Oxygen in V/Q mismatch makes no sense?

[GonefromTX]

In first aid it says when V/Q = zero, giving 100% O2 does not improve PaO2. (yeah no **** patient is as good as not breathing with a ventilation of zero.)

It also says when V/Q = infinity, 100% O2 DOES improve PaO2. This is wrong. V/Q of infinity means NO BLOOD FLOW AT ALL. You are oxygenating a lung that does not participate in gas exchange AT ALL.

The explanation they give is to assume <100% dead space ie in pulmonary embolus. Well if you can assume <100% dead space in V/Q = infinity why not assume <100% obstruction in V/Q = zero? Giving 100% O2 SHOULD improve PaO2 because you're getting more oxygen in the lung ie when some air still passes though an aspirated peanut (provided there's not complete obstruction), increasing V!

Am I missing something here?

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[673441]

In first aid it says when V/Q = zero, giving 100% O2 does not improve PaO2. (yeah no **** patient is as good as not breathing with a ventilation of zero.)

It also says when V/Q = infinity, 100% O2 DOES improve PaO2. This is wrong. V/Q of infinity means NO BLOOD FLOW AT ALL. You are oxygenating a lung that does not participate in gas exchange AT ALL.

The explanation they give is to assume <100% dead space ie in pulmonary embolus. Well if you can assume <100% dead space in V/Q = infinity why not assume <100% obstruction in V/Q = zero? Giving 100% O2 SHOULD improve PaO2 because you're getting more oxygen in the lung ie when some air still passes though an aspirated peanut (provided there's not complete obstruction), increasing V!

Am I missing something here?

Simple math.
V/Q => ventilation/perfusion
Ventilation = 0
Then V/Q = 0

Ventilation = non-zero number
Perfusion = 0
Then V/Q = an infinite number since dividing by zero is a no-no in math. Don't believe me? Try it on a calc lol.

 

[GonefromTX]

Simple math.
V/Q => ventilation/perfusion
Ventilation = 0
Then V/Q = 0

Ventilation = non-zero number
Perfusion = 0
Then V/Q = an infinite number since dividing by zero is a no-no in math. Don't believe me? Try it on a calc lol.

Read my question please..?

 

[Womb Raider]

In first aid it says when V/Q = zero, giving 100% O2 does not improve PaO2. (yeah no **** patient is as good as not breathing with a ventilation of zero.)

It also says when V/Q = infinity, 100% O2 DOES improve PaO2. This is wrong. V/Q of infinity means NO BLOOD FLOW AT ALL. You are oxygenating a lung that does not participate in gas exchange AT ALL.

The explanation they give is to assume <100% dead space ie in pulmonary embolus. Well if you can assume <100% dead space in V/Q = infinity why not assume <100% obstruction in V/Q = zero? Giving 100% O2 SHOULD improve PaO2 because you're getting more oxygen in the lung ie when some air still passes though an aspirated peanut (provided there's not complete obstruction), increasing V!

Am I missing something here?

I'm not sure this is right, but this is how I think about it:

In the case of flow obstruction (e.g. PE), the blood that would have gone through the blocked vessel is now diverted elsewhere. This increases the flow through other pulmonary vessels. By increasing the partial pressure of O2 of inspired air, you increase the diffusion rate of inspired oxygen --> blood. (Diffusion = A*D*(P1-P2/T)) This helps your body maintain adequate oxygenation of blood despite increasing flow rates of blood.

In the case of airway obstruction, the blood that flows through the segment of lung is NOT diverted to a better ventilated area. (Well, in reality it is due to the pulmonary vasoconstriction, but I don't think this corrects perfectly, especially not with large obstructions blocking a large volume of lung.) Thus, the blood is never capable of being oxygenated in the lung, and re-enters the circulation unoxygenated. If you're having trouble grasping this just imagine a PFO - no amount of increased inspired O2 is going to help the PaO2.

 

[gregoryhouse]

In first aid it says when V/Q = zero, giving 100% O2 does not improve PaO2. (yeah no **** patient is as good as not breathing with a ventilation of zero.)

It also says when V/Q = infinity, 100% O2 DOES improve PaO2. This is wrong. V/Q of infinity means NO BLOOD FLOW AT ALL. You are oxygenating a lung that does not participate in gas exchange AT ALL.

