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By Reilly Fogarty
Header photo courtesy of DAN
Oxygen toxicity is a controversial subject among researchers and an intimidating one for many divers. From the heyday of the “voodoo gas” debates in the early 1990s to the cursory introduction to oxygen-induced seizure evolution that most divers receive in dive courses, the manifestations of prolonged or severe hyperoxia can often seem like a mysterious source of danger.
Although oxygen can do great harm, its appropriate use can extend divers’ limits and improve the treatment of injured divers. The limits of human exposure are tumultuous, often far greater than theorized, but occasionally–and unpredictably–far less.
Discussions of oxygen toxicity refer primarily to two specific manifestations of symptoms: those affecting the central nervous system (CNS) and those affecting the pulmonary system. Both are correlated (by different models) to exposure to elevated partial pressure of oxygen (PO2). CNS toxicity causes symptoms such as vertigo, twitching, sensations of abnormality, visual or acoustic hallucinations, and convulsions. Pulmonary toxicity primarily results in irritation of the airway and lungs and decline in lung function that can lead to alveolar damage and, ultimately, loss of function.
The multitude of reactions that takes place in the human body, combined with external risk factors, physiological differences, and differences in application, can make the type and severity of reactions to hyperoxia hugely variable. Combine this with a body of research that has not advanced much since 1986, a small cadre of researchers who study these effects as they pertain to diving, and an even smaller group who perform research available to the public, and efforts to get a better understanding of oxygen toxicity can become an exercise in frustration.
Piecing together a working understanding involves recognizing where the research began, understanding oxygen toxicity (and model risk for it) now, and considering the factors that make modeling difficult and increase the risk. This article is the first in a two-part series. It will cover the history of oxygen toxicity research, our current models, the external risk factors we understand now, and what the future of this research will look like.
After oxygen was discovered by Carl Scheele in 1772, it took just under a century for researchers to discover that, while the gas is necessary for critical physiological functions, it can be lethal in some environments. The first recorded research on this dates back to 1865, when French physiologist Paul Bert noted that “oxygen at a certain elevation of pressure, becomes formidable, often deadly, for all animal life” (Shykoff, 2019). Just 34 years later, James Lorrain Smith was working with John Scott Haldane in Belfast, researching respiratory physiology, when he noted that oxygen at “up to 41 percent of an atmosphere” was well-tolerated by mice, but at twice that pressure mouse mortality reached 50 percent, and at three times that pressure it was uniformly fatal (Hedley-White, 2008).
Interest in oxygen exposure up to this point was largely medical in nature. Researchers were physiologists and physicians working to understand the mechanics of oxygen metabolism and the treatment of various conditions. World War II and the advent of modern oxygen rebreathers brought the gas into the sights of the military, with both Allied and Axis forces researching the effects of oxygen on divers. Chris Lambertsen developed the Lambertsen Amphibious Respiratory Unit (LARU), a self-contained rebreather system using oxygen and a CO2 absorbent to extend the abilities of U.S. Army soldiers, and personally survived four recorded oxygen-induced seizures.
Kenneth Donald, a British physician, began work in 1942 to investigate cases of loss of consciousness reported by British Royal Navy divers using similar devices. In approximately 2,000 trials, Donald experimented with PO2 exposures of 1.8 to 3.7 bar, noting that the dangers of oxygen toxicity were “far greater than was previously realized … making diving on pure oxygen below 25 feet of sea water a hazardous gamble” (Shykoff, 2019). While this marked the beginning of the body of research that resembles what we reference now, Donald also noted that “the variation of symptoms even in the same individual, and at times their complete absence before convulsions, constitute[d] a grave menace to the independent oxygen-diver” (Shykoff, 2019). He made note not just of the toxic nature of oxygen but also the enormous variability in symptom onset, even in the same diver from day to day.
The U.S. Navy Experimental Diving Unit (NEDU), among other groups in the United States and elsewhere, worked to expand that understanding with multiple decades-long studies. These studies looked at CNS toxicity in: immersed subjects with a PO2 of less than 1.8 from 1947 to 1986; pulmonary toxicity (immersed, with a PO2 of 1.3 to 1.6 bar, and dry from 1.6 to 2 bar) from 2000 to 2015; and whole-body effects of long exposures at a PO2 of 1.3 from 2008 until this year.
The Duke Center for Hyperbaric Medicine and Environmental Physiology, the University of Pennsylvania, and numerous other groups have performed concurrent studies on similar topics, with the trend being a focus on understanding how and why divers experience oxygen toxicity symptoms and what the safe limits of oxygen exposure are. Those limits have markedly decreased from their initial proposals, with Butler and Thalmann proposing a limit of 240 minutes on oxygen at or above 25 ft/8 m and 80 minutes at 30 ft/9 m, to the modern recommendation of no greater than 45 minutes at a PO2 of 1.6 (the PO2 of pure oxygen at 20 ft/6 m).
