Connect with us

Education

NEDU Deep Stop Summary

Published

on

The NEDU stop study remains the most detailed deep stop research done to date. It may well remain this way for some years to come and conceivably even indefinitely. This is because such research is expensive and because the issue appears largely settled in the minds of those with the budgets needed to explore this topic. Other studies are being developed but likely with a much smaller budget and fewer controls. Moreover, the kind of study tech divers would like to see may well fail to identify enough difference between dissolved gas and deep stop profiles to be meaningful. This latter problem is a good place to start our summary of the current research since it also helps contextualize some of the decisions made by NEDU researchers.

In order to be useful a study should demonstrate some difference between the things being measured. All things being equal one might as well stay with the long-used and widely successful dissolved gas models if deep stops and bubble models appear “similar” in outcomes. This means that a study should use a provocative decompression in order to develop some decompression sickness by which to measure a difference in models. In this case, the NEDU study dived US Navy divers without thermal protection on air to a depth of 170 feet/52meters where they conducted work for 30 minutes before ascending over a 144 minute decompression. Divers were often shivering upon surfacing, reducing perfusion and increasing risk of DCS. Some research indicates cold of this sort would be like doubling one’s bottom time when considering the effect of reduced blood flow in cold divers. The NEDU abstract provides a nice overview of the study which can be reviewed in entirety here.

We should first acknowledge this study was a US Navy test designed to evaluate whether there was any benefit to move toward bubble-based models including deep stops. The procedures of tech divers vary considerably from those of most US Navy diving and so it was inevitable that tech divers would find such a study lacking as a useful comparison. These differences complicate evaluation of deep stop in the minds of some tech divers. The main complications relate to 1) the amount of decompression time, 2) the unusual decompression stop arrangement, 3) the breathing gases used, and 4) the temperature of the water. We shall take each of these into consideration in an attempt to outline the reasons for these choices and the primary discontent. However, readers are again encouraged to review in detail these assessments, so they can develop a more informed opinion. 

The amount of decompression and arrangement of stops derive from the US Navy algorithms selected. The total decompression time was based upon the gas content (dissolved gas), VVAL18 Thalmann algorithm which formed the baseline by which to compare a deep stop schedule as generated by the probabilistic BVM(3) bubble model. The bubble model was set to optimize a 174-minute decompression with the lowest possible risk, developing stops that would control bubbles in a way consistent with its model parameters. These aspects have aroused some disagreement in the technical community who argue the total time and associated “deep stops” are longer than reasonable and a far departure from what any tech diver might consider for decompression. However, the dissolved gas model accurately predicted and did result in relatively low incidence of DCS for “shallow stop” protocols. Meanwhile, the argument for deep stops is largely that they should limit supersaturation and bubble formation in a way that provides more benefit than the increase in gas dissolved in slow compartments that result from the stops. This study demonstrates this does not appear to be true, at least within the scope of these profiles. For a variety of reasons, most experts do not believe changing the stop distribution would have a significant effect on this failure of deep stops to work as it was hoped they might. Nonetheless, the additional time when compared to a common deep-stop, gradient approach of 20/85 resulted in 59 minutes of additional “deep stop” minutes, eliciting reasonable discontent among some.

Deep stop proponents also took issue with the use of air diving though most made less of this than the previous discussion revolving around the length and distribution of stops. We don’t have a good reason to believe the value of deep stops should be negated by certain breathing mixes. If deep stops control bubbling in a useful way, they should do so independent of the gasses breathed. Some argue that the value of hyperoxic mixes in concert with deep stops might have an additive value though no evidence appears to exist that supports that contention. 

Finally, some argue that the cold experienced by divers worked in concert with the added time at depth to disadvantage divers on the deep stop profile. The argument is that these divers were ascending while following an unreasonably long, deep-stop schedule and were thus reaching critical parts of their offgassing much later in the dive when they were very cold and where perfusion was greatly reduced. Meanwhile, the argument goes, the shallow-stop divers had finished the bulk of their decompression before they became cold. Some have even argued that this experiment was more about testing thermal issues than deep stops though most experts appear unified in disagreeing with that view. The experts argue that both groups suffered from the same thermal stress and that the low but relevant DCS incidence in the shallow-stop profile support this contention. 

