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Understanding Oxygen Toxicity Part II: Hypotheses and Hyperoxia

Diver Alert Network’s Reilly Fogarty examines the latest research on the mechanisms behind CNS and pulmonary oxygen toxicity to tease out what we think we know and what it means for your diving. Watch those PO2s!

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by Reilly Fogarty
Header photo by Stephen Frink, Research conducted at the US Navy Experimental Diving Unit.

You can read Part I of this series here.

The history of oxygen toxicity research serves well to set the stage for the complication and nuance of modern research, but it’s important to recognize that what we are currently working with is a series of compounded hypotheses on the effects of oxygen in the body. They’ve been tested to varying degrees and serve as the basis for compounding theories and practices both medical and academic in nature, but the more we learn about the function of oxygen in the human body, the more we realize what we don’t yet know. The specificity of the mechanisms combined with the concurrent reactions required to make those mechanisms possible fills the pages of more than one textbook, but here’s a real-world look at what we think we know, and what it means for divers.

The production of ATP during the breakdown of sugar at normal (normoxic) oxygen partial pressures. Diagram courtesy of aquaCORPS.

Starting Small

Most modern theories of oxygen toxicity focus primarily on the function of oxygen free radicals and lipid peroxidation, in a mechanism that mimics inflammatory processes in the body. Oxygen free radicals, or reactive oxygen species (ROS) are ions (atoms or molecules having an unpaired electron in an outer orbital) that are highly reactive. The pairing or loss of the lone electron results in the generation of an additional free radical, leading to a continuous chain of species production. Their initial creation is primarily the result of an oxi-reductive process in the electron transport chain, the result of which is superoxide, hydrogen peroxides, hydroxyl, and water (Chawla, 2001). These free radicals result in lipid peroxidations (a type of oxidative lipid degradation) in cell membranes, damage to cellular enzymes and interference with nucleic acid and protein synthesis. Exposure to high partial pressures of oxygen increase free radical production and may result in damage to the pulmonary epithelium, intra-alveolar edema, interstitial thickening and several other conditions (Cooper, 2019). 

The production of ATP and reactive oxygen species during the breakdown of sugar at elevated (hyperoxic) oxygen partial pressures.
Diagram courtesy of aquaCORPS.

The general mechanism for central nervous system (CNS) toxicity resulting in tonic-clonic seizures (convulsions involving both muscle stiffening and twitching or jerking) involves hyperoxia-induced free radical production overwhelming specific neural pathways, combined with localized neuron depolarization and hyperexcitability. This theory suggests that exposure to high partial pressures of oxygen results in an increase  in the firing rate of specific neurons, notably those of a part of the brain called the caudal Solitary Complex (cSC), a portion of the dorsal medulla oblongata which is important in cardiorespiratory control and has some neurons that are particularly sensitive to hyperoxia and pro-oxidants (Ciarlone, 2019). The effect of this hypersensitivity combined with increased free radical production is theorized to be the stimulus for the seizure evolution seen in CNS oxygen toxicity, although other mechanisms bring epilepsy models into the fold and propose looping and self-amplifying circuits of neurons that result in seizure evolution. An additional mechanism proposes seizure onset as a result of hyperoxia induced enzyme inhibition, notably of Gama Amino Butyric Acid (GABA). GABA is an inhibitory neurotransmitter, and inhibition of its production is theorized to result in neuronal excitation resulting in seizure (Treiman, 2001). These mechanisms are not exclusionary and in some instances may combine, overlap or catalyze each other. 

Fig. 1.
Fig. 1 courtesy of Divers Alert Network (DAN).

Pulmonary oxygen toxicity is typically proposed to follow a similar inflammatory mechanism caused by free radical production and lipid peroxidation. These mechanisms involve redox and inflammatory damage throughout the body, primarily to the capillary endothelium and alveolar epithelium resulting in impaired gas exchange and neutrophil infiltration leading to respiratory failure (Ciarlone, 2019). The visible effect of this inflammatory reaction is the irritation of the airway, decreased gas exchange and eventual thickening of alveoli and damage to the alveoli and airway tissues. 

