Questions on respiratory system?

[sameeralord]

Hello everyone,

Here are some questions I have on the respiratory system. I would appreciate any help. Thanks These are true or false questions. I don't have answers.

1. Alveolar diffusion capacity is directly proportinal to its partial pressure.
I think it is false, because this is not measuring speed of diffusion.
2. Alveolar diffusion capacity is increased in exercise?
I know this is true but I don't understand why. First of all they say capillary venous pressure changes from 40 to 25 mmHg so more oxygen enter the blood with high gradient. But wouldn't a high gradient cause lower oxygen partial pressure. For example let's say I inspire oxygn at 200 mmHg and capillary venous is 100 mmHg. 50 mmHg would be passed and equilibrium would be reached at 150 mmHg. If capillary venous becomes 50, 75 mmHg would be passed and equilibrium would be reached at lower partial pressure 125 mmHg. Also I know increasing blood flow happens in exercise, but how can a high gradient cause higher partial pressure of oxygen? Also in exercise they say arterial partial pressure of oxygen remain unchanged, but the textbook also says capillary venous pressure changes from 40 to 25 mmHg ?
3. Intrapleural pressure is lower in patients with emphysema?
Why is this? Do the alveolar sac converge make it lower.
4. Hypoxic hypoxia is a recognized feature in anaemia?
I don't understand why partial pressure oxygen remains normal when, Hb is reduced. Does the blood flow increase such a high amount for dissolved oxygen to maintain partial pressure of oxygen.
5. Hypoxic hypoxia is a recognized feature in increased bronchiolar tone?
I don't know
6. Coughing reflex is inhibited during anaesthesia?
Is it?
7. Carbon dioxide transport in blood results in an increase in the haemotocrit in venous blod when compared to arterial blood?
How does a chloride shift create swelling in the red cell. Is it highly osmotically active?
8. The vital capacity is a good index of the lung capacity of an individual?
This must be false right, it tests the function more.
9. Pulmonary surfactant is reduced in the fetal lung when thyroxine is low?
Is it?
10. Defense mechanism of lung include pulmonary surfactant?
This stops alveoli collpsing. So should you consider it as a defense mechanism. I think false.

 

[mtc1973]

1. see the other thread - in short flux volume increases as pressure gradient increases so DL should stay resonable constant. Since DL is the ratio of flux/gradient.
2. Huge increase in blood flow hence larger blood volume in lungs and more DL.
3. Lower elastic recoil of lungs because elastic alveolar walls are no longer present.
4. PO2 depends upon diffusion - diffusion is not affected in anemia - only capacity because we have less Hb. Think dissolved oxygen when talking about PO2 - not bound.
5. Increased tone as in asthma - usually its V/Q mismatch leading to hypoxemia but I guess if bronchoconstriction is bad then there is low ventilation.
6. Not sure.
7. No. Are you talking about long term adaptive response to hypoxia??
8. Vital capacity is a good measure - because it gives the functional volume usable by the lung. But yes - it doesn't tell you the total capacity. But the useful capacity is what matters.
9. thyroxine and glucocorticoids both accelerate type II cell maturation and hence surfactant production.
10. Surfactant proteins are thought to be involved in lung defense.


Hey what is this -- homework?

 

[sameeralord]

1. see the other thread - in short flux volume increases as pressure gradient increases so DL should stay resonable constant. Since DL is the ratio of flux/gradient.
2. Huge increase in blood flow hence larger blood volume in lungs and more DL.
3. Lower elastic recoil of lungs because elastic alveolar walls are no longer present.
4. PO2 depends upon diffusion - diffusion is not affected in anemia - only capacity because we have less Hb. Think dissolved oxygen when talking about PO2 - not bound.
5. Increased tone as in asthma - usually its V/Q mismatch leading to hypoxemia but I guess if bronchoconstriction is bad then there is low ventilation.
6. Not sure.
7. No. Are you talking about long term adaptive response to hypoxia??
8. Vital capacity is a good measure - because it gives the functional volume usable by the lung. But yes - it doesn't tell you the total capacity. But the useful capacity is what matters.
9. thyroxine and glucocorticoids both accelerate type II cell maturation and hence surfactant production.
10. Surfactant proteins are thought to be involved in lung defense.


Hey what is this -- homework?

