Shunt -> hypoxemia and dead space -> hypercarbia?

[bomgd3]

This whole situation blows my mind, and I have never gotten a satisfactory answer from any of my friends or professors. Why the heck does shunt cause hypoxemia, while dead space causes hypercarbia? The way I think of it is that ANY V/Q mismatch causes both hypoxemia and hypercarbia, because there simply isn't gas exchange going on in both situations.

I would LOVE it if someone could clear this up for me. It's making my brain melt. Thanks!

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[jdh71]

This whole situation blows my mind, and I have never gotten a satisfactory answer from any of my friends or professors. Why the heck does shunt cause hypoxemia, while dead space causes hypercarbia? The way I think of it is that ANY V/Q mismatch causes both hypoxemia and hypercarbia, because there simply isn't gas exchange going on in both situations.

I would LOVE it if someone could clear this up for me. It's making my brain melt. Thanks!

Dead space and shunt are just the extreme ends of the the V/Q equation.

Basically dead space causes the hypercarbia because your effective minute ventilation is reduced from baseline.

Minute ventilation is fine in shunt, you're simply putting blood in parts of the lung that can't participate in oxygenation or mixing right sided blood with left sided blood.

 

[calvnandhobbs68]

If you want it broken down totally here's my take on it:

Dead Space:
Like jdh said, you're reducing your effective minute ventilation. What this means is that you're only getting half as much air into exchange areas as you usually would. For instance, lets take a simple example. Lets say half your alevoli are dead space because of some type of perfusion interruption.

Let's say normal ventilation is 5L/min and we'll put none of that in anatomic dead space for simplicity sake. ALL your alveoli are getting perfused at 5L/min BUT only 2.5L/min are participating in gas exchange, so its basically as if you were inspiring 2.5L/min.

Since your blood flow is non existent for half your lung, all that blood has to go past your good alveoli. Now all your blood is equilibrating with only half the air volume its used to. Your O2 sat will still be okay because your blood is gonna pull that O2 from the air until it equilibrates. Remember that there's still usually a ton of residual O2 left in air you expire...a person can breathe on the air they expire. So there's still enough O2 left to saturate that extra blood.
Not so with CO2, which is equilibrating the other way. Normal air has no CO2, so when that air is equilibrated its done...no more CO2 is gettin in there. Thus you get hypercarbia but no hypoxemia.

On a side note, this relates into why people inhale their air when they hyperventilate right? There's plenty of O2 in the air but that air is already equilibrated with respect to CO2. Thus, their body won't blow off anymore CO2, bringing your blood CO2 levels back up and keeping you from passing out from respiratory alkalosis. Also why we can do CPR...plenty of O2 left in your breath for a person to absorb.

Shunt:
Opposite case, now you've got blood flowing where its not wanted. In this case ALL 5L/min of your air is equilibrating with your blood because its only going to the good alveoli. Half your blood isn't participating in exchange at all though (lets say you have pneumonia that fills up half your space).

Now half your blood isn't equilibrating with respect to O2, bringing your O2 sat down to the average between the alveoli. So blood 100% sat on one half and 75% sat on the other will be 87.5% sat overall. That's no good...hypoxemia.

Now half the blood isn't equilibrating with respect to CO2 either but the half that is is equilibrating with twice the volume of air it usually would. Remember CO2 is equilibrating OUT of the blood,so this matters. This brings the PPCO2 down for half the blood to a level lower than the normal equilibration PP. This will mix with the blood still at venous PPCO2 and bring you to an over CO2 that's pretty close to normal. Thus, no hypercarbia.

Obviously I'm ignoring all kinds of compensatory/complicating mechanisms that kick in (vasoconstriction for example) but thats the extreme generalization.

 

[bomgd3]

Thanks! That helps a lot. And in both shunt and dead space (or any V/Q mismatch), AaDO2 is elevated right?

I also have a tough time understanding the relevance of the whole dead space -> hypercapnia/shunt -> hypoxemia thing. It seems like there is not a single disease where this distinction breaks down well. For example, if you threw a massive PE and gave yourself a giant dead space, you become both hypoxemic and hypercapnic right? And if type A pink puffers tend to have more dead space, then why do they also tend to have normal ABG or be slightly hypoxemic? Similarly, type B blue bloaters tend to have more shunt, so why do they tend to be both hypoxemic and hypercapnic?

To me, it seems like pulmonologists are trying to categorize very complex processes into an overly simple schema which does not do a very good job of predicting actual pathophysiology.

