"Profound hypoxemia may ensue if the oxygen is discontinued. This is because even if the ventilation does return to its previous level, the patient may take many minutes to unload the large accumulation of CO2 in his or her tissues because of the large body stores of this gas."

Now this doesn't really make sense. So what if the body has a lot of CO2? As soon as ventilation ramps back up, O2 should hit its steady-state right?? I mean, what the heck does body stores of CO2 have to do with O2?

Thanks in advance! This West book really has me scratching my head at times.

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[cmage]

Actually CO2 does play a role in O2 levels. If you remember there are 5 causes of hypoxemia and one of them is hypoventilation. As patient is hypoventilating after taken off ventilator, assuming tidal volume remains constant, CO2 increases. Increase CO2 leads to a decrease in alveolar O2 (law of partial pressure), which leads to hypoxemia.

 

[armybound]

usually the big warning about O2 and COPDers is about STARTING them on O2.

I guess I don't understand the confusion about taking a COPDer off of O2.. they're on O2 because they're chronically hypoxemic. They don't ventilate well.. this is what's causing their debilitating illness in the first place.

the issue with CO2 is that COPDers are also chronically hypercarbic. Usually we respond swiftly to hypercarbic states, actually more quickly than we respond to hypoxemia. COPDers get used to having high CO2 and it becomes less of a drive for them to breathe.. they reset their set point to a more hypercarbic state. Hypoxemia becomes the main respiratory drive.

I would assume that removing their hypoxemia and their hypercarbia and then taking them off of O2 would leave them with a pretty poor respiratory drive altogether..

 

[bawer234]

They become hypoxemic b/c their aveoli are trashed....ventilation and oxygenation are two different concepts. Ventilation refers to (among other gases) CO2 while oxygenation refers to O2 exchange. COPDer's need supplemental O2 because room air is inadequate to provide an appropriate level of oxygenation. Take them off the O2 and they be hypoxemic.

Due to COPDers' emphysema, their airways begin to close off sooner (look up closing capacity) due to lack of cartilagenous support so respiration becomes more difficult (this is why they breath through "pursed lips", so they can provide "auto-PEEP" to prevent closure of the airways). If supplemental O2 is not maintained they may go into respiratory distress. Additionally, low O2 (as well as high CO2) promotes hypoxic pulmonary vasocontriction which increases pulm vascular resistance and over the long term this leads to pulm HTN and right heart failure. Suplemental O2 helps to limit pulm vasc resistance the symptoms that accompany hypoxemia...also its proven to prolong life in these pts.

Similar to what armyman said, there is a danger in placing these pts on too high a supplemental O2 value. Since their body becomes less responsive to PaCO2 levels, their chemoreceptors only really respond to PaO2 levels. If you give them too much O2 their respiratory drive is only driven by PaO2 (which should be more than adequate with excess supplemental O2) and neglects a steady climbing PaCO2 level which can lead to somnolence, coma, and death.

 

[mishaS]

Actually CO2 does play a role in O2 levels. If you remember there are 5 causes of hypoxemia and one of them is hypoventilation. As patient is hypoventilating after taken off ventilator, assuming tidal volume remains constant, CO2 increases. Increase CO2 leads to a decrease in alveolar O2 (law of partial pressure), which leads to hypoxemia.

Hmmm... So, correct me if I'm wrong, but the majority of respiratory rate is set by chemo receptors via blood pCO2 and pH correct? While adding pure O2 into the mix will greatly increase pO2 that is inspired, it really shouldn't have a large displacement effect on the small amount of atmospheric pCO2 that is inspired, since the vast majority of the CO2 at the level of the alveoli comes from our body, and stays because expiratory reserve and dead space is not being ventiliated, so shouldn't giving oxygen have a very small effect on pCO2? What I'm confused about here is that shouldn't someone with COPD be chronically hypercapnic, regardless of oxygen uptake, because of their inability to ventilate their alveoli?

the patient may take many minutes to unload the large accumulation of CO2 in his or her tissues because of the large body stores of this gas

Hmm.. maybe this means that if you discontinue oxygen, patient becomes hypoxic, there is more lactate formed, and blood pH drops. Because of chronic hypercapnia and respiratory acidosis, the kidneys have been secreting H+ out of the body, and pulling in more HCO3-, so blood HCO3- is disproportionately high. When the blood pH drops from lactate production, because of the high blood HCO3-, maybe there is a large shift in the carbonic anhydrase reaction, causing more severe hypercapnia. The higher level of CO2 causes more CO2 to bind to hemoglobin, lowering its affinity for O2, which is exacerbated by the lower pH, so less of the O2 that actually makes it to the alveoli gets bound to hemoglobin (assuming the binding curve moved far enough to the right). The higher pCO2 and lower pH should further increase ventilation, as should the lowered pO2 if it gets bad enough, but because COPD makes it hard to increase alveolar ventilation, even if the patient tries very hard, it might take a while to unload the high blood CO2, to allow hemoglobin to bind O2 more effectively.

That's my guess, I just pulled it out of my ass, because we never covered that, so I could be wrong.

 

[mishaS]

Similar to what armyman said, there is a danger in placing these pts on too high a supplemental O2 value. Since their body becomes less responsive to PaCO2 levels, their chemoreceptors only really respond to PaO2 levels. If you give them too much O2 their respiratory drive is only driven by PaO2 (which should be more than adequate with excess supplemental O2) and neglects a steady climbing PaCO2 level which can lead to somnolence, coma, and death.