There are several additional and notable mechanisms for both CNS and pulmonary toxicity that involve other sources of free radical damage catalyzing neural misfiring, damage to proteins and resulting immune responses, and inappropriate oxidative signals as a result of exposure to hyperbaric oxygen — what’s important to understand in this is not the specifics of the proposed models as much as the applied cause and effect. Exactly why each of these mechanisms functions as it does remains unclear in some instances, but the proposed hypotheses bring us closer to understanding what inputs can be altered to understand and eventually address the resulting symptoms of oxygen toxicity. What’s interesting to note is the significant overlap in many of the proposed mechanisms, many of which provide reactants for or accelerate other similar mechanisms, as well as the recent convergence of many theories on the concept of oxygen toxicities effects being inflammatory or autoimmune in nature. 

Jarrod and Paolo Macciachini during oxygen decompression. Photo courtesy of the GUE archives.

Day-to-Day Variability

The single most significant issue in applying what we know about oxygen toxicity isn’t the unknown nature of specific mechanisms, but the huge variability in the exposures that result in symptom evolution, even in the same individual on two separate days. This variability is partially a function of the many contributing factors in oxygen toxicity, resulting from differences in factors that contribute to, inhibit, or result in the catalysts involved in the mechanisms discussed above. The majority of this variability is proposed to be the result of both the multitude of pathways that result in injury, and factors like antioxidant defense levels, neurotransmitter levels, genetic factors, nitric oxide production rates, and hormone levels — particularly concerning thyroid function, epinephrine production and ACTH levels (Shykoff, 2019). 

This variability is so great that some models propose that CNS toxicity can be affected by inert gases, visual input, and circadian rhythm (Mathieu, 2006). The result of all of this is that the list of variables that contribute to oxygen toxicity risk of all kinds is both incomplete, and so long and variable that they cannot possibly be controlled for in their entirety. In the real world this means that we must apply enormous levels of conservatism to what amounts to an educated guess at the average limits of divers. Comparison of models created by military researchers (using exceptionally fit young males performing difficult work underwater as a model), and academic models (using samples that more closely resemble the diving population) result in significant variability both by model and by acceptable risk. 

NOAA Oxygen Exposure Limits.

For the most part we, as an industry, have found some success in settling for the current NOAA oxygen exposure guidelines, but even these see unexpected injuries in use. The management of some primary diving-related risk factors for oxygen toxicity has resulted in the ability of some divers to far exceed recommended guidelines seemingly without symptoms, but because of this variability we are largely unable to quantify the risk they face — it’s as of yet unclear if the diver performing hours long decompressions in a habitat is taking a gamble with each dive or maintaining a moderate safety margin with the controls they’ve put in place. 

Carbon Dioxide

Carbon dioxide may be the greatest controllable risk factor in CNS oxygen toxicity, and unmitigated CO2 production and retention has been correlated with significantly increased seizure risk. This risk is primarily the result of the combination of CO2 production from exercise, combined with increased retention as a result of increased gas density, hydrostatic compression of the lungs, and dead space ventilation caused by the length of tubing in a breathing apparatus (Carlione, 2019). While breathing a hyperoxic gas may initially inhibit ventilation, continued exposure stimulates ventilation and decreases CO2 retention as long as that CO2 is effectively eliminated. The result of this is increased CO2 production and retention to increase arterial PCO2 and the production of respiratory acidosis. This is exacerbated by the oxygen induced interference with CO2 transport in the body, resulting in a higher dissolved PCO2 and decreased bicarbonate and carbamino concentrations (Carlione, 2019). 

The resulting hypercapnic acidosis increases free radical species formation via a cascade of mechanisms involving an increase in hyperoxic blood delivery to the brain, and an interaction called the Fenton Reaction that in combination results in increased free radical production, which accelerates oxidative stress and increases seizure risk. Like the mechanisms above, this is a broadly accepted but still unproved hypothesis that results in an increase in seizure risk, but while the specifics of the interaction may be variable, the effect of CO2 on convulsion risk have been strongly correlated. 

