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Hello all,

Long time lurker, 1st time poster. So I am going through RR path and came across something that I don't quite understand. I am reviewing the A-a gradient and how it can be used to distinguish between causes of hypoxemia.

I understand that a large A-a gradient indicates one of the following problems:

1.) Right to Left Shunt (basically, an extreme ventilation defect)
2.) A diffusion defect
3.) Low Vdot/Qdot (ventilation defects)

What I do not understand is how a perfusion defect (High Vdot/Qdot) can cause an increased A-a gradient. If we have an alveolus that is ventilated normally, but has a reduced perfusion, the pulmonary capillary blood leaving that alveolus will still be completely oxygenated (PaO2=100mmHg). Therefore there should not be hypoxemia and there should not be an A-a gradient. However, Goljan lists perfusion defects as being one cause of increased A-a gradient hypoxemia. Is this an error? I am confused about this...
 

Knicks

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Hello all,

Long time lurker, 1st time poster. So I am going through RR path and came across something that I don't quite understand. I am reviewing the A-a gradient and how it can be used to distinguish between causes of hypoxemia.

I understand that a large A-a gradient indicates one of the following problems:

1.) Right to Left Shunt (basically, an extreme ventilation defect)
2.) A diffusion defect
3.) Low Vdot/Qdot (ventilation defects)

What I do not understand is how a perfusion defect (High Vdot/Qdot) can cause an increased A-a gradient. If we have an alveolus that is ventilated normally, but has a reduced perfusion, the pulmonary capillary blood leaving that alveolus will still be completely oxygenated (PaO2=100mmHg). Therefore there should not be hypoxemia and there should not be an A-a gradient. However, Goljan lists perfusion defects as being one cause of increased A-a gradient hypoxemia. Is this an error? I am confused about this...
I think the bolded portion is where you're wrong. You, yourself, said that there is reduced perfusion; so while there's oxygen in the alveolus, it's not making it to the capillary blood ---> hypoxemia ---> increased A-a gradient.


Someone double-check my explanation; if it's not accurate, please correct.
 

WellWornLad

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Any V/Q mismatch can potentially cause an increased A-a gradient, whether the problem is ventilation or perfusion. In either case, the mismatch has to be sufficiently large to overcome the compensatory mechanisms of the lung. In the case of a perfusion defect, this usually means a massive PE.

I think you're concentrating too much on the "single alveolus/capillary" model. The A-a gradient is about total blood oxygenation, not whatever is leaving that single capillary in that idealized model they usually teach. If you shut down enough capillaries with a PE, at some point the remaining capillaries are not going to exchange enough oxygen to meet the basic metabolic needs of the body and PaO2 - an average of all blood leaving the lungs - is going to decrease.
 
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Hello all,

Long time lurker, 1st time poster. So I am going through RR path and came across something that I don't quite understand. I am reviewing the A-a gradient and how it can be used to distinguish between causes of hypoxemia.

I understand that a large A-a gradient indicates one of the following problems:

1.) Right to Left Shunt (basically, an extreme ventilation defect)
2.) A diffusion defect
3.) Low Vdot/Qdot (ventilation defects)

What I do not understand is how a perfusion defect (High Vdot/Qdot) can cause an increased A-a gradient. If we have an alveolus that is ventilated normally, but has a reduced perfusion, the pulmonary capillary blood leaving that alveolus will still be completely oxygenated (PaO2=100mmHg). Therefore there should not be hypoxemia and there should not be an A-a gradient. However, Goljan lists perfusion defects as being one cause of increased A-a gradient hypoxemia. Is this an error? I am confused about this...
It's not an error. In terms of V/Q mismatching a perfusion defect is simply dead space. Dead space is ventilation without perfusion. In other words the alveoli (PAO2) are just fine in terms of oxygenation however what's crossing the a/c membrane and being picked up in arterial blood (PaO2) is where the problem is. A normally oxygenated alveolus means nothing if the O2 cannot perfuse into arterial blood. When arterial blood lacks oxygenation it will cause a patient to be hypoxemic. What's causing the diffusion defect needs to be diagnosed.

I know exactly what you are talking about in regards to "the pulmonary capillary blood leaving that alveolus will still be completely oxygenated (PaO2=100mmHg)" and that is true under normal circumstances. O2 enters the arterial blood at 100 torr and comes back in venous blood at 40 torr. But if there's a perfusion defect a normal O2 torr of 100 in arterial blood will be lower thus causing an increase in the A-a gradient.

So in conclusion I agree that perfusion defects account for increased A-a gradient hypoxemia.

Hope this helps and I apologize for any info that you might already know.
 
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turkeyjerky

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I love how people always just repeat dogman they're been told w/o thinking about it. When someone questions it, they just say the same thing, but louder.

