lung physiology questions..please help !!

[ketap]

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hello, i don't know where to put this questions because basically it's mostly contained with pathophysiology questions ( i think) ..so i decided to put it in the physiology subforum...if this is inappropiate, the moderator is very welcome to move this thread to the right place..

friends, i am learning about respiratory physiology and patophysiology right now...and i found some confusions, some are solved after i thought it for a while, but some aren't answered yet...so i decided to bring it to this forum for a discussion..please help me, thx u ...

1. why with a higher inspired concentration of oxygen, there will be more rapid gas diffusion? is there any law explain this?

2. what is the difference between right to left shunt and v/q mismatch?because as we know, they both can be alike: right to left shunt : v/q= 0, and v/q mismatch : low v/q

3. and why does v/q mismatch will response to oxygen therapy but, the right to left shunt will not?

4. is there such thing as extra alveolar and intra alveolar vessels? what and where are they? because it is very confusing me why they are compressed when low and high volume, respectively?

5. i have read this :
Quote:
If the proximal airways are obstructed, for example by mucus plugs, the gases in the alveoli gradually empty into the blood along the concentration gradient, and are not replenished: the alveoli collapse, a process known as atelectasis
i don't really understand some of this statement..does the alveoli really eventually empty all of it contents to zero? if it does, how can the alveoli collapse? where are the surfactant and alveolar interdependence?

sorry for asking many questions..i am quiet confuse about them, so i decided to bring this up to the forum ....

please help,, thx u warm regards, Ketap

 

[Ableton]

All of these questions can easily be answered by picking up a physiology textbook. In the future, I urge you to do so, but here we go for now:

1. why with a higher inspired concentration of oxygen, there will be more rapid gas diffusion? is there any law explain this?

Diffusion rates depend on the partial pressure difference, surface area of the membrane and the permeability.

J = PA(Cout - Cin)

2. what is the difference between right to left shunt and v/q mismatch?because as we know, they both can be alike: right to left shunt : v/q= 0, and v/q mismatch : low v/q

Right-to-left shunts are anatomical defects where a certain amount of the blood bypasses the pulmonary circulation, resulting in hypoxemia. The blood never has the chance for gas exchange.

With a low V/Q, you just have low ventilation relative to perfusion. Less air is getting into the lugs for gas exchange.

3. and why does v/q mismatch will response to oxygen therapy but, the right to left shunt will not?

You should be able to answer this now that you know the difference between the two.

4. is there such thing as extra alveolar and intra alveolar vessels? what and where are they? because it is very confusing me why they are compressed when low and high volume, respectively?

I don't know a lot about this, since it seems fairly useless. My best guess would be when the alveoli are filled with air, the extra-alveolar vessels are compressed and blocked; when the alveoli are emptied, these vessels become distended with blood flow (similar concept to coronary blood flow only taking place during diastole). Someone feel free to correct me on this if they know the answer.

5. i have read this :
Quote:
If the proximal airways are obstructed, for example by mucus plugs, the gases in the alveoli gradually empty into the blood along the concentration gradient, and are not replenished: the alveoli collapse, a process known as atelectasis
i don't really understand some of this statement..does the alveoli really eventually empty all of it contents to zero? if it does, how can the alveoli collapse? where are the surfactant and alveolar interdependence?

The oxygen in the alveoli will never really reach zero, but it will come into equilibrium with the venous blood, so no gas exchange will be taking place. A decrease in alveolar oxygen partial pressure results in hypoxic vasocontrsiction. This reduces the blood flow to areas of the lungs where gas exchange is inefficient and perfusion would be wasted. No new air is coming in to distend the alveoli, so they will collapse.

 

[McGillGrad]

Read BRS

 

[ketap]

hi, Ableton and McGillGrad: thx a lot for the input..i really appreciate it..thx u very much...🙂

i actually had read 3 physiology books..guyton, Sherwood, and West respiratory physiology books...but all the questions i am asking wasn't there and some of them confuse me (sometimes, because it is hard for me to understand), so i dicided to discuss it in this forum..🙂

i can see well a lot of great answer from Ableton..thx u very much 🙂
but if it is ok, i would like to ask...
1.

Diffusion rates depend on the partial pressure difference, surface area of the membrane and the permeability.

i know that principal too..but i always think that principle is more correlated to the amount of a gas transported than the rapidity of a moving gas..am i wrong?

2.

I don't know a lot about this, since it seems fairly useless. My best guess would be when the alveoli are filled with air, the extra-alveolar vessels are compressed and blocked; when the alveoli are emptied, these vessels become distended with blood flow (similar concept to coronary blood flow only taking place during diastole). Someone feel free to correct me on this if they know the answer.

actually, that is very true..i read it from a critical care medicine textbook, but, what i am confuse is not that..but , the real confusion to me is if there is such thing called as intraalveolar vessels?? i tried to find the pics of it to understand where it is and what it is..but i can't find anything called intraalveolar vessels..😕

 

[ACSurgeon]

hi, Ableton and McGillGrad: thx a lot for the input..i really appreciate it..thx u very much...🙂

i actually had read 3 physiology books..guyton, Sherwood, and West respiratory physiology books...but all the questions i am asking wasn't there and some of them confuse me (sometimes, because it is hard for me to understand), so i dicided to discuss it in this forum..🙂

i can see well a lot of great answer from Ableton..thx u very much 🙂
but if it is ok, i would like to ask...
1.

i know that principal too..but i always think that principle is more correlated to the amount of a gas transported than the rapidity of a moving gas..am i wrong?

