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>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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