The OP is right, perfusion defects cannot account for the hypoxemia seen in pulmonary embolism. Rather, hypoxemia is due to associated inflammation causing V/Q mismatching, shunting, atelectasis and functional inactivation of surfactant.
 
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I love how people always just repeat dogman they're been told w/o thinking about it. When someone questions it, they just say the same thing, but louder.

The OP is right, perfusion defects cannot account for the hypoxemia seen in pulmonary embolism. Rather, hypoxemia is due to associated inflammation causing V/Q mismatching, shunting, atelectasis and functional inactivation of surfactant.

First off, try being a team player instead of insulting those of us helping to answer the OP questions.

So you're telling me that if a patient is not perfusing they will show no signs of hypoxia? I find your reasons fascinating because shunting IS one end of the V/Q mismatching spectrum. Atelectasis and functional inactivation of surfactant - among other conditions - where there is perfusion without ventilation are conditions OF shunting. Do your research on the other end of the V/Q mismatching spectrum called Dead Space. I guarantee that hypoxemia is a condition seen when there is ventilation with no perfusion. How else are the tissues going to get supplied with O2 if there's nothing there to absorb O2 and transport it?
 
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I love how people always just repeat dogman they're been told w/o thinking about it. When someone questions it, they just say the same thing, but louder.

The OP is right, perfusion defects cannot account for the hypoxemia seen in pulmonary embolism. Rather, hypoxemia is due to associated inflammation causing V/Q mismatching, shunting, atelectasis and functional inactivation of surfactant.

"Acute respiratory consequences of pulmonary embolism include increased alveolar dead space, pneumoconstriction, hypoxemia, and hyperventilation."

Source: http://emedicine.medscape.com/article/300901-overview
 

turkeyjerky

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First off, try being a team player instead of insulting those of us helping to answer the OP questions.

So you're telling me that if a patient is not perfusing they will show no signs of hypoxia? I find your reasons fascinating because shunting IS one end of the V/Q mismatching spectrum. Atelectasis and functional inactivation of surfactant - among other conditions - where there is perfusion without ventilation are conditions OF shunting. Do your research on the other end of the V/Q mismatching spectrum called Dead Space. I guarantee that hypoxemia is a condition seen when there is ventilation with no perfusion. How else are the tissues going to get supplied with O2 if there's nothing there to absorb O2 and transport it?
I was going to call you a douche for accusing me of not being a team player (on the internet, of all places...), but then I see that you're a just an RT student--so I guess that's all you really have to fall back on.

Anyway, your post leaves me with the distinct impression that you don't know the definition of many of the terms you use. I'm not quite sure what they teach you exactly in RT school--most of the stuff you're talking about is basic material from week 1 of respiratory physiology,(did you really think think that I don't know what dead space is?) concepts the the OP clearly understands better than you do.
 

turkeyjerky

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"Acute respiratory consequences of pulmonary embolism include increased alveolar dead space, pneumoconstriction, hypoxemia, and hyperventilation."

Source: http://emedicine.medscape.com/article/300901-overview
Thanks for proving me right. You do know that the quotation you've provided does absolutely nothing to support your argument (other than simply restating it). I can play that game too:

Impaired gas exchange due to PE cannot be explained solely on the basis of mechanical obstruction of the vascular bed and alterations in the ventilation to perfusion ratio. Gas exchange abnormalities are also related to the release of inflammatory mediators, resulting in surfactant dysfunction, atelectasis, and functional intrapulmonary shunting
UptoDate
 

coldweatherblue

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pulmonary pathophys...

A perfusion defect in the base (PE..) will lead to widespread hypoxic bronchoconstriction (because of j-receptors, inflammatory mediators, etc) in areas of the lung that are normally well ventilated (like at the apex.) So the defect in perfusion causes a reflex that shunts MORE blood to areas of the lung that are suffering from reflex bronchoconstriction, leading to V/Q mismatch and resultant A-a gradiant.

just remember, the mechanism of hypoxemia in PE is NOT just the deadspace ventilation caused by an area being ventilated but not perfused (ie, the area of the defect.) the main cause of hypoxemia in PE is the reflex bronchoconstriction of other areas of the lung that are normal, which leads to V/Q mismatch (ie, low V, high Q, which is the opposite of the area affected by the PE.)
 

45408

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I was going to call you a douche for accusing me of not being a team player (on the internet, of all places...), but then I see that you're a just an RT student--so I guess that's all you really have to fall back on.
Really? Stay classy.
 
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cetona

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Hello all,

Long time lurker, 1st time poster. So I am going through RR path and came across something that I don't quite understand. I am reviewing the A-a gradient and how it can be used to distinguish between causes of hypoxemia.