 

[jdh71]

Thanks! That helps a lot. And in both shunt and dead space (or any V/Q mismatch), AaDO2 is elevated right?

I also have a tough time understanding the relevance of the whole dead space -> hypercapnia/shunt -> hypoxemia thing. It seems like there is not a single disease where this distinction breaks down well. For example, if you threw a massive PE and gave yourself a giant dead space, you become both hypoxemic and hypercapnic right? And if type A pink puffers tend to have more dead space, then why do they also tend to have normal ABG or be slightly hypoxemic? Similarly, type B blue bloaters tend to have more shunt, so why do they tend to be both hypoxemic and hypercapnic?

To me, it seems like pulmonologists are trying to categorize very complex processes into an overly simple schema which does not do a very good job of predicting actual pathophysiology.

With massive PE, you usually increase your resp rate to keep up with minute ventilation, so you only really get shunt.

And pulmonologists don't "categorize very complex processes into an overly simple schema" - your physiology textbook does. If anyone knows the complex interplay between that happens between the heart, the lungs, and the gas exchange, it's us pulmonologists. They're trying to teach you this crap in a vacuum, hoping that if you understand the concept in isolation, you'll be able to apply it in a more practical sense later when you're able to tie together the rest of the patient.

 

[Knicks]

good thread

 

[Ian]

Resurrecting a thread since I have a similar question. In COPD, hypoxemia usually occurs earlier than hypercapnia, with hypoxemia occuring when FEV1 is <50% and hypercapnia when FEV1 is <25%. Does this mean that a shunt occurs earlier than dead space? Is it because the compensatory vasoconstriction which produces dead space occurs at a later time?

 

[bdc142]

Been googling for about an hour and can't find this answer...can anyone explain why SUTM why V/Q mismatch and pulmonary shunt (they treat the two as separate entities) are reasons for type 1 respiratory failure (low O2, normal to low CO2) but dead space is a cause for type 2 respiratory failure (low O2, high CO2)???

Really appreciate some help

 

[Romeo Nedham]

Glad to find this thread. Really love calvnandhobbs68's explanation. To truly understand what he said you need to google "alveolar ventilation equation".

Also, this lecture helps much!

 

[Peach Newport]

What kind of uncultured savage calls hypercapnia "hypercarbia?"

 

[Ramaq Chishti]

Resurrecting a thread since I have a similar question. In COPD, hypoxemia usually occurs earlier than hypercapnia, with hypoxemia occuring when FEV1 is <50% and hypercapnia when FEV1 is <25%. Does this mean that a shunt occurs earlier than dead space? Is it because the compensatory vasoconstriction which produces dead space occurs at a later time?

Hi, did you get any answer to this?

 

[Ramaq Chishti]

If you want it broken down totally here's my take on it:

Dead Space:
Like jdh said, you're reducing your effective minute ventilation. What this means is that you're only getting half as much air into exchange areas as you usually would. For instance, lets take a simple example. Lets say half your alevoli are dead space because of some type of perfusion interruption.

Let's say normal ventilation is 5L/min and we'll put none of that in anatomic dead space for simplicity sake. ALL your alveoli are getting perfused at 5L/min BUT only 2.5L/min are participating in gas exchange, so its basically as if you were inspiring 2.5L/min.

Since your blood flow is non existent for half your lung, all that blood has to go past your good alveoli. Now all your blood is equilibrating with only half the air volume its used to. Your O2 sat will still be okay because your blood is gonna pull that O2 from the air until it equilibrates. Remember that there's still usually a ton of residual O2 left in air you expire...a person can breathe on the air they expire. So there's still enough O2 left to saturate that extra blood.
Not so with CO2, which is equilibrating the other way. Normal air has no CO2, so when that air is equilibrated its done...no more CO2 is gettin in there. Thus you get hypercarbia but no hypoxemia.

On a side note, this relates into why people inhale their air when they hyperventilate right? There's plenty of O2 in the air but that air is already equilibrated with respect to CO2. Thus, their body won't blow off anymore CO2, bringing your blood CO2 levels back up and keeping you from passing out from respiratory alkalosis. Also why we can do CPR...plenty of O2 left in your breath for a person to absorb.

Shunt:
Opposite case, now you've got blood flowing where its not wanted. In this case ALL 5L/min of your air is equilibrating with your blood because its only going to the good alveoli. Half your blood isn't participating in exchange at all though (lets say you have pneumonia that fills up half your space).

