Sign up for our monthly newsletter so you never miss the latest from InDepth!
by Jarrod Jablonski
This four-part series will explore the historical development of Global Underwater Explorers’ (GUE) decompression protocols with a focus on technical diving and the evolving trends in decompression research. The series will include aspects important in recreational diving but with a greater focus on the variables affecting technical divers. Those with less technical experience will hopefully benefit from a substantial number of reference materials linked throughout the series. These support materials and the balanced perspectives I am striving to present are designed to encourage a broader grasp of this complex subject. I also wish to take a few chances with this series by presenting some controversial positions in the hope they will stimulate open discussion and deeper consideration on all sides.
In the interest of disclosure, I would like to foreground my belief that it is impossible to reach a definitive conclusion regarding the most efficient or the safest decompression procedures, though such determinations depend largely on how you define these terms. Indeed, it is a lack of certainty that motivates me to write this series since most of us will experience our entire diving careers with uncertain knowledge and while evaluating contradictory advice. It is my intent to provide a balanced overview while asserting that one should pursue a measured response to the dictates of pundits on all sides of the debate, myself included. Most importantly, I will explore the idea that many details may not be as significant as we typically imagine. For the sake of informed consideration, we will even explore the idea that both sides—in fact, all of us—are wrong and that we might know less about decompression sickness than it appears.
One last word on the structure of this series. My intent here is more about establishing a broad perspective and less about arguing a narrow view of this elaborate subject. To this end, I hope you will join the discussion by posting in our comments, or that some of these ideas might stimulate discussions in your various communities. Let’s get started.
Part One: Contextualizing the problem of decompression.
Humans have been exploring the underwater world for hundreds of years, driven by a seemingly insatiable curiosity to reach ever farther below the mysterious surface. The brevity of early breath-hold dives gave way to technology with advances in diving bells in the 16th and 17th century and led to the development of independent diving with the Fleuss rebreather unit around 100 years later. The Fluess device was a self-contained underwater breathing apparatus (scuba) and helped develop the future of untethered diving, although excursions would remain short and/or shallow for many years to come.
Developing technology that could support extended time while working underwater was a necessary part of the construction of bridges such as the Brooklyn Bridge during the 1870s. This was accomplished by constructing underwater rooms that were pressurized to keep them dry. Few people would think of these immersions as “diving,” but the extended time breathing gas at pressure highlighted a problem that would become known as decompression sickness, which was later included as one of two distinct pathophysiologies.
The desire to understand and ultimately prevent the occurrence of decompression-related injury spans the life and interest of many researchers, nations, and individuals. In order to better appreciate some historical context, we can refer to the early work of Robert Boyle (1627 – 1691) who identified pressure-related problems when he spotted bubbles in the eye of a decompressed snake. Those not familiar with Robert Boyle may be familiar with J.S. Haldane (1860 – 1936) who is credited with establishing the first set of decompression tables while under commission by the Royal Navy.
Meanwhile, individuals like Albert Buhlmann (1923 – 1994) helped develop the science of decompression during a rich university career, including work for military, commercial, and even recreational diving interests. Decompression enthusiasts are likely familiar with early work done by researchers like Brian Hills (1934 – 2006) who focused on incorporating the formation of bubbles into decompression algorithms. Certainly, these few people do not properly represent the science of decompression, and we could list dozens of other important individuals who heavily shaped the science. My intent here is only to highlight the span of more than 5,000 years during which humans have been reaching ever farther below the watery surface. This history also includes roughly 200 years of research by a wide range of individuals, organizations, and governments seeking to understand the complications of breathing gas under increased pressure.
The development of decompression practices proved successful even in their first use with caisson work, notably reducing the problems associated with breathing gas while under pressure. This progress extended into diving activity, and included the first tables produced by Haldane in 1908 for the British Admiralty. His tables remained in use by the Royal Navy until 1955. These developments supported longer and more aggressive diving activity, inaugurating a new age of discoveries and their associated challenges.
Advancement tends to remove some or even many risks but also creates the possibility for new problems. These might develop from the ability to push boundaries farther or because more people can become involved in a given activity. We tend to build upon early success, refining safety protocols and treating a progressively smaller subset of incidents. Over time, the strategies to reduce injury become more refined and, to some extent, more individualized.
