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Date: Thu, 07 Sep 2000 19:32:13 -0500
To: techdiver@aquanaut.com
From: Scott Hunsucker <swhac@pc*.gu*.ne*>
Subject: answers to 80/20 questions and more on O2
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>Scott,
>
>Thanks for popping your head in every now and then on these discussions,
>no matter how much it seems you're talking to a brick wall.  :-)

My pleasure.

>I have one question for you (well, I have many, but I'll limit it to one
>for now :-).

Fire away, but it usually takes me a couple of days to get to it.

>One thing that hasn't been brought up in this discussion so far is the
>vasoconstriction caused by staying on high PO2 mixtures (regardless of
>whether it's 80/20, 100%, etc).

Correct, there is vasoconstriction that occurs from breathing oxygen at 
higher PO2s.  More specifically there is vasoconstriction secondary to 
hyperoxia at the precapillary sphincter; yet, the large increase in oxygen 
diffusibility greatly outweighs any concerns that would be created by the 
constriction.  In short, oxygen is able to get around the vasoconstriction 
and still effectively replace the nitrogen, which greatly offsets any 
possible problem.  Breathing O2 at higher PO2s also allows a reduction in 
interstitial pressure and reduces edema:  Which, one could postulate, if 
this did not happen the effects of the edema could also lead to problems 
with DCS.  Oxygen at high PO2s also leads to mild bradycardia, a slight 
decrease in cardiac output, and an increase systemic vascular resistance, 
none of these are problems for fit people (yet another reason to stop 
smoking and quit eating 1lb of peanut M&Ms a day, true cave instructor 
vices) and are considered inconsequential.  There are studies, both animal 
and human, that have shown there can be interference with offgassing of 
nitrogen caused by oxygen induced vasoconstriction, but this effect is NOT 
SEEN until PO2s exceed 2.0.  I realize that someone will read this and try 
to twist it into some convoluted argument (probably someone who smokes and 
eats peanut M&Ms, or better yet like Black and Morin, who don't even do 
this stuff), against using oxygen, but the information needs to be known 
for informed decisions to be made.

>  I was under the impression that a large
>reason for the breaks (and a large reason for the fact that they don't
>have to be subtracted from the deco) is that the high PO2's cause
>vasoconstriction, which in turns reduces efficacy of offgassing.

Fair statement, but if the efficiency of deco is reduced by something, 
would it not make sense that the time spent at deco would thereby have to 
be increased?

>  By going off the high PO2 for a while you encourage vasodilation and thus
>increase the efficiency of the offgassing.

It takes approximately one hour for tissues to become saturated with 
O2.  Of course different tissues are affected at different rates:  blood 
changes are seen within five minutes, soft tissues peak within one 
hour.  Once we stop breathing high PO2 O2 the blood returns to normal in 5 
minutes (odd how BG (back gas) breaks are recommended for 5-6 minutes don't 
you think? ;-)) and muscle drops within two hours and soft tissues within 
four hours.  So you see the short BG breaks are only long enough to just 
allow the blood to return to normal values and not really time to offset 
any possible negative effects of vasoconstriction; which in turn is offset 
by taking one hour (on O2 which is longer than most people will spend 
decoing on O2) to saturate tissue and thereby have a systemic effect, as 
well as the high diffusibility of oxygen in the first place.

>Is this correct?

Not quite, but I do hope that I have answered your question, and maybe some 
others along the way.
Sincerely,
Scott Hunsucker


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<html>
<br>
<blockquote type=3Dcite cite>Scott,<br>
<br>
Thanks for popping your head in every now and then on these
discussions,<br>
no matter how much it seems you're talking to a brick wall. 
:-)</blockquote><br>
My pleasure.<br>
<br>
<blockquote type=3Dcite cite>I have one question for you (well, I have
many, but I'll limit it to one<br>
for now :-).</blockquote><br>
Fire away, but it usually takes me a couple of days to get to it.<br>
<br>
<blockquote type=3Dcite cite>One thing that hasn't been brought up in this
discussion so far is the<br>
vasoconstriction caused by staying on high PO2 mixtures (regardless
of<br>
whether it's 80/20, 100%, etc). </blockquote><br>
Correct, there is vasoconstriction that occurs from breathing oxygen at
higher PO2s.  More specifically there is vasoconstriction secondary
to hyperoxia at the precapillary sphincter; yet, the large increase in
oxygen diffusibility greatly outweighs any concerns that would be created
by the constriction.  In short, oxygen is able to get around the
vasoconstriction and still effectively replace the nitrogen, which
greatly offsets any possible problem.  Breathing O2 at higher PO2s
also allows a reduction in interstitial pressure and reduces edema: 
Which, one could postulate, if this did not happen the effects of the
edema could also lead to problems with DCS.  Oxygen at high PO2s
also leads to mild bradycardia, a slight decrease in cardiac output, and
an increase systemic vascular resistance, none of these are problems for
fit people (yet another reason to <b>stop smoking</b> and <b>quit
eating
1lb of peanut M&Ms a day</b>, true cave instructor vices) and are
considered inconsequential.  There are studies, both animal and
human, that have shown there can be interference with offgassing of
nitrogen caused by oxygen induced vasoconstriction, but this effect is
NOT SEEN until PO2s exceed 2.0.  I realize that someone will read
this and try to twist it into some convoluted argument (probably someone
who smokes and eats peanut M&Ms, or better yet like Black and Morin,
who don't even do this stuff), against using oxygen, but the information
needs to be known for informed decisions to be made.<br>
<br>
<blockquote type=3Dcite cite> I was under the impression that a
large<br>
reason for the breaks (and a large reason for the fact that they
don't<br>
have to be subtracted from the deco) is that the high PO2's cause<br>
vasoconstriction, which in turns reduces efficacy of offgassing.
</blockquote><br>
Fair statement, but if the efficiency of deco is reduced by something,
would it not make sense that the time spent at deco would thereby have to
be increased?  <br>
<br>
<blockquote type=3Dcite cite> By going off the high PO2 for a while
you encourage vasodilation and thus<br>
increase the efficiency of the offgassing.  </blockquote><br>
It takes approximately one hour for tissues to become saturated with
O2.  Of course different tissues are affected at different
rates:  blood changes are seen within five minutes, soft tissues
peak within one hour.  Once we stop breathing high PO2 O2 the blood
returns to normal in 5 minutes (odd how BG (back gas) breaks are
recommended for 5-6 minutes don't you think? ;-)) and muscle drops within
two hours and soft tissues within four hours.  So you see the short
BG breaks are only long enough to just allow the blood to return to
normal values and not really time to offset any possible negative effects
of vasoconstriction; which in turn is offset by taking one hour (on O2
which is longer than most people will spend decoing on O2) to saturate
tissue and thereby have a systemic effect, as well as the high
diffusibility of oxygen in the first place.<br>
<br>
<blockquote type=3Dcite cite>Is this correct?</blockquote><br>
Not quite, but I do hope that I have answered your question, and maybe
some others along the way.<br>
Sincerely,<br>
Scott Hunsucker<br>
<br>
</html>

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