Partial pressure of gases in various parts of the respiratory system

AI Thread Summary
Understanding the respiratory system requires clarity on concepts like anatomic dead space and residual volume. Anatomic dead space refers to air in the conducting zones that does not reach the alveoli, while residual volume is the air remaining in the lungs after exhalation, which cannot be forcibly expelled. The partial pressure of oxygen (P02) in alveoli is lower than in inspired air due to the mixing with residual volume and the presence of water vapor, while expired air has a higher P02 due to mixing with dead space air. Arterial P02 is primarily determined by oxygen dissolved in blood and is influenced by shunting, with a typical value around 95 mmHg. The partial pressure of carbon dioxide (PCO2) in arterial blood stabilizes at around 40 mmHg due to equilibrium with alveolar PCO2, despite the presence of bicarbonate in the bloodstream.
sameeralord
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Hello everyone,

Ok to understand the respiratory system, proper understanding of this diagram is essential. Something I don't have, so if anyone can help me with these questions I would be very greatful. Thanks :smile:

http://img515.imageshack.us/img515/8923/rightbv.jpg

1. Anatomic dead space and residual volume?
I know what anatomic dead space is but residual volume is confusing me. Is it in the conducting zone as well and non technically isn't it like some kind of anatomic dead space.

2. Why does the alveoli have less partial pressure of oxygen than inspired air? I can understand how addition of water vapour can reduce it but residual volume just confused me. Does oxygen from residual volume get mixed with this as well increasing P02.

3. Why does the expired air have higher P02 of oxygen than alveoli?
I can understand how mixing with dead space would archieve it. Does the residual volume affect it as well. Residual volume is confusing me.

4. What creates the P02 in arterial blood and why it is 95?
So it is basically oxygen dissolved in blood right that causes the partial pressure of oxygen.We consider the haemoglobin bind oxygen as part of dissolved blood right? 95 is due to shunting right?

5. Why is PC02 in alveoli 40 and what creates PC02 in arterial blood?
Is it 40 in alveoli because CO2 diffuses into it from the capillaries. So C02 from tissues goes to capillarie-->veins--->capillaries---->alveoli so from where does arterial PC02 come from.

Your help would be greatly appreciated. Thanks :smile:
 
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Before I offer any help, are these questions for an assignment, or questions you have formed on your own while studying?
 
Moonbear said:
Before I offer any help, are these questions for an assignment, or questions you have formed on your own while studying?

No no not assignment. I have given my own explanation for each question. This is not homework help. :smile:
 
sameeralord said:
No no not assignment. I have given my own explanation for each question. This is not homework help. :smile:
Okay then. Just checking; these sound like the sort of questions I might torture my students with. :wink:

sameeralord said:
1. Anatomic dead space and residual volume?
I know what anatomic dead space is but residual volume is confusing me. Is it in the conducting zone as well and non technically isn't it like some kind of anatomic dead space.
Anatomic dead space is in the air passages; the portion of air that never gets to the lungs (i.e., in the trachea, bronchi, bronchioles). Residual volume is the air left in the lungs that can't be forcibly exhaled.

2. Why does the alveoli have less partial pressure of oxygen than inspired air? I can understand how addition of water vapour can reduce it but residual volume just confused me. Does oxygen from residual volume get mixed with this as well increasing P02.

3. Why does the expired air have higher P02 of oxygen than alveoli?
I can understand how mixing with dead space would archieve it. Does the residual volume affect it as well. Residual volume is confusing me.

4. What creates the P02 in arterial blood and why it is 95?
So it is basically oxygen dissolved in blood right that causes the partial pressure of oxygen.We consider the haemoglobin bind oxygen as part of dissolved blood right? 95 is due to shunting right?

5. Why is PC02 in alveoli 40 and what creates PC02 in arterial blood?
Is it 40 in alveoli because CO2 diffuses into it from the capillaries. So C02 from tissues goes to capillarie-->veins--->capillaries---->alveoli so from where does arterial PC02 come from.

Your help would be greatly appreciated. Thanks :smile:

I thought this was going to be easy to answer, and then I looked again at your diagram. Where did you get it from? It's quite misleading the way it is drawn, because it doesn't represent that pulmonary veins contain the oxygenated blood returning to the heart to be distributed to the body via the systemic arteries, and then systemic veins return low-oxygenated and higher CO2 blood to the heart for return to the lungs via pulmonary arteries. It seems to mix up the concepts of arteries and veins in a very confusing way.

Generally, the concept to understand is that partial pressures of gases are traveling in a concentration gradient from high to low as gas exchange occurs. Oxygen is picked up from air at higher levels than carbon dioxide, because air has a higher partial pressure of oxygen than carbon dioxide. Carbon dioxide gets picked up by venous blood from the tissues as a waste product.

The reason you don't see a large difference in CO2 between venous and arterial blood, like you do for O2, is that a lot of the CO2 is maintained as bicarbonate in the blood, not as free CO2 or bound to hemoglobin.
 
Thanks Moonbear!

I still have one question. Why does arterial carbon dioxide contain relatively high pressure.
So carbon dioxide in veins is 46 and in alveoli it is 40 so shouldn't the carbon dioxide in arteries be somewhere like 46-40=6. However it is 40. I don't get it. So having bicarbonate should reduce pressure of CO2 in arterial blood further right. Thanks a lot for your help!
 
Again, you need to remember the direction of concentration gradients. When the excess of CO2 is in venous blood, and exchange occurs in the direction of dumping out CO2 into the alveoli, you can't get a concentration lower than what is present in the alveoli. Once an equilibrium between PCO2 in the alveoli and arteries is reached, no more exchange occurs.
 
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