Ventilation/Perfusion question

[sab3156]

This is from firecracker:

"Pulmonary blood vessels constrict in response to low PO2, which decreases pulmonary blood flow to poorly ventilated alveoli and indirectly promotes blood flow to well ventilated alveoli. This hypoxic vasoconstriction is unique to the lungs, and helps maximize the efficiency of gas exchange."

However, in areas of low ventilation, there is actually HIGHER PO2 in the alveoli. In areas of high ventilation, there is LOW PO2 in the alveoli. So how does this make any sense? Shouldn't this be opposite? We also learned this same thing in class, so I am a bit confused as to how this can be reconciled (in other words, how do you reconcile the high PO2 and low ventilation in Zone 1 with the fact that Zone 1 vasculature is vasoconstricted compared to Zone 3? Shouldn't it be vasodilating due to high O2?)

EDIT: Better way of asking my question:

Increasing ventilation to a group of alveoli (Group 1) results in increasing perfusion to those alveoli. However, increasing ventilation will also decrease PO2 in those alveoli. So what exactly is the mechanism here that increases the perfusion to these alveoli (Group 1) compare to other alveoli (Group 2), because it is not consistent with the mechanism in the pulmonary vasculature in which hypoxia induces vasoconstriction. For simplicity, assume that all of those alveoli in both Groups (1 and 2) exist in the same zone and originally had the ventilation and perfusion.

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[68PGunner]

Look up what’s low ventilation vs high ventilation and you will get your answer, as in why is Zone 3 considered high ventilation and why is Zone 1 considered low ventilation?

Hint: it has to do w/ the top and possibly middle lobes weighing on the lower lobe and pushing all the air out of the lower lobe during expiration.

 

[sab3156]

Look up what’s low ventilation vs high ventilation and you will get your answer, as in why is Zone 3 considered high ventilation and why is Zone 1 considered low ventilation?

Hint: it has to do w/ the top and possibly middle lobes weighing on the lower lobe and pushing all the air out of the lower lobe during expiration.

Of course, but that is not my question. My question is why high ventilation of the Zone 3 is said to cause vasodilation even though it is hypoxic compared to Zone 1. Pulmonary vasculature vasoconstricts in hypoxic conditions, but it seems that there is a contradiction here...

 

[68PGunner]

Of course, but that is not my question. My question is why high ventilation of the Zone 3 is said to cause vasodilation even though it is hypoxic compared to Zone 1. Pulmonary vasculature vasoconstricts in hypoxic conditions, but it seems that there is a contradiction here...

Your two paragraphs in your original post talk about two separate things with a separate reason for each. They have nothing to do with each other.

Paragraph 1 talks about oxygen exchange efficiency. You don't want blood perfusion in your capillaries through areas of dead alveoli. This is a physiology change if your body is disrupted from its equilibrium set points due to some pathologies that will result in destroyed or collapsed alveoli.

Paragraph 2 talks about the situation of remnant oxygen being left in Zone 1 vs Zone 3 after each breath. Because of the anatomical weight of other lobes pushing on the lower lobe after each expiration, almost close to zero oxygen is left in Zone 3 after each breath, meaning low oxygen whereas there will be remnant oxygen at the apex meaning high oxygen. During inspiration, due to less oxygen being at Zone 3, there will be more oxygen ventilated through that area.

 

[sab3156]

Thanks for the explanation. Logically, I can understand that the areas of high ventilation should be receiving the most blood. But I'm still confused because... the blood leaving Zone 1 is constantly high in PO2, so why is it not causing vasodilation of the vasculature in Zone 1? Zone 3, since it has the lowest PO2 in the blood, should be vasoconstricting, correct? Zone 3 has way less alveolar PO2.

 

[Rahas]

Are you talking about hypoxic vasoconstriction? That depends on alveolar PO2.

The blood leaving all alveoli should have the same PO2 (assuming theres no pathology).

 

[sab3156]

Are you talking about hypoxic vasoconstriction? That depends on alveolar PO2.

Exactly, so why is hypoxia induced vasoconstriction attributed to areas of "low ventilation" when in fact they have the highest alveolar PO2? On the other hand, areas of lowest alveolar PO2 ("high ventilation") are described as having vasodilation induced by this high ventilation... it makes no sense to me.

The blood leaving all alveoli should have the same PO2 (assuming theres no pathology).

