Bonairetrip
Contributor
A great example of really poor decision making is at
Confessions of a Mortal Diver
Confessions of a Mortal Diver
Emergency Surface from 250 FT and reascent procedures
- Thread starter Jerrod
- Start date
Please register or login
Welcome to ScubaBoard, the world's largest scuba diving community. Registration is not required to read the forums, but we encourage you to join. Joining has its benefits and enables you to participate in the discussions.
Benefits of registering include
- Ability to post and comment on topics and discussions.
- A Free photo gallery to share your dive photos with the world.
- You can make this box go away
manni-yunk
Contributor
Disagree - as I use them all the time. Wireless Comms have come a long way - and are extremely reliable.
Yes - Gas changes are complicated - but can be done.
Back up regulators require a lot of practice is ditching the mask and going to a back up mask
Co2 build up has been pretty much taken care of as well with the oral-nasal pocket and directed gas flow.
FFMs are phenominal - but not main stream in tech diving which amazes me. I have one dive buddy that has it rigged up for multiple gas changes through a block - and it works well.
A lot of the "negatives" of comms ad FFMs of today are hanging around from years ago, and no longer true.
I suppose our use of relative terms varies. I certainly don't rate hard-wire communications used by commercial divers as "extremely reliable'. Wireless will always be even less reliable at diver depths. Acoustic signals are unreliable deep inside wreaks by any measure, physics hasn't changed.
I concur, but it isn't something I want to deal with deep inside a wreak.
Nonsense. Oral-nasal masks with directed gas flow have been available since the early 1970s. The internal volume of an oral nasal mask is added to the regulator or mouthpiece and is usually about 3x more. Oral-nasal masks have measurably higher CO2 levels -- especially when trying to minimize gas consumption at depth. It gets even worse for rebreather divers. Even nasal breathing increases CO2 levels in the mask and becomes a real issue when deep.
I have an AGA mask from 1974, which is virtually identical to the ones sold today. We used them in underwater welding habitats and experimented with them for standby divers in the bell. I don't understand what "negatives" you are describing unless you are referring to the 1960s.
Don't get me wrong, I like FFMs and hats even more, in the right application. Their attributes don't come free and are best suited to umbilical supplied diving with virtually unlimited gas supplies and people to manage them. I would not use them on Scuba in a demanding environment like the Doria, U-869, or on any multi-gas dive.
http://www.scubaboard.com/forums/ba...divers-safety-stand-down-day.html#post6100318
Last edited:
CT-Rich
Contributor
Not that I have a real clue, but a wireless comm would be virtually useless inside a steel wreck. No direct path for sound and the hull would shield any radio signals from anything other than line of sight.
It is interesting to hear about using PPO2 at 60'. The compression of the bubbles and high oxygen make sense but wouldn't the O2 be toxic at that depth?
It is interesting to hear about using PPO2 at 60'. The compression of the bubbles and high oxygen make sense but wouldn't the O2 be toxic at that depth?
manni-yunk
Contributor
I guess "reliable" is defined by us differently. In the last 100+ dives, with my buddy - we have had zero issues with our wireless comms. Also - zero issues with communicating back to the boat. And - we have the LESS powerful wireless comm system.
Second - no one is saying that the laws of physics have changed, but technology has adapted to those laws. Acoustic signals will not penetrate the wreck - but if you are communicating with a buddy within line of site - it works great - even if inside a wreck.
Your AGA mask from 1974 probably is the same as the AGA sold today - but fro mmy own observations - the AGA isnt selling as much as the guardian these days. So - the real comparison would be with the Guardian. It seals better for most faces - therefore a significant improvement.
"especially when trying to minimize gas consumption" - what do you mean. If you are inferring that short shallow breathing, or skip breathing is used to minimize gas consumption, then yes.....Co2 retention coul dbe a problem. But - if you just breath normally - I done see how it could be any significant statistical difference.
I believe that I am a CO2 retainer. When I skip breath (on a regular second stage) - I get horrible, horrible Co2 headaches. As soon as I learned not to do so - I have never had one. I could replicate it in one dive at any time. That being said - I know I am a co2 retainer. I have had the FFM down to 150fsw for deco dives, and never had the Co2 headache - so my personal conclusion is that there is no significant difference in Co2 levels and a diver - when the diver breathes corrently.
The perceived "negatives" that I hear about are commonn discussed on here - usually from people that have never dove ffm. For instance - "increased gas consumption". That is a complete pile of crap. If a FFM is leaking throughout a dive - then yes, gas consumption will clearly increase. If a diver is overly "chatty" - then yes - they will breathe more. I have tracked my SAC rate with standard dive gear and FFM - and it is 100% identical. So the "increased gas consumption" garbage comes from people that had a mask that didnt seal correctly, they were not comfortable with, or the couldnt shut up.
