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SWBO - all lies!

Thread Status: Hello , There was no answer in this thread for more than 60 days.
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Ben Gowland

Aplysia gowlandicus
Apr 4, 2002
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Ha ha - now I've got your attention.......

This is an old thought that has popped back into my head due to 2 recent threads which I've brought into one (denounce me at will :D )

SWBO - 'traditional' theory claims that in the last 10m of ascent the pressure drops so significantly that Oxygen 'offloads' from the blood into the lungs.

There is a difference between oxygen LEAVING the blood to go into the lungs and; the rate of diffusion from lungs to blood REDUCING. Either one could cause a SWBO, but the former requires the PO2 in the alveolar gas to be lower than the PO2 in the pulmonary artery.

Now, ahem, it's been a while since I read any of the classic literature on SWBO. Does anyone have a reference that PROVES that alveolar PO2 gets so low and that pulmonary artery PO2 exceeds it?

The 'exhale in last 5m' technique is based on the common theory - i.e. that if oxygen has to leave the blood to enter the lungs - you'd want the volume of gas that it is joining to be as small as possible so that the ppO2 of alveolar gas increases faster and thus results in less 'offloading'.

However, if the O2 transfer is merely reducing and hasn't 'reversed', then exhaling could aggrivate the situation by reducing the amount of O2 molecules available to transfer to the blood (albeit at a slow rate).

None of this takes account of any of the blood flow or arterial pressure aspects of exhaling v holding it in - which probably have a greater bearing - but I thought it was worth pointing out.

Any comments/refs from those still in touch with the classic literature?

Ben
 
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efattah

Well-Known Member
Mar 2, 2001
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Ben,

I have thought of this a lot.

There is a problem with the 'vacuum theory.'

The idea is this:
- At the end of the dive, your arterial oxygen saturation may be very low (perhaps 60% or even less)
- It is easy to calculate the lung pO2 which would result in an SaO2 of < 60%
- From that data some people then conclude that the lungs suck O2 out of the blood, BUT
- In reality, it is VENOUS blood which is passing by the lungs, not arterial
- The venous blood saturation SvO2 at the end of the dive is probably extremely low, perhaps SvO2=15% or even less
- The lung pO2 required to suck oxygen out of blood with SvO2=15% is ridiculously low
- In my opinion, in the last few meters, the lungs do not suck oxygen out of the blood; instead, the flow rate of O2 from the lungs to the blood slows dramatically, but it is still beneficial to have air in the lungs

- The only factor not taken into consideration is that if the flow rate of O2 from the lungs to the blood is very slow (close to zero), then exhaling in the last few meters might have the effect Sebastien Murat has spoken of, namely, avoiding the strange blood shunts which occur from rapidly expanding lungs (which, according to him, could compromise blood flow to the brain)

- So, even if exhaling in the last few meters might help, I don't think it would be because of a vacuum effect (lungs sucking O2 from blood)
 

feign

Well-Known Member
Jun 30, 2003
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Eric makes a good point to remind everyone that pulmonary arteries are carrying venous blood.

The term artery can be misleading, but they are called arteries because the blood is moving away from the heart. In this case from the right side of the heart, filled with the deoxygenated blood.
 

cebaztian

Well-Known Member
Oct 3, 2003
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lies

So what about the idea/theory that it is pressure on the heart that causes the BO. Like a packing BO. Caused by too much air in the lungs in addition to bloodshift and less room in the lung on ascent. (A cardiologist told me this).
 

cdavis

Well-Known Member
Jan 21, 2003
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Sounds like Murat and the cardiologist have similar ideas. They begin to make more sense. Same cure though.

Connor
 

ADR

Well-Known Member
Jan 21, 2004
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great thread ben!!

Ben and eric this is fascinating and has been playing on my mind as well lately. The benefits of exhaling prior to surfacing if the vacuum theory is false would be if I understand this correctly
1. Reduced thoracic pressure resulting in greater blood flow to the brain
2. The ability to inhale immediately on surfacing rather than the delay and exertion associated with exhaling first plus reinhaling some of the expired gases
Both of these could be outweighed by the loss of o2 if the transfer has only slowed.
 

