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High Pressure Problems on Über-Deep Dives: Dealing with HPNS

If you’re diving beyond 150 m/490 ft you’re likely to experience the effects of High Pressure Nervous Syndrome (HPNS). Here InDepth’s science geek Reilly Fogarty discusses the physiology of deep helium diving, explains the mechanisms believed to be behind HPNS, and explores its real world implications with über-deep cave explorers Dr. Richard “Harry” Harris and Nuno Gomes. Included is a list of sub-250 m tech diving fatalities.

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By Reilly Fogarty
Header image: Original Photo by Sean Romanowski, effects by the team at GUE HQ

There aren’t many technical divers exploring deeper than 153 m/500 ft on a regular basis—the logistical and physiological demands alone make sure of that. The small group of divers who do reach those depths without saturation chambers or other professional accoutrements face a daunting host of new concerns. At these depths, decompression models aren’t as well validated, and dives require precise gas planning and acknowledgement of extreme environmental exposures. 

As if decompression illness (DCI) and oxygen toxicity risks weren’t enough, divers must prepare to deal with the possibility that they may get to depth and experience vertigo, confusion, seizures, and a varied list of other neurological maladies—sometimes without warning. These symptoms are the result of high-pressure nervous syndrome (sometimes called high-pressure neurological syndrome) or HPNS. Symptoms of HPNS are highly variable but primarily affect those who descend rapidly to 153 m/500 ft or deeper. HPNS may have played a role in the death of legendary cave explorer Sheck Exley, and it may have caused numerous close-calls in deep cave and wreck explorations. But, the extreme depth required to experience onset has relegated research and education on HPNS to a niche corner of the diving community—one with significant interplay with the commercial saturation diving world and the most extreme sport communities. 

The Physiology of Deep Helium Diving

In 1961, G.L. Zal’tsman, who headed the Laboratory of Hyperbaric Physiology, St. Petersburg, Russia, first identified what would eventually become known as high-pressure nervous syndrome. The political climate of the period limited access to his work in the west, so credit for the discovery is often shared with Peter Bennett, D.Sc, who published a paper on the subject in 1965. While politics and international tensions separated them, both researchers described what they called “helium tremors” that occurred during experiments with military subjects. Using gases with the high helium content required to manage narcosis at depth, participants in these studies were observed experiencing uncontrollable muscle tremors upon compression in a chamber. 

At the time, it was unknown if this was a function of the helium in their breathing gas or an effect of depth. The term “high-pressure nervous syndrome” originated just a few years after Zal’tsman’s study, when R.W. Brauer identified changes in the conscious states and electroencephalography data from subjects in a chamber dive to nearly 368 m/1,200 ft. In the decades since, several studies further illuminated what we now know as HPNS, primarily as a result of research into deep sea exploration from the 1970s to early 1990s. As it stands now, HPNS is primarily identified by a decreased mental status, dizziness, visual disturbances, nausea, drowsiness, muscle tremors, and seizures in divers rapidly reaching depths of 153 m/500 ft or more, or exploring the extremes of depth closer to 306 m/1,000 ft at any rate of compression while breathing a high helium content gas. 

The prevailing theory is that a combination of speed of compression during descent, and the absolute pressure at depth, cause these symptoms. Symptoms are rare during dives above 153 m/500 ft, but dives that exceed that depth, or that reach depth quickly, increase the likelihood of symptom evolution. Symptoms do not appear to correlate to each other, and individual susceptibility is highly variable, which makes predicting onset difficult. Some researchers also theorize that there are two separate conditions caused individually by compression (the symptoms of which diminish at depth) and total pressure (the symptoms of which persist throughout the bottom portion of a dive). This two-part explanation for HPNS symptoms provides some interesting avenues for future research and could help solidify some of the theorized mechanisms underlying the condition, but it has yet to be expanded upon in a significant way. 

