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Wreck in Depth: USS Saratoga (CV-3)

The third installment of our historical wreck series brought to you by shipwreck diving travel specialists at Dirty Dozen Expeditions. Are you ready to make the jump?

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By Martin Cridge
Header image courtesy of US Navy

Marc Mitscher pulled the control stick of his aircraft to the side, bringing his plane around and lining up for the first ever aircraft landing on the USS Saratoga (CV-3). Stretched out below him was the 264 m/866 ft flight deck of the newly commissioned carrier.

Marc Mitscher on the deck of the USS Saratonga CV-3. Photo by US Navy.

Mitscher would go on to lead the U.S. Fast Carrier Task Force during World War II on a number of daring missions including Operation Hailstone, the fast carrier attack on Truk Lagoon in February 1944. But in January 1928, he was concentrating on bringing his aircraft safely down onto the flight deck of Saratoga. After his successful landing, the rest of his air group followed, and Saratoga went on to conduct her first shakedown cruise before heading to the Pacific via the Panama Canal. Although she was originally designed to pass through the canal, Saratoga knocked down a number of lamp posts on her way through the locks due to the large overhang of her flight deck. 

Saratoga would spend the rest of her career assigned to the Pacific Fleet, although she would occasionally take part in exercises or fleet reviews on the east coast during the interwar years. 

USS Saratoga (CV-3) transiting the Panama Canal on 4 March 1930. Photo by Naval History & Heritage Command.

Saratoga was laid down at the Camden, New Jersey yard of the New York Shipbuilding Corporation in September 1920, originally as a Lexington class battlecruiser. In February 1922, the Allies adopted the Washington Naval Treaty, which aimed to prevent a post-World War I arms race. The treaty placed restrictions on the number, size, and armament of certain naval vessels as well as which types of new vessels could be built. As a result of the treaty’s restrictions, the Navy scrapped their plans to build six Lexington class battlecruisers. Part of the treaty, however, allowed two vessels that were already under construction to be converted into aircraft carriers. 

USS Saratonga (CC-3) under construction, 1921. Photo courtesy of Wikimedia Commons.

So, on  July 1, 1922, the Navy selected Saratoga and her sister Lexington to become the fleet’s first aircraft carriers. Japan followed suit and converted the battlecruiser Akagi and the battleship Kaga into aircraft carriers. Aircraft carriers weren’t exempt from the Washington Naval Treaty’s limits on the size and armaments of naval ships. Per the treaty, the vessels were limited to 36,000 tons maximum standard displacement, which included 3,000 tons for antiaircraft and torpedo defenses. This benchmark proved difficult to achieve, and both the Saratoga and Lexington exceeded their limit while the treaty was in force.

USS Saratonga in a dry dock at the Puget Sound Naval Shipyard on 17 November 1930. Photo by US Navy.

Saratoga became the Navy’s first purpose-built fleet carrier to be launched when she glided down the slipway into the Delaware river on April 7, 1925. She was commissioned for the first time at the Philadelphia Navy Yard on November 16, 1927, and sailed for the first time under the command of Captain Harry E. Yarnell. While the original role of aircraft carriers was perceived to be fleet reconnaissance, anti-submarine patrol, and spotting for the big guns of capital ships, the  Navy spent the interwar period developing tactics and multi-mission capabilities of aircraft carriers through a number of fleet training exercises and war games. 

Naval Aviation grew to become a key component of fleet battle tactics and was constantly developed to improve and project the fleet’s strike power over the horizon. Other scenarios were played out in exercises that developed the Navy’s ability to attack other aircraft carriers and shore bases, as well as to offer support for amphibious operations. In one fleet problem exercise in 1938, Saratoga successfully launched a surprise air attack on Hawaii in what was an almost identical scenario to the Japanese attack in December 1941.

The Aftermath of Pearl Harbor

At the start of the Pacific war, when Japan attacked Pearl Harbor, Saratoga was in San Diego, having  just completed a dry dock and maintenance period. After embarking her air group, she managed to get underway within 24 hours of the Japanese attack for her first mission of the war—carrying reinforcements for the U.S. garrison on Wake Island. Ultimately, the mission was cancelled before Saratoga could reach Wake, and the island fell into Japanese hands.

View from directly opposite the damage showing torpedo bulkhead No. 1 and the forward edge of the hole. Photo by Naval History & Heritage Command.

In January 1942, the Japanese submarine I-6 torpedoed Saratoga for the first time, forcing her to return to the west coast for repairs. Returning to the fleet just before the Battle of Midway, the fighting was finished by the time she reached Pearl Harbor where she loaded replacement aircraft for both the Hornet and Enterprise so that they could replace the planes they lost in the battle.

Torpedo Damage Diagram. Photo by Naval History & Heritage Command.