Between 1935 and 1986, dozens of studies were performed looking at oxygen toxicity in various facets, with exposures both mild and moderate, in chambers both wet and dry. After 1986, these original hyperbaric studies almost universally ended, and the bulk of research we have to work with comes from before 1986. For the most part, research after this time has been extrapolated from previously recorded data, and, until very recently, lack of funding and industry direction coupled with risk and logistical concerns have hampered original studies from expanding our understanding of oxygen toxicity.
Primary Toxicity Models
What we’re left with are three primary models to predict the effects of both CNS and pulmonary oxygen toxicity. Two models originate in papers published by researchers working out of the Naval Medical Research Institute in Bethesda, Maryland, in 1995 (Harabin et al., 1993, 1995), and one in 2003 from the Israel Naval Medical Institute in Haifa (Arieli, 2003). The Harabin papers propose two models, one of which fits the risk of oxygen toxicity to an exponential model that links the risk of symptom development to partial pressure, time of exposure, and depth (Harabin et al., 1993). The other uses an autocatalytic model to perform a similar risk estimate on a model that includes periodic exposure decreases (time spent at a lower PO2). The Arieli model focuses on many of the same variables but attempts to add the effects of metabolic rate and CO2 to the risk prediction. Each of these three models appears to fit the raw data well but fails when compared to data sets in which external factors were controlled.
The culmination of all this work and modeling is that we now have a reasonable understanding of a few things. First, CNS toxicity is rare at low PO2, so modeling is difficult but risk is similarly low. Second, most current models overestimate risk above a PO2 of 1.7 (Shykoff, 2019). This does not mean that high partial pressures of oxygen are without risk (experience has shown that they do pose significant risk), but the models cannot accurately predict that risk. Finally, although we cannot directly estimate risk based on the data we currently have, most applications should limit PO2 to less than 1.7 bar (Shykoff, 2019).
For the majority of divers, the National Oceanic and Atmospheric Administration’s (NOAA) oxygen exposure recommendations remain a conservative and well-respected choice for consideration of limitations. The research we do have appears to show that these exposure limits are safe in the majority of applications, and despite the controversy over risk modeling and variability in symptom evolution, planning dives using relatively conservative exposures such as those found in the NOAA table provides some measure of safety.
The crux of the issue in understanding oxygen toxicity appears to be the lack of a definitive mechanism for the contributing factors that play into risk predictions. There is an enormous variability of response to hyperoxia among individuals–even between the same individuals on different days. There are multiple potential pathways for injury and distinct differences between moderate and high PO2 exposures, and the extent of injuries and changes in the body are both difficult to measure and not yet fully understood.
Interested in the factors that play into oxygen toxicity risk and what the future of this research holds? We’ll cover that and more in the second part of this article in next month’s edition of InDepth.
- Shykoff, B. (2019). Oxygen Toxicity: Existing models, existing data. Presented during EUBS 2019 proceedings.
- Hedley-Whyte, John. (2008). Pulmonary Oxygen Toxicity: Investigation and Mentoring. The Ulster Medical Journal 77(1): 39-42.
- Harabin, A. L., Survanshi, S. S., & Homer, L. D. (1995, May). A model for predicting central nervous system oxygen toxicity from hyperbaric oxygen exposures in humans.
- Harabin, A. L., Survanshi, S. S. (1993). A statistical analysis of recent naval experimental diving unit (NEDU) single-depth human exposures to 100% oxygen at pressure. Retrieved from https://apps.dtic.mil/dtic/tr/fulltext/u2/a273488.pdf
- Arieli, R. (2003, June). Model of CNS O2 toxicity in complex dives with varied metabolic rates and inspired CO2 levels.
- NOAA Diving Manual. (2001).
Two Fun (Math) Things:
CALCULATOR FOR ESTIMATING THE RISK OF PULMONARY OXYGEN TOXICITY by Dr. Barbara Shykoff
Reilly Fogarty is a team leader for risk mitigation initiatives at Divers Alert Network (DAN). When not working on safety programs for DAN, he can be found running technical charters and teaching rebreather diving in Gloucester, MA. Reilly is a USCG licensed captain whose professional background includes surgical and wilderness emergency medicine as well as dive shop management.
The Thought Process Behind GUE’s CCR Configuration
GUE is known for taking its own holistic approach to gear configuration. Here GUE board member and Instructor Trainer Richard Lundgren explains the reasoning behind its unique closed-circuit rebreather configuration. It’s all about the gas!
