by Doug Ebersole M.D.
Header image courtesy of Virginie Papadopoulou. Remaining images courtesy of Doug Ebersole.
Patent foramen ovale (PFO) is an important topic in diving as the appreciation of its relationship to decompression illness (DCI) grows within the community. More than 1200 scuba divers from around the world are affected each year by DCI. Although the incidence of DCI is relatively low, ranging from about 1 episode per 10,000 dives (0.01% per dive) to about 10 episodes per 10,000 dives (0.1% per dive), depending on the nature of the dive, the presence of a PFO is felt to increase the risk five to 13-fold (1, 2, 3). As a result, an understanding of the link between PFO and DCI, as well as various treatment options, is vitally important to divers, and the health professionals who treat them.
Incidence and Anatomy
A PFO is an integral part of the normal fetal circulation. Normally, a portion of the blood from the inferior vena cava passes from the right atrium to the left atrium through the PFO during fetal life, bypassing the lungs. At birth, pulmonary blood flow increases greatly, increasing left atrial pressure. The resulting atrial pressure differences compress the septum primum against the septum secundum, functionally closing the PFO. Anatomic closure of the PFO occurs later in infancy in most people but is incomplete in approximately 25% of the population (4, 5), leaving these individuals at risk for right to left shunting.
PFO diameters are quite variable in size ranging from 1-19 mm/0.04-0.75 in, with the average size being larger in older adults (4), suggesting PFOs may continue to enlarge during life. The cause of this is unknown, but in part may be due to known elevations in right heart pressures with aging causing the pressure difference between the left atrium and right atrium (which keeps the PFO closed) to lessen. This may result in “larger” PFOs in older adults.
The Relationship of PFO to DCI
In 1986, it was first suggested by Wilmhurst and colleagues that a cardiac right to left shunt may be important for a paradoxical gas embolism in scuba divers (6). Subsequently, the importance of PFO for DCI in divers has been further investigated (1,7, 8, 9). As mentioned above, the risk of DCI in sport divers is quite low but is increased by at least five-fold in the presence of a PFO (1, 2, 3). Additionally, the average number of ischemic brain lesions as seen on MRI in experienced divers with PFO has been reported to be twice as high as in divers without PFO (11). The etiology and clinical significance of these findings are unclear but may represent multiple subclinical paradoxical embolic events across the PFO.
Both transthoracic echo (TTE), a cardiac ultrasound performed from the chest wall, and transesophageal echo (TEE), a cardiac ultrasound performed from the esophagus, have been used for the diagnosis and assessment of PFO. TTE is considered the preferred diagnostic test of choice as it is noninvasive. However, given its better visualization of the atrial septum, TEE, while more invasive, is much more accurate than TTE and can be used if, despite a negative TTE, there is still a high index of suspicion that the patient has a PFO.
Including a “bubble study” with the echocardiogram, either TTE or TEE, will increase the likelihood of diagnosing a PFO if it is present. This is done by connecting two syringes of saline with a small amount of air with a stopcock and then “swishing” the two syringes back and forth to “agitate” the saline, making small “microbubbles” that will be seen on ultrasound imaging. Visualization of microbubbles passing from the right to left atrium through the visualized foramen ovale is diagnostic of a PFO. In clinical practice, the actual site of right-to-left shunting may not be convincingly visualized or recorded for technical reasons. If the echo demonstrates microbubbles appearing in the left atrium immediately after arriving in the right atrium, then the presence of a PFO can be presumed. If bubbles appear in the left atrium more than five beats after they appear in the right atrium, then the possibility of shunting from another cardiac source (such as an anomalous pulmonary vein) or from a pulmonary source (such as a pulmonary arteriovenous malformations) must be considered.
Of note, while the injection of “agitated saline” is routinely done via an arm vein due to convenience, it has been shown that using a femoral vein in the leg is more accurate (12-13).
No specific guidelines exist for PFO closure in people who have decompression illness, but the options are to stop scuba diving, decrease the depth and/or time of dives to limit the inert gas load, or undergo percutaneous PFO closure. Some divers decide that they have many other interests and diving is not that important to them. These divers will frequently give up the sport.
Other divers who enjoy the sport but dive infrequently often opt for diving “conservatively” to limit their bubble-load. This might involve no-decompression diving, limiting depths to less than 30m/100ft, diving nitrox on air profiles, making prolonged safety stops (greater than the recommended 3-5 min) at approximately 4-6m/15-20 ft at the end of their dives, and limiting the number of dives per day to one or two. Tech divers could also opt to dive more conservatively depending on their risk tolerance.
