Why does hypoventilation not increase A-a gradient?

[Ven0m]

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I found this on another thread, but it didn't explain it well. So I started a new thread.

If V/Q is less than 1, then A-a gradient will increase.
e.g. pulmonary edema: fluid in alveoli prevents capillary blood from being 100% saturated, then that blood mixes with saturated blood from non-fluid filled alveoli, lowering PaO2.

But if I breathe really slowly, doesn't this also decrease PaO2?
Blood is being perfused at a normal rate, but ventilation has decreased, right? And since PAO2 is normal, but I'm just breathing so slow that I can't fully saturate all the blood that's being perfused, wouldnt this increase the A-a gradient and be considered a V/Q mismatch?

edit: nvm, i realized that with hypoventilation, PAO2 goes down, which causes PaO2 to follow, which maintains the A-a gradient. Silly me.

 

[aspiringmd1015]

just know why our PA02 is going down, its because of your PACa02 going up, ventilation effects PAc02, not PA02.

 

[Ven0m]

just know why our PA02 is going down, its because of your PACa02 going up, ventilation effects PAc02, not PA02.

Wait.. doesn't the O2 in the alveolus diffuse to blood as it comes? Doesn't this lower the PAO2 as well?

 

[aspiringmd1015]

no, the only things that can lower the PA02 are in the gas equation, Patmosphere, PAc02, and Fio2(normally being .21)

 

[Xzuk]

Goljan actually explains this pretty well. I'll try to explain it to the best of my memory (been a while since I did the step). So anyway A: alveolar PO2, a: arterial PO2. Essentially: any changes in ventilation should not change A-a gradient as oxygen should be able to freely diffuse across the alveoli and into the bloodstream (remember oxygen is perfusion limited under normal conditions meaning that PaO2 equilibrates before blood has cleared the alveoli) and thereby increase PaO2 to the same level as PAO2 (hence hypo or hyperventilation will not cause an increase in A-a gradient). Likewise, small changes in perfusion should not cause a change in A-a gradient as whatever oxygen is in the alveoli will equilibrate with arterial blood.

What then causes increased A-a gradient?
1. Diffusion problems: If oxygen is unable to leave alveoli what happens is that oxygen cannot enter blood resulting in a high PAO2 (closer to atmospheric PO2) and low PaO2 (closer to venous PO2): Pulmonary oedema is one such cause, ARDS is another, fibrosis is another
2. Serious perfusion problems (e.g. pulmonary embolism) resulting in dead-space. Since no blood is able to flow through the ventilated alveoli, it is "shunted" to other regions without being adequately oxygenated before returning to the pulmonary veins resulting in a step down in PaO2
3. Shunts within the heart (any cause of eisenmenger complex) resulting in R --> L shunt. Since deoxygenated blood enters arterial system --> PaO2 decreases (while PAO2 is actually unaffected).

I'm sure there are other causes but from my limited memory and understanding, I hope I have explained this a little better.

Cheers,
Matt

 

[Ven0m]

Thanks Matt! So if I held my breath for an extended period of time, the PAO2 wouldn't change, even though the blood is still actively perfusing and taking away oxygen? Like the blood equilibriates to 100 mm Hg, as the initial PAO2, then leaves and new, unsaturated blood comes. The PAO2 remains constant even if I hold my breath?

Or is PAO2 just referring to the initial fresh air that was able to be inspired?

e.g. If we graphed PAO2 on Y, with time breath held on X... Would the line be going down?

 

[Phloston]

I found this on another thread, but it didn't explain it well. So I started a new thread.

If V/Q is less than 1, then A-a gradient will increase.
e.g. pulmonary edema: fluid in alveoli prevents capillary blood from being 100% saturated, then that blood mixes with saturated blood from non-fluid filled alveoli, lowering PaO2.

But if I breathe really slowly, doesn't this also decrease PaO2?
Blood is being perfused at a normal rate, but ventilation has decreased, right? And since PAO2 is normal, but I'm just breathing so slow that I can't fully saturate all the blood that's being perfused, wouldnt this increase the A-a gradient and be considered a V/Q mismatch?

edit: nvm, i realized that with hypoventilation, PAO2 goes down, which causes PaO2 to follow, which maintains the A-a gradient. Silly me.

just know why our PA02 is going down, its because of your PACa02 going up, ventilation effects PAc02, not PA02.

Goljan actually explains this pretty well. I'll try to explain it to the best of my memory (been a while since I did the step). So anyway A: alveolar PO2, a: arterial PO2. Essentially: any changes in ventilation should not change A-a gradient as oxygen should be able to freely diffuse across the alveoli and into the bloodstream (remember oxygen is perfusion limited under normal conditions meaning that PaO2 equilibrates before blood has cleared the alveoli) and thereby increase PaO2 to the same level as PAO2 (hence hypo or hyperventilation will not cause an increase in A-a gradient). Likewise, small changes in perfusion should not cause a change in A-a gradient as whatever oxygen is in the alveoli will equilibrate with arterial blood.

What then causes increased A-a gradient?
1. Diffusion problems: If oxygen is unable to leave alveoli what happens is that oxygen cannot enter blood resulting in a high PAO2 (closer to atmospheric PO2) and low PaO2 (closer to venous PO2): Pulmonary oedema is one such cause, ARDS is another, fibrosis is another
2. Serious perfusion problems (e.g. pulmonary embolism) resulting in dead-space. Since no blood is able to flow through the ventilated alveoli, it is "shunted" to other regions without being adequately oxygenated before returning to the pulmonary veins resulting in a step down in PaO2
3. Shunts within the heart (any cause of eisenmenger complex) resulting in R --> L shunt. Since deoxygenated blood enters arterial system --> PaO2 decreases (while PAO2 is actually unaffected).

I'm sure there are other causes but from my limited memory and understanding, I hope I have explained this a little better.

Cheers,
Matt

By far the highest yield etiology for normal A-a gradient on Step 1 is opioid-induced hypoventilation.