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 help! lung physiology questions  



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Author3 Posts
  #1

hello, i am new here and really excited to find this forum...hopefully i can contribute and learn as much as possible in this forum...smiling face

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 ...smiling face

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 smiling face




  #2

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

rate of gas diffusion = A/T × d × (p1-p2)
from the equation there're 2 structural factors and 2 gas factors affect rate of diffusion
structural are ==> [A = surface ares / T = thickness of the membrane ]
gas factors are ==> [D = diffusion constant (solubility) / (p1-p2) = pressure gradient ]
so as you notice the rate of diffusion is directly proportional to pressure gradient
and as you increase the inspired concentration of oxygen you'll increase the pressure gradient across the alveolar membrane resulting in increase in the rate of gas diffusion across the membrane .

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

V/Q mismatch means that V/Q ratio may increase or decrease
if V/Q = 0 ==> airway obstruction (shunt)
and if V/Q = infinity(high value) ==> blood flow obstruction
SO right to left shunt is a condition having low V/Q ratio and charactrized by the 5T's (Tetralogy/Transposition/Truncus/Tricuspid/TAPVR)

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

V/Q mismatch will response to oxygen therapy ONLY if it has high value so 100% O2 will improve PO2 , while RIGHT TO LEFT SHUNT as you said has LOW v/q ratio which means airway obstruction (shunt) so if the airway is obstructed there'll be NO USE of oxygen therapy and 100% O2 will not improve PO2 .

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?

Alveolar (capillaries) and extra alveolar vessels (arteries and veins) have different surrounding pressures.
Alveolar vessels are surrounded by alveolar pressure (measured relative to pleural pressure). Transmural pressure is capillary pressure minus alveolar pressure.
Extra alveolar vessels are approximately surrounded by intrapleural pressure. They can be thought of as being tethered to the lung parenchyma.

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?


Obstructive (or resorptive) atelectasis results from blockage of an airway. Air retained distal to the occlusion is then resorbed from nonventilated alveoli. Over time, the affected regions become totally airless. The rate at which atelectasis develops, and the extent of collapse, depend upon several factors, particularly the degree of collateral ventilation and the composition of inspired gas.

i hope that help you , GL


  #3

hello, almsamim..thx u so much for the respond. i very appreciate that.. smiling face
i enjoy your answers ,thx a lot smiling face but, if u don't mind , i would like to ask you some again that still confuse me...

so, in absorption atelectasis , what is the true cause of the alveoli collapse?

is it the affected alveoli that really empty its gas to zero? or is it actually , the gas in the alveoli that overtime will equilibrated with the low mix venous blood ( 40 and 40, respectively) so, there will be no further gas diffusion?

thx a lot smiling face





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