By Richard Lundgren
Header photo by Ortwin Khan
Numerous incidents over the years have resulted in tragic and fatal outcomes due to inefficient and insufficient bailout procedures and systems. At the present time, there are no community standards that detail:
- How much bailout gas volume should be reserved
- How to store and access the bailout gas
- How to chose bailout gas properties
Accordingly, Global Underwater Explorers (GUE) created a standardized bailout system consistent with GUE’s holistic gear configuration, Standard Operating Procedures(SOP), and diver training system. The system was designed holistically; consequently, the value and usefulness of the system are jeopardized if any of its components are removed.
Bailout Gas Reserve Volumes
The volume of gas needed to sustain a diver while bailing from a rebreather is difficult to assess, as many different factors impacts the result— including respiratory rate, depth and time, CO2 levels, and stress levels. These are but a few of the variables. All reserve gas calculations may be appropriate under ideal conditions and circumstances, but they should be regarded as estimates, or predictions at best.
The gas volume needed for two divers to safely ascend to the first gas switch is referred to as Minimum Gas (MG) for scuba divers. The gas volume needed for one rebreather diver to ascend on open-circuit during duress is referred to as Bailout Minimum Gas (BMG). The BMG is calculated using the following variables:
Consumption (C): GUE recommends using a surface consumption rate (SCR) of 20 liters per minute, or 0.75 f3 if imperial is used.
Average Pressure (AvP or average ATA): The average pressure between the target depth (max depth) to the first available gas source or the surface (min depth)
Time (T): The ascent rate should be according to the decompression profile (variable ascent rate). However, in order to simplify and increase conservatism, the ascent rate used in the BMG formula is set to 3 meters/10 ft per minute. Any decompression time required before the gas switch (first available gas source) must be added to the total time. One minute should be added for the adverse event (the bailout) and one minute additionally for performing the gas switch.
BMG = C x AvP x T
Note that Bailout Minimum Gas reserves are estimations and may not be sufficient! Even though catastrophic failures are unlikely, other factors like hypercapnia (CO2 poisoning) and stress warrants a cautious approach.
Decompression bailout gas volumes are calculated based on the diver’s actual need (based on their decompression table/algorithm), and no additional reserve is added.
It should be noted that GUE does not endorse the use of “team bailout,” i.e. when one diver carries bottom gas bailout and another diver carries decompression gas based on only one diver’s need. A separation or an equipment failure would quickly render a system like this useless.
Common Tech Community Rebreather Configuration
- Backmount rebreather (note side mount rebreathers are gaining in popularity)
- Typically, three-liter oxygen and a three-liter diluent cylinder on board (each hold 712 l/25 f3)
- Bailout gas in one or more stage bottles which could be connected to an integrated Bailout Valve (BOV).
Containment and Access
Rather than carry bailout minimum gas (BMG) in a stage bottle, which is typical in the rebreather diving community, GUE has designed its bailout system as a redundant open-circuit system consisting of two 7-liter, 232 bar cylinders (57 f3 each) that are integrated into the rebreather frame, and called the “D7” system, i.e. D for doubles, 7 for seven liter. Note that GUE has standardized the JJ-CCR closed-circuit rebreather for training and operations.
These cylinders, each with individual valves, are linked together using a flexible manifold. This system holds up to 3250 liters of gas (114 f3), of which only about 10% is used by the rebreather as diluent. Hence, close to 3000 liters (106 f3) is reserved for a bailout situation. This gives a tremendous capacity and flexibility in a relatively small form factor for dives requiring additional gas reserves (when direct ascent is not possible or desirable).
The following advantages were considered when designing the bailout system:
- The D7 system is consistent with existing open-circuit systems utilized by GUE divers. A bailout system that is familiar to the user will not increase stress levels, which is important. A GUE diver will rely on previous experience and procedures when most needed.
- The system contains the gas volumes needed according to the GUE BMG calculations as well as the diluent needed for a wide range of dive missions.
- The system is fully redundant and has the capacity to isolate failing components, like a set of open-circuit doubles and still allowing full access to the gas.
- The overall weight of the system is less, compared to a standard system with an AL11 liter (aluminum 80 f3) bailout cylinder. In addition, it contains 800-900 liters/20-32 f3 more gas available for a bailout situation compared to the AL11 liter system. Weight has been traded for gas.
- The system does not occupy the position of a stage bottle which allows for additional stages or decompression bottles to be added.
- If the ISO valves on each side were closed, the flex manifold can be removed and the cylinders transported individually while still full.
