Apnea, vasoconstriction, and dynamics

[sebastien murat]

A reversal (weakening) DR upons ascent occurs only during F-dives but not during E-dives, at least not in humans. In fact, E-dives may further accentuate the DR during ascent. This reversal is caused by lung decompression per se, but only to the extent that lung volume increases above FRC. The greater the increase in lung volume and the greater the rate of lung decompression, as when nearing the surface, for example, the greater the reversal in the DR. This reversal is accompanied by hypotension, largely as a result of a reduction in peripheral vascular resistance (i.e., vasodilation). Despite an increase in cardiac output and tachycardia, blood flow to the brain is compromised. Depending on the degree of hypoxia already incurred this may be or may not develop into a problem. Indeed, ascent-tachycardia is a usual feature of diving in mammals, birds and reptiles, but then again they rarely push the envelope since it adversely affects their ability to dive frequently. Reversal of the DR increases the risk of SWB, and in my opinion is an important contributing factor for it.

Tachycardia is the usual sign of a reversal, but at large inflation pressures this may revert to bradycardia. Bradycardia in this case is not evidence of improved O2-conservation, rather it probably a sign of a impeded venous blood return to the heart (due to excessive lung re-expansion) and contraction of a largely empty ventricular chamber. This may invoke the Bezold-Jarisch reflex (apnea, hypotension, bradycardia, asystole, cardiovascular collapse and syncope).

In seals who E-dive (e.g., elephant seals, etc.), ascent tachycardia still occurs because their anatomy is such that the thorax (chest + lungs) actually stretches the pulmonary membrane during ascent, since their lungs do not become congested with blood. In humans, this is not the case however. Once lung volume increases above about RV (since the actual measure of FRC depends on the depth and can be reduced to RV) there is stretching of the lung mebrane, which triggers pulmonary stretch receptors and invokes the lung inflation vasodepressor reflex (peripheral vasodilation, tachycardia and hypotension). Because FRC with head-out immersion reduces the dry FRC value by as much as 50 % or more, once several E-dives have been undertaken, it means that diving FRC is not much greater than RV. Actually, once one factors in lung-shrinkage associated with breath-holding per se, FRC probably equates to very cose to RV, meaning: no stretch and no vasodepressor reflex.

All that being said, it would seem that, some species may be able to exert volitional control of the DR even during lung expansion.


Seb

 

[cdavis]

Seb,

It would seem that your first paragraph argues strongly for full lung divers to exhale slowly in the last 20 ft or so in order to keep lung volume near FRC and preserve the DR to the max. Do I have that correctly?

Thanks

Connor

 

[sebastien murat]

It is tempting to think that perhaps the notion of exhaling to minimize lung volume expansion may seem like a wise way of reducing the risk of SWB, presumably as it does in seals (Hooker et al. 2005). Unlike seals, however, airway collapse in humans occurs in non-respiratory bronchioles before more distal, respiratory airways, so that any such maneouver is not likely to prevent gas-exchange, but actually promote it. In addition, ventilatory maneouvers, such as exhaling underwater have been found to reverse the DR in seals (Harrison 1960).

A common mistake divers make is that they assume that once they surface and breathe, they are then safeguarded. The dive is not actually over until vital organs a reoxygenated which can still take about 4-6" during F-dives.

Seb

 

[Shallow russian]

Guys, thanks for great and amasingly clear and interesting discussion!
But, what would be final answer? Never exhale before surfacing when diving on full lungs?
Never doing even slight exhale 1-2 meters before surface?
And when you are packed?
If all these practical questions make sense in that case.

 

[Will]

Provided that this bradycardia is the result of an emotive response and not one associated with increased oxygen extraction (why would it if there is no physical tension), then, actually, venous blood O2 stores will increase (i.e., SvO2).

Assuming that the athlete has attained a level (and very few have) where they can maintain 100% muscular relaxation even during emotional stress, then the major 'O2 extractors' will be the royal organs:
1. Lungs
2. Heart
3. Brain
Breathing (lungs) can be controlled, but the heart and brain will be burning O2 at a much greater rate than in the absence of emotional stress. This creates an 02 defecit before the dive has begun - not a problem for a diver like Seb, who is as far as I know limited by muscular failure rather than hypoxia, but it can be a problem for me. This is why I choose to get stressed during the dive (if at all) where it has the opposite effect on 02 stores (conserving them).

