Some iscience on SWB

[sciencemike]

Splinter thread from....
http://forums.deeperblue.net/general-freediving/78948-praise-shallowness-2.html#post722758.

Hey Trux- or anyone else,
Sorry to derail, but there is soo much bad information out there on SWB. So much confusion, and it is the most serious problem spearos face(as someone wiser than me said).

I have often wondered a couple of things. Maybe i should just use the search forum or start a new thread. Upon surfacing from a very deep dive gas bubbles can come out of your blood stream, even when just free diving (as evidenced by free divers even getting the bends, which is an extreme case of bubbles). When these bubbles (assuming they are larger than 8 um) get lodged in your pulmonary capillary bed to be destroyed, they have been shown to dramatically increase the blood pressure in the pulmonary artery. My question to you is have you ever seen reports of this adding to the SWB? Lets say if someone did 20 or so deep dives.


Secondly, blood pH affects heme/O2 binding. When acidic (muscle capillary bed), O2 is released from Heme and when its basic (pulmonary capillary bed) it binds - well lets not say it binds but is more sequestered out of solution into a complex with hemoglobin, thusly reducing its partial pressure. This dramatically affects the partial pressure of O2 in the lungs and in the muscle. Can anyone correlate this with changing blood pH when you dive? Does the blood pH drop at the end of the dive in the lungs, whereby reducing the pH gradient allowing for O2 to be released back into the lungs? Because otherwise O2 will never be allowed to backflow like we have talked about.

Mod please remove the i in the title iscience.

 

[trux]

As for the influence of bubble building on SWB or hypoxemia in general, I am not aware of any studies, but will try to look up if there are some related documents.

As for the releasing of O2 into lungs, I actually do not think it really happens. Although the vacuuming of O2 from the blood is often referred to, it is not really exact. My statement in the other thread about the reverse diffusion was not correct from this point of view.

During the ascent, O2 continues to be consumed, but the partial pressure rapidly drops (due to the changing environmental pressure). And since it is not really the amount of oxygen that determines the oxygen supply to tissues, but rather the partial O2 pressure, it can easily happen that it drops below the functional minimum rapidly during the ascent, abruptly cutting off so the oxygen supply. So the "vacuuming" does not actually mean oxygen is being physically removed from the blood, but rather that its arterial partial pressure rapidly drops below the functional limit.

As for the blood pH during the ascent, it actually does not drop, but may possibly even grow. During the descent the releasing of CO2 from blood to lungs is hindered by the growing PACO2 (partial alveolar pressure of CO2), leading to rapidly increased PaCO2 (partial arterial pressure of CO2) in the blood (causing low pH). This excess CO2 then starts diffusing into lungs as you ascent. With the increased diffusion, the CO2 in blood starts dropping (or at least slows increasing) and the pH may grow (or slows dropping). In consequence it has influence on the Bohr saturation curve, and helps the alveoli to bind the remaining oxygen better, despite it's low partial pressure. This effect actually slightly helps coping with the depressurizing effect, that would be more deadly otherwise.

EDIT: Some links about Shallow Water Blackout / Latent Hypoxia: swb @ APNEA.cz

 

[ILDiver]

Please tell me if my understanding is correct. I was in a bit of a hurry reading the other thread during my brief stop at home and after reading a certain post I had trouble focusing

Ok, he is my understanding. I do two separate dives, first one is a deep dive. I leave the surface with 21% O2 (a little less really, but my numbers are not going to be accurate, just illustrative) in my system. When I get to 30m I have 17% O2 level. But Partial Pressure, I have a higher concentration of O2 in my blood and tissue and with PP factored in it's like I've got an equivalent to 30% O2 level. I'm coming back up and at 10m I'm at 13% O2 in my system, but with PP factored in I'm at an equivalent of 20% O2, then the surface I'm at 11% O2 level and no effects of PP.

Second dive I go to 10m. I stay there for X minutes. My O2 level drops to the same 13%. With PP I would have the same equivalent 20%. The accent to the surface would have the same affects.

As far as SWB and a Deep Blackout, I'm not sure I get how your using the terms. I thought SWB was blacking out while surfacing in the top 10m, regardless of max depth? So a blackout from a static attempt is just a blackout. Is this not correct.

I will read the other thread closer and thanks for the help. The physics and Physiology are two parts of scuba and freediving classes I like. Just not remembering all the formulas.

 

[azapa]

Chris, I am reading FIT's course notes here like you are.

Your math is correct, but the gradient, or speed of the reduction of O2 is a major aggravation in SWB. I like the term "vacuum effect" although it is not literal, it kinda describes it for me: O2 being "sucked" out, or in realty, falling fast.

