~Anne Keckler
ACSM Certified Personal Trainer
Read the latest post on my fitness blog!
http://www.annekeckler.com
Photos: http://www.flickr.com/photos/annekeckler
Mom to Patrick Keckler, child actor:
http://www.patrickkeckler.com
--- On Fri, 6/3/11, tallyscubac...@googlegroups.com <tallyscubac...@googlegroups.com> wrote:
From: tallyscubac...@googlegroups.com <tallyscubac...@googlegroups.com>
Subject: Digest for tallysc...@googlegroups.com - 5 Messages in 3 Topics
To: "Digest Recipients" <tallyscuba...@googlegroups.com>
Date: Friday, June 3, 2011, 7:52 AM
Group: http://groups.google.com/group/tallyscubaclub/topics
b1draper <b1dr...@gmail.com> Jun 02 07:13AM -0700
^
So far I've received deposits from Mike and Nancy. I'm looking into
the possibility of rolling O2 and BloodBorn Pathagen training into the
class. If you're interested in taking this class and have not paid
your deposit please do so by Monday June 6th as I need to place an
order with the Red Cross and give them time to fill it. The total cost
for the class is $100, including the $50 deposit.
If I cancel the class I'll refund the deposit. However if a student
ellects not to show up to class on the 18th, the deposit will not be
refunded as I will have already purchased supplies for the class.
b1draper <b1dr...@gmail.com> Jun 02 06:13AM -0700
^
This applies to all divers...
http://www.diverite.com/education/rebreather/tips/o2toxicityandrebreathers/
Oxygen Toxicity and CCR Diving
Dr. K. David Sawatzky is a diving medical specialist on contract at
Defence Research and Development Toronto from 1998 to 2005. Previously
he was the Canadian Forces Staff Officer in Hyperbaric Medicine at
DCIEM (1986-1993) and later the Senior Medical Officer at
GarrisonSupport Unit Toronto (1993-1998). He has been on the Board of
Advisors for the International Association of Nitrox and Technical
Divers (IANTD) since 2000, and is an active cave, trimix and closed
circuit rebreather diver/instructor/instructor trainer.by Dr. K. David
Sawatzky
_________________________________________________________________________________________
I recently had the privilege of spending five days in Florida with
Lamar Hires, the owner of Dive Rite. That was the longest time we have
managed to spend together since he ‘certified’ me as a full cave diver
in 1988 (I already had over 100 exploratory cave dives in Canada).
Although I am an Inspiration CCR IT (I have been diving the
Inspiration since 2000 and the Megalodon since 2005), I did the full
Optima CCR course with Lamar as he had other students to train. During
this time Lamar and I had hours to chat and it quickly became apparent
that there are some serious mistakes being made by CCR divers as a
result of their lack of understanding of oxygen (O2) toxicity in the
CCR diving environment. Lamar asked me to write this article to
address some of those mistakes. Other articles that I have written on
oxygen toxicity and diving are posted on this website. I strongly
suggest you stop and read them now as you need to know what they say
to fully understand this article.
Oxygen toxicity is a consequence of biochemical damage that occurs in
cells as a result of oxygen free radicals. Whenever oxygen is present,
oxygen free radicals are formed. Our cells have several mechanisms to
inactivate oxygen radicles and to repair the damage that they cause.
These defenses are able to keep ahead of the damage at normal partial
pressures of oxygen (pO2) but they fall behind when the pO2 exceeds
about 0.45 atmospheres (ata).
At pO2s of 0.45 to 1.3 ata the lungs are usually the first tissue in
the body to show the effects of oxygen damage. Mild cough and painful
inspiration progress to uncontrollable cough and very painful
inspiration. Exposure times of “days” are usually required to
experience symptoms. Levels of discomfort that will be tolerated by a
diver will completely heal in about 4 weeks.
At pO2s of 1.3 to 1.6 ata divers can experience oxygen damage to the
eyes (hyperbaric induced myopia) where the diver becomes near-sited.
This usually requires exposure times in the range of 30 or more hours
over 10 or so days. I had one diving companion who developed this
problem after 33 hours CCR diving using a pO2 set point of 1.3 ata
over 11 days. The myopia largely resolves over a few months but the
diver may be left with a small permanent visual change, and they may
be more susceptible to recurrence of the problem in the future.