 

[OceanMan]

Hi,

Just to point out this thread
http://forums.deeperblue.net/showthread.php?t=65936&highlight=exhale+ascent
where I posted a scientific paper about seals exhaling during ascent and where I wonder if it could be beneficial for freedivers.

Unlike seals, however, airway collapse in humans occurs in non-respiratory bronchioles before more distal, respiratory airways, so that any such maneouver is not likely to prevent gas-exchange, but actually promote it

Seb, even if that is true, when exhaling during ascent will the reduced volume of the lung not induced a much smaller gaz exhange than in full re expanding lungs?
Ok it will not make the respiratory bronchioles collapse again. But the total volume of air in the lung will be greatly reduced which should reduce gaz exchange anyway. As the lung volume is way smaller, a much smaller quantity of O2 can return from the blood to the lungs. Don't you think?

I hope I make myself clear.

Matthias

 

[sebastien murat]

Salut Matthias,

Clear enough!

You need to go back and look at the ideal gas law (PV =nRT). Lung shrinkage effects aside, you are are normally a closed system so that all variable, bar P & V are constant. If you exhale you are no longer a closed system: n (the no. of molecules) can vary also. This is bad news because just as V increased when you held your breath, resulting in a reduction in PO2 in the lungs, now you've substituted V with n resulting in a similar effect....you've gone full-circle. Worse yet you actually increase the rate of gas-exchange. How? Keeping the lungs at FRC by passively exhaling ensures the centralization of blood volume. Though some believe that reductions in the surface area reduces the rate of gas-exchange, they overlook an important fact, i.e., the pulmonary capillaries are distended and engorged with blood. We know that increases in pulmonary capillary blood volume will actually increase the rate of gas-exchange. In my view this will increase the potential for SWB. Nevertheless, many divers are in the habit of exhaling upon ascent. The only advantage this might have is ensuring that the lungs don't expand so much as to restrict blood from returning to the heart, etc., since we know that it is possible to faint by packing. But this generates problems all its own once again. No matter how you configure it, if you think you've solved it with F-dives you create another problem, and there does not seem to be any way around it...sadly.

Seb

 

[sebastien murat]

Shallow Russian ..... I assume you mean shallow like in the pool!

There are many recipes, and some are better than others. One must decide, based on where one is, how best to get to where one wants to be and what level of safety one wants to have. I dive on empty because my DR (and my large blood O2 stores) allow me to do so, consequently, I don't have any of the problems most people speak of. Though such a recipe would similarly serve anyone else, performance-wise they may be better served, at least initially, by diving on full lungs. In my opinion its all a matter of whether you're in a hurry to prove yourself and feel like gambling with your life, despite having the knowledge and understanding of the risks, or, whether you have the patience and persistence to travel on the road less travelled, despite seemingly insurmountable odds.

I have plenty of time and am in no hurry, which makes the decision easy.

Seb

 

[OceanMan]

This is very interesting. That really makes sense indeed. Merci Seb.

I don't want to seem to persist in my ideas, I just want to recap my thoughts.

So:

As you say, there is nothing one can do about the reduction in PO2 in the lungs, the only factor one can play with is V (by reducing n by breathing out).
If one want to stop O2 from returning from the blood to the lungs, the idea is not to prevent gaz exchange.
The idea is to allow little room in the lungs for O2 coming from the blood. Eventually, when exhaling during ascent, you might have less O2 returning from the blood to the lungs EVEN if the gaz exchange is greater but just because this O2 has only a small volume to go into. So even if this small volume is rapidly filled with O2, there will less O2 in it than in a greater volume.

But I don't really believe in it myself. I am almost sure you're right, breathing out during ascent must not be a good idea. And who the hell will have the courage to try anyway rofl

 

[cdavis]

Seb,

I should have known it was more complicated than it looked, but I'm still very curious. Sorry if it seems like I am laboring the point.
Entirely aside from the possibility that 02 is returning to the lungs on ascent, it would seem that maintaining the max DR by keeping lung volume at or below FRC all the way to the surface would be beneficial. If you are doing Fdives, properly timed exhale should do that. What am I missing?

Thanks for your input. Any possibilty of doing a clinic in the US?

Connor

 

[wet]

Thanks Seb. Seems to me, the human E-dive maintains O2 conservation maximally throughout the entire dive until surface exhalation-inhalation.

