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Heart Rate Variability, or simply HRV, is becoming more and more used in different fields, from an instrument able to diagnose cardiovascular anomalies, to a tool instrumental in improving high performance sports training. Many of us who are seriously into physical activities and sports practicing are familiar with or even have used one of the many apps available for watches or smart phones. But do we really know what they are?
Well, HRV is simply the variance in the interval between two heat beats. Or to be more precise, the changes in the interval between successive normal heartbeats. Usually, this is assessed through the timing between QRS complexes, which are main spikes as seen in a continuous electrocardiographic recording (ECG). HRV is the result of the balance between the sympathetic and the parasympathetic branches of the autonomic nervous system (ANS), as well as of other non-neural sources of variation. From a practical standpoint, it is as simple as a collection of time intervals, or for those more familiar with mathematical terms, it is a time series (a series of data points indexed by time).
Typically, these time intervals are not fixed or static but can vary widely moment to moment in response to input from the sympathetic and the parasympathetic branches of the autonomic nervous system, which control the contraction and relaxation of the cardiac muscle. Each system is activated by multiple receptors, responding to arterial pressure (baroreceptors), oxygen, and CO2 levels, as well as endogenous substances, emotions, immunological alterations, among other stimuli.
The parasympathetic branch, which regulates your energy and helps your body recover during rest periods, is mediated mainly by acetylcholine and is responsible for maintaining homeostatic heart frequencies and contractility without exhausting. It is responsible for short-term fluctuations of the heart frequency, and it operates in a frequency between 9 to 25 cycles per minute or 0.15Hz to 0.4Hz. Note that Hertz (Hz) is an international metric of frequency and is defined as one cycle per second (cpm).
Conversely, the sympathetic branch, which regulates your “fight or flight” stress impulses, is mediated mainly by norepinephrine, and its activity is triggered by stress, increasing cardiac energy demand by increasing heart rate . This branch is responsible for longer-term fluctuations of the heart frequency, operating in a lower bandwidth of 0.04Hz to 0.15Hz (or 2 to 9 cycles per minute).
HRV is commonly studied in the time and frequency domains, that is as a function of time and frequency. Different HRV indicators have been associated with sympathetic or parasympathetic activity. Additionally, there is an important association between specific frequencies and the baroreflex function, which provides a rapid negative feedback loop to adjust our heart frequency in order to maintain blood pressure at nearly constant levels.
But wait, what do time and frequency domains mean?
Let us start with the simpler one, time domain. In mathematics, the domain of a function is the set into which all of the input of the function is constrained to fall; therefore, when the term time domain is used, it simply means that we are doing our analysis based on time intervals extracted from the ECG recording. There are many indicators that have been created to study the variance in the intervals but here we will discuss only two of them, SDNN and RMSSD.
SDNN is the standard deviation, a measure of variation, of the time interval between heart beats (the R-R interval), and reflects all the cyclic components responsible for variability. The greater the SDNN, that is the variation between beats, the better. RMSSD is the square root of the mean squared differences of successive R-R intervals, or the variance of the variance of our time series, and is considered to be related to the parasympathetic activity. Both, SDNN and RMSSD are powerful indicators of our cardiovascular health, since the loss of variance between intervals is associated with many cardiovascular and/or inflammatory diseases. As shown below in Figure 3, we want our heart rate frequency to fluctuate a lot over time.
Now that the main time domain indicators have been defined, let us move to the frequency domain. But first, we need to understand one important math concept: any function or time series—think of the graph of a curve—can be re-written as a summation of sine and cosine functions, which are used to model phenomena such as sound and light waves. This idea was first introduced by Jean Baptiste Fourier in 1882 in his work Théorie analytique de la chaleur and later became known as Fourier series.
Figure 1 shows an example, using an arbitrarily chosen function:fx=x3+ x2+3x+5, plotted in the interval ]-π to π [. The resulting data shown as a curve can be reconstructed using a summation of sines and cosine functions through a Fourier series. In this case, twenty sine/cosine functions were used to approximate the curve, while in Figure 2, fifty functions were used.
It is easy to see from the diagrams that, the more functions we use, the greater the precision in the reconstruction of the original data. In both cases, we are using the sum of sine and cosine or “wave” functions to approximate the curve fx=x3+ x2+3x+5 in an ordered way. Each of the component sine and cosine functions correspond to a specific frequency. In this way, a curve can be broken down into its constituent frequencies.