Ok, this is the detail we haven't learned (yet). I didn't know that the body loses chemo-receptor response to pCO2. That pretty much made my whole convoluted guess moot 😀.

 

[ensuii]

They become hypoxemic b/c their aveoli are trashed....ventilation and oxygenation are two different concepts. Ventilation refers to (among other gases) CO2 while oxygenation refers to O2 exchange. COPDer's need supplemental O2 because room air is inadequate to provide an appropriate level of oxygenation. Take them off the O2 and they be hypoxemic.

Due to COPDers' emphysema, their airways begin to close off sooner (look up closing capacity) due to lack of cartilagenous support so respiration becomes more difficult (this is why they breath through "pursed lips", so they can provide "auto-PEEP" to prevent closure of the airways). If supplemental O2 is not maintained they may go into respiratory distress. Additionally, low O2 (as well as high CO2) promotes hypoxic pulmonary vasocontriction which increases pulm vascular resistance and over the long term this leads to pulm HTN and right heart failure. Suplemental O2 helps to limit pulm vasc resistance the symptoms that accompany hypoxemia...also its proven to prolong life in these pts.

Similar to what armyman said, there is a danger in placing these pts on too high a supplemental O2 value. Since their body becomes less responsive to PaCO2 levels, their chemoreceptors only really respond to PaO2 levels. If you give them too much O2 their respiratory drive is only driven by PaO2 (which should be more than adequate with excess supplemental O2) and neglects a steady climbing PaCO2 level which can lead to somnolence, coma, and death.

This is what I was taught in MS2 as well

 

[turkeyjerky]

Guys, please stop promoting the whole "don't give O2 to a COPDer" myth. That's a myth and a dangerous one. The whole "hypoxic drive theory" is (mostly) bullsh*t--there's a ton of info on this if you look for it, including on uptodate, published articles and editorials and blogposts across the interwebs. Here's a quick one: http://paramedicblog.wordpress.com/2009/11/19/hypoxic-drive-theory-myth-the-why-and-how/

 

[gravitywave]

Guys, please stop promoting the whole "don't give O2 to a COPDer" myth. That's a myth and a dangerous one. The whole "hypoxic drive theory" is (mostly) bullsh*t--there's a ton of info on this if you look for it, including on uptodate, published articles and editorials and blogposts across the interwebs. Here's a quick one: http://paramedicblog.wordpress.com/2009/11/19/hypoxic-drive-theory-myth-the-why-and-how/

👍 O2 and morphine live together in my head for this very reason. Never deprive a patient of either one who demonstrates a clinical need for them.

 

[Rendar5]

Guys, please stop promoting the whole "don't give O2 to a COPDer" myth. That's a myth and a dangerous one. The whole "hypoxic drive theory" is (mostly) bullsh*t--there's a ton of info on this if you look for it, including on uptodate, published articles and editorials and blogposts across the interwebs. Here's a quick one: http://paramedicblog.wordpress.com/2009/11/19/hypoxic-drive-theory-myth-the-why-and-how/

Perhaps the mechanism of why bringing a bad COPDer to 100% oxygen is bad is a myth, and personally I do agree with the fact that it's a myth. However, if you have enough experience, you will see that it's true that they will desaturate if you overoxygenate. Doesn't matter what the pathophysiology behind it actually is (it's actually explained as a V/Q mismatch by overoxygenating deadspace by those doctors who know better). The truth is that bad things do happen to COPDers at very high SpO2's in those with a poor baseline and I have personally seen it. Not to mention there's no reason to bring a COPDer to 100%SpO2 anyway. 92-93% is perfectly fine and doesn't appear to do any damage.

Bottom Line:
Bad COPD exacerbation, titrate oxygen. Both withholding oxygen and overoxygenating are bad. You have so many options ranging from NC with 2-4L, to Venti-Mask going up to 50% O2 to NRB that provides up to 70%. You can place them on BiPap which can titrate up to 100% FiO2. And the same when they're intubated. Titrating SpO2 levels to the low 90%'s is pretty easy.

 

[turkeyjerky]

Perhaps the mechanism of why bringing a bad COPDer to 100% oxygen is bad is a myth, and personally I do agree with the fact that it's a myth. However, if you have enough experience, you will see that it's true that they will desaturate if you overoxygenate. Doesn't matter what the pathophysiology behind it actually is (it's actually explained as a V/Q mismatch by overoxygenating deadspace by those doctors who know better). The truth is that bad things do happen to COPDers at very high SpO2's in those with a poor baseline and I have personally seen it. Not to mention there's no reason to bring a COPDer to 100%SpO2 anyway. 92-93% is perfectly fine and doesn't appear to do any damage.

Bottom Line:
Bad COPD exacerbation, titrate oxygen. Both withholding oxygen and overoxygenating are bad. You have so many options ranging from NC with 2-4L, to Venti-Mask going up to 50% O2 to NRB that provides up to 70%. You can place them on BiPap which can titrate up to 100% FiO2. And the same when they're intubated. Titrating SpO2 levels to the low 90%'s is pretty easy.

Agree completely, although I do believe it's important to understand the underlying patophysiology since it informs therapy if the patient develops worsening hypercapnia.

 

[CaptainSSO]

That all seems ridiculously complicated, and makes me want to crawl into a hole with my Xbox and ice cream.

 

[Rendar5]

That all seems ridiculously complicated, and makes me want to crawl into a hole with my Xbox and ice cream.

dead space gets 100% oxygen, perfusion to that area increases whereas it was very low before, now you're perfusing dead-space, i.e., non-ventilatory space. Thux V-Q mismatch.