Can a series of moderate depth E-dives (10 sequentially) be done, or is there an accumulating risk with each additional dive? (eg. repeated F-dives accumulate N2, so risk of DCS gradually increases) Must the Surface intervals be lengthened after each additional E-dive? DDeden

 

[sebastien murat]

It's possible that that the DR could be maintained by exhaling during ascent. But this doesn't circumvent the fact that O2 will be lost during the exhale. That's bad news, but there's worse to come yet...wait for it...

As part of my research into SWB here at the university, I've discovered that there is another culprit for SWB, to the extent that it may possibly more significant than the either a loss of the DR or a fall in PAO2 (in the lungs) associated with decompression. It goes something like this:

F-dives are liley to be associated with a large transfer of CO2 out of the lungs during ascent, whether you exhale or don't. During rapid decompression to high altitude, which is essentially equivalent to ascending from depth (I've attached a pic) the hypocapnia and alkalosis that develops is of a magnitude that can only be achieved by severe hyperventilation, hence why there is a decreased urge to breathe during ascent. Though this effect would result in a (rapid) left-shift in the HbO2-dissociation curve (Bohr shift) and improve O2-uptake by the blood (in the lungs), it would, unfortunately, also restrict desaturation at the tissues, so that tolerance to hypoxia can be expected to be critically reduced. In other words, tolerance to hypoxia would be markedly decreased.

Not finished yet...it gets worse

Despite the potent vasodilatory effects of acute hypoxiema on the cerebral vasculature the cerebral vessels are more sensitive to decreases in PaCO2. The cardiovascular responses during hypocapnic hypoxia involve vasodepression and inadequate cerebral perfusion. In fact, there is cerebral vasoconstriction and peripheral vasodilation. Considering that the normal brain ordinarily receives 20 % of the cardiac output, despite the fact that it makes up only 2.5 % of the total body mass, a redistribution of cardiac output to the periphery may itself adversely affect cerebral perfusion. Even if the hypocapnia was only of a mild intensity this would still be enough to blunt or abolishes the vasodilatory stimulus of severe hypoxia. E-dives minimize such effects.

So, there it is....pick your poison

Seb

PS: No courses in the US, Cdavies, but look me up in Mallorca as of this September. Thw website (sub7seas.com) will be revamped by the end of the month.

 

[sebastien murat]

Wet,

It's hard enough getting bendt with F-dives, let alone E-dives! Studies on rats have shown that reducing lung volume by just 5 % reduces the incidence of DCI by as much as 50 %. Lung volume is reduced by a lot more than just 5 % with E-dives. I very much doubt you would be able to get bent. Certainly, some of the dives I've done have shown that event to depths in excess of 100m with E-dives, narcosis (an indicator of the inert gas burden) is totally absent, whereas it could be felt at depths as shallow as 40 m (in ideal conditions but with exercise and 60 m with no exercise).

Seb

 

[sebastien murat]

Correction:

...at 60m with no exercise with F-dives.

Seb

 

[fogish]

Sebastien things are just starting to make sense to me, I just had to read it about 20 times. Do you happen to know why the cerebral vasculature responds in such a way to a decrease in PaCO2? Is the response solely because of the exchange of O2 and CO2 in the lungs? It seems to me that there would be an increase of O2 in the blood and a decrease of CO2, why would the body react to that by vasoconstriction of the cerebrum and vasodilation of the peripheral? Is it just resupplying your muscles with O2 at the expense of the brain?

I think I am missing something vital here, sorry if it is simple, I am just beginning to figure all of this out.

 

[sebastien murat]

Fogfish,

Sorry, your questions don't make sense....don't know exactly what your asking. PO2 does not increase during breath-holding, except during descent. I don't know why hypocapnia aver-rides the vasodilatory effects of hypoxia. Would strongly suggest that your review other threads to get a better handle on the topic.

Seb

 

[cdavis]

Seb,

Thank you for such a detailed reply, I appreciate the time it took.

I assume there is a typo in paragraph 3 , C02 should be passing from the blood to the lungs on ascent. This makes it all fit together, I think.