At pO2s of 1.3 to 1.6 ata divers can also experience convulsions (CNS
toxicity). The risk of convulsing is related to the pO2, the time of
exposure, the work level, the level of carbon-dioxide, and individual
variation. The problem is that the risk of convulsing is highly
variable in the same person from day to day. What this means is that
you might tolerate a very high O2 exposure without problem on one day
but convulse at a relatively low O2 exposure another day. There is
absolutely NO WARNING before the convulsion starts and if you are in
the water when you have a convulsion you will most likely drown or
embolize.
NOAA has come up with a conservative set of exposure limits that will
protect most divers most of the time. However, these limits are
designed for open circuit bounce dives and NOT for CCR diving. Many
CCR divers are using procedures based on assumptions that are NOT
physiologically correct.
For example, many CCR divers push the pO2 limits to reduce the amount
of required decompression. The bottom line is that a small increase in
the pO2, say from 1.3 ata to 1.4, 1.5, or even 1.6 ata will only
remove a few minutes from your decompression time while drastically
increasing your risk of an O2 convulsion. Most CCR manufacturers
recommend that you NEVER have a pO2 in the breathing loop of more than
1.3 ata. I have been strongly supportive of this philosophy since I
started CCR diving in 2000.
As a result of hyperbaric induced myopia, some CCR divers are using a
pO2 of 1.2 ata or even less as their maximum on any dive. Certainly if
you are going to dive more than three hours in one day or if you are
going to be doing several consecutive days of CCR diving you need to
reduce the pO2 to 1.2 or even to 1.1 ata avoid O2 toxicity. I know a
few CCR divers who never use a pO2 of more than 1.0 ata.
The biggest mistake many CCR divers make is to elevate the pO2 at the
end of the dive, during decompression. The logic is that they are at
rest and therefore the risk of an O2 convulsion is reduced. This logic
is correct, but it fails to consider several other factors.
CNS O2 toxicity is a result of cumulative damage in the cells. At the
end of a CCR dive that requires decompression a significant amount of
damage has occurred. If you then increase the pO2 you will increase
the rate of damage and you will dramatically increase the risk of
suffering an O2 convulsion, even if you are at rest.
I was absolutely convinced of this point in 2000 when I started diving
CCR and flatly refused to perform this procedure even though the VERY
senior instructor (not Lamar) on my CCR Trimix course strongly
recommended it. Since then I have reviewed several CCR fatalities
where death was almost certainly as a result of an O2 convulsion
secondary to pushing the pO2s.
I stated previously that you may do the same dive with high pO2s many,
many times without problem and then suffer a seizure on the next dive.
However, there are several reasons CCR divers are more likely to
suffer an O2 seizure than OC divers.
While diving CCR the diver is often exposed to the maximum pO2 for the
entire dive. Diving OC the diver is exposed to the maximum pO2 only
when they are at the maximum depth of the dive and during the first
decompression stop after a gas switch.
While diving CCR the diver is often exposed to an elevated partial
pressure of carbon-dioxide (pCO2). There are several reasons all
divers are exposed to elevated pCO2 but when diving CCR there are more
reasons and the elevation of CO2 can be greater. Failure of the one-
way values sometimes occurs (usually not installed correctly) but by
far the most common reason is failure of the CO2 absorbent due to a
number of problems that are almost always the diver’s fault. Diver’s
don’t pack the absorbent correctly, it settles during a long car or
boat ride, divers remove and then refill the canister with the same
absorbent, channeling can occur, etc. but most commonly divers simply
dive too long on one fill to try and save a few dollars.
So let’s return to the practice of elevating the pO2 during
decompression. Not only is the brain at the highest risk of convulsing
due to the accumulated damage that occurred during the dive, but the
pCO2 is most likely to be elevated as the absorbent is partially or
mostly used up.
So why does pCO2 matter so much in O2 toxicity? Quite simply, pCO2
controls the blood flow to the brain. As the pCO2 rises, the blood
flow to the brain is increased. As the blood flow to the brain is
increased, more O2 (and O2 radicals) will be delivered to the brain
even if the pO2 remains constant! More O2 radicals results in more
damage to the cells. On top of this, if the diver then also increases
the pO2 ……. is it any wonder that they convulse?