Martin teaches a passive exhale at about 3M before the surface, just to reduce this nasty gradient (or vacuum- please, i know it is not a vacuum, its just a term that explains it well for me) by reducing a little the pressure whilst still with pressure on the chest. Also preps for the first inhale.

What I am personally very unhappy with on the pre-surface passive exhales is use of optimal weighting on a thick suit. You do loose a lot of buoyancy and ONLY a buddy will save your butt if something goes wrong.

I sometimes feel the the pre surface exhale is ONLY good on demanding line dives with good buddies around.

Enter TRUX

 

[trux]

Chris, your logic is basically correct, although using the percent values is little bit misleading, because they do not change, and because you usually use percents for the SaO2 and SvO2 values (arterial and venous saturation), which change with a different logic.

So let's put your example into the right terms. I'll use only approximate values, the exact ones are depending on many factors, like atmospheric pressure, CO2 level, individual physiological differences, etc:

You lose consciousness (black out) at venous partial pressure (PvO2) of 17-19 mmHg. The venous pressure is lower than arterial pressure (PaO2), hence the PaO2 limit is roughly 20-35 mmHg. The alveolar pressure (PAO2) would need to be slightly higher to assure successful diffusion of oxygen through the alveolar wall - so the critical limit for the pressure in lungs may be as high as 40 mmHg.

On surface, the PaO2 is around 100 mmHg (without hyperventilation). Now, you are right that at depth, the pressure grows, so at 10m it would be double of that, at 30m four times higher.

When you are 30m deep the gas exchange works indeed better due to the higher PAO2, so you can stay down consuming O2 until it drops for example to 80 mmHg, and still have no hypoxic signs (I deliberately do not speak about CO2 yet). When you start surfacing - at 10m the 80 mmHg will drop to half due to the ambient pressure change. That makes 40 mmHg and it is already pretty close to the critical limit. By ascending higher, the PAO2 drops to 20 mmHg (on the surface), which is already deep in the blackout zone.

Note: I ignored the continuing O2 consumption during the ascent.

Fortunately for us, the above mechanism is greatly controlled by CO2. When in depth, the alveolar partial pressure of CO2 also grows proportionally, hence the CO2 stops diffusing into lungs, and cumulates in blood and tissue instead. It increases blood acidity, shifts the gas dissociation curve - helps discharging O2 better in the tissue, but prevents the efficiency of binding O2 remaining in lungs. It also causes lower blood pH, which then controls your urge to breath. So normally, in depth, due to the reduced diffusion of CO2 into lungs, you start feeling the urge to surface and breath earlier than on surface. The problem is if you hyperventilated - the CO2 level will be lower, the pH higher, and the urge to breath may come too late.

When you start ascending, the CO2 starts flowing into the lungs, because the gradient of PaCO2/PACO2 changes, the arterial CO2 level drops, and the Bohr oxyhemoglobin dissociation curve gets shifted on the other side, helping to bind O2 remaining in lungs. The dropping CO2 level (climbing pH) also causes that you start feeling fine while ascending despite fast falling PaO2, and do not see the SWB coming.

Note: in reality it depends on the speed of ascent, and the level of physical effort whether the PaCO2 really drops during the ascent. In fact it may continue to grow, just the speed will be considerably reduced by the depressurizing. I did not see yet any specific study of CO2 levels during ascent, showing empiric values.

This is why hyperventilating before a dive is extremely dangerous. Proper level of CO2 is much more important for your safety than at surface apnea. Although there it is important too, because besides it signalling function, shifting Bohr effect, it also greatly influences the tolerance to hypoxemia - high CO2 level allows the PaO2 to drop lower without blacking out, than with low CO2.

As for the definition of Shallow Water Blackout (by Wikipedia called Deep Water Blackout), and blackout at statics: basically they are both caused by too low PaO2, but at SWB, the sudden drop is initiated by the ascent, and by the slowed or reversed CO2 level growth during the ascent causes that it often comes without any warning signals.

Unfortunately, Wikipedia completely screwed out the definitions - what we understand under SWB, and what has historical reasons to be called so, they define as Deep Water Blackout. For the author there, Shallow Water Blackout is a plain hypoxic blackout (i.e. at static or dynamic apnea). Although, they are definitely wrong, it may confuse many people, hence I prefer referring to SWB as Latent Hypoxia, Depressurizing BO, or Ascent BO.

 

[trux]

Martin teaches a passive exhale at about 3M before the surface, just to reduce this nasty gradient (or vacuum- please, i know it is not a vacuum, its just a term that explains it well for me) by reducing a little the pressure whilst still with pressure on the chest. Also preps for the first inhale.