The mechanism behind HPNS has yet to be proven, but most researchers choose to work upon the basis of a few reasonable theories. The first relies on the compression of the cell membranes in the central nervous system. In this model, the rapid compression of the lipid components of these membranes may alter the function of the inter-lipid structures that facilitate signal transmission within the central nervous system. This change in structure could facilitate hyperexcitability of some nervous system pathways and cause the types of tremors and seizures associated with serious HPNS cases. This membrane compression could also alter the signaling pathways required for motor function and cognition, resulting in  confusion and assorted neurological symptoms that sometimes occur in divers with HPNS. 

Another model focuses on the role of neurotransmitters themselves, rather than their signaling receptors. The various iterations of this model examine the effects of pressure and varying helium/oxygen exposures on the production or reception of these transmitters. In some ways, this method resembles our understanding of oxygen toxicity mechanisms, which could lead to some interesting interplay between future research projects and the balancing of oxygen and helium exposures at extreme depth. Some of the more promising studies in this area show evidence of NMDA receptor antagonists reducing convulsions in animal models, and describe the effectiveness of increased dopamine release in preventing increased motor activity under extreme pressure in rat models

A third model focuses on the effect of helium on HPNS risk. This model functions on a yet-unidentified mechanism, but explores the potential distortion of lipid membranes by helium at depth. The data from these studies suggests that high pressure helium—not high hydrostatic pressure—may alter the tertiary structure of protein-lipid interactions and change signaling pathways within the nervous system. Numerous other avenues for research exist in this niche, including  projects working on a great number of neurotransmitter related conditions and pre-treatment protocols for HPNS, oxygen toxicity, and possibly related normobaric diseases. Any of these models could prove accurate, but the interplay between the many neurotransmitters makes it most likely that a combination of these models will best illustrate what occurs in-situ. 

Real-World Experiences

Experienced firsthand, HPNS is far less academic, but equal parts confounding and terrifying. The variable onset and sometimes ambiguous symptom presentation make it difficult to discern from other conditions, and mild symptoms can be easily written off. By the same token, however, a serious bout of tremors or confusion as a result of a rapid descent to deep water can leave a diver terrified and unable to act. Dr. Richard “Harry” Harris, SC OAM, is a physician and technical diver with years of exploration in deep caves and shipwrecks. His experiences with HPNS mirror that of many. Most often, he’s observed symptoms like trembling hands or loss of coordination that could be attributed to either HPNS or the adrenaline rush of a fast hot-drop from a boat in heavy seas. 

Richard “Harry” Harris in the main shaft of Pierce Resurgence, New Zealand. Photo by Simon Mitchell.

On one recent dive to 150 m/490 ft, Harris described becoming temporarily incapacitated on the bottom due to minor tremors, finding himself unable to clip his strobe to the shot line. The symptoms resemble common descriptions of mild HPNS symptoms, but the relatively shallow (in terms of HPNS, at least) depth still gives him pause when he tries to discern the specific cause of the symptoms. Dives past 200 m/656 ft have provided similar conundrums, but Harris has experienced tremors at extreme depths with enough regularity to notice that he is somewhat more susceptible than his regular dive buddy Craig Challen. “This [variation in symptom onset and presentation] has really made me question again the role of the mental state, approach, and perhaps even intentional mindfulness on these symptoms,” explains Harris. 

Harris wearing dual Megalodon rebreathers. Photo by Simon Mitchell.

By focusing on gas choices that strike a balance between gas density and the high concentrations of helium that can cause HPNS symptoms, and by descending relatively slowly, Harris has managed to alleviate symptoms on much deeper dives. A recent 245 m/799 ft dive with an intentionally slowed descent gave him none of the same complaints as his rapid descents to shallower water and felt “like a [much shallower] 150 m/490 ft dive.”

Wet Mules in their element. Photo by Simon Mitchell.

It’s worth noting at this point that Harris and Challen are extraordinarily capable and experienced divers, and HPNS is a condition that shouldn’t be taken lightly. Their approach—a combination of conservatism and safety—is likely key to their management of HPNS on extremely deep dives. Other divers, some equally experienced, have not been as fortunate in the past. 

