??? - usmlestudy1

[ArchivalUser]

what is perfusion limited and diffusion limited situation?

[ArchivalUser]

These are annoying terms that make people dislike respiratory physiology.

I like to keep things simple, so here's how I think about it clinically:

Only 3 things really matter in respiratory physio-

1) Gas in alveoli
2) Blood in pulmonary capillaries
3) The space in between (endothelial cells, alveolar wall, interstitium)

Perfusion vs diffusion limited basically depends on how fast the gas can cross from #1 into #2 and vice versa.

For the gasses we care about -oxygen and CO2 - they move very fast across the membrane. For these guys, diffusion isn't an issue at all! If you can get blood to the capillaries, these gasses will exchange quickly. Of course, you have to get the blood there.... so we say these gasses are "perfusion limited" because that's the only thing potentially stopping them. Pathologically, this would be something like a pulmonary embolus.

For diffusion limited, these gasses don't really like to cross membranes. You can pump a river of blood through those capillaries, but the gas is going to take its sweet time moving across and the same amount is going to cross regardless. Carbon monoxide is a typical example of this.

So lets talk pathology and how these terms might be tested. I doubt anyone will ask a direct question about diffusion vs perfusion limited; the concepts are what's important.

So what would happen to oxygen, a perfusion-dependent gas, if I increased the interstitial space between the capillaries and alveoli? This is actually what happens in ARDS as inflammatory cells and fluid extravasate into the pulmonary iterstitium and ultimately the alveoli themselves. This also happens in your chronic interstitial lung diseases, but lets focus on ARDS right now because it's a high yield test topic.

In ARDS, you have all this edema that makes it harder for oxygen to move from the alveoli to the blood. The result is that you've got deoxygenated Hgb just passing through the lungs before oxygen has a change to get to it. In this case, oxygen has become diffusion limited and the patient has a real problem. These patients will have a very high A-a gradient, again because they can get O2 to the blood before Hgb passes by.

For the CK folks, this mechanism in ARDS guides management. We put these people on mechanical ventilation so we can maximize their FiO2 as well as give them additional positive pressure to keep alveoli from collapsing. We give them diuretics like furosemide to reduce the edema in the lung interstitium and improve gas exchange (this would actually be a fair step 1 question since it really gets at the mechanism for ARDS).