questions on pulmonary ventilation

[SamarEsawy]

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Hello,world

1- the -ve intrapleural pressure is preventing the lung from collapsing.if the pleural pressure became equal to the atm. Pressure,the lung would recoil and collapse


that’s okay but how?I can’t imagine..what makes negative pressure prevent lung from collapsing?this is going over my head.


2- Each elastic structure has a volume where it’s neither stretched nor compressed.


This volume is called relaxation volume.
If the relaxation volume of the lungs is 1 litre and that of the thoracic wall is 5 litres
Then at the end of normal expiration when all respiratory muscles are relaxed ,the volume of lung and thoracic wall equals 2.3 litres
I don’t understand this at all Can you explain it for me?


3- What is meant by the surface tension of the fluid lining the alveoli? And how does this tension make the alveoli tend to shrink?
4- Do Intrapleural pressure changers during inspiration and expiration precede lung volume changes?how
5- Work required to expand the lungs against the lungs and chest wall elastic forces is called “compliance or elastic work”


Oh that’s horrible..why against chest wall elastic forces?I know that chest has a continous tendency to expand outwards.


6- How is the resistance of medium sized bronchi greatest ?greater than resistance of small bronchioles?oh man you must be kiddin me
7- What makes fall in PCO2 cause bronchoconstriction?
“Even following a maximum expiration , some air is left in the lungs and air ways because the negative intrapleural pressure prevents complete collapse of the lungs. This air aerates blood between breaths and hence prevets marked changes in blood PCO2 and PO2”


Exaplain this please
People I’m feeling so stupid when I started reading about pulmonary ventilation in my text book ..
I can’t understand all of this at
Thanks in advance

 

[Little Soldier]

ok, ill try from the beginning.

negative means relative to atmospheric, so -5mmHg means 760 - 5 = 755mmHg. imagine the mouth and vocal cords open, this fills the lung with atmospheric pressure air, since it is greater than 755mmHg, the alveoli dont collapse because its being pushed outwards at a force of 760mmHg. i think youre applying the negative pressure in the wrong direction, the negative pressure is between the layers of the pleura, since the parietal end is stuck to the chest wall its being held at that area, the visceral is stuck around the lungs and so as the lungs try to collapse inwards, the chest wall is simultaneously being pulled outwards creating the negative pressure. this means that the negative pressure is literally dragging the lungs out wards. someone please correct me if im mistaken.

for question 2, im not sure where you got those figures, if you could paste them here ill try to help

3 - the surface tension is the tension of the molecules in the alveoli trying to stick together, like if you have tiny droplets of water near eachother they draw together. if you dont understand this then its best you look it up

4 - yes, they do. basically as the chest wall and diaphragm move outwards, they pull the pleura, increase the magnitude of negative pressure and thus pull the lungs outwards. and vice versa. make sure you look up transpulmonary, transrespiratory and transthoracic pressure. dr najeebs pulmonary mechanics series is a good place to start and would explain all of these things to you more clearly than i could.

5 - the chest has a tendency to contract inwards following inspiration, during inspiration you need to overcome this force and also the surface tension/ elastic forces in the lungs to expand outwards. this force is provided by the external intercostals and diaphragm (mainly ).

6- i have never heard that before, but its been a while. i will try and look it up.

7 - if you have a fall in pco2, then it usually indicates a v/q mismatch. fall in co2 means theres no perfusion in that area to give oxygen, the lungs recognise this via chemoreceptors and since it realises that theres no eprfusion there its kind of like a dead space so rather than waste air going into a alveolar sac with no blood to do gas exchange, it closes it off and redirects the air to the rest of the lungs where it can be of more use. look up the exact mechanism.

im 90% sure my answers are correct, if anyone has any errors please point them out.

 

[evilbooyaa]

The chest wall has a tendency to expand outwards. The lungs have a tendency to collapse inwards. The balance between the two is achieved by the pleural sac. Intrapleural pressure is normally negative because the chest wall is pulling the lungs open in a suction-like manner.

Focus on that and most of your pleural pressure questions will be answered.