Sheck Exley reported a particularly bad case during a dive to 210 m/689 ft, with vision blurred to the extent that he was “looking through small circles with black dots, and started convulsing.” Despite these symptoms, he continued his dive, and proceeded to a maximum depth of 263 m/863 ft. It’s thought that Exley’s eventual death during an attempt to descend past 305 m/1,000 feet in the Mexican Zacatón cave system could have been caused in part by HPNS symptoms exacerbated by narcosis. 

Sheck Exley and Nuno Gomes at Boesmansgat in 1993. Photo by Andrew Penny and Charles Maxwell.

Nuno Gomes, a technical diver who holds several Guinness World Records for depth in open water and in caves, has also become intimately acquainted with HPNS, experiencing the following during a world record dive: 

Nuno Gomes decompressing after his 271 m/889 ft record dive in the Red Sea. Photo by Krzysztof Starnawski.

“As I descended past 250 m/816 ft, the HPNS set in. At first, relatively mild, then fairly strong. And later on, the symptoms became so extreme that my whole body shook uncontrollably. One other problem was lack of coordination of movement. I felt severely narcosed on my bottom trimix of 3.15/85. It had only a calculated END of 40 m/131 ft. From my experience, a more realistic narcosis level was 78 m/256 ft as calculated using the Total Narcotic Depth (TND). When I reached the tag marked 315 m/1,033 ft at an actual depth of between 322 m/1,056 ft and 323 m/1061 ft, I realized that this was as far as I was able to go. I was not sure that I would be able to return if I went any deeper. At that stage, I was not sure that I would be able to swim up from that depth.”

Gomes’s regular attempts to reach extreme depth made him uniquely prepared to identify symptoms of HPNS as they appeared, but even with his breadth of experience, the effects of the condition could have become lethal if allowed to continue. 

Nuno Gomes during decompression following his 271 m/889 ft record dive. Photo by Krzysztof Starnauski.

Statistically, there just aren’t enough documented cases of HPNS to make for a meaningful analysis, but these incidents can provide a basis for education. The symptom severity and onset variability is enormous, but there are some trends that can be pulled from the stories of Harris, Exley, and Gomes. How to integrate those in your dive plan without meaningful data to back them up, however, falls to personal choice. 

Diver Fatalities Beyond 250 meters/816 Feet. Note that numerous divers have died at shallower depths seeking to break records. Complied by Nuno Gomes

Planning for the Future

There are more than a few good reasons not to end this piece with a “how-to” on diving past 153 m/500 ft. With regard to HPNS specifically, the reality is that we just don’t know enough about the mechanisms that cause the symptoms divers experience. What we have is an understanding that high helium content and rapid descents likely contribute to HPNS risk, some people are more susceptible than others, and the symptom presentation is not uniform or predictable. Beyond these fundamental constants, we must piece together what we know from the limited research we do have and the experiences of others. 

The data on compression speed appears to be pretty clear: HPNS symptoms may not be entirely preventable, but the risks can be somewhat ameliorated by slowing our descent speeds. There also appears to be an opposing effect between helium and nitrogen content in our breathing gas. This is likely due to changes in the structures of the membranes surrounding our central nervous system caused by helium and other inert gases, requiring divers to balance potential narcotic effects and HPNS risk in gas planning. 



Using nitrogen as a protective gas seems counterintuitive, but in some extremely deep dives, adding just 5% nitrogen to a heliox mixture appeared to dramatically reduce HPNS symptoms in divers. However, the extent of practical efficacy remains to be seen. Promising studies researched using hydrogen to minimize HPNS risk, but this avenue of research is prohibitively expensive and logistically challenging due to the inherent fire risk. 

The onset of HPNS symptoms also appears to be relatively gradual, although it’s important to recognize that not all data supports this and rapid onset can occur. With slow descent rates and intelligent gas choices, it seems unlikely that divers would experience HPNS severe enough to incapacitate them before they had a chance to turn their dive, but that is not to say that it cannot happen or should be ignored as a real concern. Symptoms of HPNS still haven’t been found to correlate with each other, and not only can new symptoms arise quickly, but also the nature of the ailments means that a diver may not be able to identify symptoms until it is too late to react. 