This is not true - the lowest ventilation regions of the lungs have the highest PO2 and lowest blood perfusion, and therefore the blood leaving these low ventilated regions has the highest PO2.

 

[68PGunner]

Thanks for the explanation. Logically, I can understand that the areas of high ventilation should be receiving the most blood. But I'm still confused because... the blood leaving Zone 1 is constantly high in PO2, so why is it not causing vasodilation of the vasculature in Zone 1? Zone 3, since it has the lowest PO2 in the blood, should be vasoconstricting, correct? Zone 3 has way less alveolar PO2.

Where did you get that the PO2 in the blood leaving Zone 1 is constantly high in PO2 vs Zone 3? O2 is perfusion limited, meaning that the equilibrium between the PO2 between the alveoli and the capillary vessels will be hit WAY before the end of the capillary. In other words, the PO2 in all capillary vessels AFTER oxygen has been exchanged to an equilibrium between the alveoli and the capillary vessels, whether they are hitting Zone 1, Zone 2, or Zone 3 will be close to 100 mm Hg.

 

[68PGunner]

This is not true - the lowest ventilation regions of the lungs have the highest PO2 and lowest blood perfusion, and therefore the blood leaving these low ventilated regions has the highest PO2.

In term of low blood perfusion at Zone 1 vs high blood perfusion at Zone 3, the reason for that is due to more capillaries being concentrated at Zone 3 vs less capillaries being concentrated at Zone 1. It's not due to the level of cardiac output.

 

[sab3156]

Where did you get that the PO2 in the blood leaving Zone 1 is constantly high in PO2 vs Zone 3? O2 is perfusion limited, meaning that the equilibrium between the PO2 between the alveoli and the capillary vessels will be hit WAY before the end of the capillary. In other words, the PO2 in all capillary vessels AFTER oxygen has been exchanged to an equilibrium between the alveoli and the capillary vessels, whether they are hitting Zone 1, Zone 2, or Zone 3 will be close to 100 mm Hg.

From Costanzo:

Blood perfusion is low, ventilation is low, and alveolar PO2 is high, leading to high PO2 in the blood leaving Zone 1.

 

[68PGunner]

From Costanzo:

View attachment 226161

Blood perfusion is low, ventilation is low, and alveolar PO2 is high, leading to high PO2 in the blood leaving Zone 1.

Ah, I see. To answer your question, let's remember what the formula for diffusion from alveoli to the capillary, which is equal to DL x change in pressure. Let's remember that change in pressure is directly correlated to flow, which can be written as change in pressure/resistance. Therefore, my guess is that a hypoxia condition would cause you to vaso-dilate Zone 3, because there's where you have more capillaries running through and also bc of higher flow.

 

[sab3156]

Ah, I see. To answer your question, let's remember what the formula for diffusion from alveoli to the capillary, which is equal to DL x change in pressure. Let's remember that change in pressure is directly correlated to flow, which can be written as change in pressure/resistance. Therefore, my guess is that a hypoxia condition would cause you to vaso-dilate Zone 3, because there's where you have more capillaries running through and also bc of higher flow.

Hypoxia in the pulmonary vasculature causes vasoconstriction, not vasodilation. This was the basis for my original question.

 

[Rahas]

I don't believe I've read about hypoxic vasoconstriction in the context of lung zones. The perfusion (and ventilation) differences have to do with the effect of gravity. Hence the eradication (or mitigation) of lung zones in a supine person.

 

[Rahas]

ie while the higher O2 tension in zone I alveoli will promote vasodilation, they'll still receive less flow than zone III because:

1.blood still has to climb uphill against gravity to reach zone I (flow to zone III is aided by gravity)
2.pulmonary vasculature is highly compliant, so decreased blood flow to zone I vessels should cause a passive reduction in vessel diameter

 

[68PGunner]

From Costanzo:

View attachment 226161

Blood perfusion is low, ventilation is low, and alveolar PO2 is high, leading to high PO2 in the blood leaving Zone 1.

I just notice something. Are you sure that PaO2 is alveolar partial pressure of oxygen instead of arterial partial pressure of oxygen? From my notes, A usually means alveolar whereas a usually means arterial.

 

[sab3156]

I don't believe I've read about hypoxic vasoconstriction in the context of lung zones. The perfusion (and ventilation) differences have to do with the effect of gravity. Hence the eradication (or mitigation) of lung zones in a supine person.