Thanks for the help I have some queries though. In question 2 you didn't address my question on lower partial pressure of oxygen. In question 3 how does lower elastic recoil of lungs make pleural pressure lower. In inspiration, it is the elastic recoil of lung and the expansion of chest wall, that makes pleural cavity more negative, when there is no elastic recoil shouldn't it make it more positive. In question 5, during inspiration bronchioles dilate so ventilation must not be affected? In question 7 I'm talking about acid base balanc inside an erythrcyte, where there is chloride shift. Does that pull water with it. In question 8, is the answer true or false, the question is not asking about useful capacity right. This is not homework just some questions I did to improve my knowledge.

 

[mtc1973]

Thanks for the help I have some queries though. In question 2 you didn't address my question on lower partial pressure of oxygen. In question 3 how does lower elastic recoil of lungs make pleural pressure lower. In inspiration, it is the elastic recoil of lung and the expansion of chest wall, that makes pleural cavity more negative, when there is no elastic recoil shouldn't it make it more positive. In question 5, during inspiration bronchioles dilate so ventilation must not be affected? In question 7 I'm talking about acid base balanc inside an erythrcyte, where there is chloride shift. Does that pull water with it. In question 8, is the answer true or false, the question is not asking about useful capacity right. This is not homework just some questions I did to improve my knowledge.

I think you have a fundamental to correct. When the air in the alveolus with a PO2 of say 100 mmHg comes into contact with the blood - the blood PO2 will rise and get to the PO2 in the alveolus. We assume constant ventilation - and therefore there is not a drop in the PO2 in the alveolus. So think of the PO2 in the alveolus as constant - because there is constant ventilation. It does not drop as O2 transfers into the blood.


The elastic recoil of the lung favors collapse of the lung - which generates a low pleural pressure (or negative pressure if we are using PATM = 0). The higher the recoil - the more negative the PIP. But at rest PIP is never positive since there is always a tendency for the lung to collapse inward and the chest wall to pop outward - therefore there is always a negative pressure (forget forced expiration). The higher the recoil force the more negative the PIP, the lower the recoil force then a less negative PIP is developed.

Remember increased bronchiolar tone - means decreased radius. Tone of the muscle increases.

As for a chloride shift. You are swapping 1 osmotic particle (chloride ion) for 1 osmotic particle (bicarbonate ion) - so looking at that transporter in isolation there is no net gain or loss of osmolytes for that transporter alone.

And - if summarizing the question : does FVC measure total then no - but you knew that!

 

[mtc1973]

See the balance of forces - ER = lung elastic recoil. CWR = chest wall recoil. So decreasing ER - makes the PIP less negative i.e. say -2 instead of -5.

 

[sameeralord]

I think you have a fundamental to correct. When the air in the alveolus with a PO2 of say 100 mmHg comes into contact with the blood - the blood PO2 will rise and get to the PO2 in the alveolus. We assume constant ventilation - and therefore there is not a drop in the PO2 in the alveolus. So think of the PO2 in the alveolus as constant - because there is constant ventilation. It does not drop as O2 transfers into the blood.


The elastic recoil of the lung favors collapse of the lung - which generates a low pleural pressure (or negative pressure if we are using PATM = 0). The higher the recoil - the more negative the PIP. But at rest PIP is never positive since there is always a tendency for the lung to collapse inward and the chest wall to pop outward - therefore there is always a negative pressure (forget forced expiration). The higher the recoil force the more negative the PIP, the lower the recoil force then a less negative PIP is developed.

Remember increased bronchiolar tone - means decreased radius. Tone of the muscle increases.

As for a chloride shift. You are swapping 1 osmotic particle (chloride ion) for 1 osmotic particle (bicarbonate ion) - so looking at that transporter in isolation there is no net gain or loss of osmolytes for that transporter alone.

And - if summarizing the question : does FVC measure total then no - but you knew that!

Thanks that was a wonderful answer Cleared many of my major misunderstandings. You have stated lower the recoil force then a less negative PIP is developed, less negative means increase pressure right. So the answer must be false. I'm still struggling a bit to understand how hypoxia occur in asthma. This is what I'm thinking, in asthma bronchioles are obstructed, in inspiration bronchioles dilate so it is not much of a problem, but in expiration very difficult, now how is this causing a mismatch. I'm not talking about question I understand your answer there, just asking about asthma.

