USMLE Perfusion limited, A-a gradient is not zero

[mgimou]

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FA17 says that normal A-a gradient for oxygen is 10-15 mm Hg. Doesn't this mean that normally oxygen is diffusion limited?

I am a little bit confused here, as multiple sources (including FA17) say that oxygen normally (in a healthy person at rest) is perfusion limited.

If oxygen is really perfusion limited, shouldn't A-a gradient be zero?

Any ideas highly appreciated. Thanks in advance.

 

[ERDOC555]

One potential reason for a small gradient could be the venous mixing when the bronchial veins empty into the left atrium, bypassing pulmonary oxygenation, and thus leading to less oxygenated blood.

 

[mgimou]

Thank you, Dermpire. This does make sense. But this would, IMHO, justify A-a gradient not only for oxygen, but also for any other gas.

But I really like your idea, thanks again.

Can there be any "oxygen-specific" causes?

One potential reason for a small gradient could be the venous mixing when the bronchial veins empty into the left atrium, bypassing pulmonary oxygenation, and thus leading to less oxygenated blood.

 

[Surgeria]

as long as I know Oxygen compared to Carbon monoxide is diffusion limited. For example CO2 can pass through the thick alveolar walls in pulmonary fibrosis, but O2 cannot. If you are having fibrotic disease and inspire normal room air and get 150 mmHg of O2 in the alveoli, most probably not to much will pass to the blood because of fibrosis, so gradient will be way more higher than 10-15. On the other hand CO2 will diffuse from the blood to the alveoli leaving slightly higher blood CO2 (maybe 45), but most of it will diffuse out of the blood and be blown in the air. I learned this from B&B and Uworld. So it means that CO2 is more perfussion limited (you just need to drag some CO2 to the alveolar vessels, and thats it, you will blow it out) and O2 is more diffusion limited? I guess CO2 is just way more lipid soluble? This is the difference?

 

[mgimou]

Thank you, Surgeria, for your input. I'm not I sure I totally understand what you mean though. Especially the part about oxygen being more diffusion limited than carbon monoxide. Did you mean carbon dioxide?

as long as I know Oxygen compared to Carbon monoxide is diffusion limited. For example CO2 can pass through the thick alveolar walls in pulmonary fibrosis, but O2 cannot. If you are having fibrotic disease and inspire normal room air and get 150 mmHg of O2 in the alveoli, most probably not to much will pass to the blood because of fibrosis, so gradient will be way more higher than 10-15. On the other hand CO2 will diffuse from the blood to the alveoli leaving slightly higher blood CO2 (maybe 45), but most of it will diffuse out of the blood and be blown in the air. I learned this from B&B and Uworld. So it means that CO2 is more perfussion limited (you just need to drag some CO2 to the alveolar vessels, and thats it, you will blow it out) and O2 is more diffusion limited? I guess CO2 is just way more lipid soluble? This is the difference?

 

[Surgeria]

Thank you, Surgeria, for your input. I'm not I sure I totally understand what you mean though. Especially the part about oxygen being more diffusion limited than carbon monoxide. Did you mean carbon dioxide?

right, carbon dioxide. CO2 diffuses more easily through the alveolar wall compared to O2. So CO2 is not diffusion limited, it means that in states of "bad" diffusion like in pulmonary fibrosis, you will not retain CO2 because it is very lipid soluble and passes even through fibrotic alveolar walls. I hope you got the idea. In same scenario of pulmonary fibrosis, O2 will not pass rapidly so you will develop A-a Gradient (more o2 in alveoli, and less in the blood)

 

[mgimou]

I see what you are saying, and thank you for the nice summary. I've been wondering why O2 in a healthy person at rest is considered perfusion limited despite the fact that normal A-a gradient for O2 is not zero.

Dermpire suggested that it might be because of some venous blood bypassing oxygenation. This blood dilutes oxygenated blood in the left atrium, and this leads to O2 partial pressure in arterial blood less than O2 partial pressure in the alveoli. This is seems like a valid explanation to me, but I am open to other alternative reasoning. I would greatly appreciate any other possible explanations.

Thank you.

right, carbon dioxide. CO2 diffuses more easily through the alveolar wall compared to O2. So CO2 is not diffusion limited, it means that in states of "bad" diffusion like in pulmonary fibrosis, you will not retain CO2 because it is very lipid soluble and passes even through fibrotic alveolar walls. I hope you got the idea. In same scenario of pulmonary fibrosis, O2 will not pass rapidly so you will develop A-a Gradient (more o2 in alveoli, and less in the blood)

 

[Fewa Fibroblast]

Normally oxygen is limited by the perfusion of the lungs as oxygen equillibrates early (after travelling 1/3rd of capillary length). Ideally A-a gradient should be 0 but A-a gradent of about 5 is created as
a)the ventilation perfusion matching is not perfect/ideal(also increases with age as it progressively becomes less ideal).(nothing is ideal)
b)Presence of normal anatomical shunts
But in emphysema or fibrosis oxygen is limited by diffusion and A-a gradient rises further.

CO2 can diffuse in normal as well as fibrosed lungs so it is most of the time perfusion limited.
CO is always diffusion limited as it doesnot equilibrate even at the end of cappilaries.
Hope it helps.