The explanation they give is to assume <100% dead space ie in pulmonary embolus. Well if you can assume <100% dead space in V/Q = infinity why not assume <100% obstruction in V/Q = zero? Giving 100% O2 SHOULD improve PaO2 because you're getting more oxygen in the lung ie when some air still passes though an aspirated peanut (provided there's not complete obstruction), increasing V!

Am I missing something here?

When you have V/Q=zero this is called a shunt. Examples of shunts include R to L shunts (i.e., Tetralogy of Fallot) this means that there is an area of perfusion that is not receiving ventilation. No matter how much oxygen you give it will not correct the issue, because that area of perfusion is bypassing the lung and staying unoxygenated.

A V/Q=infinity is an area of dead space where there is ventilation without perfusion. An example of this would be a PE. That area of lung is not being perfused but by sending blood to other areas of the lung you can overcome the deadspace.

V/Q= infinity and V/q=zero are incompatible with life, they are just used as a reference to understand the extremes. Real life examples fall in between. a high V/Q ratio will still not improve with oxygen if large enough because there is not enough functional lung to overcome the mismatch or there is a AV shunt that bypasses the lung altogether.

You can also think about it in terms of severe ARDS, these patients are very hard to keep oxygenated even with intubation and high FIO2 because they have such little functional lung volumes left. Blood is flowing through areas of collapsed alveoli and no matter how much oxygen you give it will not correct because there are not enough open alveoli.

An analogy would be like water flowing through a water filter. If the filter stops working (alveoli collapse) or you have a hole in the pipe that lets water escape before going through the filter (R to L shunt) then no matter how good a filter you have, the water that comes out will remain contaminated. If the pipe bringing the water gets clogged (PE) but you have another pipe for the water to go through that has a water filter attached to it (blood goes to other areas of the lung), the water will still come out clean.

Not a perfect analogy but hope it helps.

 

[sovereign0]

In first aid it says when V/Q = zero, giving 100% O2 does not improve PaO2. (yeah no **** patient is as good as not breathing with a ventilation of zero.)

It also says when V/Q = infinity, 100% O2 DOES improve PaO2. This is wrong. V/Q of infinity means NO BLOOD FLOW AT ALL. You are oxygenating a lung that does not participate in gas exchange AT ALL.

The explanation they give is to assume <100% dead space ie in pulmonary embolus. Well if you can assume <100% dead space in V/Q = infinity why not assume <100% obstruction in V/Q = zero? Giving 100% O2 SHOULD improve PaO2 because you're getting more oxygen in the lung ie when some air still passes though an aspirated peanut (provided there's not complete obstruction), increasing V!

Am I missing something here?

I think the issue is that the whole lung isn't gonna have V/Q = 0 or infinity, it's just regional. So in the case of V/Q = infinity, there is an area of the lung with ventilation but no perfusion. Why is there no perfusion? Blood isn't reaching that part of the lung. But there's still a constant volume of blood in circulation. So it has to go somewhere.

All that extra cardiac output will go to the perfused region of the lung. Now in that area, you're getting twice (conceptually) the perfusion per the same unit ventilation. All the blood in circulation is still undergoing gas exchange, there just isn't as much lung as there is blood. Oxygen becomes diffusion limited - there's so much blood going through that you just can't load it all with oxygen. By increasing PAO2, you can increase the driving force for diffusion, allowing the extra perfusion to get a little bit more oxygenation.

This is in contrast to a shunt, where you have blood that is not undergoing gas exchange. No matter how much oxygen you give, there's no point where that oxygen can get into the blood.

 

[mw18]

I think the issue is that the whole lung isn't gonna have V/Q = 0 or infinity, it's just regional. So in the case of V/Q = infinity, there is an area of the lung with ventilation but no perfusion. Why is there no perfusion? Blood isn't reaching that part of the lung. But there's still a constant volume of blood in circulation. So it has to go somewhere.

All that extra cardiac output will go to the perfused region of the lung. Now in that area, you're getting twice (conceptually) the perfusion per the same unit ventilation. All the blood in circulation is still undergoing gas exchange, there just isn't as much lung as there is blood. Oxygen becomes diffusion limited - there's so much blood going through that you just can't load it all with oxygen. By increasing PAO2, you can increase the driving force for diffusion, allowing the extra perfusion to get a little bit more oxygenation.

This is in contrast to a shunt, where you have blood that is not undergoing gas exchange. No matter how much oxygen you give, there's no point where that oxygen can get into the blood.