In the end, these are not issues that can resolve through additional debate as evidenced by hundreds of posts and extensive argumentation. However, most divers and especially most experts appear convinced the NEDU study supports an argument that deep stops are actually less efficient because they do not appear to control bubbling enough to overcome the additional gas absorbed by slow tissues during the additional time at depth. The experts argue that all aspects of concern for tech divers i.e. use of air, cold water and extended stop time are not arguments in support of deep stops. Adjustments in these areas through use of shorter deep stops and hyperoxic mixes might reduce the difference but would merely be masking the lack of improved efficiency. 

The NEDU study appears reasonably convincing to most, at least with respect to a lack of compelling value in favor of deep stops, though with some complications as discussed. I will come back to some of these complications but first our review should conclude with the apparent relevance of other studies seeking to establish the value of deep stops. In 2005 a French study evaluated deep stops by measuring venous gas bubbles. We previously discussed the complexity of relying upon such measures though the technique likely remains broadly useful for considering decompression stress across a diving population. The French study suggested that none of the deep models appeared superior in venous bubble control and one was rated inferior. A Ljubkovic Study conducted in 2010 again used venous gas emboli (bubbles) to see how effectively the varying permeability model (VPM) controlled bubbles. They determined it was not particularly effective in this regard although they did not compare its success to bubbles present with other strategies. The Spisni Study in 2017 compared a ratio-deco, rule-based approach to a dissolved-gas, gradient-factor approach and concluded that adding longer and/or deeper stops was not more effective as based upon higher post-dive inflammation associated with deeper stops. 

When all these pieces are considered alongside the more compelling NEDU research, it appears that deep stops are not bringing the long-imagined benefit sought by proponents, at least not in a way that is easily qualified. Anti-inflammatory markers and venous bubbles are both imperfect markers and leave ample room to argue against these studies. Yet, our efforts should be less about resisting developing knowledge and more about learning what we can from accumulated wisdom. To this end, we can merge three of these conclusions into growing sense that deep stops do not appear to be controlling venous bubbles in a pronounced way. This adds an interesting dimension but is it important? We would be hard pressed to argue that increased venous bubbling is a positive development even while acknowledging it is a relatively common occurrence for blood leaving tissues in the process of off-gassing. 

On the one side, deep-stop advocates can argue 1) that venous gas bubbles are not a useful diagnostic measure of DCS, 2) that anti-inflammatory markers show contradictory results in various studies, and 3) that the NEDU study is not representative of technical diving profiles and therefore not an effective indictment of deep stops as commonly used. On the other side, one can argue that 1) deep stops do not appear to effectively control venous bubbles which are very problematic for some forms decompression illness and generally correlated with DCS likelihood across populations of divers, 2) that several studies hint at a weakness in deep stops with the most detailed study to date showing a clearly increased risk of DCS, and 3) no objective study to date appears to support the value of deep stops.

An objective review of the developing science does appear to support the idea that deep stops fail to provide compelling value and may, in fact be less efficient. Some find the evidence compelling, some feel swayed but promote a measured response and some remain entirely unconvinced. Is there anything else we might interpret from the trending science on deep stops? We will return to this subject in part four of our series.

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!

Published

on

By

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.

Continue Reading

Classical decompression algorithms limit hypothetical tissue gas contents and prescribe decompression schedules with most of the total stop time (TST) allocated to shallow decompression stops. More recent bubble-model-based algorithms limit hypothetical bubble profusion and size and prescribe decompressions with TST skewed toward deeper stops. A large man-trial compared the efficiency of these approaches. Divers wearing swimsuits and tshirts, breathing surface-supplied air via MK 20 UBA, and immersed in 86 °F water were compressed at 57 fsw/min to 170 fsw for a 30 minute bottom time during which they performed 130 watt cycle ergometer work. They were then decompressed at 30 fsw/min with stops prescribed by one of two schedules. The shallow stops schedule, with a first stop at 40 fsw and 174 minutes TST, was prescribed by the, deterministic, gas content, VVAL18 Thalmann Algorithm. The deep stops schedule, with a first stop at 70 fsw, was the optimum distribution of 174 minutes TST according to the probabilistic BVM(3) bubble model. Decompression sickness (DCS) incidence following these schedules was compared. The trial was terminated after the midpoint interim analysis, when the DCS incidence of the deep stops dive profile (11 DCS/198 dives) was significantly higher than that of the shallow stops dive profile (3/192, p=0.030, one-sided Fisher Exact). On review, one deep stops DCS was excluded, but the result remained significant (p=0.047). Most DCS was mild, late onset, Type I, but two cases involved rapidly progressing CNS manifestations. Results indicate that slower tissue gas washout or continued gas uptake offsets the benefits of reduced bubble growth at deep stops.