2. If you are at baseline (not inspiring, not expiring) you have a certain amount of volume. After you are finished expiring and before you start inspiring, you have the least amount of air in your lungs that is physiologically possible. That is why there are volume differences.

3. Look at this article for basics: http://en.wikipedia.org/wiki/Pulmonary_surfactant
Without surfactant, the surface tension increases, and the pressure required to keep the alveoli from collapsing increases. As the pressure required increases, the likelihood of alveoli collapsing (due to the intrapleural pressure not able to offset the now increased pressure requirements) increases.

4. Agree with above.
5. Only thing I'll edit is that the board answer is that only the diaphragm is working during passive inspiration. Also to add, the less compliance you have, the higher the pressure, and thus the work, that is required to inflate to the same volume.

6. http://en.wikipedia.org/wiki/Airway_resistance

While the assumptions of the Hagen–Poiseuille equation are not strictly true of the respiratory tract it serves to show that, because of the fourth power, relatively small changes in the radius of the airways causes large changes in airway resistance.
An individual small airway has much greater resistance than a large airway, however there are many more small airways than large ones. Therefore resistance is greatest at the bronchi of intermediate size, in between the fourth and eighth bifurcation.

7. Agree with above.

 

[SamarEsawy]

guys your answers are great and I'm getting better at pulmonary ventilation but I'm still confused about the compliance of lung and thorax together
It says in my textbook that the work of breathing overcomes the elastic recoil of the lungs as well as the elastic recoil of the chest walls. I understand that the elastic recoil of the lungs is inwards (casuing lungs to collapse) which must be overcome to expand them. However why does work need to be done to overcome the elastic recoil of the chest walls?
sorry I still can't imagine this

one more question
What makes PO2 higher at the apex of the lung while PCo2 lower at the apex of the lung than the base?

 

[evilbooyaa]

To your first question: Chest wall generally wants to expand, but is limited by the lungs. The increased pressure during an inspiration allows the force to be a net expansion. Only thing I could think of is that when they say work of breathing, they also mean (forced) expiration. This will cause the alveolar pressure to decrease beyond it's equilibrium point, thus 'fighting' the standard recoil of the chest wall. I can't see how inspiration fights the natural tendency of the chest wall.

As to your second question, that is much more straight-forward. Most of the time, your pulmonary blood flow is heavily shunted to the inferior parts of your lung (the bases). However, alveoli fill up nearly similar throughout a normal lung. Therefore, with the same inspired PO2 and less blood flow, that means the apex has decreased O2 taken into the blood/RBCs, and less CO2 deposited into the aleveoli within lung apices. This results in a higher PO2/lower PCO2 in the apices than in the bases. It's a physiologic V/Q mismatch (V = same across the board, Q = higher at bases)

 

[SamarEsawy]

As to your second question, that is much more straight-forward. Most of the time, your pulmonary blood flow is heavily shunted to the inferior parts of your lung (the bases). However, alveoli fill up nearly similar throughout a normal lung. Therefore, with the same inspired PO2 and less blood flow, that means the apex has decreased O2 taken into the blood/RBCs, and less CO2 deposited into the aleveoli within lung apices. This results in a higher PO2/lower PCO2 in the apices than in the bases. It's a physiologic V/Q mismatch (V = same across the board, Q = higher at bases)

that's clearly explained and easy to imagine,although we have less ventilation at the apex of the lung due to decreased compliance of alveoli at the apex, but the decrease in ventilation is not as much as the decrease in perfusion which is even greater according to the ventilation perfusion ratio

To your first question: Chest wall generally wants to expand, but is limited by the lungs. The increased pressure during an inspiration allows the force to be a net expansion. Only thing I could think of is that when they say work of breathing, they also mean (forced) expiration. This will cause the alveolar pressure to decrease beyond it's equilibrium point, thus 'fighting' the standard recoil of the chest wall. I can't see how inspiration fights the natural tendency of the chest wall.

that's completely goinn over my head,the compliance of the lungs alone is twice that of both lung and chest wall and this is driving me to craziness
I googled this and found this simple model about the balancing forces of lung and chest wall which I can't understand ..may be it's the only way
http://advan.physiology.org/content/28/3/125.full
can you explain in to me?