 

[mtc1973]

Thanks that was a wonderful answer Cleared many of my major misunderstandings. You have stated lower the recoil force then a less negative PIP is developed, less negative means increase pressure right. So the answer must be false. I'm still struggling a bit to understand how hypoxia occur in asthma. This is what I'm thinking, in asthma bronchioles are obstructed, in inspiration bronchioles dilate so it is not much of a problem, but in expiration very difficult, now how is this causing a mismatch. I'm not talking about question I understand your answer there, just asking about asthma.

Thats right less negative means the pressure is higher - but it is still below the pressure in the lung - and therefore is still a distending pressure (i.e. the transpulmonary pressure is still positive - PA - PIP).

Well in asthma there is a V/Q mismatch - which means some areas of lung do not oxygenate blood well, and some areas do. The tendency is to generate overall hypoxemia - because a fraction of your blood never gets well oxygenated.
In very bad asthma - requiring a trip to ER, the ventilation can become so low that you get hypoxemia just from the very bad ventilation (hypercapnia is also seen in this case - whilst hypercapnia is not a feature of most asthmatics). In the majority of functional asthmatics though - it is V/Q mismatch that generates hypoxemia. Just think of some areas of lung not getting adeqaute ventilation but blood is still passing through - so that fraction of the blood is poorly oxygenated.

 

[sameeralord]

Thats right less negative means the pressure is higher - but it is still below the pressure in the lung - and therefore is still a distending pressure (i.e. the transpulmonary pressure is still positive - PA - PIP).

Well in asthma there is a V/Q mismatch - which means some areas of lung do not oxygenate blood well, and some areas do. The tendency is to generate overall hypoxemia - because a fraction of your blood never gets well oxygenated.
In very bad asthma - requiring a trip to ER, the ventilation can become so low that you get hypoxemia just from the very bad ventilation (hypercapnia is also seen in this case - whilst hypercapnia is not a feature of most asthmatics). In the majority of functional asthmatics though - it is V/Q mismatch that generates hypoxemia. Just think of some areas of lung not getting adeqaute ventilation but blood is still passing through - so that fraction of the blood is poorly oxygenated.

Hey thanks again

Intrapleural pressure is lower in patients with emphysema?

However I'm bit fuzzy with the wording here, what lower means lower pressure or less negative (which is higher pressure). So the question should be worded properly right? For example if normal intrapleural pressure at rest is -4, and emphysema patient it is -2, it means pressure is higher. I have one other quick question, why do they call the expansion force of the chest wall, elastic recoil force of chest wall, I don't undertand where elasticity is coming to chest wall, isn't this due to contraction of muscles?

 

[mtc1973]

""For example if normal intrapleural pressure at rest is -4, and emphysema patient it is -2, it means pressure is higher. "" -- right!

so e.g. ATM = 760 mm Hg = 0 cm H2O in respiratory physiology everything is relative to Zero (convention) - i.e. atmospheric

so if PIP is -5 cm H20 - that is less than 760 mm Hg i.e. less than atmospheric

so if in emphysema it is -2 cm H20 - that's just a little bit less than atmospheric, i.e. higher than the previous example.




In terms of transpulmonary pressure less elastic recoil and less negative, i.e. like -2 rather than -5. So in your example

if PA = 0

and PIP is -2 (emphysema) or -5 (normal)

Then PTP is +2 and +5

i.e. so the transpulmonary pressure is higher in the normal case - because the recoil is higher. Make sense?

Well muscle contraction moves the chest wall - and then when the muscles relax the chest wall moves elastically back to a natural set point. Its like a spring. That would take a long time to explain fully!

 

[sameeralord]

""For example if normal intrapleural pressure at rest is -4, and emphysema patient it is -2, it means pressure is higher. "" -- right!

so e.g. ATM = 760 mm Hg = 0 cm H2O in respiratory physiology everything is relative to Zero (convention) - i.e. atmospheric

so if PIP is -5 cm H20 - that is less than 760 mm Hg i.e. less than atmospheric

so if in emphysema it is -2 cm H20 - that's just a little bit less than atmospheric, i.e. higher than the previous example.




In terms of transpulmonary pressure less elastic recoil and less negative, i.e. like -2 rather than -5. So in your example

if PA = 0

and PIP is -2 (emphysema) or -5 (normal)

Then PTP is +2 and +5

i.e. so the transpulmonary pressure is higher in the normal case - because the recoil is higher. Make sense?