By August 7, 1942, Saratoga was in the Solomon Islands supporting the U.S. offensive on Guadalcanal. At the end of August, Saratoga was torpedoed for a second time, this time by submarine I-26. After repairs at Pearl Harbor, Saratoga returned to the South Pacific.

Saratoga spent most of 1943 operating from Nouméa in New Caledonia supporting operations in and around the Solomons. She was, for a while, the only operational U.S. carrier in the Pacific. In November, Saratoga supported the U.S. offensive in the Gilbert Islands and Nauru before heading back to the west coast for a much needed refit.

January 1944 saw Saratoga back in action, this time supporting operations in the Marshall Islands before joining the British Eastern Fleet, which was operating in the Indian Ocean. During operations with the British, Saratoga carried out a number of successful raids on both Sumatra and Java during April and May.

In June that year,  the Saratoga was back in dry dock at the Bremerton yard in Washington, and when she emerged in September, she had a new, special role. Saratoga was chosen to develop night fighting tactics and to train pilots for night fighter operations.

Saratoga on fire after a kamikaze attack. Photo by US Navy.

In 1945, Saratoga returned to frontline duty, and in February was tasked to provide air cover for the amphibious landings on Iwo Jima. On February 21, she was hit by kamikaze planes and bombs in two separate attacks by the Japanese. Although the forward part of her flight deck was seriously damaged, she managed to recover her aircraft before retiring from the operation and returning to the U.S. for further repairs.

During the repairs, the Navy decided to convert Saratoga permanently into a training carrier. The aft aircraft elevator was welded in the up position and all its associated machinery was removed. A larger forward elevator was fitted and its operating machinery upgraded. Finally, parts of the hangar deck were converted into accommodations and classrooms. Saratoga spent the remaining months of the war as a training venue for pilots operating out of Pearl Harbor. 

Once the Japanese had surrendered, Saratoga took part in Operation Magic Carpet, the repatriation of American servicemen. In the end, she took over 29,000 American servicemen home, more than any other ship. Since Mitscher’s first landing in January 1928, over 98,500 planes had touched down on Saratoga’s flight deck, setting a U.S. Navy record. 

USS Saratoga (CV-3) during Operation Magic Carpet in 1945. Photo by US Navy.

As a result of technical advancements made during the war, the Saratoga had become obsolete, and she was selected to take part in Operation Crossroads, the first atomic tests at Bikini. She departed from the U.S. mainland for the last time on May 1, 1946, sailing out under the Golden Gate bridge from San Francisco for her date with destiny at Bikini Atoll.

For test Able, Saratoga was deliberately positioned some distance from the planned zero point so that she could be used later in test Baker. After the Able test she suffered some minor damage, mainly from fires on her teak-covered flight deck, but these were soon extinguished. 

Some of her crew even moved back onboard the ship for a couple of weeks while preparations for the Baker test were made. Despite being placed in the expected fatal zone for the Baker blast, some of these crew members left their kits and personal belongings onboard, believing the Saratoga wouldn’t sink.

But she did.

USS Saratonga (CV-3) sinking in Bikini Atoll, 25 July 1946. Photo by US Navy.

Diving One of the Largest Shipwrecks in the World 

As built, Saratoga‘s official standard displacement was 36,000 tons (43,055 tons full load), and she was 270 m/888 ft long. Modifications to the vessel in 1945 increased her full load displacement  to 49,552 tons and her overall length to 277 m/909 ft, making her one of the largest diveable shipwrecks in the world. 

The Saratoga now sits upright in 51 m/167 ft of water with the top of her superstructure reaching 18 m/60 ft and the flight deck averaging 27 m/90 ft. 

USS Saratonga schematic. Courtesy of Dirty Dozen.

First dives on the Saratoga are truly awe-inspiring. This is a big wreck, and just orienting yourself  can take a number of dives.

The effects of two atomic explosions, war damage, and general deterioration from over seventy years of resting on the lagoon bottom are now starting to show, with parts of her superstructure, hull, and flight deck collapsing in recent years. None of this, however, diminishes the impressive nature of this wreck.

After the Baker bomb exploded underneath LSM-60, the Saratoga was hit by a number of massive tidal waves which lifted the mighty vessel and smashed into her sides, causing serious damage to her side plating. Two million tons of coral, sand, and water were thrown up into the air by the explosion, which then came crashing down onto the flight deck.

Five-inch guns on the flight deck. Photo by Martin Cridge.

Saratoga was built with an unarmored flight deck. This maximized hangar space and was more easily repaired but was obviously not as strong as an armored deck. Although original reports by Navy divers after Saratoga sank said that the flight deck was largely intact, it was seriously dished from the aft elevator to the stern over the hangar deck area. It’s likely that it was seriously damaged and would have been unusable had the ship not sank. Now, large parts have collapsed onto the hangar deck below. 

A plane inside the collapsed flight deck of Saratoga. Photo by Aron Arngrimsson.