The past decade has failed to provide much in significant data on HPNS as it pertains to recreational divers, certainly almost nothing in comparison to the deep-diving heyday that brought about the COMEX tables and Atlantis projects. Going forward, it seems likely that HPNS will become a greater concern. Technical divers will continue to explore the limits of depth with the widespread adoption of rebreathers, persisting in their search for deeper caves and unexplored wrecks. Hopefully, this ongoing—perhaps even increasing—activity will spur more research into HPNS and the potential interplay between the mechanisms of narcosis and oxygen toxicity. Until then, we’ll have to continue to glean what we can from the data we have and the experiences of the more ambitious among us. 

References:

  1. Naquet, R., Lemaire, C., J.-C. Rostain, & Angel, A. (1984). High Pressure Nervous Syndrome: Psychometric and Clinico- Electrophysiological Correlations [and Discussion]. Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences, 304(1118), 95-102. Retrieved May 21, 2021, from http://www.jstor.org/stable/2396156 
  2. Talpalar, Adolfo. (2007). High pressure neurological syndrome. Revista de neurologia. 45. 631-636.
  3. Understanding Oxygen Toxicity: Part 1 – Looking Back
  4. Pearce PC, Halsey MJ, MacLean CJ, Ward EM, Webster MT, Luff NP, Pearson J, Charlett A, Meldrum BS. The effects of the competitive NMDA receptor antagonist CPP on the high pressure neurological syndrome in a primate model. Neuropharmacology. 1991 Jul;30(7):787-96. doi: 10.1016/0028-3908(91)90187-g. PMID: 1833661.
  5. Kriem B, Abraini JH, Rostain JC. Role of 5-HT1b receptor in the pressure-induced behavioral and neurochemical disorders in rats. Pharmacol Biochem Behav. 1996 Feb;53(2):257-64. doi: 10.1016/0091-3057(95)00209-x. PMID: 8808129.
  6. Bliznyuk, A., Grossman, Y. & Moskovitz, Y. The effect of high pressure on the NMDA receptor: molecular dynamics simulations. Sci Rep 9, 10814 (2019). https://doi.org/10.1038/s41598-019-47102-x
  7. High Pressure Neurological Syndrome, DIVER (2012) by Dr. David Sawatzky

Additional Resources:

InDepth: Diving Beyond 250 Meters: The Deepest Cave Dives Today Compared to the Nineties by Michael Menduno & Nuno Gomes

World Record Cave Dive – 282.6 m (927 feet) – Nuno Gomes

Pearse Resurgence 2020-Richard Harris and Craig Challen

Diver Records Doom | Last Moments-Dave Shaw

aquaCORPS:Accident Analysis Report from aquaCORPS #9 Wreckers (JAN95):What happened to Sheck Exley? by Bill Hamilton, Ann Kristovich And Jim Bowden

InDepth: Thoughts on Diving To Great Depths by Jim Bowden

InDepth: Playing with Fire: Hydrogen as a Diving Gas By Reilly Fogarty


Reilly Fogarty is an expert in diving safety, hyperbaric research, and risk management. Recent work has included research at the Duke Center for Hyperbaric Medicine and Environmental Physiology, risk management program creation at Divers Alert Network, and emergency simulation training for Harvard Medical School. A USCG licensed captain, he can most often be found running technical charters and teaching rebreather diving in Gloucester, Massachusetts.

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The Role of Agency When Discussing Diving Incidents: An Adverse Event Occurs—An Instructor Makes a Mistake

Human Factors educator and coach Gareth Lock examines the role of our innate attribution biases and language, in forming our collective judgements when incidents occur—in this case, by considering a student diving injury that occurred during a class. Was the instructor to blame? Was anyone?

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by Gareth Lock

Header Photo by Alexandra Graziano

What do you think when you read the following? Who is at fault? Where do you think the failures lie?

“The instructor failed to notice that the gas pressure in one of their four student’s cylinders was dropping faster than was expected, and consequently, missed that this particular student had run out of gas. The student then panicked and bolted for the surface which ended up with them having an arterial gas embolism.”

It would be normal for the majority of Western-cultured divers to believe that the fault would lie with the instructor, especially as I framed your thought processes with the subtitle, ‘An Instructor Makes a Mistake’. 