Well muscle contraction moves the chest wall - and then when the muscles relax the chest wall moves elastically back to a natural set point. Its like a spring. That would take a long time to explain fully!

Thanks Its making sense. Just with the last question again. You mentioned "But at rest PIP is never positive since there is always a tendency for the lung to collapse inward and the chest wall to pop outward" Here the tendency of the chest wall to pop forward, is this due to the contraction of muscles, or elastic recoil of the chest wall.I think I saw somewhere can't remember for sure, that elastic recoil of the chest wall is in opposite direction, to elastic recoil of lung, is this true?

 

[mtc1973]

Yes - chest wall is being pulled inward by the low pressure in the pleural space. So at FRC the natural tendency is for the chest wall to recoil outward and the lungs to recoil inward (elasticity). The balance of the outward chest recoil and the inward lung recoil - is what determines FRC. So FRC is defined as when the inward lung recoil is matched by the outward chest wall recoil under relaxed conditions.
So during a pneumothorax - when the pleural space is unable to develop a low pressure - the lung is allowed to collapse in on itself - and the chest wall pops out to its natural zero tension state.

Since lung recoil is a factor here - imagine - if we change lung recoil, e.g. fibrosis or emphysema - we change the balance mentioned above and FRC will change.

 

[sameeralord]

Yes - chest wall is being pulled inward by the low pressure in the pleural space. So at FRC the natural tendency is for the chest wall to recoil outward and the lungs to recoil inward (elasticity). The balance of the outward chest recoil and the inward lung recoil - is what determines FRC. So FRC is defined as when the inward lung recoil is matched by the outward chest wall recoil under relaxed conditions.
So during a pneumothorax - when the pleural space is unable to develop a low pressure - the lung is allowed to collapse in on itself - and the chest wall pops out to its natural zero tension state.

Since lung recoil is a factor here - imagine - if we change lung recoil, e.g. fibrosis or emphysema - we change the balance mentioned above and FRC will change.

Thanks agan But I'm sill not clear. At FRC the muscles are contracting and pulling the chest wall outward. How can we call this elastic recoil of chest wall. It is not recoiling just been pulled by the muscles.

 

[mtc1973]

No - at FRC everything is relaxed. It is the low pressure of the pleural space that pulls the chest inward.

 

[sameeralord]

No - at FRC everything is relaxed. It is the low pressure of the pleural space that pulls the chest inward.

Oh I think I understand. So at rest if I have to describe the lung, I have to talk about the elastic recoil force of the chest walll, as you have said pleural pressure pulls lung inward and chest wall elastically recoils outward. So at rest I call this elastic recoil force of chest wall. Now when you inspire muscles contract, so now I can't call this elastic recoil force of chest wall but I have to call it expansion force of the chest wall. Did I get it right. If I did thanks a lot for your help

 

[mtc1973]

More or less - I'll post minor correction when I get time. But yes recoil is after we relax muscles.

 

[sameeralord]

I was thinking too much again and I have few more clarifications.

Why is intrapleural pressure more negative in inspiration and positive in expiration?
Ok I know we discussed this before but I have some questions. So the expansion of chest wall makes it negative. Now I'm confused with them calling expiration a passive process. Now when inspiratory muscles contract, how do they decide when to relax, does it automatically happen after some time or does the elastic recoil of the lung cause this. What if the elastic recoil of the lung is lot higher than the passive expiration of muscles, Then wouldn't that create a big gap in intrapleural space and create negative pressure. Simple if they ask this question somwhere, and I say this is because, there is the large expansion of chest wall, and the natural tendencey of the lung to recoil creates greater negative intrapleural pressure in inspiration is it correct.

Periods of voluntary hypeventilation are followed by hypoventilation?
Now this is where my lack of understaning of regulation of respiration becomes a problem. Ok I understand when you hyperventilate carbon dioxide is low and you lose the central chemoreceptors respiratory drive. Now it is said that respiratory centre receives input from peripheral chemoreceptors. Then how come central chemoreceptors is the main respiratory drive. Since they are in medulla do they comunicate with respiratory centre. Also they are stimulated by increase carbon dioxide, so is their respone always hyperventilation to remove CO2, or do they do what is needed by the body by considering all variables. So in this case,
I know since loss of respiratory drive, apnea would occur and partial pressure of oxygen would decrease. Now this would activate peripheral chemoreceptors. Now my question is I'm thinking that a response for low oxygen is hyperventilation to increase oxygen. Why is it hypoventilation?