A number of planes and various pieces of military equipment were staged on the flight deck for the Baker test. The planes were all swept off the deck during the test, and the remains of some of them are now scattered around the Saratoga on the seabed, some still in surprisingly good condition. Planes were also stowed on the hangar deck, although these are now mostly inaccessible due to the collapse of the flight deck over the hangar. It’s still possible to see into the cockpits of some of them, but these planes are now, sadly, in poor condition. 

500-lbs bombs. Photo by Aron Arngrimsson.

Some of Saratoga’s main ship armaments were removed prior to Operation Crossroads, but a representative number were left onboard, including 2x twin 38 caliber 5″ dual purpose gun mounts, a number of single 5″ dual purpose gun mounts on the sponsons down each side of the ship, along with an array of 40mm Bofor and 20mm Oerlikon guns.

Lots of munitions were also onboard when the Saratoga was sunk. These include 159 kg/350 lb and 227 kg/500 lb bombs, air drop torpedoes, rockets, 5” gun cartridges, and depth charges, all of which can still be found scattered in and around the wreck today.

Forward of the forward aircraft elevator, the flight deck is still largely intact apart from a small area towards the bow. This is one of the  areas where Saratoga was hit when she was off Iwo Jima—in February 1945—and was hastily repaired. Now the damaged area allows access to the bow area under the flight deck, including the emergency radio room—with all of its vacuum tubes and dials—and the lamp locker with some lamps still in place.

Saratoga Bridge. Photo by Aron Arngrimsson.

Inside the Saratoga

The interior of the Saratoga is vast, and probably no more than 10% of the ship has been properly explored since her sinking. The Saratoga was heavily compartmentalized, and the majority of her watertight doors and hatches were closed when she sank, hindering today’s explorations. Most of the penetrations go forward from the forward elevator shaft at various levels.

Illustration of penetrations inside the elevator shaft. Photo by Aron Arngrimsson.

In some areas, permanent lines have been laid, but care is still needed, as a fine silt is present that is easily stirred up within most parts of the vessel. Needless to say, excellent buoyancy skills are a must to avoid silt outs, and divers need to be constantly aware of their surroundings. Divers with the necessary skills and experience who do venture inside are richly rewarded with a number of unique sights. A maze of passageways lead off in all directions to storerooms, workshops, galleys, pantries, mess decks, accommodation decks, and bathrooms.

Operation Station – Command Information Center on Saratoga. Photo by Martin Cridge.

You can visit the Command Information Center, the nerve center of the ship when it was operating at war. The cabins and bathrooms used by Admirals and Captains are nearby. Divers can visit the ready room where pilots were briefed on their upcoming missions, and the machine shops packed with lathes, grinding wheels, bench drills, and metal- and wood-working tools. Probably the most impressive area, however—especially for those not suffering from dental-phobia—is the dentist’s surgery and sickbay. Three dentist chairs sit in the surgery, complete with dental drills, instruments, and rinse bowls. Everything is almost perfectly preserved, and if it weren’t for the fine layer of silt covering everything, the room would look like it was just waiting to receive its next patient.

Dentistry in the Saratoga. Photo by Aron Arngrimsson.

Elsewhere on the ship, countless artifacts lay scattered around, including plates, bowls, jugs, Coca Cola, bottles, and other debris, much of which has laid untouched since 1946. In store rooms, shelves full of spare parts are still crammed with items including gauges, thermometers, valves, and fittings.

Two of the more interesting and unique items for divers to see are the U.S. Navy Mark V diving helmets and standard dress drysuits. The US Navy Mark V diving helmet is one of the most well known diving helmets in the world. First introduced in 1916, it was used until 1984 and can still be purchased new today.

Dive Helmets inside the dive locker on Saratoga. Photo by Aron Arngrimsson.

All too soon, however, it is time to head back to the surface. Instead of planes, divers can see reef sharks and eagle rays cruising up and down the flight deck and turtles munching on the coral and algae. Large shoals of jacks, trevally, and rainbow runners will swim around divers as they head back up the mooring line to the surface. While divers complete their deco, they will peer out into the blue to see if the tiger sharks will turn up, and often they do. If they are really lucky, some mantas may cruise by, or even the odd whale shark or tiger shark.

Tiger shark cruising around the deco bar. Photo by Aron Arngrimsson.

Capt. Martin Cridge—Without Martin The Dirty Dozen Expeditions wouldn’t exist. A few years back, Aron and Martin spent a full year diving together in Truk Lagoon. One evening, after a day of demanding dives, they sat, had a beer, and came up with their ideal CCR wreck dive itinerary.
The first ever Dirty Dozen trip was the result of that beer and the rest is history. Martin has lived in Truk for eight years with his family and works as the skipper of our expedition vessel in Truk and Bikini.



Diving Safety

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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