I understand that a large A-a gradient indicates one of the following problems:

1.) Right to Left Shunt (basically, an extreme ventilation defect)
2.) A diffusion defect
3.) Low Vdot/Qdot (ventilation defects)

What I do not understand is how a perfusion defect (High Vdot/Qdot) can cause an increased A-a gradient. If we have an alveolus that is ventilated normally, but has a reduced perfusion, the pulmonary capillary blood leaving that alveolus will still be completely oxygenated (PaO2=100mmHg). Therefore there should not be hypoxemia and there should not be an A-a gradient. However, Goljan lists perfusion defects as being one cause of increased A-a gradient hypoxemia. Is this an error? I am confused about this...
I think this is being bogged down more than it should be. I think the best explanation to the OP's specific question was provided previously in that it's better to look at the big picture. What you say seems correct that in that individual capillary to which you refer, the blood leaving would still have a PaO2 of 100mmHg. However, when a large enough number of alveoli have decreased or no perfusion, there is not enough overall O2 and CO2 exchange, leading to hypoxemia.
 
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I was going to call you a douche for accusing me of not being a team player (on the internet, of all places...), but then I see that you're a just an RT student--so I guess that's all you really have to fall back on.

Anyway, your post leaves me with the distinct impression that you don't know the definition of many of the terms you use. I'm not quite sure what they teach you exactly in RT school--most of the stuff you're talking about is basic material from week 1 of respiratory physiology,(did you really think think that I don't know what dead space is?) concepts the the OP clearly understands better than you do.

You're right. I really have no idea the definitions of the terms that I use. They teach us a bunch of BS that has no clinical relevance. Material that is so basic that med students such as yourself mastered in one week. But who am I to compare to a med student?
 

Knicks

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Soooooo, my explanation was wrong? :confused:
 

jdover52

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I was going to call you a douche for accusing me of not being a team player (on the internet, of all places...), but then I see that you're a just an RT student--so I guess that's all you really have to fall back on.

Anyway, your post leaves me with the distinct impression that you don't know the definition of many of the terms you use. I'm not quite sure what they teach you exactly in RT school--most of the stuff you're talking about is basic material from week 1 of respiratory physiology,(did you really think think that I don't know what dead space is?) concepts the the OP clearly understands better than you do.
Wow, you think you're so special because you're in medical school? I feel bad for your future patients with that kind of attitude...please just spare them and switch professions while you can, it's not too late
 

Knicks

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I think you mixed up diffusion and perfusion.
Hmmm,, so you're saying that although less blood is reaching the gas-exchange membrane, the diffusion of oxygen is not affected, and therefore the little blood that has reached that gas-exchange membrane will still be sufficiently oxygenated?

But if less blood is going to be oxygenated, ultimately isn't that going to lead to hypoxia? This is what I was thinking in my initial post.
 

cetona

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Hmmm,, so you're saying that although less blood is reaching the gas-exchange membrane, the diffusion of oxygen is not affected, and therefore the little blood that has reached that gas-exchange membrane will still be sufficiently oxygenated?

But if less blood is going to be oxygenated, ultimately isn't that going to lead to hypoxia? This is what I was thinking in my initial post.
I could be wrong but yes, that is how I am thinking about it. In your original post you said "while there's oxygen in the alveolus, it's not making it to the capillary blood ---> hypoxemia ---> increased A-a gradient." I don't think this is true because it implies a problem with diffusion, but the oxygen in the alveolus is making it to the blood - there's just not enough overall blood where sufficient O2 and CO2 exchange is occurring, which is what you just said.
 
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I could be wrong but yes, that is how I am thinking about it. In your original post you said "while there's oxygen in the alveolus, it's not making it to the capillary blood ---> hypoxemia ---> increased A-a gradient." I don't think this is true because it implies a problem with diffusion, but the oxygen in the alveolus is making it to the blood - there's just not enough overall blood where sufficient O2 and CO2 exchange is occurring, which is what you just said.

Agreed. :thumbup: If there's sufficient O2 in the alveoli and it's not able to diffuse through the a/c membrane normally than there is an issue with diffusion. (pulmonary fibrosis, et al...) A DLCO test would be a great way to diagnositcally confirm a diffusion defect.
 

Knicks

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I could be wrong but yes, that is how I am thinking about it. In your original post you said "while there's oxygen in the alveolus, it's not making it to the capillary blood ---> hypoxemia ---> increased A-a gradient." I don't think this is true because it implies a problem with diffusion, but the oxygen in the alveolus is making it to the blood - there's just not enough overall blood where sufficient O2 and CO2 exchange is occurring, which is what you just said.
Yeah, and that's what I meant to say in my original post. :)


Soooo, I was right, right? :D
 

OveractiveBrain

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An increased alveolar-arterial gradient stems from the ability to ventilate the alveoli with sufficient oxygen but some process that limits the oxygen from getting into the capillaries.

