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To: techdiver@opal.com
Subject: decompression/breathing rate from: ddoolett
From: egray@me*.ad*.ed*.au*
Date: Tue Jul 05 12:51:38 1994
>This thought occurred to me at the weekend, so I thought I should air it (no
>pun intended :->) to get a more informed opinion. Please forgive any gross
>simplifications or theoretical cock ups - I'm here to learn.
>
>Basically, the uptake and release of gas by the blood in the lungs is
>governed by Henry's law - and the rate of absorbtion/release depends on the
>difference between the partial pressures of gas in the lungs and in the
>blood. So, when I'm swimming around during my dive, I'm breathing at a
>modest rate and tidal volume and the gas in my lungs is a pretty close match
>to the theoretical predictions so the gas absorbed by my body should follow
> the decompresion models.  However, when I'm hanging around on a line doing
>a deco stop, I become much more relaxed and expend much less effort, so my
>breathing rate (and tidal volume) plummet, so the gas in my lungs is
>exchanged much less frequently.
> Is it possible that the gas loadings in my lungs could get to the state
>where my decompression is being slowed because the rate of release is
>dropping (ie. the ppN2 in my lungs is close to the ppN2 in my blood)? Should
>I make a conscious effort to breathe deeper and more often during my stops
>to offset this, and would it make my stops any safer if I did?
>
>I know that my Aladin has a 1/2 time of about 5 minutes or so as its
>minimum, so I get 30 minutes without breathing to reach saturation on
>that...so my gut reaction is that this shouldn't be a problem, but taking it
>to its theoretical limit, a diver who didn't breathe during a stop wouldn't
>off gas at all (would they?), so it follows that a slow breathing diver
>should take longer than a quick breathing one.


In a study that measured arterial and venous PN2 after a chamber dive, 50M for 
30 minutes + 67 minute decompresion at 15,12,9,6,3M, immediately following the 
dive, the arterial PN2 was 592mmHg (0.779bar) and central venous PN2 was
560mmHg 
(0.737bar) (Radermacher,P. et al. Nitrogen partial pressures in man after 
decompression from simulated scuba dives at rest and during exercise. 
Undersea Biomed. Res. 17 (1990) 495-501).  Now to make some assumptions and do 
some sums, that is an arterial-venous difference of 0.042bar.  Multiply this 
by the solubility of nitrogen in blood 
0.042bar X 0.013ml/ml/bar = 0.000546ml/ml nitrogen lost from this blood into 
the lungs.  Multiply this by an average cardiac output and 
0.000546ml/ml X 5600ml/min = 3.06ml/min nitrogen deposited into the lungs.  
Assume a reasonable alveolar ventilation of 4200ml/min for the vital 
capacities stated in the study.  
Alveolar nitrogen = 0.75 + 3/4200 =  0.7507bar, an increase in PAN2 of 
0.0007bar for a resting alveolar ventilation.  If you doubled this alveolar 
ventilation you get alveolar nitrogen = 0.75 + 3/8400 = 0.7504bar, not much of 
a change, not much increase in the venous/alveolar nitrogen partial pressure 
difference, and therefore, presumably, not much change in diffusion of 
nitrogen from the blood into the lungs, if all other factors remain the same. 
This is calculated for the surface and would diminish with depth, assuming 
the amount of nitrogen deposited in the lungs remained the same (or possibly 
diminished) and alveolar ventilation (STPD) increased. 

However, studies show initial nitrogen offgassing rates as high as 100ml/min 
after isobaric inert gas switch after saturation (Anderson,D. et al. O2 
pressures between 0.12 and 2.5 atm abs, circulatory function, and N2 
elimination. Undersea Biomed. Res., 18 (1991) 279-292) but this rapidly 
declines.  Alveolar nitrogen would increase 100/4200 = 0.024bar in this case.
For normal bounce dives I doubt this sort or rate is ever approached.  


By all other factors one is refereing to the lung diffusing capacity for a gas, 
for nitrogen this is about 11ml/min/mmHg (8400ml/min/bar) at rest, and this 
could as much as triple with exercise (this is orders of magnitude higher than 
the amount of gas diffusing according to the calculations above).  The reason 
for an increase in diffusing capacity relies an a number of factors, the most 
important being alveolar ventilation and lung perfusion.  Ventilation/perfusion 
are normally matched to allow effective gas exchange.  If they are not matched, 
for instance if this ratio is large, poorly perfused alveoli will be
ventilated, 
and effectively, the physiological dead space will increase and gas exchange 
will not be optimal. Simply increasing breathing rate voluntarily as keith 
suggested will not necessarily improve gas exchange.  To improve diffusing 
capacity the cardiac output must increase along with pulmonary ventilation, 
as occurs with exercise.  However, the resting diffusing capacity is probably 
more than sufficient for decompression off-gassing.  Increased systemic 
circulation will theoretically reduce the time constants of the tissues in 
perfusion based decompression models, more blood flow/faster gas exchange at 
the tissue level , and it has been suggested since Haldane that mild exercise 
during decompression is beneficial.  Certainly, perfusion based decompression 
models that model inert gas wash-in and wash-out with the same time constants 
(as most do) fail theoretically if you are exercising during a dive and 
resting during decompression.

It is possible that by holding your breath that you wii prevent off-gassing 
but I do not think you need to conciously try and increase your ventialtion.

The smallest half-time on your computer does not refer to the lung or blood.  
Arterial blood gases are assumed equal to the alveolar gases and venous blood 
gases equal to the tissue tensions, in other words the blood half-times are 
too small to consider.

David Doolette
ddoolett@me*.ad*.ed*.au*

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