I have to cover one final point and that is ‘air breaks’. The risk of
CNS O2 toxicity can be dramatically reduced if the diver breathes a
gas mixture with a reduced pO2 for 5 minutes after every 20 to 25
minutes of breathing a gas mixture with a higher pO2. While sitting in
a dry chamber breathing 100% O2 at 2.0 ata, the diver can breathe O2
for twice as long before developing a specific level of pulmonary O2
toxicity if they breathe air (pO2 0.4 ata) for 5 minutes after every
20 minutes of O2. During the 5 minute “air break” the number of O2
radicals is dramatically reduced. As a result, the cells ‘catch up’
and repair some of the damage that occurred while the diver was
breathing a higher pO2.
Theoretically it is quite easy to do this while diving (switch to an
OC regulator on a tank of air or normoxic trimix if you are shallow
enough) but practically this is fairly difficult to do while diving.
In addition, it is very challenging to sort out your decompression
obligation if you are frequently switching gas mixtures.
So what is the bottom line? Taking all of the physics and physiology
into consideration, understanding oxygen toxicity as well as anyone
(there is still a lot we don’t understand) and remembering how many
CCR divers have died (many almost certainly as a result of O2
toxicity) I have the following recommendations.
CCR divers should NEVER have a pO2 in the loop greater than 1.3 ata.
There have been a few well documented convulsions in divers with a pO2
of 1.3 ata but I am not aware of any at lower pO2s. Therefore, a very
good argument can be made to never have a pO2 in the loop greater than
1.2 ata.
If you are going to be doing more than 3 hours diving in one day, or
diving CCR for several days in a row, the pO2 should be set at 1.2 ata
or less, starting with the first dive! The CO2 absorbent must be
managed properly and if you decide to ‘push’ the times a bit, ensure
your pO2s are reduced to 1.2 ata or less. Certainly the ‘pre-package’
absorbent used in the Optima eliminates many of the problems commonly
encountered with loose absorbent.
These recommendations should result in a low, but not zero risk of an
O2 induced seizure.
"Mike Redig" <mike...@nettally.com> Jun 02 09:47AM -0400
^
Very interesting research, we could apply the same pO2 exposure conservatism
towards Nitrox diving and avoid pushing the envelope so to speak on pO2
exposure limits by not exceeding depth/time limit recommendations on 32%-
40% mixtures on repeatative dives.
----- Original Message -----
From: "b1draper" <b1dr...@gmail.com>
To: "Tallahassee Scuba Club" <tallysc...@googlegroups.com>
Sent: Thursday, June 02, 2011 9:13 AM
Subject: New Research in Oxygen Toxicity
This applies to all divers...
http://www.diverite.com/education/rebreather/tips/o2toxicityandrebreathers/
Oxygen Toxicity and CCR Diving
Dr. K. David Sawatzky is a diving medical specialist on contract at
Defence Research and Development Toronto from 1998 to 2005. Previously
he was the Canadian Forces Staff Officer in Hyperbaric Medicine at
DCIEM (1986-1993) and later the Senior Medical Officer at
GarrisonSupport Unit Toronto (1993-1998). He has been on the Board of
Advisors for the International Association of Nitrox and Technical
Divers (IANTD) since 2000, and is an active cave, trimix and closed
circuit rebreather diver/instructor/instructor trainer.by Dr. K. David
Sawatzky
_________________________________________________________________________________________
I recently had the privilege of spending five days in Florida with
Lamar Hires, the owner of Dive Rite. That was the longest time we have
managed to spend together since he ‘certified’ me as a full cave diver
in 1988 (I already had over 100 exploratory cave dives in Canada).
Although I am an Inspiration CCR IT (I have been diving the
Inspiration since 2000 and the Megalodon since 2005), I did the full
Optima CCR course with Lamar as he had other students to train. During
this time Lamar and I had hours to chat and it quickly became apparent
that there are some serious mistakes being made by CCR divers as a
result of their lack of understanding of oxygen (O2) toxicity in the
CCR diving environment. Lamar asked me to write this article to
address some of those mistakes. Other articles that I have written on
oxygen toxicity and diving are posted on this website. I strongly
suggest you stop and read them now as you need to know what they say
to fully understand this article.
