osli

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Just missed a UWorld question on this, which was asking where the lowest PVR would be on a graph of lung volumes vs. time.

Their "correct" answer was at the point where FRC was labeled. Their explanation was that this was on the steepest part of the compliance curve??

I chose the point where maximum inspiration was labeled. The explanation said this was incorrect because the air-filled alveoli exerted a collapsing pressure on the vasculature, increasing resistance?

Buy would not air forcing alveoli to expand and vasculature to collapse only be the case if air was actively pumped into the lung under pressure? In normal inspiration, the alveoli are expanded because the lung parenchyma is being actively stretched by thoracic movement. i.e., the expanding alveoli draw in air, instead of the air coming in forcing alveoli to expand. And if the alveoli are being stretched via the parenchyma and not the air pressure inside, then there is tension which pulls on everything embedded in the parenchyma, including vasculature. Shouldn't that increase size and decrease resistance, thus yielding the lowest PVR at maximal inspiration?

In fact, isn't the reason why COPDers breath at an increased FRC and have expanded chests is because by keeping the lung maximally expanded the parenchymal tension pulls on the airways and helps keep them expanded? I can't see why what keeps airways expanded would collapse vasculature.

Anyone have any insight into this? Am I completely crazy? Since the average on this question was only 16%, then either the question is wrong or this isn't something covered well in schools and review books.
 

DwyaneWade

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Just missed a UWorld question on this, which was asking where the lowest PVR would be on a graph of lung volumes vs. time.

Their "correct" answer was at the point where FRC was labeled. Their explanation was that this was on the steepest part of the compliance curve??

I chose the point where maximum inspiration was labeled. The explanation said this was incorrect because the air-filled alveoli exerted a collapsing pressure on the vasculature, increasing resistance?

Buy would not air forcing alveoli to expand and vasculature to collapse only be the case if air was actively pumped into the lung under pressure? In normal inspiration, the alveoli are expanded because the lung parenchyma is being actively stretched by thoracic movement. i.e., the expanding alveoli draw in air, instead of the air coming in forcing alveoli to expand. And if the alveoli are being stretched via the parenchyma and not the air pressure inside, then there is tension which pulls on everything embedded in the parenchyma, including vasculature. Shouldn't that increase size and decrease resistance, thus yielding the lowest PVR at maximal inspiration?

In fact, isn't the reason why COPDers breath at an increased FRC and have expanded chests is because by keeping the lung maximally expanded the parenchymal tension pulls on the airways and helps keep them expanded? I can't see why what keeps airways expanded would collapse vasculature.

Anyone have any insight into this? Am I completely crazy? Since the average on this question was only 16%, then either the question is wrong or this isn't something covered well in schools and review books.
From what I remember that explanation is correct.

The PVR is at a minimum at the FRC because there are two vessels you need to be concerned about: 1) the alveolar vessels (i.e. capillaries) and 2) the extraalveolar vessels (arterioles). In order to maximize flow (and minimize PVR) you need these two to have a certain amount of flow.

At low lung volumes, the alveolar vessels are not compressed because there is no pressure on them. So flow is high through number 1. But the extraalveolar vessels run with the small airways, and since the lung volume is low there is decreased radial traction on number 2. So the diameter is smaller, and flow is minimal.

At high lung volumes, the alveolar vessels ARE compressed because of the pressure within the alveoli. So flow is low through them, even though the arterioles are pulled open by radial traction.

Thus, maximum flow is achieved at FRC, because that is where both capillaries and arterioles permit high flow, even though neither one is maximal.

So if you plot PVR versus lung volume, you will get a U-Shaped Curve since the Cap. VR curve has an inverse relationship and the Arteriole VR curve has a direct relationship
 
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osli

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Ah, now that makes some sense - I was neglecting interstitial capillaries, and it explains why the effect isn't the same on the airways. BRS Phys doesn't seem to have anything about this unless I overlooked it.

One point of clarification though... it would not be the pressure within alveoli that collapse alveolar capillaries at high lung volumes - alveolar air pressure is atmospheric at all lung volumes so long as you are not actively inspiring or expiring. It would be the tension in the alveolar wall that compresses the capillaries, squeezing them as the wall thins under tension. This is what made me think UWorld's explanation was incorrect as well, since it referred to the air pressure causing the collapsing force.

Thanks!
 

DwyaneWade

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No problem and yes, you are right about the tension versus pressure concept. BRS Phys does not address this, I remembered it and just referred back to the powerpoint slides from our lecture last fall.