Figure 3 shows the intervals between heart beats i.e., the R-R intervals extracted from a ECG recording and plotted against the time domain, which shows the variation of the heart rate frequency over time.
The next step is to approximate the waveform or curve formed by the heart beat data displayed in Figure 3 as a summation of functions through the Fourier series. This enables us to determine all the frequencies that are acting in our system. The frequency domain indicators are thought of as the “power” associated with each frequency—think of it as the relative contribution of that frequency in the re-construction of the curve formed by the data and calculated through a Fourier transform. These are usually plotted in a spectrogram, a graph where the x axis corresponds to the frequencies and the y axis to each frequency’s power or contribution, like the one displayed in Figure 4.
Now we are ready to define each one of the frequency domain indicators, categorized according to its associated frequency. They are:
- Ultra-low and Very-low Frequencies: 0.01 to 0.04 Hz, not relevant in most cases, due to the relatively short ECG recording usually used.
- Low Frequencies (LF): 0.04 to 0.15 Hz
- High Frequencies (HF): 0.15 to 0.4 Hz
In the beginning of this article, we noted that the branches of the autonomic nervous system (ANS), that is the sympathetic and the parasympathetic branches operate in different frequencies. Based on that, we can see that different HRV indicators in the frequency domain might be associated with sympathetic or parasympathetic activity.
High frequencies are highly impacted by the respiratory pattern, while low frequencies are affected by both the sympathetic and the parasympathetic branches of the ANS. Therefore, by analyzing the power or contribution associated with different frequencies, we can make inferences about the activity of each of the branches of the ANS and their interaction with other systems.
So, why does that matter?
Going back to the beginning of this article, most of the applications, i.e., “apps” used by smart phones and watches to track HRV perform their analysis are based on SDNN, which is a simple-to-calculate and powerful HRV indicator. It’s use is based on the idea that after a workout, the activity of the sympathetic branch temporarily prevails, reducing the overall variability and hence the SDNN.
In this sense, the tool can be used to avoid overtraining, adjusting the intensity of the training session according to the monitored HRV, until the measured SDNN returns to its pre-training values. The same concept can be used to measure stress levels. In theory, all other factors being the same, the more stressed we are, the less variability, and therefore a lower SDNN can be expected. In both cases, the exercise and the stress will likely induce a temporary preponderance of the sympathetic branch.
Now that we know how to analyze it and we understand that different systems are likely to be associated with different frequencies, we can understand why historically HRV was seen as a good measure of imbalances in the ANS. Probably the best way to describe HRV would be as a surrogate measure of the complex interaction between the brain and the cardiovascular system.
So how does that relate to diving?
It has been demonstrated by many studies that a reduced HRV is related to decreased life expectancy. A reduction in HRV has been reported in several cardiological and non-cardiological diseases, ranging from diabetes to renal failure, to mention a few [2,3,4]. A reduction in HRV, when analyzed in the frequency domain has also been associated with inflammatory processes [4, 5].
It is interesting to note, however, that due to huge inter-individual variance, it is difficult to establish expected HRV parameters for a population, and although some interesting studies have been published over the years, there is no consensus on standard values for each one of the HRV parameters. On the other hand, intrasubject analysis, that is the variation of HRV for the same individual over time, can offer very important insights.
Scuba diving is known to trigger oxidative and inflammatory processes, causing a variety of alterations in our physiology, ranging from loss of endothelial function , that is the capacity of the vascular endothelium to respond to vasodilator stimulus, to the activation of the innate immune system and production of microparticles  i.e., particles shed by different cells, which carry nuclear components of their originating cells, like RNA and DNA, and are involved in cell signaling and communication.
As one could imagine, scuba diving is also related to alterations in HRV  and by studying the pattern of these alterations we could infer how our bodies are responding to a dive and, in particular, to the decompression. Our recent study demonstrated that HRV is negatively associated with the production of microparticles and that, using a model built with machine learning, it was possible to predict the pre to post dive variation of the HRV, based on the variation of specific inflammatory markers, linking inflammation and oxidative stress to HRV in scuba diving.