Another is that it is "difficult" to ditch if needed. I would say that it is not much more difficult that ditching a regular mask........it just takes training and practice.
I disagree that the attributes are best suited for umbilical cord diving.
My personal opinion is that a significant number of deaths could be avoided if there was an increase usage of FFMs.
To be fair - and to completely contradict myself........as I get trained to go deeper and have more than 2 gas switches......Im not using the FFM on these dives......so - I guess I dont have it all figured out....
The simple answer is there is less stress and easier/safer management of oxygen toxicity symptoms in a chamber. This longer answer says it best. I added Red highlights to quoted text plus the Blue comments.
U.S. Navy Diving Manual Revision 6 — Volume 1, Starting on Page 3-41
3-9.2 Oxygen Toxicity. Exposure to a partial pressure of oxygen above that encountered in normal daily living may be toxic to the body. The extent of the toxicity is dependent upon both the oxygen partial pressure and the exposure time. The higher the partial pressure and the longer the exposure, the more severe the toxicity. The two types of oxygen toxicity experienced by divers are pulmonary oxygen toxicity and central nervous system (CNS) oxygen toxicity.
3‑9.2.1 Pulmonary Oxygen Toxicity. Pulmonary oxygen toxicity, sometimes called low pressure oxygen poisoning, can occur whenever the oxygen partial pressure exceeds 0.5 ATA. A 12 hour exposure to a partial pressure of 1 ATA will produce mild symptoms and measurable decreases in lung function. The same effect will occur with a 4 hour exposure at a partial pressure of 2 ATA.
Long exposures to higher levels of oxygen, such as administered during Recompression Treatment Tables 4, 7, and 8, may produce pulmonary oxygen toxicity. The symptoms of pulmonary oxygen toxicity may begin with a burning sensation on inspiration and progress to pain on inspiration. During recompression treatments, pulmonary oxygen toxicity may have to be tolerated in patients with severe neurological symptoms to effect adequate treatment. In conscious patients, the pain and coughing experienced with inspiration eventually limit further exposure to oxygen. Unconscious patients who receive oxygen treatments do not feel pain and it is possible to subject them to exposures resulting in permanent lung damage or pneumonia. For this reason, care must be taken when administering 100 percent oxygen to unconscious patients even at surface pressure.
Return to normal pulmonary function gradually occurs after the exposure is terminated. There is no specific treatment for pulmonary oxygen toxicity.
The only way to avoid pulmonary oxygen toxicity completely is to avoid the long exposures to moderately elevated oxygen partial pressures that produce it. However, there is a way of extending tolerance. If the oxygen exposure is periodically interrupted by a short period of time at low oxygen partial pressure, the total exposure time needed to produce a given level of toxicity can be increased significantly. This is the basis for the “air breaks” commonly seen in both decompression and recompression treatment tables.
CNS OxTox hits are the main ones recreational divers are concerned about since the severe symptoms are likely to drown a diver underwater using a mouthpiece.
3‑9.2.2 Central Nervous System (CNS) Oxygen Toxicity. Central nervous system (CNS) oxygen toxicity, sometimes called high pressure oxygen poisoning, can occur whenever the oxygen partial pressure exceeds 1.3 ATA in a wet diver or 2.4 ATA in a dry diver. The reason for the marked increase in susceptibility in a wet diver is not completely understood. At partial pressures above the respective 1.3 ATA wet and 2.4 ATA dry thresholds, the risk of CNS toxicity is dependent on the oxygen partial pressure and the exposure time. The higher the partial pressure and the longer the exposure time, the more likely CNS symptoms will occur. This gives rise to partial pressure of oxygen-exposure time limits for various types of diving.
Note that many of these factors are eliminated or mitigated by relaxing in a chamber.
3‑9.2.2.1 Factors Affecting the Risk of CNS Oxygen Toxicity. A number of factors are known to influence the risk of CNS oxygen toxicity:
Individual Susceptibility. Susceptibility to CNS oxygen toxicity varies markedly from person to person. Individual susceptibility also varies markedly from time to time and for this reason divers may experience CNS oxygen toxicity at exposure times and pressures previously tolerated. Individual variability makes it difficult to set oxygen exposure limits that are both safe and practical.