The instructor would have had a clear level of responsibility to make sure that the event didn’t happen the way it did, and because the student ended up with an out-of-gas situation and an arterial gas embolism, that instructor needs to be held accountable for the mistakes that were made. 

Financial compensation to the diver might be involved. As for the instructor, specific solutions for ways to prevent future mishaps would be standard. The instructor might be advised to be more aware, to monitor students more closely, and follow standards and/or training.

The problem with this approach is that it can miss significant contributory factors. Over thousands of years, we have developed a mindset that searches for the cause of an adverse event so that we can prevent the same thing from happening again. There are two parts behind this sentence that we are going to look at in this article—agency and attribution.

Agency and Attribution

Photo by Alexandra Graziano.

The first is Agency—an agent is a person or thing that takes an active role or produces a specific effect. ‘The instructor failed to notice the faster-than-normal pressure drop.’ In this example, the instructor is the agent. While we can easily identify the action and agent, we cannot determine from this simple statement whether the instructor intentionally didn’t monitor the gas, whether they accidentally missed the increased consumption rate or leak, whether the student didn’t inform the instructor, or if there was another reason. A reader of this short case study would normally assume that the instructor had some choice in the matter, that they were a free agent with free will, and that a professional with training should know better. This assumption can heavily influence how an ‘investigation’ develops from a blame-worthy event to one where wider learning can happen. 

Research has shown that the attribution of agency is subjective and is swayed by a number of different factors including culture, experience, and the language of the observer. Furthermore, the language used and how this frames the event has also been shown to directly influence the assignment of guilt, blame and/or punishment. This is especially the case if the only reports available are based around litigation and insurance claims, as these are purposely written to attribute blame. 

Societally, and developmentally, we believe that the attribution of cause behind an action is important, especially if it is an adverse event because it allows us to identify who or what needs to change to prevent the same or similar events from occurring in the future. In the out-of-gas event above, it might be obvious to some that it is the instructor who needs to change or ‘be changed’!

The Fundamental Attribution Bias

While agency is relatively clear when we describe an event, where this attribution of agency is applied is very subjective. Attribution theory was developed in the 1950s by Fritz Heider in which he described behaviours that could be attributed to internal characteristics or disposition (personality, abilities, mood, attitude, motivations, efforts, beliefs…) or to the influences external to them which were situational in nature (culture, social norms, peer pressure, help from others, organisational pressures, rules, environmental conditions…). For example, a diving student might not perform as expected despite having been given the training detailed in the course materials. This could be because of performance anxiety, lack of confidence, not paying attention to the demonstrations… (internal or dispositional attribution), or it could be caused by an argument they had had at home that morning, mortgage worries, homework which is due, promotion or threat of being fired, or poorly serviced equipment… (external or situational attribution).

Photo by Alexandra Graziano.

This subjectivity is so powerful and prevalent that there is a recognised cognitive bias called the fundamental attribution bias or error. This bias shows that there is a tendency to look for dispositional attribution when an adverse event involves someone else (they didn’t pay attention, they didn’t have the skills or experience), but the tendency to look for situational attribution when the adverse event involves us (high workload led me to be tired, the students were spread far apart, their gauge was in their BCD pocket). “When explaining someone’s behavior, we often underestimate the impact of the situation and overestimate the extent to which it reflects the individual’s traits and attitudes.” As a consequence, it is much easier to ascribe the failure to the individual rather than to look at the wider situation. This aligns with Lewin’s equation, B=f(P, E), which states that an individual’s behavior (B) is a function (f) of the person (P), including their history, personality and motivation, and their environment (E), which includes both their physical and social surroundings. 

Research has shown that culture can strongly influence how agency is attributed. Those from Western cultures e.g. Anglo-American or Anglo-Saxon European, have a tendency to be more individualistic in nature, whereas those from Far Eastern cultures have a more collective view of the world which increases collaboration, interdependence and social conformity. The research also shows that “Compared to people in interdependent societies, people in independent societies are more likely to select a single proximal cause for an event. Western cultures therefore have a tendency to erroneously attribute control and decision to the human actor closest to the event, even if this was not the case. This has huge implications when it comes to litigation and organisational/community learning.