Bailout gas can be accessed quickly by a bailout valve (BOV), which is typically configured as a separate open-circuit regulator worn on a necklace, consistent with GUE’s open-circuit configuration. However, some GUE divers use an integrated BOV. After evaluation of the situation, while breathing open-circuit from the BOV, the user can transition to a high-performance regulator worn on a long hose if the situation calls for it.
The long hose is carried under the loop when diving the rebreather. The chances of having to donate to another GUE rebreather diver is low, as both carry redundant bailout. Still, GUE maintains that the capacity to donate gas must be present. The process is more likely to involve a handover of the long hose rather than a donation.
Still, if needed, such a donation is made possible by either removing the loop temporarily or by simply donating the long hose from under the loop.
Bailout decompression gasses are carried in decompression stage bottles. If more than three bottles are needed, the bottles that are to be used at the shallowest depths are carried on a stage leash (i.e. a short lease that clips to your side D-ring to carry multiple stage bottles). Maintaining bottle-rotation techniques and capacity through regular practice is important and challenging, as this skill is rarely used with the rebreather.
Bailout Gas Properties
The choice of bailout gas is extremely important, as survival may well depend on it. It is not only the volume that is important, the individual gas properties will decide if the bailout gas will be optimal or not. As the D7 system contains both the diluent and bailout gas, both gasses share the same characteristic. The following gas characteristics must be considered when choosing gas:
The equivalent (air) gas density depth should not exceed 30 meters/100 ft or 5.1 grams/liter. This is consistent with the latest research by Gavin Anthony and Simon Mitchell that recommends that divers maintain maximum gas density ideally below 5.2 g/l, equivalent to air at 31 m/102 ft, and a hard maximum of 6.2 g/l, the equivalent to air at 39 m/128 ft. You can find a simple gas density calculator here.
Ventilation is impaired when diving, due to several factors which increase the work of breathing (WOB); when diving rebreathers, the impairment is even more so. High gas density, for example, when diving gas containing no or low fractions of helium, significantly decreases a diver’s ventilation capacity and increases the risk of dynamic airway compression. CO2 washout from blood depends on ventilation capacity and can be hindered if a high-density gas is used. The impact of density is very important, and the risk of using dense gases is not to be neglected. Note that this effect is not limited to deep diving. Using a dense gas as shallow as 30 meters/100 ft reduces a diver’s ventilation capacity by a staggering 50%.
The (air) equivalent narcotic depth should also not exceed 30 m/100 ft, or PN2=3.16. Rebreathers and emergency situations are complex enough without further being aided by narcosis.
The PO2 should be limited to allow for long exposures. GUE operating standards call for a maximum PO2 for bottom gases of 1.2 atm, a PO2 of 1.4 for deep decompression gases, and a PO2 of 1.6 for shallow decompression gases. GUE recommends using the next deeper GUE standard bottom gas for diluent/bailout when diving a rebreather in combination with GUE standard decompression gases.
Bailout gasses are not chosen in order to give the shortest possible decompression obligation. They are chosen in order to give the best odds of surviving a potentially life-threatening situation.
GUE’s D7 bailout system is flexible and contains the rebreather’s diluent as well as bailout gas reserves needed for a range of different missions. The familiarity the system, along with the knowledge that they are carrying ample gas reserves, gives GUE divers peace of mind. Choosing gases with properties that will aid a diver in duress while dealing with an emergency completes the system.
GUE did not prioritize the ease of climbing boat ladders or reducing decompression by a few minutes. These are more appropriately addressed with sessions at the gym, combined with finding aquatic comfort. Nothing prevents a complete removal of the entire system at the surface if an easy exit is needed.
Founder of Scandinavia’s Baltic Sea Divers and Ocean Discovery diving groups, and a member of GUE’s Board of Directors and GUE’s Technical Administrator, Richard Lundgren has participated in numerous underwater expeditions worldwide and is one of Europe’s most experienced trimix divers. With more than 4000 dives to his credit, Richard Lundgren was a member of the GUE expeditions to dive the Britannic (sister ship of the ill-fated Titanic) in 1997 and 1999, and has been involved in numerous projects to explore mines and caves in Sweden, Norway, and Finland. In 1997, in arctic conditions, he performed the longest cave dive ever carried out in Scandinavia. Richard’s other exploration work has included the 1999 filming of the famous submarine, M1, for the BBC; the side scan sonar surveys of the Spanish gold galleons outside Florida’s Key West in 2000; and the search for the Admiral’s Fleet, an ongoing project that has already led to the discovery of more than 40 virgin wrecks perfectly preserved in the cold waters of the Swedish Baltic Sea.
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