CO2 Retention. Hypercapnia greatly increases the risk of CNS toxicity probably through its effect on increasing brain blood flow and consequently brain oxygen levels. Hypercapnia may result from an accumulation of CO2 in the inspired gas or from inadequate ventilation of the lungs. The latter is usually due to increased breathing resistance or a suppression of respiratory drive by high inspired ppO2. Hypercapnia is most likely to occur on deep dives and in divers using closed and semi-closed circuit rebreathers.
Exercise. Exercise greatly increases the risk of CNS toxicity, probably by increasing the degree of CO2 retention. Exposure limits must be much more conservative for exercising divers than for resting divers.
Immersion in Water. Immersion in water greatly increases the risk of CNS toxicity. The precise mechanism for the big increase in risk over comparable dry chamber exposures is unknown, but may involve a greater tendency for diver CO2 retention during immersion. Exposure limits must be much more conservative for immersed divers than for dry divers.
Depth. Increasing depth is associated with an increased risk of CNS toxicity even though ppO2 may remain unchanged. This is the situation with UBAs that control the oxygen partial pressure at a constant value, like the MK 16. The precise mechanism for this effect is unknown, but is probably more than just the increase in gas density and concomitant CO2 retention. There is some evidence that the inert gas component of the gas mixture accelerates the formation of damaging oxygen free radicals. Exposure limits for mixed gas diving must be more conservative than for pure oxygen diving.
Intermittent Exposure. Periodic interruption of high ppO2 exposure with a 5-15 min exposure to low ppO2 will reduce the risk of CNS toxicity and extend the total allowable exposure time to high ppO2. This technique is most often employed in hyperbaric treatments and surface decompression. (O2 breaks are built-into most treatment tables used on recreational divers)
Because of these modifying influences, allowable oxygen exposure times vary from situation to situation and from diving system to diving system. In general, closed and semi-closed circuit rebreathing systems require the lowest partial pressure limits, whereas surface-supplied open-circuit systems permit slightly higher limits. Allowable oxygen exposure limits for each system are discussed in later chapters.
3‑9.2.2.2 Symptoms of CNS Oxygen Toxicity. The most serious direct consequence of oxygen toxicity is convulsions. Sometimes recognition of early symptoms may provide sufficient warning to permit reduction in oxygen partial pressure and prevent the onset of more serious symptoms. The warning symptoms most often encountered also may be remembered by the mnemonic VENTIDC:
The importance here is a trained chamber operator, supervisor, medic, or doctor outside the chamber and/or an attendant inside can recognize these warning symptoms even when the diver does not. They are also more easily recognized in the chamber compared to in the water.
V: Visual symptoms. Tunnel vision, a decrease in diver’s peripheral vision, and other symptoms, such as blurred vision, may occur.
E: Ear symptoms. Tinnitus, any sound perceived by the ears but not resulting from an external stimulus, may resemble bells ringing, roaring, or a machinery-like pulsing sound.
N: Nausea or spasmodic vomiting. These symptoms may be intermittent.
T: Twitching and tingling symptoms. Any of the small facial muscles, lips, or muscles of the extremities may be affected. These are the most frequent and clearest symptoms.
I: Irritability. Any change in the diver’s mental status including confusion, agitation, and anxiety. Difficult to distinguish on commercial divers
D: Dizziness. Symptoms include clumsiness, incoordination, and unusual fatigue.
C: Convulsions. The first sign of CNS oxygen toxicity may be convulsions that occur with little or no warning.
3‑9.2.1 Pulmonary Oxygen Toxicity. Pulmonary oxygen toxicity, sometimes called low pressure oxygen poisoning, can occur whenever the oxygen partial pressure exceeds 0.5 ATA. A 12 hour exposure to a partial pressure of 1 ATA will produce mild symptoms and measurable decreases in lung function. The same effect will occur with a 4 hour exposure at a partial pressure of 2 ATA.
Long exposures to higher levels of oxygen, such as administered during Recompression Treatment Tables 4, 7, and 8, may produce pulmonary oxygen toxicity. The symptoms of pulmonary oxygen toxicity may begin with a burning sensation on inspiration and progress to pain on inspiration. During recompression treatments, pulmonary oxygen toxicity may have to be tolerated in patients with severe neurological symptoms to effect adequate treatment. In conscious patients, the pain and coughing experienced with inspiration eventually limit further exposure to oxygen. Unconscious patients who receive oxygen treatments do not feel pain and it is possible to subject them to exposures resulting in permanent lung damage or pneumonia. For this reason, care must be taken when administering 100 percent oxygen to unconscious patients even at surface pressure.