2.

actually, that is very true..i read it from a critical care medicine textbook, but, what i am confuse is not that..but , the real confusion to me is if there is such thing called as intraalveolar vessels?? i tried to find the pics of it to understand where it is and what it is..but i can't find anything called intraalveolar vessels..😕

who cares? unless you're a histologist this shouldnt matter to you. Move on.

 

[bergwood]

1.

i know that principal too..but i always think that principle is more correlated to the amount of a gas transported than the rapidity of a moving gas..am i wrong?

Think of it this way:
Let's say that for every 10 molecules of O2 in the alveolus, 1 molecule would diffuse into the capillary per second. So if you had only 10 molecules of O2 total in the alveolus (ie low O2 concentrations), 1 would move across in a second, a rate of 1 molecule/second. Now lets say you had 100 molecules of O2 in the alveolus (ie high O2 concentrations), in which case 10 would move across in a second, a rate of 10 molecules/second. As such, in low O2 concentrations, less O2 is moved and at a slower rate, while at high O2 concentrations, more O2 is moved and at a faster rate.

2.

actually, that is very true..i read it from a critical care medicine textbook, but, what i am confuse is not that..but , the real confusion to me is if there is such thing called as intraalveolar vessels?? i tried to find the pics of it to understand where it is and what it is..but i can't find anything called intraalveolar vessels..😕

Intraalveolar vessels are arterioles, capillaries, and venules. They are subject to compression forces from the pressure of air in the alveoli (ie West's zone 1 conditions). When alveolar pressure gets too high (ie mechanical ventilation set too high or COPD with gas trapping), these vessels get compressed and there is less flow through them. Extraalveolar vessels are all the other vessels in the lung and are not subject to compression from the pressure of air in the alveoli; however, they can be pulled open by expansion of the lung.

 

[ketap]

lazymed and bergwood: tx u so much for the responds..🙂

Bergwood: thx u very much for that explanation ..those answers make me understand..no book could explain it better..thx u so much 🙂

i just realize, i still have 1 unclear question that haven't been answered yet...

Quote:
Originally Posted by ketap
5. i have read this :
Quote:
If the proximal airways are obstructed, for example by mucus plugs, the gases in the alveoli gradually empty into the blood along the concentration gradient, and are not replenished: the alveoli collapse, a process known as atelectasis
i don't really understand some of this statement..does the alveoli really eventually empty all of it contents to zero? if it does, how can the alveoli collapse? where are the surfactant and alveolar interdependence?

The oxygen in the alveoli will never really reach zero, but it will come into equilibrium with the venous blood, so no gas exchange will be taking place. A decrease in alveolar oxygen partial pressure results in hypoxic vasocontrsiction. This reduces the blood flow to areas of the lungs where gas exchange is inefficient and perfusion would be wasted. No new air is coming in to distend the alveoli, so they will collapse.

so, there is no air to distend the alveoli, but where are the surfactant to hold the alveoli to be still opened ?
please help me answer this question , this part still confuse me..

warm regards,Ketap

thx u 🙂

 

[Ableton]

so, there is no air to distend the alveoli, but where are the surfactant to hold the alveoli to be still opened ?
please help me answer this question , this part still confuse me..

You're really getting way to caught up in the details.

BIG PICTURE:
Hypoxia in the lung leads to vasocontriction to minimize gas exchange in areas of the lung that are not working properly. In other tissues, hypoxia leads to vasodilation to maximize tissue perfusion.

No new O2 to alveoli -> hypoxic vasocontriction of blood vessels -> cell death and tissue necrosis -> no new surfactant being made -> collapse of alveoli and probably fibrosis of the lung parenchyma

Honestly, this isn't that hard, you really should be able to put one and one together to figure this stuff out on your own rather than running to others for the answer. It will help you learn the material better in the end, not that you'd really need to know it in this much detail.

 

[Captopril]

You're really getting way to caught up in the details.

BIG PICTURE:
Hypoxia in the lung leads to vasocontriction to minimize gas exchange in areas of the lung that are not working properly. In other tissues, hypoxia leads to vasodilation to maximize tissue perfusion.

No new O2 to alveoli -> hypoxic vasocontriction of blood vessels -> cell death and tissue necrosis -> no new surfactant being made -> collapse of alveoli and probably fibrosis of the lung parenchyma

Honestly, this isn't that hard, you really should be able to put one and one together to figure this stuff out on your own rather than running to others for the answer. It will help you learn the material better in the end, not that you'd really need to know it in this much detail.

A lot of IMGs from outside of North America (I am speaking as one so I have insight) get caught up in these mundane details because we aren't really taught alot of mechanisms in Pathology. For that reason, when it's time to study for Step 1 and you open Goljan up and see that he's dropping straight SCIENCE regarding every disease, some people don't know how deep we really have to know about stuff....hence, you have dudes asking about the particular structure of the 3rd electron shell of the 4th Carbon of the Phenylalanine of the Fibrillin protein of the extra cellular matrix of the lung.

 

[ketap]

Ableton: thx for the answers n giving time to reply me..🙂 ..i really appreciate that 🙂.. actually, i have read and re-read again lots of time before posting in this forum, but i really don't get the answers, so i try to ask here..i am very sorry for bothering u for the details.. this just came up in my thinking and i can't find the answers and it's annoying me ( makes me curious) ...eg.,I have never thought of something like your answers...so , i am very thx u for giving some time for me..🙂
thx for all the replies to other friends too 🙂 u all have been so helpful 🙂