Hypothermia

Hypothermia presents as a risk factor of its own, and one that compounds the effects of CO2. The specifics of this mechanism remain unclear but the reduction in peripheral blood blow, increased cardiac output and redistribution of blood volume to the core results in increased oxygen delivery to the CNS, which may compound issues with both with CO2 retention and delivery of hyperoxic blood to the brain (Mathieu, 2006). Other factors like circadian rhythm, sleep, inert gases, diet, and gender have been similarly correlated with decreased seizure latency (the time between stimulus and seizure onset), but with varying degrees of study and theorized modeling. 

Diving in cold water might call for a higher level of conservatism. Photo by Nicole Wächter.

The real-world takeaway is that we know a little about a lot of proposed mechanisms, and a lot about very few facets of oxygen toxicity. There’s a growing convergence of theories around the idea of an inflammatory or immune response being central to the mechanisms for both CNS and pulmonary oxygen toxicity, and while these theories are quite good and have withstood significant testing, many have yet to be definitively proven. Academically the outlook is both more obscure and more hopeful — this article is just a brief summary of some of the more common models of oxygen toxicity, but there are numerous other contributory and more detailed models and mechanisms currently being researched to explain the effects of high partial pressures of oxygen on the human body. 

It’s worth noting that as divers we are primarily concerned with just CNS and pulmonary toxicity, but the effects of oxygen in the body are far more reaching and involve numerous other physiological changes. The future of research into the topic yields promise both on academic and applied fronts. Trials with inhibitors of some free radicals, anti-adrenergic and anti-epileptic drugs, ketone metabolic therapy and hyperbaric preconditioning have shown significant promise in the reduction of oxygen toxicity effects. 

Ongoing research into human exposure limits promises to improve our ability to plan real-world dives and extend out limits, and a broad field of researchers are working to overcome the gaps in knowledge that we currently have. There may not be a unique revelation in the currently published research that changes the way that you plan your dives, but the simultaneous progress on so many facets of our understanding indicates that are likely on the cusp of a new understanding of how to manage oxygen exposures and keep ourselves safe in the water. 

Thank you to Dr. Andy Pitkin, Dr. Barbara Shykoff, and Dr. Neal Pollock for their willingness to share their expertise in their respective fields. 

Additional Resources

For more information on the specific mechanisms of oxygen toxicity and the ongoing clinical trials mentioned in this article, please visit the references linked below. 

  1. Chawla, A., & Lavania, A. K. (2001). OXYGEN TOXICITY. Medical journal, Armed Forces India, 57(2), 131–133. doi:10.1016/S0377-1237(01)80133-7
  2. Cooper JS, Shah N. Oxygen Toxicity. [Updated 2019 Mar 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. 
  3. Ciarlone, G. E., Hinojo, C. M., Stavitzski, N. M., & Dean, J. B. (2019, March 9). CNS function and dysfunction during exposure to hyperbaric oxygen in operational and clinical settings
  4. Treiman, D. M. (2001, December 20). GABAergic Mechanisms in Epilepsy
  5. Shykoff, B. (2019). Oxygen Toxicity: Existing models, existing data. Presented during EUBS 2019 proceedings.
  6. Mathieu, D. (2006). Handbook on Hyperbaric Medicine. Dordrecht: Springer.

Reilly Fogarty is a team leader for risk mitigation initiatives at Divers Alert Network (DAN). When not working on safety programs for DAN, he can be found running technical charters and teaching rebreather diving in Gloucester, MA. Reilly is a USCG licensed captain whose professional background includes surgical and wilderness emergency medicine as well as dive shop management.

1 Comment

1 Comment

  1. Dominic Jeanes

    December 3, 2019 at 8:03 pm

    Best piece I have seen published on oxtox, thanks Reilly. If your research pointed you towards any info on the following questions, I’d appreciate it if you could point out further reading sources; or your own views?
    1, If metabolism doesn’t increase due to depth (from my basic understanding of CCR oxygen consumption- perhaps flawed) where does the increased production of free radicals come from? Is it due to the Fenton reaction you mentioned in your article; and if so is it therefore more due to CO2 retention than purely to depth?
    2, In all the studies we see performed, the subjects are obviously wearing full face masks, how much is the facility to nose breath and hence produce more nitrous oxide in inhaled gas effect the outcomes of CNS exposure?
    3, In more basic articles dealing with CNS Oxtox on the diver, the main concern is convulsion and loss of airway; is evidence now pointing towards there being more long term damage to the CNS and this blurring the distinction between CNS and Pulmonary/Whole body oxtox?
    Thanks for any help you can give on this matter. Cheers Dominic.