People who make their living through scuba diving—instructors and divemasters, for example—and tech divers who enjoy more aggressive types of diving such as deep wrecks, cave diving, rebreather diving, and mixed gas diving often elect percutaneous closure of the PFO. This also holds true for divers who have had recurrent “unexpected” DCI events despite diving conservatively as defined above.
The types of decompression illness that appear to be associated with PFO include cerebral (stroke-like symptoms), spinal (paralysis or urinary retention), cutaneous (skin bends), and inner ear (vertigo). DCI manifested by joint pain is felt NOT to be associated and, therefore, should not prompt evaluation for PFO.
A recent study reported the results of conservative diving practices after an episode of DCI (14). Eighteen divers in this study had a right-to-left shunt, nine were small and nine were large. Mean follow-up was 5.3 years (range 0-11 years). Four of these divers had undergone PFO closure and had no episodes of DCI in follow-up. The absolute risk of suffering DCI before examination for the remaining 14 divers with right-to-left shunt and no closure was 23.5 DCI events per 10,000 dives for those with a small shunt compared to 71.6 events/10,000 for those with a large shunt.
After following the recommendations for conservative diving practices, the DCI risk at follow-up fell to 6.0 per 10,000 dives in the small shunt group and zero in divers with the large shunt. The major limitation to this study is its small sample size, but the results suggest a need for more studies of conservative diving practices for divers with right to left shunts.
When DCI has occurred, especially after so called “undeserved” cases of DCI, divers are often encouraged to seek screening for a shunt and some diving medical societies classify these divers as ineligible to return to diving (15). There are also several diving medical specialists who recommend that divers with a history of DCI and a positive right-to-left shunt, undergo closure if it turned out to be a PFO, even though there is no clear evidence to indicate that this intervention reduces the risk of DCI or neurologic events (16-19).
However, in a 2011 study of 83 scuba divers with a history of DCI and a follow-up of 5.3 years, 28 divers had no PFO, 25 had a PFO closure, and 30 continued diving with a PFO without closure (20). At the beginning of the study, there were no significant differences between the groups in the number of dives, dive profiles, diving depth, or cumulative dives to more than 40 meters of salt water (msw).
After follow-up, while there were no differences between the groups with respect to minor DCI events, the risk for major DCI was significantly higher in the divers with PFO and no closure than in divers with PFO and closure or divers without PFO. Although this offers new evidence that PFO closure reduces the risk for major DCI, the authors do not recommend closure in all divers with a history of DCI but rather recommend further studies to confirm these results.
A recent Divers Alert Network (DAN) funded study from our institution (21) also suggested selected divers with recurrent decompression illness may benefit from PFO closure. Seventy-seven patients with recurrent decompression illness and documented patent foramen ovale were enrolled. Please note this was not a randomized trial. Patients themselves decided whether to have PFO closure or to dive conservatively after the PFO diagnosis was made. This obviously imparts some bias into the trial. Fifteen patients were excluded for various reasons, leaving 62 patients who were followed prospectively for 5-6 years.
The baseline demographics which included age, gender, years diving, total number of dives, and number of dives per year were very similar in the two groups as was the number of divers who stopped diving or dived less after suffering decompression illness. A greater proportion of divers in the “PFO Closure” group had “large” PFOs. The follow up in the PFO closure group was six years and in the Conservative group was 5.5 years.
The 42 subjects in the PFO closure group had an incidence of decompression illness of 12.9 episodes per 10,000 dives prior to PFO closure and then had a statistically significant (p<0.05) reduction to 2.7 episodes per 10,000 dives after PFO closure. The 20 participants in the Conservative group had an incidence of decompression illness of 13.4 episodes per 10,000 dives. After 5.5 years of diving conservatively without PFO closure, the incidence of decompression sickness was 3.4 episodes per 10,000 dives, but this did not meet statistical significance given the small number of subjects.
Percutaneous PFO Closure
The closure procedure for a patent foramen ovale is relatively painless and is done nonsurgically using a needle stick into a femoral vein. Imaging during the procedure is done with a combination of fluoroscopy and ultrasound imaging, either TEE or intracardiac echo. The most common device in use in the United States is the Amplatzer PFO Occluder [see photo above]. This is a wire mesh made out of nickel and a titanium alloy. The device is filled with securely sewn polyester fabric to help close the defect. It is deployed through a small catheter which has been placed across the PFO. The procedure takes about an hour and patients are usually discharged home the same day or the following morning.
