COPD and 100% oxygen

[MudPhud20XX]

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Hi all, so I think I heard this from Goljan audio. Didn't he say that you never give 100% oxygen to COPD pts? Can anyone explain this? Is this b/c the peripheral chemoreceptor responds to PO2, whereas the central chemoreceptor doesn't? Many thanks in advance.

 

[aspiringmd1015]

central receptor desensitizes, now you only have your peripheral receptor in charge of your ventilation, if you correct the patients pa02, he'll lose all resp drive, become apneic, and the dudes gone

 

[MudPhud20XX]

got it, so why does the central chemoreceptor get desensitized in COPD pts?

 

[aspiringmd1015]

persistently high c02

 

[Cardiochick]

Hi all, so I think I heard this from Goljan audio. Didn't he say that you never give 100% oxygen to COPD pts? Can anyone explain this? Is this b/c the peripheral chemoreceptor responds to PO2, whereas the central chemoreceptor doesn't? Many thanks in advance.

In COPD the brain has adapted to the low paO2!giving high concentration O2(ie: more than 28%) there will be suppression of the brain receptors and further hypoxemia occurs!

 

[Jabbed]

The concept that's being discussed is referred to as "hypoxic drive".

 

[pd1112]

In COPD the brain has adapted to the low paO2!giving high concentration O2(ie: more than 28%) there will be suppression of the brain receptors and further hypoxemia occurs!

Be careful, this is not exactly accurate. The low PaO2 is accompanied by a rise in PCO2, which is how the central chemoreceptors become desensitized, not specifically the low PaO2. I say be careful because all practice questions I've seen involving this topic have both choices as possible answers.

Interestingly, the more recent understanding is that the loss of hypoxic drive is not the most important mechanism for acute worsening of hypercapnia & hypoxemia when 100% O2 is given in acute COPD exacerbations. Too much O2 causes shifting of the CO2-Hgb dissociation curve to the right (Haldane effect), so more CO2 dissolves in the blood. More importantly, supplemental O2 removes reflex hypoxic pulmonary vasoconstriction in poorly ventilated areas, which causes a large increase in intrapulmonary shunting & worsening of the V/Q mismatch.

I don't know how relevant those two mechanisms are to Step 1, since I haven't come across them in any review resources, but it might be good to have in your back pocket in case you get a relevant question but don't see a choice related to hypoxic drive.

 

[Cardiochick]

Be careful, this is not exactly accurate. The low PaO2 is accompanied by a rise in PCO2, which is how the central chemoreceptors become desensitized, not specifically the low PaO2. I say be careful because all practice questions I've seen involving this topic have both choices as possible answers.

Interestingly, the more recent understanding is that the loss of hypoxic drive is not the most important mechanism for acute worsening of hypercapnia & hypoxemia when 100% O2 is given in acute COPD exacerbations. Too much O2 causes shifting of the CO2-Hgb dissociation curve to the right (Haldane effect), so more CO2 dissolves in the blood. More importantly, supplemental O2 removes reflex hypoxic pulmonary vasoconstriction in poorly ventilated areas, which causes a large increase in intrapulmonary shunting & worsening of the V/Q mismatch.

I don't know how relevant those two mechanisms are to Step 1, since I haven't come across them in any review resources, but it might be good to have in your back pocket in case you get a relevant question but don't see a choice related to hypoxic drive.

Thank you for the input!
Will definetly go into more details about it! 🙂

 

[Jabbed]

Be careful, this is not exactly accurate. The low PaO2 is accompanied by a rise in PCO2, which is how the central chemoreceptors become desensitized, not specifically the low PaO2. I say be careful because all practice questions I've seen involving this topic have both choices as possible answers.

Interestingly, the more recent understanding is that the loss of hypoxic drive is not the most important mechanism for acute worsening of hypercapnia & hypoxemia when 100% O2 is given in acute COPD exacerbations. Too much O2 causes shifting of the CO2-Hgb dissociation curve to the right (Haldane effect), so more CO2 dissolves in the blood. More importantly, supplemental O2 removes reflex hypoxic pulmonary vasoconstriction in poorly ventilated areas, which causes a large increase in intrapulmonary shunting & worsening of the V/Q mismatch.

I don't know how relevant those two mechanisms are to Step 1, since I haven't come across them in any review resources, but it might be good to have in your back pocket in case you get a relevant question but don't see a choice related to hypoxic drive.

