Oxygen induced hypercapnia

[chromuffin]

Can anyone explain the mechanism? UWorld QID 12141 is saying "Hyperoxia reverses pulmonary vasoconstriction, increasing physiologic dead space, as poorly ventilated alveoli are perfused."

This makes no sense to me. How can hyperoxia increase physiologic dead space? I would think excess O2 would make poorly ventilated alveoli become well ventilated. And with that, CO2 leveled would decrease.

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[mw18]

I think it's getting at the fact that, in the lung, poor oxygenation causes vasoconstriction. That way you consolidate the blood to where the oxygen is by not sending it to poorly oxygenated areas. But if you provide some oxygen to every nook and cranny, the vasoconstriction and consolidation is lost and you send blood to places that have some oxygen (due to the hyperoxia), but not enough to ventilate effectively. This is mostly just a guess, though. I can definitely see the motivation for your line of thinking.

 

[FindMeOnTheLinks]

I think it's getting at the fact that, in the lung, poor oxygenation causes vasoconstriction. That way you consolidate the blood to where the oxygen is by not sending it to poorly oxygenated areas. But if you provide some oxygen to every nook and cranny, the vasoconstriction and consolidation is lost and you send blood to places that have some oxygen (due to the hyperoxia), but not enough to ventilate effectively. This is mostly just a guess, though. I can definitely see the motivation for your line of thinking.

This is correct

 

[chromuffin]

This is correct

Ok so let me try and make sense of this.
I get that giving O2 would theoretically increase the PaO2 to allow for blood flow through all alveoli again. And so, since they have damaged alveoli, those malfunctioning alveoli couldn't allow for diffusion (since emphysema causes a decreased DLCO). This would then prevent CO2 diffusion out of those capillaries, effectively causing hypercapnia.

However, here is my question. Emphysema is essentially a V/Q mismatch, right? And per B&B, V/Q mismatch has normal PaCO2. So.. is this true but a caveat being that 100% O2 will induce hypercapnia in emphysema due to the decreased DLCO?

 

[TheOther]

Ok so let me try and make sense of this.
I get that giving O2 would theoretically increase the PaO2 to allow for blood flow through all alveoli again. And so, since they have damaged alveoli, those malfunctioning alveoli couldn't allow for diffusion (since emphysema causes a decreased DLCO). This would then prevent CO2 diffusion out of those capillaries, effectively causing hypercapnia.

However, here is my question. Emphysema is essentially a V/Q mismatch, right? And per B&B, V/Q mismatch has normal PaCO2. So.. is this true but a caveat being that 100% O2 will induce hypercapnia in emphysema due to the decreased DLCO?

I actually just revisited the B&B pulm videos to find the exact spot that might help clear things up for you.

Firstly, yes, emphysema is a V/Q mismatch. B&B says that PaCO2 in V/Q mismatch is "often normal" because of the increase in respiratory rate. The patient in this UW question has COPD that has progressed to the point that her RR can't compensate for her diffusion deficit (decreased SpO2 due to decreased PaO2/increased PCO2). With the administration of 100% O2, pulmonary vasoconstriction becomes reversed while the damaged alveoli still can't diffuse, which is increased dead space.

Secondly, if you look at B&B's Ventilation/Perfusion slide at 16:50, he shows the equation for why hypercapnea results due to the increased dead space. Add in the Haldane effect and voila.

 

[chromuffin]

I actually just revisited the B&B pulm videos to find the exact spot that might help clear things up for you.

Firstly, yes, emphysema is a V/Q mismatch. B&B says that PaCO2 in V/Q mismatch is "often normal" because of the increase in respiratory rate. The patient in this UW question has COPD that has progressed to the point that her RR can't compensate for her diffusion deficit (decreased SpO2 due to decreased PaO2/increased PCO2). With the administration of 100% O2, pulmonary vasoconstriction becomes reversed while the damaged alveoli still can't diffuse, which is increased dead space.

Secondly, if you look at B&B's Ventilation/Perfusion slide at 16:50, he shows the equation for why hypercapnea results due to the increased dead space. Add in the Haldane effect and voila.

