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Calibrating Rebreathers Equipped With A Shearwater HUD At Altitude

Rebreather instructors Michael and Josh Thornton describe how to calibrate your Shearwater-equipped rebreather to dive at altitude; it’s something they do frequently. Are you ready to get high, and then get down? Good! Do these steps first.

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By Michael Thornton and Josh Thornton

Header Image: courtesy of Josh Thornton

Diving rebreathers at altitude requires additional steps for calibration to ensure the pO2 display is accurate. At 4500 ft/1,372 m elevation, the atmospheric pressure is an average of 859 mBar (0.85 ATA) as opposed to an average of 1013 mBar (1 ATA) at sea level. This means when the rebreather loop is flushed with 100% oxygen, the pO2 display should be reading 0.85 and NOT 1.00 (Actually 0.98 — Shearwater’s default value). 

You may ask: who dives rebreathers at altitude? Many people do. 

The altitude of Salt Lake City, Utah is approximately 4500 ft/1,372 m. Dive shops in this area frequently teach open water courses at 6,000 ft/1,829 m and frequently dive and teach at lakes such as Fish Lake, which is at altitude just shy of 10,000 ft/3,000 m. Similarly, Lake Tahoe, which straddles the borders of California and Nevada, is at an altitude of 6,220 ft/1,897 m. There are many popular dive sites at altitude. 

Photo by Josh Thornton.

If a diver decides to dive a rebreather at altitude, it is important that they know how to properly calibrate the machine for that altitude. When diving at Fish Lake, for example, the pO2 reads .15 instead of .21 (when the sensors are exposed to air), and should read .70 instead of 1.0 (when the sensors are exposed to 100% oxygen). 

Older Shearwater firmware for the primary handset allowed the diver to choose between a “sea level” setting and an “auto” setting in the altitude settings for the controller. Depending on the firmware, the diver may need to select “Auto” in order to calibrate at altitude. The specifics of this are covered in the user manual of the rebreather. 

Newer Shearwater firmware defaults to an altitude setting where the controller uses the pressure sensor to determine atmospheric pressure, and allows for an accurate calibration at higher altitudes where the atmospheric pressure is less than that at sea level.  For example at 4500 ft/1,372 m flushing with 100% oxygen and calibrating the handset in altitude mode will display the correct pO2 of 0.85. 

Courtesy of Sherwater.

However, since the Shearwater Heads Up Displays (HUDs) do not have a pressure sensor, if calibrated at 4,500 ft/1,352 m using the button interface, the HUD will incorrectly display a pO2 of 1.0 instead of 0.85. Unfortunately, if the HUD pO2 reading differs by 15% from the controller handset display, it can no longer safely be relied upon for pO2 monitoring. For example, if a diver calibrated their rebeather at Fish Lake without the proper procedure, the HUD would be off by 30%. There are, however, ways of calibrating the HUD correctly at altitude. 

Calibrating DiveCAN HUDs 

The newer Shearwater HUDs utilize the digital DiveCAN bus making them easier to calibrate at altitude (or with less than 100% oxygen) than the older analog HUDs. The diver interfaces with the DiveCAN HUD via a single button on the side of the HUD. This is used for powering on the HUD, calibrating the HUD, and acts as a wet switch. The DiveCAN HUD is connected via a cable to a circuit board located inside the head where the actual calibration is stored; the HUD itself is simply a display and an interface. There is a connector on the cable so that the HUD can be detached from the head. 

Courtesy of Sherwater.

In order to calibrate the HUD at altitude, the diver first detaches the HUD, then plugs the Shearwater controller handset (or another DiveCAN device such as a DiveCAN NERD) into the HUD connector, and then calibrates using the altitude mode and the pressure sensor in the handset. The resulting calibration is stored in the head. When the HUD is reconnected back into its original connector, it will display the pO2 correctly. In summary, the diver used the handset to calibrate the HUD port as well as the handset port. 

Another option is to use a pressure pot to pressurize the sensors to 1.0 before calibrating the HUD using the single button interface calibration procedure, but this is obviously not as convenient. The diver would need to calibrate the handset at ambient pressure, and then calibrate the HUD using a pressure pot with a pressure of 1 ATA.

Calibrating analog HUDs 

Calibrating Shearwater Analog HUDs at altitude usually requires a pressure pot. There is no way to tell the HUD that it is being calibrated using anything other than 100% oxygen at sea level. There are no connectors allowing the handset and HUD to be swapped for calibration. At lower altitudes, where the difference in pressure from sea level is small, the diver may be able to over pressurize the loop to mimic sea level pressure. After performing an altitude calibration on the primary handset at ambient pressure, the diver could then pressurize the loop until the handset reads 1.0 and then proceed to calibrate the HUD. 

Photo by Josh Thornton.

At higher altitudes, it is impossible to pressurize the loop sufficiently to reach 1.0 pressure. Ideally the rebreather head will attach to the top of a pressure pot. If such a pressure pot is not available, there are smaller pressure pots designed to accommodate only the oxygen sensors. These pressure pots are fitted with wires and connectors to enable the oxygen sensors to be plugged into the head. 

This allows the diver to isolate the oxygen sensors and pressurize them to 1 ATA to mimic 100% oxygen at sea level. With the sensors pressurized to 1 ATA (sea level) and flushed with 100% oxygen, the HUD can be calibrated. Care is needed to ensure the sensors are then placed back in the head in the correct order so that the calibration remains accurate. 

Although the removal of the sensors for placement in a pressure pot can be tedious, there is the added benefit of being able to test for current limitation and linearity above the intended pressure range of use. This same pressure pot calibration method can also be used on DiveCAN HUDs if desired. 