Self-Serving and Defensive Attribution Bias 

When it comes to an adverse event, those cultures that have high individualistic behaviours are more likely to find a way to identify someone other than ourselves as the cause i.e. “the dive center manager didn’t tell me the time had changed, and so I was late for the boat.” Conversely, when we have a successful outcome, we are more likely to look to our own performance and traits (dispositional attribution) rather than the context (situational attribution) i.e. “I had spent time practising the ascents, so my buoyancy was good for the final dive.” without noticing that their buddy was rock solid in the water and provided a very stable platform to reference against. This is known as self-serving self-attribution.

As the severity of the event increases, we mentally distance ourselves further from the traits or behaviours that would have led to this event. “I wouldn’t have done that because I would have spotted the situation developing beforehand. I am more aware than that diver.” This defensive attribution is also known as distancing through differencing.

This is a protection mechanism; if we can shift the blame to someone else because they have a different disposition (internal behaviours/traits), we can convince ourselves that what we are doing is safe, and we carry on with what we were doing in the same way we’ve always done. This might appear to be simplistic; however, much of what we do is relatively simple in theory, it is how it is weaved into our daily lives that makes things complicated or complex. 

Photo by Alexandra Graziano.

Language Matters – Invisible Meanings

The subtitle of the first section “An adverse event occurs. An instructor makes a mistake.” will have invoked a number of mental shortcuts or heuristics in the reader. We will likely make an assumption that the two events are linked and that the instructor’s mistake led to the adverse event. I purposely wrote it this way. That link could be made stronger by changing the full stop to a comma.

Language can have a large impact on how we perceive agency and causality. The problem is that how we construct our messaging is not normally consciously considered when we write or speak about events. As with many other aspects of culture, it is invisible to the actor unless there is some form of (guided) active reflection.

For example, research has shown that there is a difference between how Spanish and English-speaking participants considered the intentional or unintentional actions in a series of videos. In one example, the actor in the video would pop a balloon with a pin (intentional) or put a balloon in a box with a (unknown) pin in it and the balloon would pop (unintentional) as the balloon hit the pin.“The participant descriptions were coded as being either agentive or non-agentive. An agentive description would be something like, “He popped the balloon.” A non-agentive description could be, “The balloon popped.” The study concluded that English, Spanish, and bilingual speakers described intentional events agentively, but English speakers were more likely than the other groups to use agentive descriptions for unintentional events. Another study showed similar results between English and Japanese speakers.



Another powerful bias exists in the form of framing. This is where information is given to another party to influence their decisions and is either done consciously or not. For example, take two yoghurt pots, the first says “10% fat” and the other says “90% fat free”. The framing effect will more likely lead us to picking the second option, as it seems likely it is the healthier yoghurt. If we look at how this applies to diving incidents and agentive language “The diver ran out of gas near the end of the dive.” or “Their cylinder was empty near the end of the dive.” The first appears to put the diver at fault but we don’t know how or why this happened; whereas, the second statement is not personal and therefore allows a less confrontational conversation. Consequently, we must be careful with how we attribute agency as it limits our attention to the context immediately surrounding the person involved. If we want to learn, we have to expand our curiosity beyond the individual and look at the context.

Another example of how language matters and the shortcuts we use is the use of binary oppositions e.g., right/wrong, deep/shallow, recreational/technical, success/error, or deserved DCS/undeserved DCS. While binary modes might work for technical or mechanical systems (work/don’t work), they are not suited for systems involving people (socio-technical systems) due to the complicated and complex interactions that are present. “They didn’t use a checklist.” Is often seen as a final reason why something went wrong, as opposed to asking questions like “What sort of checklist should have been used?”, “When would the checklist normally be used?”, “What were others doing at the time”, “Which checklist? Manufacturer’s, agency’s, or their own?” 

When it comes to these socio-technical systems, we can only determine success or error/failure AFTER the event. If the actors knew that what they were doing would end up as a failure due to an error, they would do something about that ‘error’ before it was too late.

