Info Oxygen Toxicity Limits & Symptoms

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Oxygen Toxicity Limits & Symptoms​

Oxygen toxicity limits can be very confusing, especially for PPO2 (Partial Pressure of Oxygen) levels above 1.6 ATA used in chamber-based hyperbaric treatment (recompression) and decompression tables. For example, here is a chart of one of the most common DCS (Decompression Sickness) treatment tables. Note that the PPO2 of pure oxygen at 60'/18.3M is 2.82 ATA — or more than twice the normal limits recreational divers observe.

full.jpg

U.S. Navy Diving Manual, Revision 7A, 30 April 2018.
Figure 17-4. Treatment Table 5, Page 17-43 (Page 899 in Acrobat file)

Some confusion comes from recreational diving courses that only teach the minimum subset necessary for that specialty. Hopefully this, plus contributions from other ScubaBoard members, will provide a more complete understanding.


“ Why should anyone use high oxygen levels and risk oxygen toxicity? ”



The "simple answer" for divers is twofold: Rapid removal of diluent gas (nitrogen and/or helium) from the body and reducing diluent gas absorption. Hyper-oxygenation can be the objective for non-diving HBOT (HyperBaric Oxygen Treatments) for CO poisoning, gangrene, burns, etc.

The following is an excerpt from the US Navy Diving Manual, with the following modifications:

I accentuated selected text from the manual with Bold to emphasize especially important points.

Akimbo:
In addition, I included comments for added for context.

U.S. Navy Diving Manual, Revision 7A, Volume 1, 30 April 2018, starting on Page 3-42 or Acrobat Page 200


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.

Akimbo:
A CNS OxTox hit is the primary concern for recreational divers due to the high probability of drowning when using a mouthpiece. A FFM is certainly much safer during a convulsion underwater but the ability to rapidly get the diver off a pure or high PPO2 mix is essential. Also note that nausea is an OxTox symptom and vomiting in a FFM can be very dangerous, especially if preceded by convulsion.

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.

Akimbo:
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.

Akimbo:
The MK 16 is a mixed gas rebreather built for the US Navy. UBA = Underwater Breathing Apparatus.

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.

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 pres3- sure 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:

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.​
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.​

Akimbo:
Note that "air breaks" are built-in to most treatment tables used on recreational divers. It just means that the patient removes their BIBS (Built In Breathing System) oral-nasal mask and breathes air from the chamber atmosphere.


Edit 15 November 2021: Updated links for Version 7A of the US Navy Diving Manual and changed the use of colors for compatibility with different ScubaBoard Styles.
 
Allow me to put your mind at rest, your help in the post-mortem room will not be required. I certainly have not written, taught or casually suggested during a conversation with other divers, students or my neighbors over the horse rails, that a very high partial pressure of oxygen might be permissible for a very short period of time. Quite simply, I'll stand by what I've published and by the behavior and planning skills of students I've taught nitrox and mixed gas diving to during the past 20 years.

Now, any chance of an answer to the question?
 
... Akimbo, I am curious, as a saturation diver, what is the highest ppO2 that your protocols currently allow for commercial work?...

For people reading this unfamiliar with the concept, see: What is Saturation Diving

There is no reason to use high PPO2s in saturation. Most operations I have been around run the chamber around 0.3 ATA to provide leeway for controlling the atmosphere. Normal 0.21 ATA is a little too close to hypoxic limits for comfort by the time you factor-in analyzer tolerances, atmosphere mixing, response times, and margin in case of system failures. Some go as high as 0.5 ATA. This remains true even during the decompression phase. Shaving a few hours off a week of decompression isn't worth the increased fire risk when shallow.

A lot of dive supers bump it up to around 0.4 to 0.6 ATA in the bell/water. The volumes are much smaller so changes in Oxygen levels are much faster than in the chambers.
 
You mention not going over .5 because of fire risk when shallow. Do you still use nasal cannula or personal face masks for supplemental O2 to increase your off-gassing, or is this also seen as high risk or unreliable by the tender, and only use ambient chamber concentrations for deco calculations?
Thanks.
 