For example, early cities were very dangerous places before fire protection, building standards, health codes, and similar protections. These practices became more refined, focusing on workers, home dwellers, children, and others. Most advanced societies are now quite safe, and additional levels of refinement continue to tease individual safety concerns while striving for the elimination of accidents—requiring notably more effort and expense to remove progressively smaller amounts of risk. It is hard to clearly identify our place on this curve when it comes to decompression sickness, but we appear fairly well into the diminishing returns part of the process.
Exploring high-pressure environments began when elaborate mining, tunneling, and bridge-building projects resulted in problems of unknown origin. In subsequent years, we identified an arguably well-defined illness with a relatively clear causality. Many details remain vague, but our ability to characterize the problem supported the development of decompression strategies that significantly reduced injuries associated with breathing gas under pressure. These developments resulted in algorithms that predicted safe exposures and were codified into decompression tables and used for progressively deeper diving excursions.
Today, decompression-related problems are extremely uncommon, especially within the recreational diving community. We now find ourselves mostly managing problems within a small subset of incidents. We strive for clarity among these low-probability injuries, seeking to improve or at least maintain safe guidelines while expanding our understanding. We typically acknowledge some influence from pre-existing conditions that, for whatever collection of reasons, might make a person more susceptible to injury. We also strive to discourage diving activity that violates defined ascent speed or time limits while trying to establish a solid understanding of the constellation of problems we call decompression sickness.
Meanwhile, the safety of decompression among those who use algorithms within uncharted territory remains less certain. Individuals who dive very deep and/or over very long times may be outside the range where safe dives can be predicted. For example, a decompression algorithm developed for dives up to 30m/100 ft for immersions as long as one hour may or may not extrapolate for dives of longer duration and depth. It requires a great many dives in order to verify that a particular exposure will result in low risk for most people. Given the high cost, added complexity, and safety risk, these important data points are particularly limited with dives that are very deep and/or long. This is something we return to in a later discussion.
For the moment, we are mostly focused on dives with good supporting data and where notable improvement appears unlikely. Much of the sometimes raucous debate over decompression “correctness” involves teasing arguably minor benefits from already very low levels of risk. Can we change this reality? Can we find something that brings substantial improvement, perhaps allowing much longer dives with even shorter decompressions?
In thinking about the “problem” of decompression, we understand that scuba diving increases the pressure around us, also known as increased ambient pressure. We are now breathing gas that is at a higher pressure than normally exists in our body. The molecules we are breathing become dissolved in our blood, where they are transferred during normal circulation and accumulate in the tissues of our body. This occurs until the tissues are “full” or, more precisely, until they are saturated at the new inspired gas pressure. Reductions in the surrounding pressure reverse the gradient and encourage the molecules to leave the tissues through the blood.
Algorithms that strive to characterize this process are known as dissolved gas models. The transfer of dissolved gas from the tissues often results in the formation of bubbles in a way that is similar to releasing pressure from a carbonated beverage. Dissolved gas models do not ignore the risk of bubbles but also do not attempt to directly control their development. Attempts to directly limit the formation and development of bubbles are known as bubble models.
We imagine that both dissolved gas and bubbles are relevant and also that other individual factors play some role. The problems in finding the best strategy are numerous, but most will be managed in a later discussion. For now, I wish to highlight that tracking of dissolved gas has been our primary strategy, consuming all but a relative handful of the many decompression experiments through the history of decompression research.
Modeling bubbles is inevitably more theoretical and based upon mathematically derived predictions about bubble behavior, sometimes supported by lab experiments that measure the likelihood of bubble formation under certain conditions. Models can also be crafted as “dual-phase,” meaning they anticipate bubble development but also track dissolved gas, striving to ensure that both are within safe parameters. In all cases, we tend to develop more confidence in models that are tested empirically, though they may also be compared to a database of outcomes, supporting evaluation and calibration of the model particulars. The most modern approach is trending toward probabilistic models, and we will explore these in future treatment.
The presence of bubbles during decompression is well known, and to some extent is measurable by Doppler testing, which can detect bubbles in the venous part of the circulatory system. The venous system receives blood from tissues that are eliminating gas absorbed while diving, so the presence of at least some bubbles are expected. Unfortunately, there are many complications to the use of Doppler as a means to gauge decompression efficiency. Measures of venous bubbles may be useful for predicting decompression stress in populations of divers, but it fails to be a reliable measure of symptoms in an individual diver.