While explosive decompression in a high flying airplane is mechanicly similar to ascending from 30 or so meters, seems like the two situations should be pretty different. In an aircraft decompression, blood and lung C02 are quite low(normally low) to begin with, so for extreme alkylosis to occur seems reasonable. When starting to ascend from depth on an Fdive, C02 has already been forced into the blood stream from the lungs during decent, plus C02 production during the dive, should mean than the blood is quite acid and would simply be returning to a more normal PH level rather than alkylosis. I've often wondered if my strong and early urge to breathe at depth was partly related to C02 forced into the blood stream by increasing preasure and would that urge to breathe be less if I mastered Edives.

All of my above thoughts are not much more than rank speculation and I would love to see some research results on this aspect while actually diving, but it sure is fun to think about. Thank you again for all your research and willingness to share it.

This sounds crazy, but I'm going to be in Spain for Chistmas. How long will you be in Mallorca?

Connor

 

[sebastien murat]

Mia culpa! Typo on 3rd paragraph.

Yes, a paradoxical urge to breathe during descent, especially fast descent is the result of a sudden rise in Pa)2 (in the blood). If the speed of descent is excessive compared to the lung-to-chemoreceptor circulation time, then, the pressure gradient between the lungs and blood will be large and much CO2 will enter the blood stream. The diffusivity of CO2 is also very high (~ x20 that of O2) which increases this effect. Of course this problem can be circumvented by hyperventilating or increasing the circulation time relative descent speed. Warm-ups reduce this risk by: (1) increasing circulation time; and, (2). increasing the [Hb] which helps buffer the effects of hypercapnia. Consequently, 'the uglies' commonly occur on the first dive and also during weight-assisted dives where descent speed can be in excess of 3m/s. This is one of the reasons hyperventilate prior (effortless => relatively slow circulation times) to no-limits, since its can be extremely uncomfortable otherwise and the risk of a CO2 blackout is high

By a similar token, if the circulation time is slow compared to the decompression rate the blood can become alkalotic resulting in a Bohr shift. Even if it didn't, the fact is that isocapnic (normal CO2) hypoxia still results in reduced cerebral blood flow.

Hypercapnia with E-dives cannot reach the levels of F-dives (for several reasons), consequently, the urge to breathe, though it still occurs, does not need to be tolerated for long periods. Furthermore, because the metabolic rate is slower with such a strategy it means that that increasing frequency with which contractions develop is at notime as high as F-dives.


Xmas (proper?) Mallorca: no can do as I'll be in Sweden, but 2 weeks before and 3 weeks after I'll be back.

Seb

 

[sebastien murat]

Mia culpa! Typo on 3rd paragraph.

Yes, a paradoxical urge to breathe during descent, especially fast descent is the result of a sudden rise in Pa)2 (in the blood). If the speed of descent is excessive compared to the lung-to-chemoreceptor circulation time, then, the pressure gradient between the lungs and blood will be large and much CO2 will enter the blood stream. The diffusivity of CO2 is also very high (~ x20 that of O2) which increases this effect. Of course this problem can be circumvented by hyperventilating or increasing the circulation time relative descent speed. Warm-ups reduce this risk by: (1) increasing circulation time; and, (2). increasing the [Hb] which helps buffer the effects of hypercapnia. Consequently, 'the uglies' commonly occur on the first dive and also during weight-assisted dives where descent speed can be in excess of 3m/s. This is one of the reasons hyperventilate prior (effortless => relatively slow circulation times) to no-limits, since its can be extremely uncomfortable otherwise and the risk of a CO2 blackout is high

By a similar token, if the circulation time is slow compared to the decompression rate the blood can become alkalotic resulting in a Bohr shift. Even if it didn't, the fact is that isocapnic (normal CO2) hypoxia still results in reduced cerebral blood flow.

Hypercapnia with E-dives cannot reach the levels of F-dives (for several reasons), consequently, the urge to breathe, though it still occurs, does not need to be tolerated for long periods. Furthermore, because the metabolic rate is slower with such a strategy it means that that increasing frequency with which contractions develop is at notime as high as F-dives.

I'll be doing some blood gas-monitoring, either later this year or early next year as part of my research.

Xmas (proper?) Mallorca: no can do as I'll be in Sweden, but 2 weeks before and 3 weeks after I'll be back.

Seb

 

[Will]

As I wrote somewhere else descent hypercapnia and subsequent CO2 narcosis are a good sign, as they indicate minimal ventilation during the breathe-up, and are normally followed by an easy contraction-free ascent all the way to the surface.
In my experience hypercapnia brings on the DR faster than anything else, so this could be an advantage of inhale diving if it doesn't develop as much during exhale descents?