Blood shift and Exhale(FRC) diving, musings

[efattah]

When I do my series of extreme full exhale dives, I never cough, I can exhale fully no problem (no wheezing). My diving ability goes up dramatically, in particular I can do semi active full exhale (fun) dives for 1'20" to 1'40".

However, I have had edema before, in 2000, when I did excessive exhale dives. Then, I was wheezing, coughing a bit, and my diving ability immediately afterwards dropped dramatically.

 

[Mullins]

Probably depends on your current state of dive fitness - if you have a very flexible chest then you won't end up with such a big pressure gradient across the alveolar membrane. But then, you also wouldn't get as much bloodshift because your chest would be collapsing further and overall thoracic volume would be lower... no?

 

[trux]

Does anybody know what volume of blood is normally in the lungs and/or how much might be accumulated through blood shift in the area in or after the alveolar capillaries?

I do not remember the numbers from the top off of my head, but I believe having seen values over 2 litres. It depends, of course on diverse factors. I think I have somewhere a study with some rather precise quantification. The only thing I had at the hand right now was the blood-shift you have on surface - the increase was measured to be 0.7 liter.

In addition to a predive increase in TLC, a redistribution of blood from the periphery to the intrathoracic blood-containing structures, a “blood shift,” allows the RV to decrease below normal. An increase in intrathoracic blood volume of 700 ml is observed during mere head-out immersion,...

 

[Simos]

Thanks for the clarification Connor, I do see the difference. I thought that blood shift was the general term used for describing the constriction of peripheral blood vessels and concentration of blood around the lungs (despite of the fact that if you push things too much it might lead to oedema when the limit of how much the lung blood vessels can swell).

I have to admit that it's still a bit unclear to me of what the benefits of FRC might be when it comes to blood shift and deep dives. Blood shift will occur in shallower depths for sure if diving FRC and the way I understand it is that you'll then reach the limit of how your lung vessels can swell earlier - pushing beyond this point will probably lead to oedema. Comparing with diving full lung, the same exact things will happen only in greater depths.

So essentially it should mean that if you want to dive as deep as possible you are better off diving full lung and perhaps if you are planning shallower dives then FRC will help you get the blood shift effect that you'd otherwise only experience in greater depths? I guess it depends on what the max limits of swelling of lung vessels - if the limit is not exceeded, maybe there is some benefit with FRC even if going deep...

 

[trux]

Kind of, but 1. it's mostly plasma and
2. it isn't in blood vessels, so it wouldn't improve the rate of gas exchange. If anything it would hinder gas exchange by reducing gas volume and coating the alveolar wall.

Dave, why do you tell the blood is not in blood vessels? Don't you consider the alveolar capillaries to be blood vessels, or are you referring to leaking of blood plasma through the alveolar wall inside the alveolar space? The second can indeed happen, but to my best knowledge that's already pathological, not what we call blood-shift. The plasma would dilute the surfactant layer, and increase the alveolar surface tension, keeping it then collapsed even upon surfacing. Without the presence of similarly big pressure gradient in the opposite way, the plasma would take much longer to be absorbed back (if at all). It would then reduce the lung efficiency on surface. In other words, it is in fact pulmonary oedema. It certainly happens rather frequently at extreme competitive dives, but I do not think it is what we really want to achieve when diving. And especially not at repetitive diving.

Normally, the blood-shift associated with the hydrostatic pressure at depth, and the vasoconstriction of extremities, moves blood to the core, hence the alveolar capillaries and blood vessels are engorged with blood. They do contain also red cells, so the elevated volume of hemoglobin in the alveoles does help better gas exchange. In the same time you are right that it also reduces the intrapulmonary volume. At repetitive FRC dives it is not a big problem though, because the diver can regulate the exhaled (or inhaled) volume accordingly.

 

[Mullins]

Talking about oedema, Trux. I was responding to the question: "isn't a oedema an increased bloodvolume?"

 

[efattah]

Generally speaking, edema = lung squeeze. It can take different forms and causes, but plasma or blood inside the lungs, interfering with the surfactant, is definitely not good and not normal.

 

[Mullins]

I don't imagine it's particularly good either, but I think it's probably very common. Wasn't interstitial water detected in 70% of athletes at 2007 WCs?

I get it fairly regularly, but it resolves quickly and doesn't seem to have any effects on dive performance over subsequent days.