In a single Alveolar-capillary model, a total perfusion defect will create an alveolus with all the oxygen it can handle, but no where for it to go. The expired oxygen from that alveolus will be enormous (Alveolar O2 very high). The blood "leaving" that system will have no oxygen (Arterial O2 very low).

Now spread this to a larger model of 5 alveoli-capillary systems. If there is a defect in just one perfusion, the expired air will greater from that one alveolus. Combined with the normal alveoli, the alveolar O2 will be higher than normal. While the blood leaving the other 4 will be normal (you cannot hypersaturate blood with oxygen in any meaningful manner), the alveolar oxygen is now elevated. Normal arterial O2, High Alveolar O2, increased A-a gradient. The increased A-a gradient stems from a relatively NORMAL arterial oxygen, but an increased Alveolar oxygen, a result of the inability to get oxygen out of the alveolus with the perfusion defect.

To expand this model to the millions of alveoli in the lung, there would have to be a significant perfusion defect to dent the normal expired alveolar O2. In that case the A-a gradient would likely be overshadowed by the massive heart strain, but in any case, thats the physiology.

In the case of a particular perfusion defect, called a pulmonary embolus, the isolated, tiny defect in perfusion produces almost no impact on the A-a gradient. Platelet derived mediators impact the global lung simultaneously, increasing capillary permeability and causing fluid to leak into the interstitium. This increases the diffusion distance (the thickness of the wall between alveolus and capillary essentially increases), limiting diffusion of oxygen. This happens at a global level, and is therefore a very large diffusion defect.
 
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OveractiveBrain

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Rather than get into the fight, Ill just offer my own explanation, and hope it works out for everyone.

An increased alveolar-arterial gradient stems from the ability to ventilate the alveoli with sufficient oxygen but some process that limits the oxygen from getting into the capillaries.

In a single Alveolar-capillary model, a total perfusion defect will create an alveolus with all the oxygen it can handle, but no where for it to go. The expired oxygen from that alveolus will be enormous (Alveolar O2 very high). The blood "leaving" that system will have no oxygen (Arterial O2 very low).

Now spread this to a larger model of 5 alveoli-capillary systems. If there is a defect in just one perfusion, the expired air will greater from that one alveolus. Combined with the normal alveoli, the alveolar O2 will be higher than normal. While the blood leaving the other 4 will be normal (you cannot hypersaturate blood with oxygen in any meaningful manner), the alveolar oxygen is now elevated. Normal arterial O2, High Alveolar O2, increased A-a gradient. The increased A-a gradient stems from a relatively NORMAL arterial oxygen, but an increased Alveolar oxygen, a result of the inability to get oxygen out of the alveolus with the perfusion defect.

To expand this model to the millions of alveoli in the lung, there would have to be a significant perfusion defect to dent the normal expired alveolar O2. In that case the A-a gradient would likely be overshadowed by the massive heart strain, but in any case, thats the physiology.

In the case of a particular perfusion defect, called a pulmonary embolus, the isolated, tiny defect in perfusion produces almost no impact on the A-a gradient. Platelet derived mediators impact the global lung simultaneously, increasing capillary permeability and causing fluid to leak into the interstitium. This increases the diffusion distance (the thickness of the wall between alveolus and capillary essentially increases), limiting diffusion of oxygen. This happens at a global level, and is therefore a very large diffusion defect.
 

Knicks

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^^ Perfect
 

ZIMAgo

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Rather than get into the fight, Ill just offer my own explanation, and hope it works out for everyone.

An increased alveolar-arterial gradient stems from the ability to ventilate the alveoli with sufficient oxygen but some process that limits the oxygen from getting into the capillaries.

In a single Alveolar-capillary model, a total perfusion defect will create an alveolus with all the oxygen it can handle, but no where for it to go. The expired oxygen from that alveolus will be enormous (Alveolar O2 very high). The blood "leaving" that system will have no oxygen (Arterial O2 very low).

Now spread this to a larger model of 5 alveoli-capillary systems. If there is a defect in just one perfusion, the expired air will greater from that one alveolus. Combined with the normal alveoli, the alveolar O2 will be higher than normal. While the blood leaving the other 4 will be normal (you cannot hypersaturate blood with oxygen in any meaningful manner), the alveolar oxygen is now elevated. Normal arterial O2, High Alveolar O2, increased A-a gradient. The increased A-a gradient stems from a relatively NORMAL arterial oxygen, but an increased Alveolar oxygen, a result of the inability to get oxygen out of the alveolus with the perfusion defect.
Except no blood is actually leaving that single alveolar unit... which contradicts the otherwise perfect explanation.

The point that the A-a gradient isn't seen except in a massive PE and likely implies a hemodynamic instability because the capacity of blood to circulate through the remaining vasculature is close to being met or exceeded- resulting in a low V/Q mismatch in the non affected pulmonary units.

My pulmonary attending used to hate when people brought up the A-a gradient when pimped about PEs. :)
 
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