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Billy BA
08-17-2006, 12:01 PM
Anyone ever wondering why it is in Type I Respiratory Failure that there is low pCO2 along with low pO2? The thing that keeps getting me is that I can see why you might low pCO2 and low pO2 when there is some diffusion problem b/c CO2 has a much greater capacity for diffusion. But I can't come up with a mechanism for why it is that CO2 is getting blown off and PO2 isn't diffusing properly into the blood.

Say you get a PE and get the situation of increased physiologic dead space. Well, the blood gets shunted to other functional units and the CO2 gets blown off but the pO2 doesn't rise proportionally. I was thinking that maybe has to do w/ the increased flow and the O2 not being able to equalize, but then in exercise when the cardiac output increases the O2 still has time to equalize, just towards the end of the capillary bed so I can't really buy that idea. Anyone got any ideas for the pathophysiology of this? I have tried looking up it for days on the internet, asked my residents and attendings and have yet to get a decent answer. If you know of any good physiology resources online or know the answer, it would be greatly appreciated!

md90
08-17-2006, 02:25 PM
Think in a clinical/practical sense... what is the body doing in each situation?

First remember:
1. ventilation is matched to perfusion.. so that there can be adequate gas exchange--this is the goal!!!
2. ventilation and perfusion are greater at the base of the lung
3. wasted ventilation at apex of lung
4. wasted perfusion at base of lung

With exercise.. what is going on? there is increased cardiac output therefore there is vasodilation.. meaning that there is better gas exchange (ventilation and perfusion are very close to being matched).. very little wastage...

So if there is an obstruction (eg fibrosis).. how can oxygen get through that?? think of a dense forest.. and you have to get through that.. it can be very difficult especially if you don't the route OR the route gets changed; OR if the space is limited (vasoconstriction).. very little can get through the space..

Hope that this helps... also try drawing out a picture, and writing out the information that you know... sometimes a visual will help to understand..:p

Anyone ever wondering why it is in Type I Respiratory Failure that there is low pCO2 along with low pO2? The thing that keeps getting me is that I can see why you might low pCO2 and low pO2 when there is some diffusion problem b/c CO2 has a much greater capacity for diffusion. But I can't come up with a mechanism for why it is that CO2 is getting blown off and PO2 isn't diffusing properly into the blood.

Say you get a PE and get the situation of increased physiologic dead space. Well, the blood gets shunted to other functional units and the CO2 gets blown off but the pO2 doesn't rise proportionally. I was thinking that maybe has to do w/ the increased flow and the O2 not being able to equalize, but then in exercise when the cardiac output increases the O2 still has time to equalize, just towards the end of the capillary bed so I can't really buy that idea. Anyone got any ideas for the pathophysiology of this? I have tried looking up it for days on the internet, asked my residents and attendings and have yet to get a decent answer. If you know of any good physiology resources online or know the answer, it would be greatly appreciated!

Billy BA
08-17-2006, 03:42 PM
md90,

I am not sure if you really understood the question that was posted. I understand the normal physiology of the lung. I also understand how it is that a diffusion impairment (fibrosis) will affect the pO2 before it affects the pCO2 due the CO2 being much more soluble than O2.

What I am questioning is how it is that w/ an increased V/Q mismatch (pulmonary emboli...ventilation w/o perfusion) shows up with Type I respiratory failure (low pO2, low pCO2). Low CO2 by definition is alveolar hyperventilation. Now, there is a reason that for the low O2 in the face of low CO2. I have read in some sources that it has to do with the different disassociation curves for pCO2 and pO2. The pCO2 being a more linear relationship and pO2 having the sigmoidal relationship. Another source said that the acute pulmonary hypertension from a PE will override the hypoxic vasoconstriction and establish a right to left shunt. Neither explanation makes much sense to me.

If the CO2 is reaching the a patent alveolus to be blown off, why is that the O2 is not diffusing properly into the capillaries?




Think in a clinical/practical sense... what is the body doing in each situation?

First remember:
1. ventilation is matched to perfusion.. so that there can be adequate gas exchange--this is the goal!!!
2. ventilation and perfusion are greater at the base of the lung
3. wasted ventilation at apex of lung
4. wasted perfusion at base of lung

With exercise.. what is going on? there is increased cardiac output therefore there is vasodilation.. meaning that there is better gas exchange (ventilation and perfusion are very close to being matched).. very little wastage...

So if there is an obstruction (eg fibrosis).. how can oxygen get through that?? think of a dense forest.. and you have to get through that.. it can be very difficult especially if you don't the route OR the route gets changed; OR if the space is limited (vasoconstriction).. very little can get through the space..

Hope that this helps... also try drawing out a picture, and writing out the information that you know... sometimes a visual will help to understand..:p

md90
08-17-2006, 05:02 PM
md90,
I am not sure if you really understood the question that was posted. I understand the normal physiology of the lung. I also understand how it is that a diffusion impairment (fibrosis) will affect the pO2 before it affects the pCO2 due the CO2 being much more soluble than O2.

What I am questioning is how it is that w/ an increased V/Q mismatch (pulmonary emboli...ventilation w/o perfusion) shows up with Type I respiratory failure (low pO2, low pCO2). Low CO2 by definition is alveolar hyperventilation. Now, there is a reason that for the low O2 in the face of low CO2. I have read in some sources that it has to do with the different disassociation curves for pCO2 and pO2. The pCO2 being a more linear relationship and pO2 having the sigmoidal relationship. Another source said that the acute pulmonary hypertension from a PE will override the hypoxic vasoconstriction and establish a right to left shunt. Neither explanation makes much sense to me.

If the CO2 is reaching the a patent alveolus to be blown off, why is that the O2 is not diffusing properly into the capillaries?

To answer your question.. I went back and looked at what respiratory failure was... inadequate gas exchange r/t hypoxemia with or without hypercapnia. With Type I: both pO2 and pCO2 are both low... but there are various causes to this type of respiratory failure...and it can be either acute or chronic; And from what I gathered from the sources, we must first ask, what is the underlying cause for the failure? The causes: asthma, PE, pulmonary edema, pulmonary fibrosis, ARDS (acute causes); the initial finding: Low pO2 and High pCO2... leading to the conclusion:

that the hypocapnia is the result... at least in most of the sources that I read.. the person will first go into a hypercapnia and hypoxemia (appears as if it's a compensation made by the body)... b/c our bodies are trying to bring the pH back to normal...

here is one of the sources that I checked: http://www.gpnotebook.co.uk/simplepage.cfm?ID=-979763191

What do you think? This is a good test question...to place on the USMLE step 1 exam, and I thank you for asking it... and will continue to research for possible answers on my breaks... :rolleyes:

Billy BA
08-17-2006, 05:13 PM
I see that we are speaking in riddles. Master your fear or fear will master you. To be one with the world will make the world one with you.

md90
08-17-2006, 05:41 PM
sorry.. I push the "submit" button before completing my thought...; Then I realized that I might be looking at this wrong.. and changed my thinking and the focus from the O2 to the CO2... and how the pathophysiology of the "causes" would lead to the respiratory failure..... don't know if I'm making sense... I'm thinking as I am writing....

PS:
Master your fear or fear will master you. To be one with the world will make the world one with you. I like it... and so true..







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