Thanks

 

[bobze]

I was thinking too much again and I have few more clarifications.

Why is intrapleural pressure more negative in inspiration and positive in expiration?
Ok I know we discussed this before but I have some questions. So the expansion of chest wall makes it negative.

Covering your lung is a serous pleura layer, a visceral and parietal layer. Embryologically it derives from the same thing, so at the hilus (or root) of the lung, the visceral (surface of the lung) and parietal layers are continuous. Further out the surfaces merely touch together, but the layer is composed of specialize epithelium that secrets a serous fluid.

Have you ever tried to pull apart two wet glass microscope slides? The effect is similar. The parietal pleura is tightly adhered to the thoracic wall. Which moves in three directions during expansion, down from the diaphragm, a out expansion (like lifting up on a bucket handle) and in another direction visually like lifting the pump of a water pump--From other muscles like the external and innermost intercostals.

Since the parietal pleura is adhered to the thoracic wall it is forced to follow the motion of the wall. And since the "wet glass" effect predominates the interaction between the visceral and parietal pleura, the visceral pleura is pulled outward as well. Creating a negative pressure gradient (not really negative, just subatmospheric, pressures can't really be negative and when we say they are we just mean relative to another pressure--In this case that of the atmosphere we define as "0").

Now I'm confused with them calling expiration a passive process.

So at the end of inspiration, your muscles relax. You muscles were doing work against the thoracic cage which is packed with lots of tissue, cartilage, elastic fibers etc which want to keep it at a resting size. So after inspiration, when your muscles cease doing this work, the thoracic wall "springs" back into place. This is why we call it a passive process. It doesn't require an "energy investment" on your part and simply the result of the energy you put into the system.

Now when inspiratory muscles contract, how do they decide when to relax, does it automatically happen after some time or does the elastic recoil of the lung cause this.

In the lung and chest wall, you have specialized mechanoreceptors called stretch receptors. As the lung stretches they increase their firing rate which sends afferent sensory input signals to the brain via the vagus nerve. Particularly to a place called the "pontine respiratory group" located somewhere in the medulla or pons (sorry I can't recall at the moment and I'm too tired to look ). The PRG contains a specialized input center called the "inspiratory off switch" (IOS). The IOS then sends efferent signals out to the respiratory muscles which say "stop inspiration".

This is done without you having to think about it, because it occurs in the brain stem and is reflexive. There is lots of other reflexive receptors which provide input to your respiratory center (most notably the dorsal respiratory group in the medulla which has inspiratory neurons and ventral respiratory group containing both inspiratory and expiratory neurons).
Interestingly, there are people born with certain genetic mutations which takes away the automaticity of breathing and they have to consciously think to breath (and require positive pressure ventilators, often through permanent tracheotomy). Can you imagine that!?

What if the elastic recoil of the lung is lot higher than the passive expiration of muscles, Then wouldn't that create a big gap in intrapleural space and create negative pressure. Simple if they ask this question somwhere, and I say this is because, there is the large expansion of chest wall, and the natural tendencey of the lung to recoil creates greater negative intrapleural pressure in inspiration is it correct.

You don't have passive expiration muscles, passive expiration is just the system returning to its starting point. Its kind of like picking a marble up and placing it on top of a slide. You had to put energy into the marble to get it to the top, but gravitational energy provides the ride back to the bottom. Likewise inspiration is like picking that marble up, while expiration (at least during eupnea) is like it rolling down the slide.

I'm not aware of any pathologies that increase elastic recoil of the lung (I am by no means a lung expert). Certain pathological conditions, particularly obstructive lung disease like; emphysema, chronic bronchitis, asthma etc, increase the compliance of the lung. Specifically emphysema is in part a decrease in the number and quality of elastic fibers in the lung. So during inhalation more air is inspired than can be exhaled (kind of a "black hole" for air). Resulting in increasing FRC, TLC, RV and a decreasing VC.