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No Fault DCI? The Story of My Wife’s PFO

What does it mean if you keep getting bent, even when you follow all the rules? Avid tech diver James Fraser recounts his and his wife’s Deana journey of discovery that led them to realize she had a PFO. Does any of this sound familiar? Read on!

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Breathing O2

by James Fraser

All photos courtesy of James Fraser

When you follow all the rules and still get decompression illness, what’s up?

The person I hold most dear in this life has now had three incidents of decompression illness (DCI) over a two-year period. The latest episode required recompression, so we began investigating her frequent illness to determine if there was a possible solution. Deana is a very conservative diver, diving within her training, computer limits, and dive planning tools such as Deco Planner. On all of the dives where she had DCI, her training, tools, and dive profiles say she should not have gotten bent. But she got bent just the same.  

DCI is a risk for any diver, even when following the rules. However, we have to remember that DCI is a potential sports injury, no different than a football player risking a concussion. Despite this fact, DCI seems stigmatized, and people feel ashamed to admit it happened to them. So Deana and I decided to share her experiences with DCI, to help others realize, Sh*t, I mean, DCI happens! Experiences with DCI should be shared, so that the diving community can continue to learn, grow, and be safer divers. 

Some background

Deana Fraser has been a registered nurse (RN) for over 25 years, and received her BSN in 2002. Throughout her career, she has specialized in ER, ICU, and OR nursing. Currently, she manages the Overlake Operating Roomin Bellevue, Wash. When Deana is not managing the OR, she is usually diving in the extreme conditions of the Pacific Northwest (PNW), where all dives are cold (46-55℉/8-13°C), dark, and wonderful. Deana has been a recreational diver since 2004, and loves diving in Seattle and the surrounding areas as often as three days a week. It is her number one passion. 

She just completed her Global Underwater Explorers (GUE) Technical 1 course (normoxic trimix) in September 2019, and as of this article she has completed over 500 dives, 150 during 2019 alone. Deana always looks forward to expanding her skills and experience in the recreational and technical diving arena. 

Deana is also a breast cancer survivor; she was diagnosed with Stage Two breast cancer in May 2016, and underwent a lumpectomy and six weeks of radiation treatment, until July 2016. She is in full recovery, but continues to take Tamoxifen (20mg) daily. This information is not intended to draw any type of correlation of breast cancer and DCI, but to give all details about Deana’s fitness and health in respect to her history with DCI.

Deana is one of those people that lets nothing hold her back. She was not able to dive for a few months after her radiation treatment, so she turned to her second love: hiking. She proceeded to hike over 200 miles (dragging her husband with her) over the next six months while she was recovering. Deana has been cancer free for over three years now and is back to her first love of diving. When she returned to diving, she pursued her dream of technical diving and signed up for GUE Fundamentals in 2017. She has been unstoppable since then and again has dragged her husband along for the ride. 

After cancer treatment, Deana spent a lot of time building up her strength and dexterity in order to pack double 100s over the rocky beaches of the PNW. She trained relentlessly to reach the goal of being a GUE Tech 1 Diver, a mission that she accomplished. In addition to her regular dives, Deana leads a weekly Skills Refinery Dive, offering opportunities for other local divers to hone their techniques and commit to excellence. Many are working on their GUE Tech skills to prepare for Tech 1. Deana is not done with her education and has dreams of completing GUE’s Tech 2 course in the future. Now that you know the type of person Deana is, let’s talk about the reason she and I have written this article. 

Look, James. I Got Stung by Something!