The exhaling will not reduce the depressurizing effect in any way. It may even aggravate it. However, it has the advantage (as you wrote) that you can inhale immediately after surfacing. So if your buoyancy is already positive, and you have sufficient ascent momentum not to have to need more effort to surface, it is a reasonable advice.

Another important advantage is for those diving on extremely full lungs (packing): When you fill your lungs before the immersion, with packing you may create pressure higher than the ambient pressure on surface. Now when you dive, oxygen in lungs gets consumed with a slightly higher ratio tan CO2 diffuses into lungs, hence the gas volume drops slightly at the end of apnea (roughly 2-4% volume reduction). Normally, when surfacing you wouldn't then reach the same pressure in lungs as it was just after the initial packing. The problem though is your diving response and blood shift - with progressing apnea and with increasing depth, blood is being pushed from extremities to the body core including alveolar capillaries). It has the consequence that the inner lung volume is considerably reduced. That's a very welcome effect avoiding barotrauma in depth. The real problem of the reduced lung volume is at the end of the ascent. Although the gas volume is slightly lower than at the beginning (roughly 2-4% less), the lung volume may be reduced much more than that. It would lead to extreme pressure build-up in lungs, and to consequent barotrauma (lung squeeze) just below the surface.

Hence the blowing off of some air shortly before surfacing definitely makes sense from this point of view too.

 

[ILDiver]

First, thanks Trux. I think I have a better understanding. I do recall a lot of this from the class, but there are so many details given in 4 days that I usually remember the Key points and the details of the why get confused.

Second, I understand your description of what happens while packing. Does the full lung volume also effect the heart on accent as well? It seems that the pressure on the heat in the last 3m - 10m would cause the heart to not beat as efficiently, so the exhale would allow room for the heart to pump??

 

[trux]

Second, I understand your description of what happens while packing. Does the full lung volume also effect the heart on accent as well? It seems that the pressure on the heat in the last 3m - 10m would cause the heart to not beat as efficiently, so the exhale would allow room for the heart to pump??

Yes, good note, it indeed makes sense.

 

[cdavis]

Got it, ILdiver. If you feel your body, maintaining a full lung to the surface vs soft exhale in the last few feet, you will feel more comfortable with an exhale. That discomfort is a reflection of the rapidly expanding lung displacing heart, aorta, etc. probably decreases blood preasure in the brain at a critical time.

Trux, some of your stuff is a little confusing to me. In comment #2, paragraph 4, on this page, you seem to be saying that co2 reentering the lungs and ph increasing on ascent makes one less likely to BO. Am I interpreting that right?

In comment #5 paragraph 7, seems to say the opposite and is closer to what I thought I understood.

What's the difference?

 

[trux]

Trux, some of your stuff is a little confusing to me. In comment #2, paragraph 4, on this page, you seem to be saying that co2 reentering the lungs and ph increasing on ascent makes one less likely to BO. Am I interpreting that right?

Yes, I believe that without that effect, we would see many more SWB.

In comment #5 paragraph 7, seems to say the opposite and is closer to what I thought I understood.

What's the difference?

Perhaps I look at wrong paragraphs, but I do no see anything conflicting in paragraphs 5 and 7. Can you tell what exactly confuses you?

The PAO2 drops with decreasing depth (posing a great problem for the oxygen supply), but the PACO2 drops too, facilitating little bit the pulling of the residual oxygen from lungs. Although the effect of falling PAO2 is much more serious than the one of PACO2, the lower CO2 helps coping with the O2 problem little bit (but far not enough to eliminate it). It might be worse if the blood pH raised rapidly, shifting the Bohr curve in the other direction, preventing the the transport of the remaining oxygen from lungs to blood. On the other hand, the higher CO2 increase tolerance to hypoxemia, and helps releasing O2 in tissue, so all this is rather speculative. There is certain trade off.

 

[sciencemike]

Chris, your logic . . . .as Latent Hypoxia, Depressurizing BO, or Ascent BO.

Trux, thank you so much that is exactly what i wanted to know. I will mull over that for a few days.

Any chance on you contacting wikipedia to get that changed. Also any relevent journal articles you can give for me to read? Or should i use that awesome collection on your website?

 

[trux]

Any chance on you contacting wikipedia to get that changed.

Wikipedia is actually user maintained online encyclopedia. There is no real staff who would be responsible for the content. Anyone can create new pages, or edit existing ones. The problem with the current articles on deep water and shallow water blackouts is that it is quite complex, there are several pages that would need to be completely restructured. There are also many other false statements. Additionally the articles are cross-linked among themselves, and from other pages as well. To fix it all would require already quite a lot of work and considerable time. It would be best done by someone who speaks natively English, and who is professional expert in freediving physiology. I do not feel quite competent for doing that.