Dan, the bioavailability of oral superoxide dismutase is questionable. I wouldn't rely on it to prevent O2 toxicity.

If I can paraphrase what diverdoug1 has been saying (and please correct me if this isn't what you mean): CNS O2 toxicity is CNS O2 toxicity. The mechanism and end result are the same regardless of whether it comes from a relatively low pO2 or a very high pO2. The risk with what we'd consider a "moderate" inspired pO2 over time has to do with the size of the blood vessels in the brain. Hyperoxia produces vasoconstriction when the reactive oxygen species (ROS, or free radicals) produced by excess O2 bind with nitric oxide (NO) in the bloodstream. NO is an endogenous vasodilator, that is, it's produced by the body and it makes blood vessels get bigger. ROS + nitric oxide = less nitric oxide, therefore net vasoconstriction. This is thought to be the mechanism behind the mild anti-inflammatory properties of hyperbaric oxygen. This vasoconstriction occurs throughout the body, including inside the brain. The difference is that under these conditions, production of the enzyme involved in the synthesis of NO in the blood vessels in the brain (neuronal nitric oxyide synthase, or N-NOS) is upregulated. More N-NOS = more nitric oxide in the cerebral blood vessels, which eventually leads to dilation of the cerebral blood vessels and a subsequent increase in the oxygen delivery to the brain, which can lead to CNS O2 toxicity. The longer the exposure, the greater the risk. Incidentally, the reactive nitrogen species (RNS) that form when NO reacts with ROS are thought to contribute to CNS O2 toxicity.

I've way oversimplified this and our scientists could probably explain it more elegantly but that's the basic meat and potatoes of it.

On the other hand, an extremely high pO2 (picture switching to 100% O2 deco gas vs. travel mix at 230 fsw, for example) simply puts an overwhelmingly large amount of ROS into the circulation very suddenly. The end result is the same - high levels of ROS, production of reactive nitrogen species when the ROS binds to the NO, and subsequent CNS O2 toxicity.

Best regards,
DDM
 
DDM, are you looking at liposomal drug delivery for your superoxide dismutase studies? Have you noticed differing effects across the blood-brain barrier? Paper soon? :)

:thanks:
 
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You mention not going over .5 because of fire risk when shallow. Do you still use nasal cannula or personal face masks for supplemental O2 to increase your off-gassing, or is this also seen as high risk or unreliable by the tender, and only use ambient chamber concentrations for deco calculations?
Thanks.

Chamber PPO2 all the way. Consider the logistics, misery factor (wearing a mask for hours, days on end), and the cost-benefit.

We call them BIBS masks (Built-In Breathing System) which exist as much for contaminated atmospheres as delivering treatment gasses. They are full-oral-nasal masks (the same a lot of US jet fighters use) and have demand supply and exhaust regulators. The exhaust regulator is to prevent the chamber atmosphere from being contaminated by too much O2 and so the Helium can be reclaimed.

BIBS Masks | Oxygen Therapy Systems | Amron International

As a standard decompression procedure, where are you going to get an inside tender that also isn't committed to saturation decompression? In the very rare instance where a diver gets hit on a sat decompression, some operations will treat with higher PPO2 on BIBS. In that case his chamber-mates will stay off BIBS and act as inside tenders.

More often in my experience they just blow the chamber down to the point of relief, take a rest stop (6-8 hour sleeping period) and resume normal sat decompression. Relief is often achieved in as little as 50'. That equates to about another day of decompression.

Getting bent on a sat decompression is very rare because it is cost-effective to use very conservative decompression tables -- in addition to humanitarian and legal concerns. Most sat operations are marvels of logistics. Bending a diver can hold up a highly choreographed and expensive parade.
 
Thanks Akimbo!
I am looking at dysbaric osteonecrosis of femoral heads of saturation divers, and am trying to get as many data points as I can. That is why I originally came on the site today but got distracted by other discussions. If you happen to know any sat divers with hip problems, I would be interested in possibly sending them a questionaire.
 

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