Deana and I went on a 16-day trip to the Maldives in April 2018. We spent the first week at Olhuveli Beach Resort resting, flipping our internal clocks, and doing a few recreational shore and boat charter dives. The second week, we joined up with our local Seattle dive group on Blue Force One, a fantastic live-aboard charter, for seven days of additional recreational diving; no dives on this trip were below 100 ft/30 m. On day three of diving on Blue Force, after her second dive, Deana talked to me about being stung on her abdomen. She presented with redness, point tenderness, and stinging in an area about the size of a silver dollar. She was wearing a full length 3mm wet so it definitely was not something she would have brushed against during the dive. She took a Benadryl, feeling that something stung her, got some sleep, and by the next morning it had cleared up. Deana continued diving for the rest of the trip and had no further symptoms. We now suspect that she had a minor case of skin bends, based on the other two episodes she has had since. 

Deana and I also dived in Loreto, Mexico, six months after the Maldives, in October 2018, and performed  ten dives over four days with a max depth of 80 ft/24 m; Deana showed no symptoms of DCI.

Could I Have Skin Bends?

In April this year, 2019, Deana and I were in Hurghada, Egypt, on a live-aboard dive trip with Red Sea Explorers aboard MV Nouran. Deana had completed eight recreational nitrox dives over three days, the deepest dive being 98 ft/30 m, when she showed signs of skin bends. Below are the dive profiles of the two dives the day she presented with skin bends. She again had symptoms of stinging and itching on her thighs and abdomen and point tenderness. The area was larger than the first experience she had in the Maldives.

First dive of the day: Double 12L tanks with nitrox 32 after 11 hour surface interval
Second Dive: Double 12L with nitrox 32 after 3:23min surface interval.

Deana again wondered if it was some kind of sting or allergic reaction and asked me and some of the more experienced divers for our opinions. A couple of the more senior technical divers on board agreed: Her symptoms looked and presented like skin bends. Deana went on 100% oxygen (O2) for a few hours, and the symptoms went away. She took the next day off and then continued to dive recreationally with more conservatism for the remainder of the trip. One other person on the trip who was doing Tech 1 level dives also showed signs of skin bends; they were treated with O2 and continued to dive for the rest of the trip with no further issues. 

After this episode we thought about the Maldives: Since it presented the same way and resolved itself with some time and O2, we now assumed that was also an incident of minor skin bends. 

Skin Bends Again, But Nothing a Bit of O2 Can’t Fix

Deana and I were attending Tek week at Buddy Dive in Bonaire. We were both looking forward to a week of Tech 1 dives (Max depth 170 ft/50 m, max deco: 30 min), as this was Deana’s first trip since passing her course. We had done three dives total over days one and two at recreational depths on nitrox 32 (32% oxygen, 68% nitrogen) with no required deco. 

On day three we planned to dive to 150 ft/46 m on trimix 21/35 (21% oxygen, 35% helium), with 25 min bottom time with a gas switch to nitrox 50 at 70 ft/21 m. Our decompression profile used GUE modified deco based on Deco Planner with 2 min stops from 70 ft/21 m to 30 ft/10 m and a 16 min stop at 20 ft/6 m. The total planned run time for that dive was 58 min. At the start of our ascent, our average depth was only 132 ft/40 m, as we had worked our way slowly up the reef after hitting a max depth of 152 ft/46 m.

Deco Planner Dive Profile
Perdix Shearwater Dive profile using GF20/85

After a three-and-a-half-hour surface interval, we planned a 100 ft/30 m dive on nitrox 32 with a bottom time of 40 min with a gas switch to 100% O2 at 20 tf/6 m for 10 minutes for added conservativism. Total run time for that dive was 69 min, as we extended our 20 ft/6 m stop a lot longer to just hang and enjoy the reef. 

Deco Planner for Dive 2
Perdix Shearwater Dive profile using GF20/85

Roughly two hours after this dive, Deana complained of itchy stinging skin on her hips and abdomen; she described it as being like stinging nettles. She was not concerned as this felt like what she had in Egypt, so we put her on 100% O2 for about an hour and a half and all symptoms resolved. Deana and I considered this a minor issue, and we did not talk to anyone about the symptoms since they quickly resolved. No further issues were experienced that evening. 