Oxygen toxicity is a consequence of biochemical damage that occurs in
cells as a result of oxygen free radicals. Whenever oxygen is present,
oxygen free radicals are formed. Our cells have several mechanisms to
inactivate oxygen radicles and to repair the damage that they cause.
These defenses are able to keep ahead of the damage at normal partial
pressures of oxygen (pO2) but they fall behind when the pO2 exceeds
about 0.45 atmospheres (ata).
At pO2s of 0.45 to 1.3 ata the lungs are usually the first tissue in
the body to show the effects of oxygen damage. Mild cough and painful
inspiration progress to uncontrollable cough and very painful
inspiration. Exposure times of “days” are usually required to
experience symptoms. Levels of discomfort that will be tolerated by a
diver will completely heal in about 4 weeks.
At pO2s of 1.3 to 1.6 ata divers can experience oxygen damage to the
eyes (hyperbaric induced myopia) where the diver becomes near-sited.
This usually requires exposure times in the range of 30 or more hours
over 10 or so days. I had one diving companion who developed this
problem after 33 hours CCR diving using a pO2 set point of 1.3 ata
over 11 days. The myopia largely resolves over a few months but the
diver may be left with a small permanent visual change, and they may
be more susceptible to recurrence of the problem in the future.
At pO2s of 1.3 to 1.6 ata divers can also experience convulsions (CNS
toxicity). The risk of convulsing is related to the pO2, the time of
exposure, the work level, the level of carbon-dioxide, and individual
variation. The problem is that the risk of convulsing is highly
variable in the same person from day to day. What this means is that
you might tolerate a very high O2 exposure without problem on one day
but convulse at a relatively low O2 exposure another day. There is
absolutely NO WARNING before the convulsion starts and if you are in
the water when you have a convulsion you will most likely drown or
embolize.
NOAA has come up with a conservative set of exposure limits that will
protect most divers most of the time. However, these limits are
designed for open circuit bounce dives and NOT for CCR diving. Many
CCR divers are using procedures based on assumptions that are NOT
physiologically correct.
For example, many CCR divers push the pO2 limits to reduce the amount
of required decompression. The bottom line is that a small increase in
the pO2, say from 1.3 ata to 1.4, 1.5, or even 1.6 ata will only
remove a few minutes from your decompression time while drastically
increasing your risk of an O2 convulsion. Most CCR manufacturers
recommend that you NEVER have a pO2 in the breathing loop of more than
1.3 ata. I have been strongly supportive of this philosophy since I
started CCR diving in 2000.
As a result of hyperbaric induced myopia, some CCR divers are using a
pO2 of 1.2 ata or even less as their maximum on any dive. Certainly if
you are going to dive more than three hours in one day or if you are
going to be doing several consecutive days of CCR diving you need to
reduce the pO2 to 1.2 or even to 1.1 ata avoid O2 toxicity. I know a
few CCR divers who never use a pO2 of more than 1.0 ata.
The biggest mistake many CCR divers make is to elevate the pO2 at the
end of the dive, during decompression. The logic is that they are at
rest and therefore the risk of an O2 convulsion is reduced. This logic
is correct, but it fails to consider several other factors.
CNS O2 toxicity is a result of cumulative damage in the cells. At the
end of a CCR dive that requires decompression a significant amount of
damage has occurred. If you then increase the pO2 you will increase
the rate of damage and you will dramatically increase the risk of
suffering an O2 convulsion, even if you are at rest.
I was absolutely convinced of this point in 2000 when I started diving
CCR and flatly refused to perform this procedure even though the VERY
senior instructor (not Lamar) on my CCR Trimix course strongly
recommended it. Since then I have reviewed several CCR fatalities
where death was almost certainly as a result of an O2 convulsion
secondary to pushing the pO2s.
I stated previously that you may do the same dive with high pO2s many,
many times without problem and then suffer a seizure on the next dive.
However, there are several reasons CCR divers are more likely to
suffer an O2 seizure than OC divers.
While diving CCR the diver is often exposed to the maximum pO2 for the
entire dive. Diving OC the diver is exposed to the maximum pO2 only
when they are at the maximum depth of the dive and during the first
decompression stop after a gas switch.