This is exactly the way I look at it. Right or wrong it's the way I conceptualize it.

 

[GonefromTX]

I think the issue is that the whole lung isn't gonna have V/Q = 0 or infinity, it's just regional. So in the case of V/Q = infinity, there is an area of the lung with ventilation but no perfusion. Why is there no perfusion? Blood isn't reaching that part of the lung. But there's still a constant volume of blood in circulation. So it has to go somewhere.

All that extra cardiac output will go to the perfused region of the lung. Now in that area, you're getting twice (conceptually) the perfusion per the same unit ventilation. All the blood in circulation is still undergoing gas exchange, there just isn't as much lung as there is blood. Oxygen becomes diffusion limited - there's so much blood going through that you just can't load it all with oxygen. By increasing PAO2, you can increase the driving force for diffusion, allowing the extra perfusion to get a little bit more oxygenation.

This is in contrast to a shunt, where you have blood that is not undergoing gas exchange. No matter how much oxygen you give, there's no point where that oxygen can get into the blood.

YES YOU JUST SOLVED MY 3 HOUR DILEMMA THANK YOU! V/Q =INFINITY REFERS TO ONLY ONE AREA NOT THE WHOLE LUNG!!!

 

[Psai]

YES YOU JUST SOLVED MY 3 HOUR DILEMMA THANK YOU! V/Q =INFINITY REFERS TO ONLY ONE AREA NOT THE WHOLE LUNG!!!

The best part of teaching is when you see the lightbulb go off in a student's head and you know that you contributed to their way of thinking

 

[CherryRedDracul]

The best part of teaching is when you see the lightbulb go off in a student's head and you know that you contributed to their way of thinking

Moments like that make my day.

 

[sovereign0]

YES YOU JUST SOLVED MY 3 HOUR DILEMMA THANK YOU! V/Q =INFINITY REFERS TO ONLY ONE AREA NOT THE WHOLE LUNG!!!

The best part of teaching is when you see the lightbulb go off in a student's head and you know that you contributed to their way of thinking

Moments like that make my day.

adding this thread to my CV, brb

 

[cellsaver]

YES YOU JUST SOLVED MY 3 HOUR DILEMMA...

That's what happens when you use "First Aid". However,Tao Le is very thankful and laughing all of the way to the bank.

You could have understood it in 15 minutes by reading any 1 of a dozen of textbooks in basic respiratory physiology....all of 3 pages (with diagrams)

 

[mw18]

This may be a stupid question, but can someone please explain to me how is Tetralogy of Fallot equivalent to a problem with a low V/Q ratio? In my understanding in tetralogy the blood bypasses lungs, which means lungs are not perfused. Whereas in a problem like airway obstruction the lung would be perfused well, but not ventillated.
I do understand that in both cases there would be deoxygenated blood in systemic circulation, I just don't get how can we classify Tetralogy under low V/Q if the primary issue is poor lung perfusion?
Thanks in advance!

ToF is a right to left shunt. If a shunt were to happen in the lung it would be because there was perfusion, but no oxygenation (think of it like air can't get to all the blood). Which is a low V/Q. An embolism is a situation where the lungs aren't perfused (where the blood can't get to the air).

Edit: Obviously not an expert, just my understanding.

 

[GonefromTX]

This may be a stupid question, but can someone please explain to me how is Tetralogy of Fallot equivalent to a problem with a low V/Q ratio? In my understanding in tetralogy the blood bypasses lungs, which means lungs are not perfused. Whereas in a problem like airway obstruction the lung would be perfused well, but not ventillated.
I do understand that in both cases there would be deoxygenated blood in systemic circulation, I just don't get how can we classify Tetralogy under low V/Q if the primary issue is poor lung perfusion?
Thanks in advance!

No its a good question. Been wondering the same.

ToF is a right to left shunt. If a shunt were to happen in the lung it would be because there was perfusion, but no oxygenation (think of it like air can't get to all the blood). Which is a low V/Q. An embolism is a situation where the lungs aren't perfused (where the blood can't get to the air).

Edit: Obviously not an expert, just my understanding.

The right-to-left shunt in ToF should cause a low perfusion. Blood is literally going from the right ventricle straight to systemic circulation. How is there lung perfusion?

 

[mw18]

No its a good question. Been wondering the same.