It is here that human factors really played into the scenario. Deana and I made the mistake of not talking about the issue we had just experienced. We found out later the next day that Dr. Douglas Ebersole (cardiologist and consultant to Divers Alert Network) and the late Dr. Fiona Sharp (diving physician and anesthetist) were active participants of Buddy Dive Tek week. If we had spoken up, we most likely would have been able to talk to one or both of them and potentially decide not to dive the next morning. However, hindsight is 20/20, and we just didn’t feel the need to talk about it since Deana’s symptoms had been resolved. 

The next morning Deana felt fine and showed no rash or issues from the previous day. She wanted to do the planned trimix dive to 150 ft. It was the same profile as the previous day’s dive, and the dive went without issue. We had completed an 18-hour surface interval, and Deco Planner showed we could dive the same profile with no additional decompression obligation. 

Deco Planner confirmed our assumption of being clear after 18 hours

About 45 min to an hour post dive, Deana complained of similar skin pain and stinging, but this time it extended down her thighs. When we returned to shore, we shared her symptoms with the technical diving supervisor, Mr. G, and placed her back on medical O2 for about two hours. This resolved the stinging, but Deana showed edema in her thighs, hips, and abdomen and deeper tissue pain. She had resolved to sit by the pool and have a Corona while I took a nap beside her to see if it would resolve itself. 

We Called DAN

About an hour later Deana said, “We have DAN insurance, maybe we should call them and get their advice.” She placed a call to DAN, and within minutes was talking to Dr. Matías Nochetto. After a thorough assessment, Dr. Nochetto stated that, while they cannot diagnose over the phone, there were enough signs and symptoms to recommend we go into the ER and be assessed for DCI. DAN said that Bonaire had a hyperbaric chamber with an excellent team, and they gave us contact information for some of their team members. I cannot say enough good things about how DAN took so much worry away, offered a wealth of knowledge, and confirmed the direction we should take. 

We followed DAN’s advice and told Mr. G what the plan was. Mr. G told us that Dr. Douglas Ebersole was one of the guest speakers and an active diver, and he located him for us before we went to the ER. Dr. Ebersole performed a neurological assessment in the parking lot and talked to Deana about her symptoms. He concurred that she needed to be assessed at the ER, and he felt she was showing signs of lymphatic DCI; his opinion gave us peace of mind, that while her condition wasn’t critical, it should still be checked at the ER. 

After listening to Deana’s diving history over the last few years, he suggested undergoing a Transthoracic Echo (TTE) bubble study to rule out a Patent Forum Ovale (PFO), as this could explain her susceptibility to DCI. PFOs exist in almost a third of the population; although the condition isn’t rare, the condition can be activated due to the pressures exerted on our bodies at depth.

I drove Deana to the Bonaire ER, where the nursing team did a thorough assessment and showed great care, humor, and understanding. The ER nurse who took initial care of Deana was also a paramedic and technical diver and was wonderful to work with. After a full assessment, the ER doctor, who was not a diver, suggested that Deana made a poor choice in deciding to continue diving after a possible bout of skin bends. Deana later mentioned this comment to the ER nurse, adding that the doctor was not a diver and so likely didn’t understand. The ER nurse just smiled and agreed with her. 

We were then visited by one of the hyperbaric physicians, who completed Deana’s neurological exam, which showed no signs of neurological DCI. He diagnosed her with DCI of the lymphatic system and said that recompression would be necessary to treat her symptoms. He gave her a saline IV and a Table 5 treatment in the chamber.

Deana did her 2.5 hour run in the chamber and did not notice any improvement in the pain or edema. However, her doctor told us that the pain and swelling of lymphatic DCI does not go away right after a chamber ride like with other types of DCI; DAN confirmed this when they followed up with us the next morning. We were told that the edema could take a few weeks to normalize. By the next day the pain had decreased, and Deana felt she was recovering. She did not dive any more on this trip, but still had a happy, positive demeanor, and she was the life of the party: Everyone wanted to know all about her chamber ride and experience. 