Also any relevent journal articles you can give for me to read? Or should i use that awesome collection on your website?

Yes, that would be the best starting point. If I knew about other documents, I'd certainly add them there too And if anyone else knows about some, please let me know.

 

[cdavis]

I'm definitely missing something here, at first thought it might be a typo.

My understanding: on ascent, expanding gas volume in the lungs allows 02 and co2 to increase transport into the lung gas. This drops pa02 in the blood and can contribute to a BO. It also drops paco2, which should raise blood ph. Its my understanding that 02 is bound more strongly to hemoglobin as ph rises, making it less available to the brain, so that too should contribute to BO. What is going on that makes an opposite effect? Is there some effect of co2 outside of ph?

Thanks

Connor

 

[trux]

Yes, that's correct, the raising pH (due to low CO2) has the effect you named - the stronger oxygen affinity to hemoglobin helps better binding remaining oxygen from lungs (positive effect), and in the same time makes it more difficult to release it in the tissue (negative effect). But since unlike at static or dynamic apnea, during the ascent the process of releasing CO2 into lungs occurs suddenly and quickly, the gradient of CO2 is much steeper than normally - higher at the place CO2 is being produced, and where O2 needs to be delivered (tissue / brain), and lower where it just started to be diffused out, and where remaining oxygen needs to be bound (alveoli). There is always certain gradient, but it will be amplified by the fast depressurizing.

 

[sciencemike]

Its my understanding that 02 is bound more strongly to hemoglobin as ph rises,making it less available to the brain.

The thing here to remember is that as the breath hold continues the [CO2] concentration will rise not fall. Even as more CO2 leaves during ascent, The blood pH will not go above 7.4. Remember its moving down a gradient here, and the partial pressure of CO2 in the brain and muscle is now getting very high in comparison to the blood CO2. So this brief drop in CO2 in the blood might take the pH from 7.3 to 7.35. Look at my examples below to see how high localized CO2 levels in the muscles and brain cause O2 to be released. The other thing to remember is that blood acidity is also controlled by the hydrogen ion concentration in the blood. Which will be high not just due to CO2 levels.

What is going on that makes an opposite effect? Is there some effect of co2 outside of ph?

There are both effects of CO2 outside of pH and effects of pH outside of CO2.

Most relevantly CO2 directly affects the binding of O2 to hemoglobin. High CO2 concentrations cause oxyhemoglobin to become dissociated and release the O2. This effect is much larger than the effects of pH on oxyhemoglobin. To put it in perspective with some numbers, if you look at hemoglobin and its ability to transport oxygen and dump it off you should look at it in terms of carrying capacity. Or basically what percentage of Hemoglobin is bound to oxygen. With different factors such as pH or CO2 levels you can see that hemoglobin changes its ability to dump off O2 at its terminal.

Effect of Hemoglobin + oxygen only on pO2
Lung (pO2) (100 torr )
Tissues (pO2) ( 20 torr).Hemoglobin is 98% saturated at the lungs and when hemoglobin moves to the tissues, the saturation level drops to 32%. Thus, a total of 98 - 32 = 66% of carying capacity.

Effect of Hemoglobin + oxygen with pH
Lungs = pH 7.4 and an oxygen partial pressure of 100 torr,
Active muscle = pH of 7.2 and an oxygen partial pressure of 20 torr, results in a release of oxygen amounting to 77% of total carrying capacity. Therefore 11% more than just with partial pressure alone.

Effect of Hemoglobin + oxygen with CO2
In the presence of carbon dioxide at a partial pressure of 40 torr, the amount of oxygen released approaches 90% of the maximum carrying capacity.

So as you can see many factors play into how Oxygen is released from oxyhemoglobin. There is even another factor that is important here that im not going to do the calculation on. But its the allosteric enhancement of Hemoglobin for oxygen. This makes the first number 1.7 times higher than just partial pressures alone, or about 37% if the molecule was distributed via heme with no biological enhancements.

And remember to complicate things hemoglobin itself can carry about 15% of CO2 and some of the rest can be converted into bicarbonate (HCO3-) by carbonic anhydrase. To flow through the blood with the H+ ions to be removed by the lungs.

 

[cdavis]

Thank you gentlemen, most sincerely, but, oh my aching brain! I get the gist and after reading this stuff 10 more times, I'll figure it all out (maybe). Not surprising it's more complicated than it seems at first glance.

Thanks again