Return to normal pulmonary function gradually occurs after the exposure is terminated. There is no specific treatment for pulmonary oxygen toxicity.
The only way to avoid pulmonary oxygen toxicity completely is to avoid the long exposures to moderately elevated oxygen partial pressures that produce it. However, there is a way of extending tolerance. If the oxygen exposure is periodically interrupted by a short period of time at low oxygen partial pressure, the total exposure time needed to produce a given level of toxicity can be increased significantly. This is the basis for the “air breaks” commonly seen in both decompression and recompression treatment tables.
CNS OxTox hits are the main ones recreational divers are concerned about since the severe symptoms are likely to drown a diver underwater using a mouthpiece.
3‑9.2.2 Central Nervous System (CNS) Oxygen Toxicity. Central nervous system (CNS) oxygen toxicity, sometimes called high pressure oxygen poisoning, can occur whenever the oxygen partial pressure exceeds 1.3 ATA in a wet diver or 2.4 ATA in a dry diver. The reason for the marked increase in susceptibility in a wet diver is not completely understood. At partial pressures above the respective 1.3 ATA wet and 2.4 ATA dry thresholds, the risk of CNS toxicity is dependent on the oxygen partial pressure and the exposure time. The higher the partial pressure and the longer the exposure time, the more likely CNS symptoms will occur. This gives rise to partial pressure of oxygen-exposure time limits for various types of diving.
Note that many of these factors are eliminated or mitigated by relaxing in a chamber.
3‑9.2.2.1 Factors Affecting the Risk of CNS Oxygen Toxicity. A number of factors are known to influence the risk of CNS oxygen toxicity:
Individual Susceptibility. Susceptibility to CNS oxygen toxicity varies markedly from person to person. Individual susceptibility also varies markedly from time to time and for this reason divers may experience CNS oxygen toxicity at exposure times and pressures previously tolerated. Individual variability makes it difficult to set oxygen exposure limits that are both safe and practical.
CO2 Retention. Hypercapnia greatly increases the risk of CNS toxicity probably through its effect on increasing brain blood flow and consequently brain oxygen levels. Hypercapnia may result from an accumulation of CO2 in the inspired gas or from inadequate ventilation of the lungs. The latter is usually due to increased breathing resistance or a suppression of respiratory drive by high inspired ppO2. Hypercapnia is most likely to occur on deep dives and in divers using closed and semi-closed circuit rebreathers.
Exercise. Exercise greatly increases the risk of CNS toxicity, probably by increasing the degree of CO2 retention. Exposure limits must be much more conservative for exercising divers than for resting divers.
Immersion in Water. Immersion in water greatly increases the risk of CNS toxicity. The precise mechanism for the big increase in risk over comparable dry chamber exposures is unknown, but may involve a greater tendency for diver CO2 retention during immersion. Exposure limits must be much more conservative for immersed divers than for dry divers.
Depth. Increasing depth is associated with an increased risk of CNS toxicity even though ppO2 may remain unchanged. This is the situation with UBAs that control the oxygen partial pressure at a constant value, like the MK 16. The precise mechanism for this effect is unknown, but is probably more than just the increase in gas density and concomitant CO2 retention. There is some evidence that the inert gas component of the gas mixture accelerates the formation of damaging oxygen free radicals. Exposure limits for mixed gas diving must be more conservative than for pure oxygen diving.
Intermittent Exposure. Periodic interruption of high ppO2 exposure with a 5-15 min exposure to low ppO2 will reduce the risk of CNS toxicity and extend the total allowable exposure time to high ppO2. This technique is most often employed in hyperbaric treatments and surface decompression. (O2 breaks are built-into most treatment tables used on recreational divers)
Because of these modifying influences, allowable oxygen exposure times vary from situation to situation and from diving system to diving system. In general, closed and semi-closed circuit rebreathing systems require the lowest partial pressure limits, whereas surface-supplied open-circuit systems permit slightly higher limits. Allowable oxygen exposure limits for each system are discussed in later chapters.
3‑9.2.2.2 Symptoms of CNS Oxygen Toxicity. The most serious direct consequence of oxygen toxicity is convulsions. Sometimes recognition of early symptoms may provide sufficient warning to permit reduction in oxygen partial pressure and prevent the onset of more serious symptoms. The warning symptoms most often encountered also may be remembered by the mnemonic VENTIDC:
The importance here is a trained chamber operator, supervisor, medic, or doctor outside the chamber and/or an attendant inside can recognize these warning symptoms even when the diver does not. They are also more easily recognized in the chamber compared to in the water.