Isn’t this just semantics?

All of this might appear to be semantics, and technically it is because semantics is the branch of linguistics and logic concerned with meaning. “Words create Worlds” (Heschel and Wittgenstein) for the better or worse. Think about how you frame an event or attribute agency because it WILL impact your own and others’ learning.

Look back at the original narrative in the second paragraph, which was purposely written in the manner it was, and consider where attribution has been placed, how it limits learning and what questions you can ask to improve your understanding of the event. We are cognitively efficient creatures, always looking for the shortcut to save energy. However, this efficiency comes at the expense of learning.

In this event, there were many other factors that we needed to consider, many of which would be focused on the limitations of our cognitive system. We CANNOT pay more attention; it has a limited capacity. What we can do is make it easier to prioritise and focus on the most important/and or relevant factors, and we do this by designing systems that take our limited capacity into mind. 

Monitoring four students is going to be at the limits of what is safely possible, especially when other factors are taken into consideration, such as instructor experience, visibility, current, task loading, comfort levels, etc. These factors are readily apparent and their significance obvious after the event, but in real-time with all of the other conflicting goals present, not so. When designing systems and processes, try to apply the key human factors principle: make it easier to do the right thing, and harder to do the wrong thing.

As an example of how this language can manifest itself, have a look at any agency training materials which describe adverse events or incidents, and look to see how agency and attribution are applied, and how little the context is considered. e.g. the following example is from a leadership-level training manual: a supervisor left the dive site before accounting for all of the divers in the group and two were left behind and suffered from hypothermia. The reason given for the abandonment was that the supervisor was distracted. The material then goes on to say that despite the supervisor having normally conducted good accounting procedures, this would not help in a lawsuit as a court would look at the event that occurred not what they normally did. What is missing is understanding ‘how the supervisor came to be distracted’ and what the context was. This would provide a much greater learning opportunity than the normal ‘make sure you account for everyone otherwise you could be in a lawsuit.’ “We cannot change the human condition, but we can change the conditions in which humans work.”—Professor James Reason.

Summary

We have a tendency, especially in Western cultures, to want to find out ‘who did it’ and ascribe blame to an individual agent. More often than not, the agent is the person who was closest to the event in time and space. In effect, we play the game of ‘you were last to touch it, so it was your fault’ but this rarely prevents future events from occurring. In reality, divers, instructors, instructor trainers, and dive centre managers are all managing complex interactions between people, environment, equipment and cultural/societal pressures with sensemaking only being made after the event. 

Photo by Peter Gaertner.

To be able to identify a single cause of an adverse event in diving is impossible because it doesn’t exist and yet this is what the language we use focuses on. We look for a root cause or a trigger event for an accident or incident. The research from Denoble et al, which described four stages (trigger event, disabling event, disabling injury and cause of death) of fatalities misses the context behind the trigger events and yet it is still used in incident analyses. Compare this to modern safety investigation programmes which have moved away from a root cause approach to a more systemic approach, like Accimap or Human Factors Analysis and Classification System (HFACS) that take into account systems thinking and human factors principles/models. 

A response from Petar J Denoble’s response, Click Here

There are no formal investigation and analysis programmes or tools in the sports diving sector so any data that is produced is heavily biased by personal perspectives. However, that gap will be addressed before the end of 2021 when an investigation course will be launched to the public by The Human Diver. 

This two-day programme will provide an introduction to a systems- and human factors-based approach to event learning and will be based on current best practices from high-risk industries and academia and then tailored and focused on non-fatal events in the diving industry. There will also be a number of research programmes being developed over the next year or so which look at incidents, their causality and how to report them. The methodology will be relevant to fatalities but these investigations are often undertaken by law enforcement officers or coroners.

Photo by Kirill Egorov.

For the diving community, there is a need to look at how adverse events happen, not by attributing agency to individuals, but to look wider, to the system and the context so that we can understand how it made sense for that human agent to do what they did at the time. Ivan Pupulidy covers this clearly in the US Forest Service Learning Review, “In order to change culture, you have to change the assumptions that drive the culture.”