Despite the complications, most researchers agree that bubbles (though not necessarily those detectable in the venous blood) are a critical part of the causal chain. The consensus seems to be that these bubbles either directly cause decompression sickness and/or contribute to its severity. Even if we assume bubbles cause all decompression-related symptoms, predicting their effects might be overly complicated. Albert Buhlmann, a great contributor to dissolved gas models, knew about and acknowledged the relevance of bubbles. He nonetheless focused upon refining dissolved gas strategies as a way to minimize risk of decompression sickness. We don’t yet know if this is the best strategy, but it has been quite successful at allowing a very low level of risk during most dives.
Tracking other markers that might affect symptoms of decompression sickness is conceivable and is part of a body of research that seeks to better understand the full scope of decompression problems. For example, researchers are exploring immune-response factors, including genetic influences that might be involved in the body’s reaction to decompression. We might also learn more about heart rate variability (HRV), which has become popular as a way to measure physiological stress in the world of sport and exercise, and its potential involvement in DCS. These or other techniques could conceivably be used to establish upper limits on the stress accumulation that occurs during decompression, presumably avoiding some upper threshold before symptoms become problematic.
We might also find ways to reduce decompression time by eliminating or changing the gas at the source of the problem. For example, we might eventually manage to use a liquid carrier for the oxygen that sustains our lives. By eliminating or greatly reducing use of gases like nitrogen or helium, we should be able to notably change the relevance of bubbling during changes in pressure. Or, we might develop ways to prevent or greatly reduce the risk of bubble formation by using drugs or other prophylactics that could physically alter the circumstances under which bubbles form. These ideas and many others have been explored and may hold promise, but nothing that greatly departs from current practice appears likely in the foreseeable future.
Despite reasonable uncertainty about many details in decompression sickness, including the exact incident rate of DCS, which is unknown, divers following conventional decompression tables and diving within well-established limits have a very low risk of injury with rates of 0.01-0.1% per dive or about 1-10 incidents per 10,000 dives (the higher end reflecting rates for commercial dives, the lower end reflecting technical, scientific, and recreational dives). The risk is greater for certain types of very aggressive dives, but we will explore that aspect in a later discussion. Regardless of the actual risk, few divers would knowingly choose a less efficient ascent profile if a better option was available.
The pursuit of decompression efficiency is particularly relevant for the group of divers known as technical divers. For these divers, arguably small differences can involve additional hours decompressing in the water. These divers have been particularly interested in the problem of bubbles that might develop during long ascents in deep water. Many tech divers followed early research that concluded slower ascents from depth could greatly reduce decompression time. For some years, the convention of using “deep stops” to slow a diver’s ascent seemed to be the best way forward. Yet, new research argues they are actually part of the problem. Whether or not you feel sure about the value of deep stops, I hope you will join us for some engaging online discussions and especially for future sections as we dig deeper into areas that do not commonly appear in discussions orbiting decompression or deep stops. I look forward to reading your thoughts in the comments section and hope you will join part two of our series: “Tech Divers, Deep Stops, and the Coming Apocalypse”.
Please come back in two weeks when we release the next part in this series from President Jarrod Jablonski.
Jarrod is an avid explorer, researcher, author, and instructor who teaches and dives in oceans and caves around the world. Trained as a geologist, Jarrod is the founder and president of GUE and CEO of Halcyon and Extreme Exposure while remaining active in conservation, exploration, and filming projects worldwide. His explorations regularly place him in the most remote locations in the world, including numerous world record cave dives with total immersions near 30 hours. Jarrod is also an author with dozens of publications, including three books.
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!
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.
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...
Part Three: Bubble-wise, pound-foolish. Are deep stops dangerous?
In part three, of this four-part series on the history and development of GUE’s decompression protocols, GUE founder and president,...
NEDU Deep Stop Summary
The NEDU stop study remains the most detailed deep stop research done to date. It may well remain this way...
Part Two: “Tech Divers, Deep Stops, and the Coming Apocalypse”
In part two of this four-part series on the history and development of GUE’s decompression protocols, GUE founder and president...