Now half your blood isn't equilibrating with respect to O2, bringing your O2 sat down to the average between the alveoli. So blood 100% sat on one half and 75% sat on the other will be 87.5% sat overall. That's no good...hypoxemia.

Now half the blood isn't equilibrating with respect to CO2 either but the half that is is equilibrating with twice the volume of air it usually would. Remember CO2 is equilibrating OUT of the blood,so this matters. This brings the PPCO2 down for half the blood to a level lower than the normal equilibration PP. This will mix with the blood still at venous PPCO2 and bring you to an over CO2 that's pretty close to normal. Thus, no hypercarbia.

Obviously I'm ignoring all kinds of compensatory/complicating mechanisms that kick in (vasoconstriction for example) but thats the extreme generalization.

Thank you so much! Can you please further explain the questions asked later on in the post please? Would be grateful!

 

[nimbus]

With massive PE, you usually increase your resp rate to keep up with minute ventilation, so you only really get shunt.

Actually a massive PE causes increase dead space, not shunt.

Here’s a simplified example. Say you have a massive PE that completely occludes the right main pulmonary artery. Then the entire right lung becomes dead space because there is zero perfusion but normal ventilation in that lung. All the pulmonary blood flow goes to the left lung which also has normal ventilation. There is no shunt. If the lungs are healthy and oxygen consumption is not high, many patients can maintain adequate oxygenation with venous blood being oxygenated through one healthy lung. Indeed some people walk around with one healthy lung.

An opposite example is one-lung ventilation in the operating room which is often performed for thoracic surgery. In this instance, there is perfusion to both lungs but zero ventilation in one lung. This causes a shunt resulting in poorly oxygenated entering the left side of the heart and the systemic arterial circulation. (There is some decrease in perfusion of the nonventilated lung because of hypoxic pulmonary vasoconstriction which helps partially compensate the v/q mismatch). I’ve always toyed with the idea of selectively wedging a PA catheter into the left or right main PA during one-lung ventilation to improve the shunt. This would effectively restore v/q match under one-lung ventilation. The problem is that PA catheters are not really steerable without imaging and fancy wire tricks and most often end up in the right main PA. Anyway, one-lung ventilation causes a shunt resulting in decreased arterial pO2 which we often compensate for by increasing FiO2.

 

[jdh71]

Actually a massive PE causes increase dead space, not shunt.

Here’s a simplified example. Say you have a massive PE that completely occludes the right main pulmonary artery. Then the entire right lung becomes dead space because there is zero perfusion but normal ventilation in that lung. All the pulmonary blood flow goes to the left lung which also has normal ventilation. There is no shunt. If the lungs are healthy and oxygen consumption is not high, many patients can maintain adequate oxygenation with venous blood being oxygenated through one healthy lung. Indeed some people walk around with one healthy lung.

An opposite example is one-lung ventilation in the operating room which is often performed for thoracic surgery. In this instance, there is perfusion to both lungs but zero ventilation in one lung. This causes a shunt resulting in poorly oxygenated entering the left side of the heart and the systemic arterial circulation. (There is some decrease in perfusion of the nonventilated lung because of hypoxic pulmonary vasoconstriction which helps partially compensate the v/q mismatch). I’ve always toyed with the idea of selectively wedging a PA catheter into the left or right main PA during one-lung ventilation to improve the shunt. This would effectively restore v/q match under one-lung ventilation. The problem is that PA catheters are not really steerable without imaging and fancy wire tricks and most often end up in the right main PA. Anyway, one-lung ventilation causes a shunt resulting in decreased arterial pO2 which we often compensate for by increasing FiO2.

I will do both. But your big problem is shunt because at this end of the day it's the hypoxia that will kill you the fastest. If you throw O2 at it and it doesn't improve, there is your shunt. Big PE is problem.

 

[OrgoCoop]

comes down to perfusion v diffusion limits of O2 vs CO2. Sorry if someone else already said this

 

[Iniakin]

I`m an IMG and I`ve spent days, scratching my head around V/Q issues and I wanna give this my best shot. I have to agree with Jdh in a way that "they're trying to teach you this crap in a vacuum", which sometimes actually makes things harder to understand.