You're right in that loss of hypoxic drive is no longer considered the main cause of decompensation in COPDers, although I think that the party line is still on "multifactorial causes" that are patient-specific. For test-taking purposes though there are still questions where the apparent answer assumes that the loss of hypoxic drive is the most important contributor in a particular scenario. The Haldane effect causes a leftward shift of the ODC in the lungs-- I'm not sure if it's physiologically plausible for peripheral oxygenation to be high enough such that the Haldane effect would preclude removal of CO2 from tissue.

 

[pd1112]

You're right in that loss of hypoxic drive is no longer considered the main cause of decompensation in COPDers, although I think that the party line is still on "multifactorial causes" that are patient-specific. For test-taking purposes though there are still questions where the apparent answer assumes that the loss of hypoxic drive is the most important contributor in a particular scenario. The Haldane effect causes a leftward shift of the ODC in the lungs-- I'm not sure if it's physiologically plausible for peripheral oxygenation to be high enough such that the Haldane effect would preclude removal of CO2 from tissue.

Yeah, that's essentially exactly what I said - loss of hypoxic drive is going to be the answer they're looking for probably every time. And yes, the Haldane Effect causes leftward shift of ODC, but I was talking about the CO2DC, which is shifted right because of the higher % of oxyhemoglobin in the presence of supplemental O2. With less CO2 bound to Hb, more dissolves in the blood whether you're in the lungs or peripheral tissues, resulting in a rise in PaCO2, i.e. the point of the conversation since hypercapnia is what we're trying to avoid and the reason giving 100% O2 is dangerous.

 

[Jabbed]

Yeah, that's essentially exactly what I said - loss of hypoxic drive is going to be the answer they're looking for probably every time. And yes, the Haldane Effect causes leftward shift of ODC, but I was talking about the CO2DC, which is shifted right because of the higher % of oxyhemoglobin in the presence of supplemental O2. With less CO2 bound to Hb, more dissolves in the blood whether you're in the lungs or peripheral tissues, resulting in a rise in PaCO2, i.e. the point of the conversation since hypercapnia is what we're trying to avoid and the reason giving 100% O2 is dangerous.

Ah my mistake, misread it.

 

[aspiringmd1015]

Be careful, this is not exactly accurate. The low PaO2 is accompanied by a rise in PCO2, which is how the central chemoreceptors become desensitized, not specifically the low PaO2. I say be careful because all practice questions I've seen involving this topic have both choices as possible answers.

Interestingly, the more recent understanding is that the loss of hypoxic drive is not the most important mechanism for acute worsening of hypercapnia & hypoxemia when 100% O2 is given in acute COPD exacerbations. Too much O2 causes shifting of the CO2-Hgb dissociation curve to the right (Haldane effect), so more CO2 dissolves in the blood. More importantly, supplemental O2 removes reflex hypoxic pulmonary vasoconstriction in poorly ventilated areas, which causes a large increase in intrapulmonary shunting & worsening of the V/Q mismatch.

I don't know how relevant those two mechanisms are to Step 1, since I haven't come across them in any review resources, but it might be good to have in your back pocket in case you get a relevant question but don't see a choice related to hypoxic drive.

the central chemoreceptors dont respond to pa02 though right? they only respond to H+ in the csf(co2)

 

[aspiringmd1015]

"More importantly, supplemental O2 removes reflex hypoxic pulmonary vasoconstriction in poorly ventilated areas, which causes a large increase in intrapulmonary shunting & worsening of the V/Q mismatch" now that is a sick concept, thanks.

 

[pd1112]

Ah my mistake, misread it.

No worries!

the central chemoreceptors dont respond to pa02 though right? they only respond to H+ in the csf(co2)

yessir

 

[aspiringmd1015]

yeah so even if i did see that as an answer choice, no one should be leaning towards that bc the receptor doesnt respond

 

[pd1112]

yeah so even if i did see that as an answer choice, no one should be leaning towards that bc the receptor doesnt respond

If it's asking about the central chemoreceptors, yes. If it's asking about peripheral, it'd be response to low PaO2 >>> response to high PCO2 or low pH.

 

[deleted357625]

#1 reason for becoming hypercapnic = mismatched ventilation/perfusion coupling vs. decreased binding affinity of Hb for CO2 & decreased minute ventilation
Hypercapnia can result from 2 things; an increase in CO2 production or a decrease in alveolar ventilation (most common) (if ventilation > perfusion = creates more "dead space")
COPD patients have relied on their hypoxic ventilatory/perfusion drive d/t their high sensitivity for PCO2 - once administered w/ high levels of O2, it can disrupt this adapted/homeostatic ventilation/perfusion drive leading the patient to become more hypercapnic.

 

[pd1112]

...wut