The right-to-left shunt in ToF should cause a low perfusion. Blood is literally going from the right ventricle straight to systemic circulation. How is there lung perfusion?

I think the reason that ToF is so complicated is that it has two things going on. On one hand it has the Pulmonary stenosis (which I agree with you seems like it would cause dead space similar to an embolism), and it also has a shunt through the VSD (which is obviously a shunt and no amount of oxygen will help the blood that is shunted).

I'm not sure if @jdh71 is still on here much, but I think they're a pulmonologist, and maybe can shed some light...?

 

[group_theory]

I think the reason that ToF is so complicated is that it has two things going on. On one hand it has the Pulmonary stenosis (which I agree with you seems like it would cause dead space similar to an embolism), and it also has a shunt through the VSD (which is obviously a shunt and no amount of oxygen will help the blood that is shunted).

I'm not sure if @jdh71 is still on here much, but I think they're a pulmonologist, and maybe can shed some light...?

Both V/Q mismatches can cause hypoxemia/hypoxia.

For TOF it's complicated because it's not a complete shunt. there is still blood going through the pulmonary arteries. Increasing inspired FiO2 can increase the paO2 of the pulmonary venous blood, and thus increase the overall paO2

For example: If half the blood is shunted through the VSD, and if the mixed venous pO2 to be 40mmHg. On room air at sea level, the pulmonary venous pO2 should be around 100mmHg. With 50% shunt fraction (Qs/Qt), the expected pO2 on systemic ABG should be around 70mmHg. If you apply 2L NC, the FiO2 will increase from 21% to 28%, and the pulmonary venous pO2 should be around 160mmHg, and on systemic ABG, with 50% shunt fraction, should be 100mmHg.

Now in real life the actual numbers aren't exactly what one expects on paper due to multiple moving variables - the shunt fraction can change based on pulmonary arterial pressure (which are affected by oxygen as well as degree of ventilation) which can drop/increase your shunt fraction. Increasing SVR can also affect shunt fraction as well

For Tet spells, the shunt fraction is close t0 100% so giving oxygen will have minimal impact on hypoxemia due to severely decrease pulmonary blood flow. That's why you try to increase SVR to help increase pulmonary flow. Sometimes a physical shunt is needed (systemic to pulmonary such as a modified BT shunt) to help oxygenate if corrective surgery can't be done immediately for whatever reason (e.g., pulmonary artery atresia)

*disclaimer - it's been a while since I dealt with uncorrected congenital heart disease so I may have gotten some details wrong about TOF but the main purpose of the post is to explain the VQ mismatch associated with TOF

 

[Amygdarya]

Maybe my problem with this is my definition of ventilation. I thought ventilation is the air in the alveoli. Thus, ventilation is 0 if an airway is blocked. In case of ToF everyone seems to say that ventilation of shunted blood is 0, which makes me think about the definition of ventilation.
Can I take a blood sample and say that ventiation of this blood is low, or do I need to know about the air in the lungs in order to draw conclusions about ventilation?
In kids with ToF the little blood that gets to the lungs can be oxygenated normally, because the lungs are fine. Right? Thus it seems that it is the perfusion that is low, and the V/Q is actually high?

No. I think it may help to think of ventilation/perfusion is now much oxygen gets access to what portion of blood volume (rather than actual lungs being ventilated and perfused).
Eg., as was explained so well above, in PE the whole blood volume gets redistributed in the parts of the lungs that are not affected, so that all of the blood gets access to oxygen - thus increasing %O2 will improve PaO2.
By contrast, in ToF a fraction of blood (and a significant one during test spells, as pointed out above) bypasses the lungs i.e. doesn't get any access to oxygen - thus, no matter how much oxygen you give, it will not improve PaO2 because a (significant) portion of blood is not getting oxygenated at all.

 

[SurfingDoctor]

I don't know why people are discussing ToF in the context of V/Q mismatch as V/Q mismatch in typically a discussion reserved for the isolated pulmonary circulation, not cardiac anatomy. In any case, in the setting of ToF, the measured arterial hypoxemia is related to the degree of shunting, not to reduced pulmonary blood flow, which is typically low, but can be normal or supranormal depending on the multiple factors (degree of PA stenosis, size of the VSD, degree of RVH, leaflet obstruction). Also the pulmonary circulation is compensated to some degree by the bronchial circulation (~15-20%) to provide an additional source of PBF that bypasses the valvular issues.

http://circ.ahajournals.org/content/circulationaha/35/5/904.full.pdf

As you can see in the paper (Table 2 and 3), many patients have a normal Qpa of ~3L/min in the neonate, but are still quite hypoxemic as a correlation of the Qp/Qs fraction with the larger the VSD and more the RVH/stenosis, the higher the Qs or Qao in the paper. Thus in ToF, it is all the factors that contribution to the right to left shunting, and not directly stenosis-related alterations to the PBF, that causes hypoxemia.