Walrus

Oz freediver
Oct 3, 2001
693
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Well for competition divers there is also -
3. To avoid serious injury from rapid lung overexpansion.

If you use packing for the dive then your lung volume would be greater then normal at the surface if you didn't exhale the last 5m. And it's not a slow expansion like packing would be, would happen very fast, only a few seconds. Also could contribute to BO like cebaztain was saying about increased pressure on the heart and packing blackouts. On a deep dive most people would lose some of their air from equalising mask&sinuses, specially if they don't reinhale from the mask. Still my guess would be that they don't lose all the extra air from packing. I also know quite a lot of top level divers that use packing for their warm up dives. Diving to only 15m they won't have lost much air and would be in real trouble if they didn't exhale otherwise would be close to full packing volume at the surface...

I'm not about to stop the exhale before the surface just yet. ;)


Cheers,
Wal
 

Ben Gowland

Aplysia gowlandicus
Apr 4, 2002
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Just to clarify things - I wasn't making this point to suggest that exhaling in the last few metres was the wrong thing to do - I still see many benefits to it, but I didn't want to discuss it on this thread. It was more a case that our 'textbook theory' may be technically incorrect.

Whether offloading or reduction in O2 transfer - the end result is similar - a rapid drop in arterial PO2 and thus SWBO.

My belief is that a reduction in O2 transfer would be enough to cause SWBO and the likelihood of some actually having this vacuum effect is extremely remote - i.e. they may need to BO at 30m and be brought to the surface rapidly to achieve this 'vacuum'.

One slight aside - these discussions often bring up SaO2 and pPO2. Understanding the difference between these two helps a great deal in understanding this subject. Often SaO2 is used when PO2 is more relevant and vice versa. Most of the time it is the PO2 that is most relevant to our discussions rather than SaO2 as it is the PO2 that dictates conciousness, not saturation i.e. you can BO at 95% SaO2 if the blood pressure gets too low. Conversely you can stay concious at 50% SaO2 if the blood pressure is high enough.

For those less familiar with these terms, I can appreciate that this subject can be quite confusing. DB is a great place to learn though!

Cheers

Ben
 

ADR

Well-Known Member
Jan 21, 2004
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"Well for competition divers there is also -
3. To avoid serious injury from rapid lung overexpansion. " - Wal

Hey Wal, not sure of the point of the "competition divers" addition in your post. If it's to add credibility to the statement I don't think it does as "rapid lung overexpansion" is not a function of how deep you go or whether or not you do the dive in competition or not......apart from that I agree with your point and think it's a good one. :)

Andy
 

ADR

Well-Known Member
Jan 21, 2004
655
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Hi Ben,

Your original post asked "Does anyone have a reference that PROVES that alveolar PO2 gets so low and that pulmonary artery PO2 exceeds it?"

I just remebered that Seb said he did some test with a pulse oximeter(SaO2) and also with some tube down his throat into his lungs measuring PO2 (not sure if it included a chamber or not) It sounded like a horrible thing to go through and I'm sketchy on the details but it might be worth asking him as it may have the test data you are after for validating/disproving the "vacuum theory"

regards

Andy
 

Walrus

Oz freediver
Oct 3, 2001
693
77
0
I just meant most competition divers use a lot of packing therefore are at greatest risk of lung injury if they didn't exhale before the surface. By comparison I don't think many people use packing when they spearfish or for recreational diving.
 

naiad

Apnea Carp
Supporter
Oct 11, 2003
2,897
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I wonder if some SWBO cases are just straightforward hypoxic blackouts - after all, similar things happen in static and dynamic training, where depth and pressure are not normally an issue.

Lucia
 

ADR

Well-Known Member
Jan 21, 2004
655
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Hi Wal,

Yeah that makes sense as I'd hate to see you and your 11 litres do a bounce dive down to 20m and back.

Andy
 

DrLindholm

New Member
May 31, 2004
14
1
0
There are a few different blackout things to consider

SWB is a bad terminology.