In the past decade, many studies have demonstrated that the presence of inflammatory processes are linked to lowering HRV (either in the time or frequency domains). In our study we demonstrated the inflammatory and oxidative process related to diving are also related to changes in HRV and, interestingly enough, to a preponderance of the sympathetic branch in cases where the volunteers presented more intense responses to the decompression. This fact is also probably linked to the loss of endothelial function, long observed to happen after diving, although the mechanisms are, at this point, not completely clear.
There is still a lot to be understood about the relationship of HRV alterations and diving. The hyperoxia, i.e., exposure to pressures of oxygen higher than 0.5 ATA associated with diving, has its own effects on HRV, making interpretation of HRV variations in diving even more complex. The long-term goal of our research is to better understand individual responses to decompression. We believe HRV variations can be a powerful tool to achieve this objective.
Our team has been working in cooperation with DAN Europe, which has a huge database of diving profiles and outcomes, and some interesting models are being created to model the oxidative and inflammatory processes, but there is still a long way to go before these models can be used in any practical application. However, it is a promising field, and its comprehension will surely help in the full understanding of decompression physiology, making this subject certainly something interesting for the diving community. We could even dream about being able to adjust our dive profiles based on individual responses, right? Watch this space.
- Ernst G. Heart-Rate Variability—More than Heart Beats? Front Public Heal. 2017;5(September):1-12. doi:10.3389/fpubh.2017.00240
- Malliani A, Pagani M, Lombardi F, Cerutti S. Cardiovascular neural regulation explored in the frequency domain. Circulation. 1991;84(2):482-492. doi:10.1161/01.CIR.84.2.482
- Appel ML, Berger RD, Saul JP, Smith JM, Cohen RJ. Beat to beat variability in cardiovascular variables: Noise or music? J Am Coll Cardiol. 1989;14(5):1139-1148. doi:10.1016/0735-1097(89)90408-7
- Sloan RP. Heart Rate Variability Predicts Levels of Inflammatory Markers: Evidence for the Vagal Anti-Inflammatory Pathway. 2015;(Bernik 2002):94-100. doi:10.1016/j.bbi.2014.12.017.Heart
- Adam Moser, Kevin Range and DMY. Relationship between Heart Rate Variability, Interleukin-6, and Soluble Tissue Factor in Healthy Subjects. Bone. 2008;23(1):1-7. doi:10.1038/jid.2014.371
- Brubakk AO, Duplancic D, Valic Z, et al. A single air dive reduces arterial endothelial function in man. J Physiol. 2005;566(3):901-906. doi:10.1113/jphysiol.2005.089862
- Thom SR, Bennett M, Banham ND, et al. Association of microparticles and neutrophil activation with decompression sickness. J Appl Physiol. 2015;119(5):427-434. doi:10.1152/japplphysiol.00380.2015
- Schirato SR, El-dash I, El-dash V, Natali JE, Starzynski PN, Chaui-berlinck JG. Heart rate variability changes as an indicator of decompression-related physiological stress. Undersea Hyperb Med. 2018;Mar-Apr 20:173-182.
- Schirato et al. Association between Heart Rate Variability and decompression-induced physiological stress. Front. Physiol. Front. Physiol., 03 July 2020
- Schirato’s Talk at the 2019 GUE Conference: Heart Rate Variability: What it is and Why it Matters
- From GUE’s membership magazine QUEST: Decompression: Revisiting Old Assumptions by S.Rhein Schirato
Brazilian scientist, Sergio Rhein Schirato, is a hedge fund manager and a researcher at the Laboratory of Energetics and Theoretical Physiology of the Biosciences Institute of the University of Sao Paulo (USP). He holds a PhD in Sciences, a Masters in Finance jointly granted by New York University and London School of Economics and post graduation in applied Math. His current research includes the application of neural networks in decompression modeling and heart rate variability. Additionally, he is a GUE Fundamentals and Rec 1, 2 and 3 instructor, as well as GUE Rebreather certified diver.
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.
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.
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.
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.
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.”
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.
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:
“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.
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.
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.
- 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
- Talpalar, Adolfo. (2007). High pressure neurological syndrome. Revista de neurologia. 45. 631-636.
- Understanding Oxygen Toxicity: Part 1 – Looking Back
- 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.
- 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.
- 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
- High Pressure Neurological Syndrome, DIVER (2012) by Dr. David Sawatzky
InDepth: Diving Beyond 250 Meters: The Deepest Cave Dives Today Compared to the Nineties by Michael Menduno & Nuno Gomes
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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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...