 

[fflupo]

isn t the speed on ascent while in bloodshift important to allow the pulmonary capillaries to pump the blood back, and to avoid the rupture of the alveoli which can leak and cause an edema?

i always thought that the bloodshift is an increase in the artery bloodvolume and occurs more in the artery than in the alveoli?

 

[trux]

isn t the speed on ascent while in bloodshift important to allow the pulmonary capillaries to pump the blood back, and to avoid the rupture of the alveoli which can leak and cause an edema?

When you start ascending, the lungs starts expanding, meaning that the risk of a squeeze drops (unless you have violent contractions which may induce some additional negative pressure). The expanding volume will push the blood away from the alveoli. Pulmonary capillaries do not have any pumping ability. They only have vasoconstrictive muscles controlling the blood flow. However, I do not think that they start constricting during the ascent. The change of the hydrostatic pressure is sufficient for moving some of the blood back. Not all though, and that's why at packing freedivers there may be the possibility of a barotrauma near the surface (smaller lung volume than at the moment of immersion, hence bigger pressure in lungs).

i always thought that the bloodshift is an increase in the artery bloodvolume and occurs more in the artery than in the alveoli?

Alveolar capillaries are the endings of arteries (and starting of veins), so to some extent you are right. However the volume increase is not limited to the arteries only - all blood vessels (arteries and veins) are engorged with blood. There are no constrictors between the arteries and veins, so when the arterial constrictors dilate, the blood flow into the entire rest of the system increases.

 

[fflupo]

thanx trux for your patience, appreciated

no packing, and below RV

concerning the de-constriction of the pulmonary capillaries during a high ascent speed is still not clear to me ..

i agree that there is still some blood from the shift left right after surfacing means that during the process of shifting the blood back there can be some stress (f.e. causing an edema ) on the pul. capillaries?

 

[trux]

no packing, and below RV

Yes, I know for you, but I rather described the general case.

concerning the de-constriction of the pulmonary capillaries during a high ascent speed is still not clear to me ..

What I menat is that the vasoconstriction of peripheral arteries, and the vasodilatation in the core does not stop when you start ascending, so it is not the changed blood-flow control through the arterial constrictors that changes and suppresses the blood-shift during the ascent, but rather simply the hydrostatic pressure, chest elasticity, and the resulting change in transpulmonary pressure that then push back the blood from the lungs. Well, more precisely told, there may be perhaps some smaller variation in the strength of the diving response during the ascent, and hence also in the vasoconstriction due to the decreasing pressure, but in the same time the CO2 level and acidity still increase too, so it certainly does not lead to the release of the constriction/dilatation until surfacing and inhaling.

I am not sure if I do not wrote it too complicated - in other words I wanted to tell that when you start ascending, the blood shift is still in place, and that just the blood is being pushed back from the lungs by the intrapulmonary pressure.

i agree that there is still some blood from the shift left right after surfacing means that during the process of shifting the blood back there can be some stress (f.e. causing an edema ) on the pul. capillaries?

Well, there are certainly different factors increasing the possibility of oedema (for example strong contractions), and the engorgement of the blood vessels in lungs, and the dilation of their walls is certainly a strong risk factor too, but the ascent actually reduces it, so I would not tell that the ascent adds to the risk. It is not the ascent, it is rather the time.

On the other hand, due to the collapsed alveoli in depth, some parts of lungs may not inflate, and then you can indeed suffer a barotrauma during the ascent. But that's not directly related to the blood shift.

 

[fflupo]

ok i can see your point, i think:


Pulmonary hypertension begins when tiny arteries in your lungs become narrow or blocked. This causes increased resistance to blood flow in your lungs, which in turn raises pressure within the pulmonary arteries

 

[trux]

Pulmonary hypertension begins when tiny arteries in your lungs become narrow or blocked. This causes increased resistance to blood flow in your lungs, which in turn raises pressure within the pulmonary arteries

Yes, that's valid for normobaric conditions (on surface). In depth, the same condition (pulmonary hypertension) appears even at dilated and not blocked arteries/capillaries. The hypertension is not caused by the arterial constriction in lungs, but oppositely by the peripheral constriction and the ambient hydrostatic pressure that rush the blood into the pulmonary blood vessels, increasing so the pressure there, despite their dilation. Better told not because of the ambient pressure alone, but more precisely because of the transpulmonary pressure (the difference between the ambient pressure, and the pressure inside lungs after the chest and diaphragm reach the limits of their elasticity).

 

[fflupo]

q.e.d

this was a big piece to swallow for me, thank you so much

wolf