Periods of voluntary hypeventilation are followed by hypoventilation?
Now this is where my lack of understaning of regulation of respiration becomes a problem. Ok I understand when you hyperventilate carbon dioxide is low and you lose the central chemoreceptors respiratory drive. Now it is said that respiratory centre receives input from peripheral chemoreceptors. Then how come central chemoreceptors is the main respiratory drive. Since they are in medulla do they comunicate with respiratory centre. Also they are stimulated by increase carbon dioxide, so is their respone always hyperventilation to remove CO2, or do they do what is needed by the body by considering all variables. So in this case,
I know since loss of respiratory drive, apnea would occur and partial pressure of oxygen would decrease. Now this would activate peripheral chemoreceptors. Now my question is I'm thinking that a response for low oxygen is hyperventilation to increase oxygen. Why is it hypoventilation?

Thanks

So as I said before, there are many reflexive inputs to the respiratory center. Not only reflexive, but behavioral ones as well. When you hyperventilate, you "blow off" CO2. Since the alveolar O2 partial pressure is dependent on the pressure of other gasses in the mixture (Dalton) and is given by the alveolar gas equation;

PAO2 = PIO2 -(PACO2/R),

Big "A" indicating were talking about the partial pressure in the alveoli as opposed to the artery. R is the respiratory quotient (serachable term). So decreasing PACO2, increases the PAO2. This actually has little effect on PaO2 because as pointed out in the other topic, O2 is perfusion limited.

About 98-99% is transported via oxy-hemoglobin (oHb) which equates to about 20.1 ml O2 per 100 ml blood. Only ~1-2% is actually dissolved in blood and exerts a partial pressure (O2 bound to Hb exerts no partial pressure). That's only about .3 ml O2 per 100 ml blood. Also since blood-oxygen capacity is reached about 1/3 the way down a capillary increasing the PAO2 has little change on the system.
**Of course it isn't necessarily that simple because even in a healthy lung there is ventilation-perfusion mismatching, that is to say that the "amount" of ventilation isn't perfectly matched to perfusion. But for simplicities sake, I think we can ignore such complications at the moment.

That is not the same as CO2 however, which can be blown off and the PaCO2 will decrease rapidly during hyperventilation.

During hypoventilation, your PaCO2 rises, raising your PACO2, decreasing your PAO2 and PaO2 (but not necessarily your O2-sat).

So when does this happen?

Behaviorally, you can make yourself hypo/hyperventilate. It can also happen in response to blood partial pressure/pH changes.

Your central chemoreceptors (which are the man in charge, that is they get the final word) respond only to changes in CO2 and do so "indirectly" by changes in pH of the CSF. Since CO2 readily diffuses across the blood brain barrier it increases in concentration, shifting the equilibrium of this reaction to the right;

CO2 + H2O↔H2CO3↔H+ + HCO3

The increase in H+, ie; a decrease in pH, is what prompts the central chemoreceptors to "blow off CO2"--Hopefully achieving shifting the reaction back to the right.

The problem though, during a "steady state" acidosis/alkalosis (metabolic) the brain will up regulate certain carrier channels which help to maintain the ionic composition of the CSF and mitigate the regulation by the central chemoreceptors.

**Time out for an important concept. Its important to realize that many receptors, such as these, work constitutively. That is to say, the always have a basal rate of firing. In the case of a increase H+ concentration-that activity increase. In the case of a decreasing H+ concentration (alkalosis) that activity decreases and its the increase/decrease of this activity which stimulates the DRG/VRG and sets respiratory pacing (a mechanistic concept is still ill-understood in biology)

Your peripheral chemoreceptors, found in carotid and aortic bodies, respond to changes in pH, PaO2 and PaCO2 in the plasma only. Increasing H+ (decreasing pH)--which can be from the CO2 (inhaled "volatile acid") reaction above or from fixed acid production, increasing PaCO2 or decreasing PaCO2 will increasing the firing rate of the peripheral receptors. Creating the result of hyperventilation.

Like I said you have other receptors like; pulmonary vascular "J" receptors, cardiovascular receptors, muscle/tendon receptors, airway receptors etc, which all provide input into the respiratory center--Particularly the DRG/VRG which regulate inspirational pacing (along with input from the IOS discussed above).

Does that help?

Edit:

PS. Sorry for any mistakes above, pretty tired will proof read in the morning-Pardon the English till then.
PPS. Sorry if any of this is repeated from your and MTC's conversation, I didn't read all of it.

 

[mtc1973]

Elastic recoil is increased in all of the fibrotic lung diseases. Pneumoconiosis, alveolitis etc repeat exposure to organic or mineral dust particulates. Increased recoil gives low compliance and FRC is reduced, as well as other lung volumes - but flow rates are enhanced due to increased recoil.
I'll post a graph later but the changed FRC with obstructive diseases is not actually because of the obstruction to airflow - it's the reduced recoil itself the changes the balance, irrespective of the reduced flow rates.

 

[sameeralord]

Thanks for the lengthy response Bobze

However you didn't address why period of voluntary hyperventilation is followed by hypoventilation. That was a question I had.

Other points I want to clarify

1. In hyperventilation, why do we always talk about decrease of carbon dioxide, when you hyperventilate don't you breathe in more oxygen, increasing the partial pressure of oxygen.

 

[mtc1973]

The relationship between PCO2 and CO2 content is 'linear' - the relationship between PO2 and O2 content is not - hence high alveolar ventilation results in low CO2 content but not high O2 content (higher than normal at least). This crops up in disease states too where hypoxemia can develop without hypercapnia. So it is just more reliable to look at the ventilation CO2 relationship. Remember CO2 doesn't need a carrier protein (like O2).

 

[bobze]

Elastic recoil is increased in all of the fibrotic lung diseases. Pneumoconiosis, alveolitis etc repeat exposure to organic or mineral dust particulates. Increased recoil gives low compliance and FRC is reduced, as well as other lung volumes - but flow rates are enhanced due to increased recoil.

Shame on me, you are correct

I'll post a graph later but the changed FRC with obstructive diseases is not actually because of the obstruction to airflow - it's the reduced recoil itself the changes the balance, irrespective of the reduced flow rates.

Yep, that is a good point sorry if it wasn't clear Sameer. I try and visualize it like a trash-bag that keeps filling up with water each time, while expels less water than it takes in. You are increasing the "stretchiness"--Or more appropriately the compliance of the lung. Thus increasing FRC/RV/TLC at the expense of VC (since vital capacity is VT+ERC+IRC and you are quickly shrinking your IRC!).

Thanks for the lengthy response Bobze

However you didn't address why period of voluntary hyperventilation is followed by hypoventilation. That was a question I had.

You mean voluntary hyperventilation followed by involuntary hypoventilation?

Going back up to my post, you should see all the different receptors, particularly the chemoreceptors which (remember fire at a basal rate) would decrease their firing rate when PaCO2 decreases and thus their stimulus to the breath reflex (going back again, the DRG/VRG which both posse inspiratory neurons).

Its why if you are free diving and want to "hold your breath longer", you hyperventilate first--I've never tried it, I don't fancy passing out :tongue:.

 

[sameeralord]

Thanks for the help again Bobze and mtc1973

1. However with hyperventilation and why we don't consider the increase in oxygen. Can u guys explain it fully. Like is it due to perfusion limited or how. Isn't carbon dioxide perfusion limited as well. Also in hyperventilation oxygen in alveoli as Bobze said increase, so higher gradient, now since this is perfusion limited it is not affected. Is it because despite the high partia gradient, oxygen would reach equilibrium at 100 mmhg, so no effect unless blood flow increases. Also in hyperventilation, does more oxygen bind to haemoglobin or something. Are these the reasons.

2. Also if you hyperventilate too much does apnea occur instead of hypoventilation. Meaning you remove respi drive?

 

[bobze]

Thanks for the help again Bobze and mtc1973

1. However with hyperventilation and why we don't consider the increase in oxygen. Can u guys explain it fully. Like is it due to perfusion limited or how. Isn't carbon dioxide perfusion limited as well. Also in hyperventilation oxygen in alveoli as Bobze said increase, so higher gradient, now since this is perfusion limited it is not affected. Is it because despite the high partia gradient, oxygen would reach equilibrium at 100 mmhg, so no effect unless blood flow increases. Also in hyperventilation, does more oxygen bind to haemoglobin or something. Are these the reasons.

Trying to think of an easy way to elaborate on this .

Okay, the reason we don't much talk about O2 during hyperventilation is because it is CO2 which is the driving force in changes of alveolar partial pressures. Remember back up in the that long post I made, I pointed out something from Dalton?

Remember what that guy Dalton says?

That in a mixture of gases, the total pressure of the mixture will be the sum of the partial pressures of the individual gasses in the mixture.

So when you blow off CO2 by hyperventilating, you're "making room" in that mixture for more O2, which raises your PAO2 (recall the equation PAO2=PIO2-(PCO2/R)).

It would increase your PaO2. And it would essentially do nothing to your blood O2 content under normal circumstances.

Remember I was telling you how 98/99% of the bloods O2 is bound to Hb, and only 1-2% is dissolved in the blood. It was about 20.1 ml vs 0.4 ml O2 per 100 ml blood.

Rough calculation for an example? Remember that PIO2 is equal to the (Patm-PH20 (partial pressure from water vapor))*mole fraction of O2 (which is 21)
Normal then; PAO2=149.73-(40/.8)=99
Hyperventilation where you double your breathing frequency and blow off half your CO2:
PAO2=149.73-(20/.8)=124

Small increase which would raise PaO2, but have little effect on blood oxygen content. This becomes important though, at things like high altitude. Consider on the top of a mountain where the Patm is only 350.

PIO2 then equals only 74 mmHg!
So our PAO2 without hyperventilation would be a measly 14 mmHg O2! Not all that compatible with life!

While if we hyperventilate (doubling again) we could increase our PAO2 to 34. Not great, but it will literally keep you a live at the summit of Mt. McKinely!

-Regarding the last question, no Hb doesn't bind more O2. Your Hb saturation is almost always at 98-100% leaving the alveolar capillary.

 

[sameeralord]

Thanks Bobze and mtc1973 for continuous help on this area Finally I can move on.

 

[mtc1973]

Sameerlord,

sorry been busy. Promised to post graph that explains recoil and FRC.
So on this chart the easiest to start with is the right hand graph - lung recoil and volume relationship. Which is the lung compliance curve - so recoil (or PTP, these are synonymous) and lung volume plotted on y. Basically as the volume increases (from 1 to 2 to 3) the recoil increases - makes sense - as you stretch elastic tissue you store energy and that recoil always favors collapse (by convention a positive recoil is collapse and a negative recoil is increase in volume). So you can see that no matter what volume a lung is at - the recoil favors collapse - with the highest recoil at the large lung volumes (i.e. more stretched and more stored energy). Just think balloon - more recoil energy as you fill it with more air. That is lung recoil on its own.
Now the left graph is chest wall recoil - think spring. At point 1 - this is the natural spring length (or volume in case of our thoracic cavity spring!) - no recoil inward or outward - i.e. recoil = zero. If we use muscles to contract the spring down to point 2 (smallest lung volume - RV - like when we breath out and contract the thoracic volume - think smallest spring length) - we store energy. Now when the contracted muscles relax the chest has a large recoil - i.e. high value on the x-axis - and this recoil is negative, i.e. outward. On the other hand if we use the inspiratory muscles to expand the thoracic volume to point 3 (stretch the spring) now when we relax these muscles the chest wall will recoil inwards (note it crosses axis and recoil is now a positive value - i.e. inward).
So in isolation the chest wall and the lung have associated recoil depending upon their volume. But we know that these structures are not independent - they are linked physically by the pleural membranes. So one recoil will affect the other. Now to look at the complete system and figure out the recoil of the whole system - we just add the lung recoil to the chest wall recoil. Bottom graph - but i forgot to draw the summed line!. When the entire system has zero tension (i.e. when inward lung recoil is exactly equal and opposite to outward chest recoil - the 2 forces balance - and we are at rest volume which is FRC! Point 1 on that graph.
So to get FRC in this graph just look to see where the inward lung recoil and the outward chest wall recoil are equidistant from the y-axis i.e. a net recoil of zero!
So as you can see by changing lung complaince (dotted line) - like emphysema - we increase complaince - and now the balance of forces is at a different volume - FRC has moved up. So without even worrying about airflow obstruction and air trapping - you can see why FRC changes. becuase the mechanical properties of the lung changed and the balance point now moved.
Its a complex graph - but go slwoly and if you understand it - you can predict any FRC change based on the lung complaince and the chest wall complaince.
Also if we disrupt the association between the structures - i.e. pneumothorax - each of the individual components falls to its zero tension state - hence lung collapse to near zero volume (not really though) and chest wall pops out to its zero tension state - which as you can see is higher than FRC - so the chest wall pops outward.

Good luck!