Ok, so I think I can understand If I know how this is a case of increased dead space. Wouldn't this be dead space (from the vasoconstriction) becoming a shunt, so a DECREASE in dead space? Not an increase in dead space?? Ahhhhh. I'm assuming that the 100% O2 will increase PaO2 enough to prevent vasoconstriction in some of the constricted vessels but not all? But I don't see how increasing O2 causes increased dead space when COPD is a ventilation problem, not a perfusion problem.

 

[sahanaparthasarathy]

Three mechanism explains Oxygen induced Hypercapnia:

1.v/Q mismatch: COPD is a obstructive lung disease, there will be hypoxia induced vasoconstriction in the lung. Upon oxygen administration now these vessels are vasodilated which results in increased blood flow, but the blood flow to this dilated vessels are coming from previously normally perfused area. Therefore resulting in decreased bloodflow and V/Q goes toward infinity resulting in INCREASED PHYSIOLOGICAL DEAD SPACE.

2.HALDANE effect: increased Pao2 decreases HB affinity for co2 resulting is co2 dissociation from HB which increases blood Pco2 level.

3.Hypoventillation effect: High flow o2 causes decreased peripheral chemoreceptor stimulation resulting in hpoventillation and retention of co2.

 

[Ramaq Chishti]

Ok, so I think I can understand If I know how this is a case of increased dead space. Wouldn't this be dead space (from the vasoconstriction) becoming a shunt, so a DECREASE in dead space? Not an increase in dead space?? Ahhhhh. I'm assuming that the 100% O2 will increase PaO2 enough to prevent vasoconstriction in some of the constricted vessels but not all? But I don't see how increasing O2 causes increased dead space when COPD is a ventilation problem, not a perfusion problem.

Hi, did you get an understanding of this question then? The thread is amazing.

 

[chromuffin]

Hi, did you get an understanding of this question then? The thread is amazing.

It’s been awhile since I’ve reviewed this. An increase in oxygen will vasodilate blood vessels, allowing for more blood flow in the lungs. This increased blood flow will perfuse the areas of the lungs that are bad (I.e. diseased lung). It is essential to know that COPDers have a problem with getting CO2 out. Thus, the increases blood flow (due to the increased oxygen) will allow for CO2 diffusion into the bad alveoli. This CO2 will essentially get stuck in the bad alveoli as you can’t get the CO2 out. Thus, you induce hypercapnia because the total level of CO2 rises in the body due to CO2 entrapment in bad alveoli.

 

[Mad Jack]

Ok, so I think I can understand If I know how this is a case of increased dead space. Wouldn't this be dead space (from the vasoconstriction) becoming a shunt, so a DECREASE in dead space? Not an increase in dead space?? Ahhhhh. I'm assuming that the 100% O2 will increase PaO2 enough to prevent vasoconstriction in some of the constricted vessels but not all? But I don't see how increasing O2 causes increased dead space when COPD is a ventilation problem, not a perfusion problem.

COPD is a ventilation problem that is caused by loss of functional alveoli, increased bronchial obstruction, and a decrease in pulmonary elasticity. Normal atmospheric oxygen is 20.9%, so when you give oxygen that is far beyond what the human body would normally see, it results in maximum dilation throughout the pulmonary vasculature. Under normal circumstances, highly damaged areas of the lung will have obliterated alveoli and high levels of air trapping that result in the oxygen in these areas being depleted, with a resultant decrease in perfusion due to vascular constriction. With high levels of oxygen, these areas end up having supraphysiologic O2 content due to diffusion that results in them being perused despite not being ventilated well, creating a ventilation-perfusion mismatch.

There is also the haldane effect, in which oxygen displaces CO2 from hemoglobin without an actual increase in total blood CO2, it is just more measurable on ABG due to the afformentioned displacement.

 

[Ramaq Chishti]

It’s been awhile since I’ve reviewed this. An increase in oxygen will vasodilate blood vessels, allowing for more blood flow in the lungs. This increased blood flow will perfuse the areas of the lungs that are bad (I.e. diseased lung). It is essential to know that COPDers have a problem with getting CO2 out. Thus, the increases blood flow (due to the increased oxygen) will allow for CO2 diffusion into the bad alveoli. This CO2 will essentially get stuck in the bad alveoli as you can’t get the CO2 out. Thus, you induce hypercapnia because the total level of CO2 rises in the body due to CO2 entrapment in bad alveoli.

Thank you! It makes sense.