While diving CCR the diver is often exposed to an elevated partial
pressure of carbon-dioxide (pCO2). There are several reasons all
divers are exposed to elevated pCO2 but when diving CCR there are more
reasons and the elevation of CO2 can be greater. Failure of the one-
way values sometimes occurs (usually not installed correctly) but by
far the most common reason is failure of the CO2 absorbent due to a
number of problems that are almost always the diver’s fault. Diver’s
don’t pack the absorbent correctly, it settles during a long car or
boat ride, divers remove and then refill the canister with the same
absorbent, channeling can occur, etc. but most commonly divers simply
dive too long on one fill to try and save a few dollars.
So let’s return to the practice of elevating the pO2 during
decompression. Not only is the brain at the highest risk of convulsing
due to the accumulated damage that occurred during the dive, but the
pCO2 is most likely to be elevated as the absorbent is partially or
mostly used up.
So why does pCO2 matter so much in O2 toxicity? Quite simply, pCO2
controls the blood flow to the brain. As the pCO2 rises, the blood
flow to the brain is increased. As the blood flow to the brain is
increased, more O2 (and O2 radicals) will be delivered to the brain
even if the pO2 remains constant! More O2 radicals results in more
damage to the cells. On top of this, if the diver then also increases
the pO2 ……. is it any wonder that they convulse?
I have to cover one final point and that is ‘air breaks’. The risk of
CNS O2 toxicity can be dramatically reduced if the diver breathes a
gas mixture with a reduced pO2 for 5 minutes after every 20 to 25
minutes of breathing a gas mixture with a higher pO2. While sitting in
a dry chamber breathing 100% O2 at 2.0 ata, the diver can breathe O2
for twice as long before developing a specific level of pulmonary O2
toxicity if they breathe air (pO2 0.4 ata) for 5 minutes after every
20 minutes of O2. During the 5 minute “air break” the number of O2
radicals is dramatically reduced. As a result, the cells ‘catch up’
and repair some of the damage that occurred while the diver was
breathing a higher pO2.
Theoretically it is quite easy to do this while diving (switch to an
OC regulator on a tank of air or normoxic trimix if you are shallow
enough) but practically this is fairly difficult to do while diving.
In addition, it is very challenging to sort out your decompression
obligation if you are frequently switching gas mixtures.
So what is the bottom line? Taking all of the physics and physiology
into consideration, understanding oxygen toxicity as well as anyone
(there is still a lot we don’t understand) and remembering how many
CCR divers have died (many almost certainly as a result of O2
toxicity) I have the following recommendations.
CCR divers should NEVER have a pO2 in the loop greater than 1.3 ata.
There have been a few well documented convulsions in divers with a pO2
of 1.3 ata but I am not aware of any at lower pO2s. Therefore, a very
good argument can be made to never have a pO2 in the loop greater than
1.2 ata.
If you are going to be doing more than 3 hours diving in one day, or
diving CCR for several days in a row, the pO2 should be set at 1.2 ata
or less, starting with the first dive! The CO2 absorbent must be
managed properly and if you decide to ‘push’ the times a bit, ensure
your pO2s are reduced to 1.2 ata or less. Certainly the ‘pre-package’
absorbent used in the Optima eliminates many of the problems commonly
encountered with loose absorbent.
These recommendations should result in a low, but not zero risk of an
O2 induced seizure.
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b1draper <b1dr...@gmail.com> Jun 02 07:03AM -0700
^
Exactly, given most divers use either 32% or 36%. There have been a
few deeper dives that I've done where I used 28% or 30%. I usually
keep my pO2 set to 1.3.
b1draper <b1dr...@gmail.com> Jun 02 06:10AM -0700
^
no real workout, rescue training came into play. I assessed the
situation and took control. My buddy started to panic and looked at me
wide-eyed. I grabbed his BC got his attention advised him that we were
going up. He started to bee-line to the surface and I shook him again
and directed him to the anchor line and took control of our ascent.
After exceeding the ascent for the first 10 - 15 feet (during his bee-
line) I slowed us down and made it to the surface. When we reached 15
feet he handed me my pressure guage and I came to the surface while he
decided to go back down. Knowing that I skipped the saftey stop and
initially ascended too quickly I opted to not switch regulators and go
back down.
Incase you're wondering there was enough air in the tank to make a
slow controlled ascent to the surface from 65 feet. The air ran out
just after that.
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