 

[PinusEldarica]

I think the issue is that the whole lung isn't gonna have V/Q = 0 or infinity, it's just regional. So in the case of V/Q = infinity, there is an area of the lung with ventilation but no perfusion. Why is there no perfusion? Blood isn't reaching that part of the lung. But there's still a constant volume of blood in circulation. So it has to go somewhere.

All that extra cardiac output will go to the perfused region of the lung. Now in that area, you're getting twice (conceptually) the perfusion per the same unit ventilation. All the blood in circulation is still undergoing gas exchange, there just isn't as much lung as there is blood. Oxygen becomes diffusion limited - there's so much blood going through that you just can't load it all with oxygen. By increasing PAO2, you can increase the driving force for diffusion, allowing the extra perfusion to get a little bit more oxygenation.

This is in contrast to a shunt, where you have blood that is not undergoing gas exchange. No matter how much oxygen you give, there's no point where that oxygen can get into the blood.

But won't 100% oxygen increase VaO2 in areas that are still ventilated? Would not that improve overall hypoxemia? I mean even if there is some blood shunting without oxygenation, it will eventually mix with the blood from normally ventilated area, am i getting the concept of 100% oxygen treatment wrong?

 

[chittychitty]

But won't 100% oxygen increase VaO2 in areas that are still ventilated? Would not that improve overall hypoxemia? I mean even if there is some blood shunting without oxygenation, it will eventually mix with the blood from normally ventilated area, am i getting the concept of 100% oxygen treatment wrong?

I was wondering the same thing as I was reading this thread; this was my main issue that wasn't addressed from all these explanations. However, I think the answer behind it comes from the fact that O2 is perfusion-limited (and only diffusion-limited when there is a V/Q<1). This means that in the case of shunt, the areas that are still ventilated and have a normal rate of perfusion will have already been maximally exchanging O2, and thus, 100% oxygen wouldn't have that much of an effect.

 

[alprazoslam]

Simple math.
V/Q => ventilation/perfusion
Ventilation = 0
Then V/Q = 0

Ventilation = non-zero number
Perfusion = 0
Then V/Q = an infinite number since dividing by zero is a no-no in math. Don't believe me? Try it on a calc lol.

Lolwut

 

[aldol16]

I was wondering the same thing as I was reading this thread; this was my main issue that wasn't addressed from all these explanations. However, I think the answer behind it comes from the fact that O2 is perfusion-limited (and only diffusion-limited when there is a V/Q<1). This means that in the case of shunt, the areas that are still ventilated and have a normal rate of perfusion will have already been maximally exchanging O2, and thus, 100% oxygen wouldn't have that much of an effect.

The key idea you're missing is that the solubility of O2 in water (and thus blood) is piss poor. Recall the 0.003*PaO2 term when you're calculating the O2 content of blood. Even if you administer 100% O2 at 760 mmHg, only 2.3 mmHg of that goes into blood. So the blood that's going to the ventilated regions is already maximally saturated with dissolved O2 at ambient conditions. Giving 100% O2 to those areas won't result in more O2 going into blood. The shunted blood will then mix with the blood coming from the ventilated areas, "steal" a little of the dissolved O2 to bind Hb which will make a tiny impact.

Conversely, think about V/Q = infinity. Say there is a PE at some part of the lung blocking blood flow to that area. The blood that would go through that area just goes somewhere else. This increases the "load" on the other areas of the system. But then you give supplemental O2 so that the extra O2 can then be loaded on to the Hb molecules which are actually being delivered to the perfused and ventilated areas.

In short, the key difference = where the Hb is. In shunts, the Hb is going to places that aren't being ventilated and thus can only "steal" the tiny bit of O2 that can be dissolved in the blood from the ventilated areas. In dead space ventilation, the Hb is just going to other ventilated places and so increasing O2 in the alveoli will result in direct loading of O2 onto the extra Hb.