You're right that perfusion and ventilation differences are mainly an effect of gravity, but that's not really the point here. The principle I am talking about is that hypoxia causes vasoconstriction of the pulmonary vasculature, regardless of what zones these vessels are in, thus increasing resistance and directing blood away - the question is: Why are the vessels leaving Zone 3 (which contain blood with far lower PO2 levels than the blood leaving Zone 1) vasoDILATING? High ventilation (zone 3) is said to cause VASODILATION to direct blood to those regions... but how is that consistent with "hypoxia induces vasoconstriction" (highest ventilation = lowest O2).

I guess we won't find out unless a veteran pulmonologist sees this thread.

 

[Rahas]

Pulmonary vasculature is extremely compliant, so it passively changes its radius (diameter / cross sectional area) and hence resistance depending on the amount of blood flow through it. This helps buffer pressure changes in the pulmonary circulation. (I remember this from Kaplan physiology btw, in case you need to reference it).

So in zone I, the vasodilating force would be the high O2 tension in the alveoli. However, blood must flow against gravity. Low blood flow would cause a passive constriction of the pulmonary vessels, vasoconstricting them in the process.

Zone III has the reverse position, ie the lower O2 tension wouldn't be as great a vasodilating force, but the gravity aided blood flow would cause passive stretching of the pulmonary vessels.

The fact that zone I has a high V/Q is reflective of this. I think the sequence of events could be visualized like this: Zone I lies above the heart -> due to the effects of gravity, it gets less blood --> this increases the PAO2 --> which increases the PaO2 --> the increase in PAO2 will attempt to vasodilate pulmonic blood vessels (via suppression of hypoxic vasoconstriction) --> but clearly this vasodilatory effect is unable to overcome the effects of gravity (given the PAO2 and PaO2)

The ventilation rate alone won't tell you what PAO2/PaO2 to expect, since its an interplay between ventilation and perfusion. I think the starting point of your reasoning here seems to be the high PAO2, which might be misleading you. The starting point is the low perfusion to zone I (due to the effects of gravity), which creates the high PAO2/PaO2 in the higher lung zones.

 

[sab3156]

We are getting away from the point of the question - the question has nothing to do with the points above, though they may be valid. The question phrased in another way:

Increasing ventilation to a group of alveoli (Group 1) results in increasing perfusion to those alveoli. However, increasing ventilation will also decrease PO2 in those alveoli. So what exactly is the mechanism here that increases the perfusion to these alveoli (Group 1) compare to other alveoli (Group 2), because it is not consistent with the mechanism in the pulmonary vasculature in which hypoxia induces vasoconstriction. For simplicity, assume that all of those alveoli in both Groups (1 and 2) exist in the same zone and originally had the ventilation and perfusion.

Anyone know of any physiologists/pulmonologists on the site that would be able to answer this?

 

[Rahas]

I'm not sure what you're trying to ask. Can you link me to the text / book you read which generated your confusion, so that I may read it to myself?

You seem to be saying both group 1 and group 2 alveoli initially had the same ventilation and perfusion.
This, you say, results in greater perfusion of these alveoli (due to a decrease in hypoxic vasoconstriction).
I *think* what you say next is that that the increased perfusion to these alveoli will reduce their O2 tension, thus removing the stimulus that increased perfusion to them in the first place.

Have I understood your question correctly? If I have, I can attempt to answer it. I was under the impression we were contemplating the interplay of lung zones with perfusion and PAO2/PaO2, but it seems you only used it as an example to elucidate your question.

 

[sab3156]

Assuming that the alveoli are all in the same zone, increasing the ventilation will decrease the PO2. So what is the mechanism which causes perfusion to increase in areas of high ventilation, despite the increase in relative hypoxia?

 

[Rahas]

My guess is some sort of equilibrium would be established, where both alveoli function at similar PAO2s, which would mean the higher ventilated alveolus receives greater perfusion, but not as much as one would expect based on the initial PAO2. So when the higher ventilated alveolus begins to pull blood towards itself (due to the higher PAO2), the normally ventilated one increasingly resists it (as its PAO2 increases), until an equilibrium point is reached. At this point you'd still have greater perfusion in the higher ventilated alveolus, just not as much as you'd expect if the initial alveolus offered no resistance.