Without undermining the risks associated with DCI, I want to mention the general positive outcome of this experience: we learned a great deal about Type 1 DCI, no one at our resort made Deana feel like she did something wrong, and everyone offered their support and understanding. 

In Search of a PFO

In closing, I want to offer clarity on some frequent inquiries we’ve received about this story. Some suspected that dehydration may have played a part, but as an RN, Deana had more than doubled her water intake and was always staying hydrated. While dehydration can be a contributing factor to DCI, we do not feel that it was an issue in this case. People also asked about her alcohol intake. By the time of her second DCI hit that required recompression, she had had three Coronas and one mixed drink in three days. Her alcohol consumption was not an issue.

After coming back to the United States, Deana saw Dr. James Holm, who is one of the leading hyperbaric physicians at Virginia Mason in Seattle, and was highly recommended by DAN. Dr. Holm did a follow up examination and agreed that, based on her history, dive profiles, and the lymphatic DCI experience, Deana should get a TTE bubble study to check for a PFO. Deana scheduled a TTE through Overlake Hospital’s Advanced Cardiac Imagery Department. The results revealed that she does, in fact, have a mild-to-moderate PFO.

This diagnosis was bittersweet, as it explained why Deana had frequent incidents of DCI while diving within limits, but it now puts Deana in a position to weigh the risks and determine her next course of action. Both Dr. Holms and Dr. Aviles, an interventional cardiologist who diagnosed the PFO, did not recommend rushing into a PFO repair, which they said was not a silver bullet that would guarantee a DCI-free future.

Both physicians offered several suggestions for Deana to consider: 

1. Stop diving, as this eliminates any risk of DCI in the future. For Deana this is not an option.

2. Modify her dive profile to be more conservative: diving only once per day, diving nitrox 32 but basing her profiles as if she was diving air, and/or extending her decompression profiles and safety stops.

3. Have the PFO repaired, knowing it is not a guarantee, and continue diving being as conservative as possible. 

Dr. Aviles did say that if Deana plans on continuing the frequency and type of diving she has been currently doing, getting the PFO repaired is probably her best option. These are all choices that divers who have been diagnosed with a PFO have to wrestle with, and there is no right or wrong answer. While Deana is considering her options, she will look to be more conservative with her dives. 

Like all types of higher risk sports, divers choose to accept the risk of being injured. For most divers, this is an acceptable risk, so we can enjoy the experiences we so cherish in exploring our aquatic environment. As divers we need to continually educate ourselves so we can make well-informed decisions that attempt to lower our risk of being injured. 

Deana and I highly recommend Gareth Lock’s work on human factors for understanding how our decisions play into potential diving accidents. However, even with research and advancements in technology at our disposal, we still don’t understand DCI. There is no guarantee, even if we follow all the rules, that we will not get bent unless, of course, we stop diving. It is a risk we all take when we submerge beneath the water. 

We have been amazed by the number of people we have met who discovered that they had a PFO in a way similar to Deana. Many have chosen to have their PFO corrected, though some have not, but all of them have been willing to share their experiences with us, helping us make a more informed decision. Next time you or a teammate shows any signs of DCI, tell someone and have it checked out. Sharing our experiences makes us safer, more educated divers. 

Photo by Myra Wisotzky

Additional Resources:

Gareth Lock, The Bend is Uninteresting…The Related Decisions Are Much More So


James D. Fraser is a PADI MSDT and NAUI Scuba Instructor and has been diving in the Pacific Northwest for over 30 years. James currently lives in Seattle, WA, with his wife and dive teammate Deana Fraser. Both James and Deana work at growing the local diving community and sharing their passion with all who are interested.  James recently embraced technical diving, becoming certified as a Technical 1 diver with Global Underwater Explorers. James and Deana have had opportunities to travel all over the world to experience their passion in amazing places such as Egypt and the Maldives. James currently works as a Cyber Security Director with a Fortune 500 Defense Contractor and has been a residential construction business owner as an Emergency Medical Technician (EMT). James wants to expand his knowledge in the diving field and grow his experience in technical diving.

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