V: Visual symptoms. Tunnel vision, a decrease in diver’s peripheral vision, and other symptoms, such as blurred vision, may occur.
E: Ear symptoms. Tinnitus, any sound perceived by the ears but not resulting from an external stimulus, may resemble bells ringing, roaring, or a machinery-like pulsing sound.
N: Nausea or spasmodic vomiting. These symptoms may be intermittent.
T: Twitching and tingling symptoms. Any of the small facial muscles, lips, or muscles of the extremities may be affected. These are the most frequent and clearest symptoms.
I: Irritability. Any change in the diver’s mental status including confusion, agitation, and anxiety. Difficult to distinguish on commercial divers
D: Dizziness. Symptoms include clumsiness, incoordination, and unusual fatigue.
C: Convulsions. The first sign of CNS oxygen toxicity may be convulsions that occur with little or no warning.
Fortunately, dealing with OxTox symptoms in a chamber is pretty simple. Take the diver off the oxygen mask and protect them from hurting themselves if they are having a convulsion, which subside quickly once they are off the mask.
I have been involved with hundreds of Sur-D-O2 decompression schedules and dozens of DCS treatments. I have never witnessed or heard of a confirmed OxTox hit from working colleagues. There have been MANY times we have pulled someone off the mask for a break due to a suspicious burp or twitch. In all likelihood, the vast majority were due to excessive Tabasco on breakfast or the face muscles reacting to getting out of a FFM or hat. But there is no reason to take a chance and fantastic reasons to err on the side of caution.
Here is a link to the Manual:
US Navy Diving Manual Rev. 6 with Change A
Last edited:
- Messages
- 19,807
- Reaction score
- 18,674
- Location
- Philadelphia and Boynton Beach
- # of dives
- 1000 - 2499
Interesting read Bonairetrip, thanks
The OTS Guardian is the Interspiro/AGA mask with communications added.
I mean Scuba divers train themselves to lower their breathing rates compared to commercial divers, who spend all their time in oral-nasal masks. I have also seen tests that show no significant difference on the surface where these masks are used the most (fire fighters, mine safety, etc.). The numbers change a lot as gas density increases, as measured in chamber test after chamber test.
Granted, commercial divers average much higher work levels, but typical consumption rates are 1½ Ft³/42 Liters per minute, ambient volume. It does not matter if the dead air space is in a mouthpiece, a FFM, or a hat. The higher the volume the greater ventilation rate is required to dilute it.
Carbon dioxide levels high enough to cause headaches are dangerously high by hyperbaric standards! The next symptom is usually unconsciousness. A quarter of that level is considered too high.
I think it is fair to say that it depends on the nature of the death. FFMs are a huge plus in cardiac events -- until they puke in the mask. Then they become a huge liability.
OOA events would probably be worse on average. Lets face it; a significant percentage of divers can barely handle them now. Good grief, surface swims back to the beach could become OOA events! They shouldn't, but they would.
Even small CO2 increases exacerbate narcosis and oxygen tolerance. No big deal for typical recreational divers, but the Doria and U-869 is a different matter.
Don't feel bad, nobody has. FFM and hat design is a process of compromising between desirable features and the penalty paid to achieve them. Even with unlimited budgets, the constraints imposed by physics and physiology trump.
manni-yunk
Contributor
That is not my understanding. The Guardian was redesigned from the ground up - and NOT just the AGA with comms. Different material used on the skirt, and dual seals, regulator mechanism and direction, ABV, etc Apparently they went through an intense design period to get it how they wanted it.
Surface swimming is not an issue in the guardian as it has the ambient breathing valve built in. Easy to use. I have swam a couple hundred yards in one.
I would say that a lot of incidents that ended in death, could have been more surviveable in a FFM. Certainly not OOA - but - thats a different story. I meant more health issues (pass out, MI, etc). Not to mention the obvious safety factor if the communications. Being able to communicate with other divers in the water or at the surface in the event of an entanglement - or - lost - or - almost any other situation. I dont use them for some of the more technical diving that Ive been getting into - but - every dive that Ive done 150 and less in the last 2 years has been in a FFM.
I know they are not for everyone....but I am surprised that they are no more common.
If anyone is interested, this is a chart from the Navy Manual, Figure 20-4, Treatment Table 5, Page 20-40.
Green is on an oxygen mask and light blue is an "air break" breathing from the chamber atmosphere. Table 6 adds more oxygen breathing periods at 60 and 30'.
Green is on an oxygen mask and light blue is an "air break" breathing from the chamber atmosphere. Table 6 adds more oxygen breathing periods at 60 and 30'.
Last edited:
Similar threads