I prefer separating Ascent blackout from the hyperventilation and resulting hypoxic blackout, combinations are definitely possible.

During ascent there is a shift in the direction of the flow of oxygen and the original reference is Lanphier and Rahn J.Appl.Physiol 1963: alveolar gas exchange during breath-hold diving.
If you want to read more about this I suggest a book chapter in "the lung at depth" Editors Lundgren and Miller
Dr Ferrigno and Dr Lundgren has written a chapter in this book about human breath-hold diving.
(Unfortunately this book is very expensive to buy, but if you have access to a good library you can probably borrow it/order it)

There are other blackouts as well eg if you pack to much you syncope.
 

ADR

Well-Known Member
Jan 21, 2004
655
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I went looking for that article online and might even sign up for a subscription to "Journal of Applied Physiology" as it has some great articles listed. Here is the FREE abstract for the chapter DrLindholm was referring to. It is worth noting that the tests were in a chamber to 33ft (10m) and used some "partial-rebreathing process " to measure gas samples. The abstract suggests "evidence of reversed O2 transfer".....ohh for the full article


The Article Abstract

Alveolar gas exchange during breath-hold diving
E. H. Lanphier 1 and H. Rahn 1
1 Department of Physiology, State University of New York at Buffalo, Buffalo, New York

Use of a recompression chamber permitted simulation of breath-hold dives to 33 ft of sea water (2 atm abs). Four normal subjects made such dives during rest and mild exertion while delivering alveolar gas samples at frequent intervals by a partial-rebreathing procedure. The course of alveolar gas exchange differed greatly from that in ordinary breath holding. Oxygen uptake remained at near normal levels until ascent owing to the maintenance of alveolar Po2 by increased ambient pressure. Reversal of CO2 transfer occurred during descent, and little CO2 moved in the normal direction until ascent. Greater uptake of oxygen and retention of CO2 in the body led to lower final values of both alveolar Po2 and Pco2 than in comparable breath holding at the surface. Hyperventilation made possible longer dives with harder work, and in these the Po2 reached very low values on ascent. One subject showed a final Po2 of 24 mm Hg with evidence of reversed O2 transfer . Acute hypoxia on ascent is a likely cause of drowning in breath-hold diving.

Submitted on October 17, 1962
 

ADR

Well-Known Member
Jan 21, 2004
655
62
118
I went looking for that article online and might even sign up for a subscription to "Journal of Applied Physiology" as it has some great articles listed. Here is the FREE abstract for the chapter DrLindholm was referring to. It is worth noting that the tests were in a chamber to 33ft (10m) and used some "partial-rebreathing process " to measure gas samples. The abstract suggests "evidence of reversed O2 transfer".....ohh for the full article


The Article Abstract

Alveolar gas exchange during breath-hold diving
E. H. Lanphier 1 and H. Rahn 1
1 Department of Physiology, State University of New York at Buffalo, Buffalo, New York

Use of a recompression chamber permitted simulation of breath-hold dives to 33 ft of sea water (2 atm abs). Four normal subjects made such dives during rest and mild exertion while delivering alveolar gas samples at frequent intervals by a partial-rebreathing procedure. The course of alveolar gas exchange differed greatly from that in ordinary breath holding. Oxygen uptake remained at near normal levels until ascent owing to the maintenance of alveolar Po2 by increased ambient pressure. Reversal of CO2 transfer occurred during descent, and little CO2 moved in the normal direction until ascent. Greater uptake of oxygen and retention of CO2 in the body led to lower final values of both alveolar Po2 and Pco2 than in comparable breath holding at the surface. Hyperventilation made possible longer dives with harder work, and in these the Po2 reached very low values on ascent. One subject showed a final Po2 of 24 mm Hg with evidence of reversed O2 transfer . Acute hypoxia on ascent is a likely cause of drowning in breath-hold diving.

Submitted on October 17, 1962
 

cdavis

Well-Known Member
Jan 21, 2003
4,006
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Very interesting. Does the "reverse co2 transfer" explain why my urge to breath comes on much faster and harder in cw than in dynamic?

Connor
 
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