Deadspace as a CO2 problem

[OrbitalOverload]

Hey guys,

Can someone help me understand deadspace conceptually. I understand the concept of anatomic and physiologic deadspace - that is that the airways without alveoli constitute anatomical deadspace and that damaged alveoli or underperfused alveoli represent physiologic deadspace.

What I don't get is how deadspace can be seen primarily as a CO2 problem without a necessary drop in PaO2. To reiterate, I was taught the shunt is primarily a PaO2 problem, (which makes sense - if less blood sees alveolus, less O2 diffusion will occur since O2 exchange is flow-limited, but CO2 can be compensated for through hyperventilation).

I don't understand how PaO2 can remain normal in deadspace with abnormal PaCO2. If part of the lung is not being perfused, than blood is being forced through other areas in the lung that constitute the alveolar ventilation area, right? Is this how PaO2 can be maintained in deadspace? Well if this is true, why can't CO2 similarly diffuse and create a situation where there is no increase in PaCO2 and no decrease in PaO2.

Please help!!!!

Thank you

Orbital

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[Hernandez]

Vast over simplification for explanation purposes.....it takes more volume of capillary to alveoli contact to remove co2 than it does for oxygen to uptake oxygen as hemoglobin makes oxygen uptake a more active process as there is not intr-alveoli co2 binder.

 

[Mad Jack]

Oxygen takes longer to cross the AC membrane, but once it crosses, hemoglobin actively grabs it, allowing a smaller amount of space to take up a much larger amount of oxygen. CO2, however, crosses the membrane quickly, but requires a much higher rate of exchange due to the largely passive nature of CO2 transport (yeah, some of it is on hemoglobin, but it's not nearly as efficient as oxygen transport for various reasons). I'm really tired, and it's actually kind of a difficult topic, but this concept is why you end up with PEEP largely effecting oxygenation, while breaths per minute largely affects ventilation (until you drop below a certain minimum threshold).

 

[HuskyMD Emeritus]

Hey guys,

Can someone help me understand deadspace conceptually. I understand the concept of anatomic and physiologic deadspace - that is that the airways without alveoli constitute anatomical deadspace and that damaged alveoli or underperfused alveoli represent physiologic deadspace.

What I don't get is how deadspace can be seen primarily as a CO2 problem without a necessary drop in PaO2. To reiterate, I was taught the shunt is primarily a PaO2 problem, (which makes sense - if less blood sees alveolus, less O2 diffusion will occur since O2 exchange is flow-limited, but CO2 can be compensated for through hyperventilation).

I don't understand how PaO2 can remain normal in deadspace with abnormal PaCO2. If part of the lung is not being perfused, than blood is being forced through other areas in the lung that constitute the alveolar ventilation area, right? Is this how PaO2 can be maintained in deadspace? Well if this is true, why can't CO2 similarly diffuse and create a situation where there is no increase in PaCO2 and no decrease in PaO2.

Please help!!!!

Thank you

Orbital

VD/VT, V/Q mismatch and shunt all cause hypoxemia, none of them are specifically a PaO2 or PaCO2 problem.
High VD/VT will result in low PaO2.

 

[OrbitalOverload]

Thanks all.

My understanding now is;

The strong Hb-O2 interaction allows O2 to be saturated in deadspace because once blood sees ventilated alveolus, O2 saturation takes place unless diffusion is impaired. Conversely, while CO2 is more soluble, it effectively takes longer to unload it into the alveolus, and this necessitates hyperventilation to compensate in deadspace. In shunt, hyperventilation can compensate to normalize PCO2, but since less blood is seeing alveoli, 100% o2 is needed.

Not so intuitive but I think I get it. Would someone mind confirming that my rationale make sense?