1. Shunting:
​

- cause: foreign body inhalation -> obstruction of airways.
- side of obstruction: V/Q = 0, since there`s no ventilation, but perfusion is still happening -> you won`t be able to get O2 and to give off CO2.
- side without obstruction: V/Q = 1, blood still goes here like it was before, everything is fine.
- result: when blood on the side with obstruction (low O2, high CO2) mixes with blood on the side without obstruction (normal O2, normal CO2) -> you`re getting hypoxemia and hypercapnia.
- response: hyperventilation, which is capable to fix hypercapnia, but is unable to fix hypoxemia. Why is that? Well, as calvnandhobbs68 noticed, CO2 equilibrates out, so your CO2 removal is directly dependent on ventilation. If you breath fast enough, CO2 will be able to equilibrate, but it doesn`t change PaO2 a lot, since high V/Q regions (part of physiologic dead space that will start to participate in the gas exchange, when obstruction happens) have little capacity to absorb additional O2 and compensate for regions with V/Q = 0. Down below on the left you can see the graph that shows this concept:

Also important to notice that O2 therapy won`t fix hypoxemia in shunt. The reason why is because the blood that is going to well-ventilated areas are already extracting the maximum O2 that they can. Another words, PaO2 on the side without obstruction is normal (75-100) and, therefore, SaO2 is normal (95-100%). So if you`ll give O2 therapy, O2 will go to these already well-ventilated areas, so you`ll increase PaO2 from 100 to 400-500 or whatever, but it won`t change SaO2 on the side without obstruction, because SaO2 will stay the same at the level of PaO2 of 100 and at the level of PaO2 of 500. The graph on the right upper side shows this idea.

- does it mean that shunt can`t lead to hypercapnia? No, it actually can and it all depends on the fraction of the shunt. With shunt fraction >50%, you`ll get hypercapnia, so it depends on how much alveoli can`t participate in the ventilation. Think about this as about a spectrum.

- treatment: resolve the shunt.

2.1 Pure dead space:
​

- cause: pulmonary embolism.
- side of emboli: V/Q = infinity, because ventilation is happening, but no blood flow at all.
- side without emboli: V/Q = 1. It`s very important to notice that the whole "dead space" concept can only work out if you consider the presence of so called "pure dead space". What does it mean? It means that there`s no hypoxic vasoconstriction that actually happens in real life. So you just have to assume that the blood that is found on the side with emboli just stays there and doesn`t go anywhere else (this is so stupid). If you`ll make this assumption - everything is going to work out.
- result: side with emboli (pure dead space) doesn`t go anywhere, but side without emboli goes to systemic circulation, so you`re getting hypercapnia without hypoxemia.
- response: hyperventilation won`t be able to fix hypercapnia here, because you can imagine that all that air that you inhale will go to alveoli that participate in the gas exchange and can accept CO2 and to those alveoli that do NOT participate in gas exchange, because of the emboli present in the blood vessels that supply them. This is the opposite of what you see in the shunt: all air goes ONLY to the functional alveoli that are capable to give off CO2, while here air goes to dysfunctional alveoli (dysfunctional because of the presence of emboli in the blood vessel) AS WELL AS functional alveoli, so it makes it`s impossible to compensate.
- treatment: O2 can`t help in pure dead space for the same reasons as in the shunt.
- conclusion of pure dead space: hypercapnia, no hypoventilation, O2 therapy doesn`t help.

2.2 Real-life dead space:
​

Now what happens in real life is completely different (which makes it`s so funny and so sad at the same time, when I remember how much time I`ve spent to understand all this):
1. Hypoxic vasoconstriction actually happens, so all that deoxygenated blood on the side with emboli (V/Q = infinity) goes to the side without emboli with oxygenated blood -> mixing -> hypoxemia.
2. Since perfusion on the right side increases (since it starts to receive deoxygenated blood from the side with obstruction due to hypoxic vasoconstriction), but ventilation stays the same -----> V/Q < 1, so it`s actually V/Q mismatch case here.
3. Patient will hyperventilate so much that he`ll be able to resolve hypercapnia and even will enter respiratory alkalosis state from low CO2.
4. Since V/Q < 1, then O2 therapy actually can help. I think about this as about increasing V in V/Q mismatch and, therefore, getting closer to V/Q = 1.
5. Conclusion of real-life dead space: hypoxemia, hypocapnia, O2 therapy works.

3. V/Q Mismatch:​

- cause: pulmonary edema.
- side with pulmonary edema: V/Q <1, since perfusion is the same and ventilation can`t happen effectively in the presence of fluid.
- side without pulmonary edema: V/Q = 1, so everything is fine.
- result: blood on the left side (low O2) mixes with blood on the right side (normal O2) and you`re getting hypoxemia.
- treatment: since V/Q < 1, O2 therapy is going to help.













At last, I`d like to leave this graph from B&B, which actually helps to keep these things straight in your mind: