Breathing physiology... whats best for off-gassing

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Genesis once bubbled...
I'm not "getting it"

I cannot say I am surprised, Genesis. You might benefit from doing a liitle reading of a physiology text. I will try and find you a reference later today and attach it.

Try and think of the lung as a sort of sponge but unlike a natural sponge all the material from which it is made is hollowed out with very,very thin elastic walls containing blood, and in addition all the air pockets are interconnected. In addition think of the sponge being held in a zero gravity situation (more of this later). Thus all the blood in the sponge is separated from the air cells within it by a thin wall only microns thick, which is no barrier to diffusion at all. In consequence all the blood in this lung will be at equilibrium with the gasses in the air sacs and visa versa.

If these air sacs are now inflated with 100% oxygen at the surface, (at 1 bar) the blood on the "lung" will rapidly reach a partial pressure of oxygen of about 1 bar as the oxygen rapidly diffuses into it. Also if the blood contains carbon dioxide at 0.5 bar the pp CO2 in the air sacs will very rapidly again approach 0.5 bar as the carbon dioxide diffuses from the blood into the oxygen added to the air cells. The only real barrier to such diffusion being the pressure gradients. If the lung is then deflated the CO2 in the cells is removed to the atmosphere. If this cycle is repeated over and again, eventually all the CO2 in the "blood" will be removed and it will only contain oxygen at 1 bar.

In life the pressures differ but the principle is the same. The partial pressure of carbon dioxide in the blood is determined by the diver's metabolism and is continuously being replaced and the oxygen is removed by the blood which circulates around the body.

Moth-eaten lungs!

If you were to take a soldering ion and burn holes in the centre of the sponge to destroy, say, half of the lung's tissue you produce a large air sac with no blood in close proximity to the gasses in the centre of it. Thus, even if the large sac of air is ventilated very little gas exchange takes place because there is no blood at the centre of the air sac. The ventilation in the centre of the sac is normal but perfusion is completely absent:- An extreme form of VQ mismatch where the ventilation greatly exceeds the perfusion. This is what happens in advanced chronic obstructive pulmonary disease (COPD) such as emphysema.

If there is a blockage to an airway leading to a part of the lung, due to a foreign body for example, no ventilation can take place in that part of the lung. The perfusion greatly exceeds the ventilation. This is what is seen in asphyxia.

There other examples at the other end of the spectrum - affecting the circulation - such as pulmonary shunts (too much) and pulmonary emboli (too little perfusion), where there is also a major VQ mismatch.

The net result of all these examples of VQ mismatch is that the blood will simply pass through the affected area of the lung largely unaltered. At least gas exchange in these areas is less efficient.

In life

Gravity is present in life but the lung is held inflated against the chest wall (due to the pressure exerted by the regulator in the mouth agaist a near vaccum in the pleural cavity) which very effectively keeps all the alveloli inflated with the aid of surfactant. If this "sponge" is taken out of the rib cage (or the vacuum seal is broken as in pulmonary barotrauma) the air cells simply collapse due to their inherent elasticity. In addition if it is allowed to hang upright gravity will pull all the blood to the bottom, sqashing all the air cells and forcing any remaining air to the top.

The lungs' internal elasticity keeps its structure reasonably uniform when it is held inflated within the chest cavity in life;- effectively stuck to the cest wall.

However there is known to be a small gradient in VQ mismatch due to gravity, which of course causes the blood WITHIN the rib cage to exert a marginally greater pressure against the avleoli at the positional bottom of the lung than at the top, dilating the lower pulmonary capillaries, proprtionaltely increasing blood flow and reducing alveolar size and thus reducing ventilation. If the lung is 30 cms in height the amount of this pressure differential will be 0.03 bar. (At the surface the pressure in the alveoli of 1 bar this represents a differential of 3%).

This gradient will be present whether the diver is immersed or not but while it is not a great problem for humans, it does cause problems to large animals such as elephants.

Thus the only part of the lung to have both air and blood at ideal poportions is in the centre but this is not due to any external pressure gradient, it is simply due to gravity acting on the blood within the chest cavity and this gradient will be present whatever the diver's attitude in the water, although when horizontal this differential is less because the lung "height" is less.

When you take a deep breath, which all of us do regularly, any alveoli that may have collapsed are reinflated. Yawning is thought to be a reflex mechanism ensuring they remain patent and the lungs therefore as efficient as possible.

When you exercise you do not just take deeper breaths, both ventilation and perfusion increase together and in proportion. You take deaper breaths to increase ventilation and your cardiac output rises to increase perfusion.

I hope this helps.

:doctor:
 
OK folks, I have spent a few hours drawing the attached diagram using Excel. I hope they can be downloded without problem.

First fact.

The pressure within the thoracic cage is a constant throughout. In a scuba diver it is that provided by the regulator and will vary according the the phase of the resiratory cycle. In a freediver it will be at ambient pressure depending upon the ability of the right side of the heart to compensate for the pressure changes in consequence of a reduction in the volume of the air cells during the descent and the ability of the left side of the heart to evacuate blood from the pulmonary bed during the ascent as the air cells re-expand.

Second fact.

The lungs are suspended against the vacuum of the pleural cavity which keeps ALL the alveoli relatively patent.

Third fact.

At any particular phase of respiration the volume of the chest cavity will be kept constant by the reflex control mechanisms operating on the chest wall and diaphragm.

Diagram

This represents a normal healthy lung with some VQ mismatch. De-oygenated (nitrogen loaded) blood enters the lungs from the right side of the heart (blue) and passes though minute vessels in intimate contact with air in the alveoli. As it passes through the lungs the blood gradually takes oxygen from the air and carbon dioxide and nitrogen diffuse into the air cells until the air is in equlibrium with the blood when it reaches the pulmonary veins (red). Ventilation and perfusion are only equally matched throughout in genuine zero gravity, which represents peak efficiency.

VQ gradient

This shows, schematically, what happens if there is a significant VQ gradient. The top of the lung is overventilated and underperfused. The bottom of the lung is underventilated and overperfused. The smaller quantity of blood in the apices is rapidly saturated with oxygen and also rapidly loses any CO2 and nitrogen but much of the air is "wasted" as there is liitle blood to oxygenate. In the bases, since ventilation is relatively poor less gas exchange takes place. The overall effect is that the blood leaving the lungs has less oxygen and contains larger quantities of carbon dioxide (and nitrogen) than in zero gravity.

As I have said before, if a significant VQ gradient exists in divers it will be present whatever the orientation of the diver but the lungs are not the limiting factor in off-gassing.
 
The file attatched to this post and the next were too big to attach as a single page.

They are simplified out of all proportion but I hope they help to explain normal lung function.

The first, attached to this post is the ideal siuation where there is no VQ mismatch at all, which can only be found in a completely healthy lung in zero gravity.
 
B) Pulmonary embolus

A serious medical condition. (PE is the worst example of the "economy class syndrome" due to a deep vein thrombosis). A blockage of the pulmonary arteries means that a large part of the lung is not perfused, the vessels shrink and the air cells enlarge to compensate. No gas exchange takes place in the affected part of the lung so the blood leaving the lungs overall has less oxygen and still contains large quantities of carbon dioxide (and nitrogen).

In addition, of course, if the right heart can cope the whole cardiac output will pass through the healthy half of the lung which will be overperfused. This condition is life-threatening because of the strain put on the right side of the heart, which will also receive poorly oxygenated blood at lower than normal pressure.

C) Asphyxia

A foreign body in the airway prevents ventilation of that part of the lungs. Once more no gas exchange takes place in the affected part of the lung so the blood leaving the lungs has less oxygen and still contains large quantities of carbon dioxide (and nitrogen).
 
What I understood in part, you have explained more fully with detail I had not imagined. I was going to quote BRW's book where in essence he says one of the biggest fallacies is to trust causal relationships derived from one atmospere in a hyberbaric environment. There are just TOO many variables to be able to extrapolate accurately.

That being said, I see no room for extrapolation in your treatise, and concur completely.

As a side note, I re-read some of the first posts in this thread, where I said I would listen to a medical doctor on this. Thanks Dr Paul... youdaman!
 
Hi Netdoc,

Can I quote a part of my first post on this thread?

Dr Paul Thomas once bubbled...
. . .

However, I understood the limiting factor for deco is not gaseous exchange in the lungs but gaseous exchange at the periphery, particularly in the slower tissues?. . .

The problem with vertical hangs, as I see it, is the very real difference in hydrostatic pressure along the length of the entire, erect, immersed, human body. Someone who is 1.5 M tall will have a pressure differential of 0.15 bar along the body when erect, and an erect stop at 3 metres head-height is a 3.5 M stop at the waist and a 4.5 M stop at the ankles. The off-gassing pressure gradient at the ankles is less than at chest height and so offgassing from these tissues will be less.

If you lie horizontally in the water for your stops all of your body is close to the stop, not above it nor below it.

So there are good theoretical reasons why an erect stop is less efficient overall at off gassing.

Forgetting trim, bouyancy control etc. etc. surely that is the point? In a vertical hang the "centre of decompression" is lower.

However, this has been very much an academic exercise since decompression tables are very conservative and I suspect the differences between horizonal and vertical hangs are marginal to say the least, so I doubt there is any point in taking this any further.
 
is there a signifigant difference in BP from your ankles to your head? and would this not be so out of the water as well as in (gravity). AND since offgassing is far faster out of the water, would you reccomend to lie down immediately after leaving the watery environs?

As I pointed out before, what sounds reasonable on the surface or as an intuitive extrapolation to beneath the surface is still conjecture until such time as someone figures out a way of measuring or quantifying ALL of the variables... ei, not just gravity, but delta pressures along the body as well.

In other words, there are far more unsubstantiated theories then there are unqualified facts. To be able to say "one" attitude in the water is "obviously" better than another attitude because of off-gassing is pure conjecture without hard empirical datum.

To give other reasons that are far more reasonable makes sense, such as the drag created by your body when horizontal allowing you to slip forward but retarding vertical movements, etc, etc.

Your case about VQ is compelling though and very well presented. AND I agree that the greatest variable in this gas exchange is NOT the pressure exerted outside of the lungs, but the pressure of gravity within the lungs and that is something we deal with on the surface as well, and is a non-issue for most. At least I hope that I am reading you correctly.
 
Dear Readers:

I have not check this thread for a while since it seemed to drift into a zone well handled by others (and my time is limited).

Gas Exchange

As was mentioned earlier in the thread, gas exchange at the lung is not the limiting factor for a healthy diver. This is true even when there are a “large number” (there are not a large number) of Doppler-detectable bubbles. I do not believe that there is anything yet in the “DOCTORDECO” supplements, but one can check Powell, MR.; MP Spencer; and O von Ramm (l982). “Ultrasonic Surveillance of Decompression”. In: The Physiology and Medicine of Diving. 3rd Edition. PB Bennett, and DH Elliott, eds. Bailliere Tindall, London. We measured gas exchange inequalities with VERY large decompression bubble loads and found that there are not any. This is different from the operating room setting when exchange inequalities do appear when there has been an accidental introduction of air into the heart and pulmonary artery.

Some meter manufacturers have added a “microembolization factor” in their deco meters. This is probably a good stratagem to amend additional conservatism, but laboratory evidence is against this as the true mechanism.

Off gassing at Depth

There is not any evidence that gas exchange in the tissues at any given depth is any different from another depth, that is, it is depth independent. This is why the half times for the compartments in tables and meters are constant for all depths. (The m-values will change, however.

Off gassing on the Surface

This is a function of blood flow to the tissues and is diver dependent. Currently deco meters are not adaptive to allow for blood flow changes. (I do this for my calculations of NASA decompressions, but this is a different arena.) Thus, divers can protect themselves by performing some movement when in the water (cycling movements in the arms and legs) while in safety of deco stops. While on the surface, you can lie down but again the arms and legs should be moved. This activates what is known as “the muscle pump” and is a very important mechanism to increase tissue perfusion

Dr Deco
:doctor:

PS. All portions of the body are in pressure equilibrium unless a condition to produce a “squeeze” exists. Pressure is equalized though the blood of the vascular system in accordance with Pascal’s Principle. This includes the lungs and brain.
 
That's what my understanding of how fluids work (including air), but these explanations clarify and put it into practice...
 
Dr Deco once bubbled...


Off gassing at Depth

There is not any evidence that gas exchange in the tissues at any given depth is any different from another depth, that is, it is depth independent. This is why the half times for the compartments in tables and meters are constant for all depths. (The m-values will change, however.

I agree, Dr Deco I have spent far too much time on this forum, of late!

I fear I have caused some confusion. I am now convinced there is no "centre of decompression" and offgassing will only depend on the pressures at the regulator, which alone determines the partial pressures of the inert gasses in the alveoli and therefore in the arterial blood.

Let us assume a diver is breathing air and a particular tissue compartment is saturated with nitrogen at 10 metres, since the diver has been at this depth for at least six half times for that compartment.

(Forgetting about dilution due to water vapour and CO2, which will both be relatively constant), with the regulator at 10 metres the pp N2 in the inspired air, the alveoli, the blood and the tissue and will be 0.79 bar x 2 = 1.58 bar throughout. There will be no offgassing at all because, by definition, the system is in equilibrium and this tissue is saturated.

The diver now instantly ascends to a regulator depth of 6 metres so the ambient pp N2 will be 1.26 bar as will the pp N2 in the arterial blood. The tissue will now be effectiverly supersaturated with nitrogen at 1.58 bar. There now exists an offgassing gradient of 1.58 - 1.26 = 0.32 bar, which will cause nitrogen to leave this tissue since the blood bathing the tissues in all parts of the body will have the lower pp N2 derived from the inspired air.

If the diver only rises to 8 metres regulator depth the ambient pp N2 will be 0.79 x 1.8 = 1.42 bar. The offgassing gradient will be 1.58 - 1.42 = 0. 16 bar, which is half that at 6 metres so the offgassing rate will be halved.

Dr Deco, is this is what you mean when referring to M values?

I apologise for creating some confusion. As ever, it is far more complicated than we originally assume. I fell into the trap of wrongly assuming that the liquid pressure gradient from head to foot of about 0.15 bar in the erect position would affect the partial pressures of the inert gasses in the blood, but these are derived from the inspired gas mix alone. It would now seem that no such gradient can exist, as the partial pressures of inert gasses in the arteries can only come from the regulator which is a set depth, with constant partial pressures for any given depth (at least in open circuit diving).

Since all the soft tissues of the body, apart from those within the chest cavity, are in direct contact with water at ambient pressure and have approximately the same density as water, they are all at ambient pressure and there will be no venous pooling as there is when the body stands erect in air. However, the pressures within the arterial tree are increased by the muscular activity of the heart, raising intra-arterial pressure over and above ambient pressure solely in order to move the blood around the body against vascular resistance (and gravity, when present). From this I postulate that the pressure of the blood in any part of the body is quite irrelevant with respect to offgassing, what is important for offgassing is an adequate circulation to all parts of the body, Netdoc, and I am now convinced that regulator depth and gentle movement, not attitude are the determining factors.

Now for the twist in the tale?

Netdoc, you say
since offgassing is far faster out of the water, would you recommend to lie down immediately after leaving the watery environs?

Offgasing can only be faster if the offgassing gradient is increased. I strongly suspect that when I am decompressing at 3 or 6 metres on 100% oxygen the offgassing of nitrogen is much greater than it is on the surface because after surfacing I am breathing a mix that contains an opposing nitrogen partial pressure of 0.79 bar, which was not there before. (Not so with helium). However I do agree that if you have not decompressed on oxygen or nitrox on an air dive, the opposing nitrogen pressure is less after surfacing.

If you wish to increase offgassing after surfacing, rather than lying down, it would be much more effective to breath 100% oxygen. Indeed, as you know, this is the basis of the early treatment of any DCI with oxygen.

:wink:
 

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