Calibrating with less than 100% oxygen

In many remote destinations, oxygen is produced with oxygen generators, which are often only capable of producing 92-94% oxygen. Calibrating a Shearwater DiveCAN HUD with less than 100% oxygen requires special procedures.

On the primary handset in “System Setup” the diver can edit the percentage of oxygen to whatever is in the calibration cylinder. So when set to 92% after a full flush, it will calibrate at 0.92 ATA (or slightly less depending on altitude/barometric pressure etc). The DiveCAN HUD can be calibrated using the same procedure as outlined above for altitude calibration. (Plug the handset into the HUD connector and calibrate using the appropriate oxygen percentage and using the pressure sensor of the handset).

Courtesy of Sherwater.

Calibrating an analog HUD once again usually requires the use of a pressure pot. However, after calibrating the handset the diver may be able to over pressurize the loop to achieve a pO2 of 1.0 inside the loop if the percentage of oxygen is not too low. With less than 100% oxygen, the diver will need to pressurize the sensors over sea level pressure until the previously calibrated handset displays a pO2 of 1.0. It may be easier to keep a bottle of 100% oxygen purely for calibrating the HUD to avoid these extra steps. 

Additional considerations when using less than 100% oxygen

Even after correct calibration has been achieved, there are dangers associated with using less than 100% oxygen. When oxygen is produced using an oxygen generator, which again yields only 92-94% oxygen, the remaining gas is mostly argon. Unfortunately, argon is extremely narcotic at depth, and with a density of 1.78g/l compared to nitrogen’s 1.24g/l, will cause a higher work of breathing.

Photo by Josh Thornton.

On a fully closed rebreather, at a constant depth, only “oxygen” is injected into the loop. However, if the injected oxygen contains argon, the fraction of argon in the loop will continually rise throughout the dive, as the body metabolizes the oxygen, leaving a residual of argon in the loop with each injection. To counteract this, periodic loop flushes need to be performed, any time less than 100% oxygen is being utilized.

Note from Shearwater Research: Note that the Shearwater user-adjustable default value is actually 0.98 vs 1.0, so handsets could read 0.98 after normal calibrations, not 1.00 depending on the value the user defines. 

Also, another method for altitude calibration is to calibrate the handset and HUD at sea level (or in a pressure pot on bench at home), then travel to the dive site (and just maintain previous calibration).  Remember that calibrations are NOT required before every dive, and in fact less frequent calibrations have benefits.

It is probably also worth mentioning the DiveCAN connectors are not intended for very frequent plug/unplug cycles, so it is best to keep these to a minimum.  Also a note to take care not to overstress and the connectors when doing the plugging/unplugging and to inspect for any damage or corrosion.

Additional Resources: 

He needed to calibrate! GUE explorer Martin McClellan was determined to conduct an extensive photogrammetric survey on the wreck of the 19th century steamship SS Tahoe, which rests intact on a steep underwater slope at a maximum depth of 470ffw (144mfw) beneath Glenbrook Bay in Lake Tahoe, Nevada, at an altitude of 6,220 ft/1,897 m. Pushing the Altitude: The Quest to Document the SS Tahoe


Michael Thornton started diving in 1998 and has been an addict ever since. He was certified OC Full Cave at age 15 and began teaching technical diving courses through the family dive store, Dive Addicts, Draper, UT in 2006. Michael is a rebreather, cave, and advanced mixed gas Instructor Trainer through TDI and IANTD. Recently he became a GUE Fundamentals instructor. He and his family launched SubGravity in 2014, which emerged out of a desire to safely explore and experience the underwater world in some of the most extreme and demanding environments imaginable. Michael is also a co-founder of TEKDiveUSA, the biannual North American advanced and technical diving conference.

Josh Thornton, a co-founder of TEKDiveUSA, has been diving for 23 years, and teaching for 17 of those. Josh took his OC Full Cave Course in 2004 and has been completely obsessed with cave diving ever since. He is the training director at Dive Addicts, and a CCR adv mixed gas Instructor Trainer and CCR cave instructor for TDI and IANTD. He is also a co-founder of SubGravity. 


Education

Understanding Oxygen Toxicity: Part 1 – Looking Back

In this first of a two-part series, Diver Alert Network’s Reilly Fogarty examines the research that has led to our current working understanding of oxygen toxicity. He presents the history of oxygen toxicity research, our current toxicity models, the external risk factors we now understand, and what the future of this research will look like. Mind your PO2s!

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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. 

Early Research

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.  


Comparison of predicted and recorded oxygen toxicity incidents by proposed model (Shykoff, 2019).

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).  

NOAA Oxygen Exposure Limits  (NOAA Diving Manual, 2001).

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.

Additional Resources:

  1. Shykoff, B. (2019). Oxygen Toxicity: Existing models, existing data. Presented during EUBS 2019 proceedings.
  2. Hedley-Whyte, John. (2008). Pulmonary Oxygen Toxicity: Investigation and Mentoring. The Ulster Medical Journal 77(1): 39-42.
  3. 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
  4. 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
  5. Arieli, R. (2003, June). Model of CNS O2 toxicity in complex dives with varied metabolic rates and inspired CO2 levels
  6. NOAA Diving Manual. (2001). 

Two Fun (Math) Things:

CALCULATOR FOR ESTIMATING THE RISK OF PULMONARY OXYGEN TOXICITY by Dr. Barbara Shykoff

The Theoretical Diver: Calculating Oxygen CNS toxicity


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.

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