After note: The article was heavily influenced by the work of Crista Vesel whose referenced paper examined agentive language and how it influenced how the US Forest Service moved from Serious Accident Investigation Guide to a Learning Review. The review allowed more genuine inquiry to occur and find out the real reasons why serious events, including fatalities, occurred. You can find Vesel’s paper here: “Agentive Language in Accident Investigation: Why Language Matters in Learning from Events.”

Footnotes:

1. Lexico. Explore: agent. http://www.lexico.com/en/definition/ agent (accessed July 30, 2021). 

 2. Agentive Language in Accident Investigation: Why Language Matters in Learning from Events Crista Vesel ACS Chem. Health Saf. 2020, 27, 1, 34–39. 2020 3. Myers, D. Social Psychology, 11th ed.; McGraw-Hill: New York, 2013; pp 100−117

4. Fausey, C.; Long, B.; Inamon, A.; Boroditsky, L. Constructing agency: the role of language. Frontiers in Psychology 2010, 1, 1−11. 

5. Dekker, S. Why We Need New Accident Models; Lund University School of Aviation: Sweden, 2005.

6. Fausey, C. M.; Boroditsky, L. In English and Spanish Speakers Remember Causal Agents Differently, Proceedings of 30th Annual Meeting of the Cognitive Science Society, Washington, DC, July, 2008. https://escholarship.org/uc/item/4425600t (accessed November 13, 2019).

7. Denoble, P.J; Caruso J.L.; de L Dear G.; Pieper C.F. and Vann R.D. Common Causes of Open Circuit Recreational Diving Fatalities. 2008

8. Learning Review (LR) Guide (March 2017); U.S. Department of Agriculture Forest Service accessed 30 Jul 2021


Gareth Lock has been involved in high-risk work since 1989. He spent 25 years in the Royal Air Force in a variety of front-line operational, research and development, and systems engineering roles which have given him a unique perspective. In 2005, he started his dive training with GUE and is now an advanced trimix diver (Tech 2) and JJ-CCR Normoxic trimix diver. In 2016, he formed The Human Diver with the goal of bringing his operational, human factors, and systems thinking to diving safety. Since then, he has trained more than 350 people face-to-face around the globe, taught nearly 2,000 people via online programmes, sold more than 4,000 copies of his book Under Pressure: Diving Deeper with Human Factors, and produced “If Only…,” a documentary about a fatal dive told through the lens of Human Factors and a Just Culture. In September 2021, he will be opening the first ever Human Factors in Diving conference. His goal: to bring human factors practice and knowledge into the diving community to improve safety, performance, and enjoyment.

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In this article published online on  September 2, 2021, Gareth Lock systematically examines the role of innate attribution biases and language, talks about agency and attribution, and explains why incident investigation may fail to help prevent similar incidents from occurring again. As an example of a failed approach, Lock refers to the paper “Common causes of open-circuit recreational scuba fatalities”, which I co-authored with my colleagues in 2008. While I appreciate Gareth’s work in general and the content of this particular article, I have to point out that our paper never intended to do what Gareth assumes and attributes to it.
1. In our paper, we do not investigate individual incidents. Instead, we attempted an epidemiological analysis based on the reported results of separate incident investigations.
2. We do not claim that triggers are the root causes. We provide clear, pragmatic definitions for all four categories we used in the paper.
3. We never attribute agency in the sense of subjective factors; our only agent is similar to an epidemiological agent, like a mechanical agent of injury (boat hitting diver), CO causing intoxication, and similar.
4. We are aware that there were causes beyond what was reported and that in most cases probably there were multiple causes, and we state it explicitly in the paper.
5. We aimed to identify contributing factors that could be targeted with preventive interventions (which we did not prescribe).
6. We assumed, that although we may never know the primordial cause(s), we still could intervene by preventing the domino effect or by interrupting the chain of events leading towards the fatal outcome. If we were not right in assuming it, why bother with teaching divers all possible corrective measures in an adverse event?I am looking forward to a bright future with much-improved incident analysis methods. I hope that my younger colleagues will have high-quality reports to work with trying to devise the best preventive interventions.

-PJ Denoble