Conclusions and Recommendations
The South Pacific Underwater Medicine Society (SPUMS), the United Kingdom Sports Diving Medical Committee (UKSDMC), and the Undersea and Hyperbaric Medical Society (UHMS) have all weighed in with formal recommendations on patent foramen ovale and decompression illness. Their recommendations are:
- A routine screening for PFO at time of dive medical fitness assessment is not necessary
- Consideration of investigating for PFO should be for divers with:
- History of DCI with cerebral, spinal, cutaneous or inner ear symptoms
- Current or past history of migraine with aura
- History of cryptogenic stroke
- History of PFO or ASD in first-degree relative
- If screening is performed:
- It should be performed in centers well practiced in the procedure
- Transthoracic echo (TTE) with agitated saline is the preferred first test
- Provocative maneuvers (Valsalva, sniff) should be performed
- In the case of positive tests: A large shunt or unprovoked shunt is associated with certain forms of DCI (cerebral, spinal, inner ear, and cutaneous). Small shunts are associated with a lower but poorly defined risk of DCI
- If a PFO is demonstrated, options include:
- Stop diving
- Dive more conservatively
- Close the PFO
- The diver should not return to diving after PFO closure until satisfactory closure has been confirmed
My final thoughts:
Should all divers be screened for a PFO?
No. There is approximately a five-fold increased relative-risk of DCI in patients with PFO, but the absolute risk is still quite small
Should all divers with DCI be screened for a PFO?
No. Twenty-five percent of the population has a PFO so one would expect a similar percentage of divers with DCI to have a PFO. Not all scuba dives have the same risk of DCI. To paraphrase James Carville’s famous quote from the first Clinton presidential campaign, “It’s the bubbles, stupid”. The issue with decompression sickness is the inert gas “bubble load”, not the PFO. However, episodes of DCI in “low-risk” dives (especially neurologic, inner ear, or “skin bends” events) or multiple “undeserved” DCI events should prompt investigation for PFO.
Should all divers with DCI and PFO have a PFO closure?
No. Options for divers with PFO and DCI include discontinuing diving, instituting more conservative diving practices, or PFO closure. Recommendations should be made on a case-by-case basis based on the DCI event(s), the type of diving being performed by the diver involved, and the risks of PFO closure.
What does the header image (above) depict?
It is an image of a heart with a PFO. Clinical bubbles were injected in the vein of the person for diagnosing the PFO, you can see that they completely fill the venous chambers (left side of the image), and because there is a PFO a few bubbles can also be seen in the arterial chambers (pointed out by the white arrows – there’s likely a lot more, if you notice the bottom of the right side is brighter compared to the rest of those chambers and that’s actually because some tiny bubbles are crossing through). Note, the “clinical bubbles” I refer to, are agitated saline contrast which are large enough that they are filtered by the lungs and don’t appear in the arterial chambers unless there is a PFO.—V. Papadopoulou
- Wilmshurst, PT, Byrne JC, Webb-Peploe MM. Relation between interatrial shunts and decompression sickness in divers. Lancet. 1989;334:1302-1306.
- Torti SR, Billinger M, Schwerzmann M. Risk of decompression illness among 230 divers in relation to the presence and size of patent foramen ovale. Eur Heart J 2004;25:1014-1020.
- Bove AA. Risk of decompression sickness with patent foramen ovale. Undersea Hyperb Med 1998;25:175-8.
- Hagan PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc 1984;59:17-20.
- Kerut EK, Norfleet WT, Plotnick GD, Giles TD. Patent foramen ovale: a review of associated conditions and the impact of physiological size. J Am Coll Cardiol 2001;38 (3): 613-623.
- Wilmhurst PK, Ellis BG, Jenkins BS. Paradoxical gas embolism in a scuba diver with an atrial septal defect. Br Med J (Clin Res Ed) 1986;293:1277.
- Moon RE, Camporesi EM, Kisslo JA. Patent foramen ovale and decompression sickness in divers. Lancet 1989;1:513-14.
- Germonpre P, Dendale P, Unger P, et al. Patent foramen ovale and decompression sickness in sport divers. J Appl Physiol 1998;84:1622-6.
- Germonpre P, Hastir F, Dendale P, et al. Evidence for increasing patency of the patent foramen ovale in divers. Am J Cardiol 2005;95;912-15.
- Gempp E, Blattearu J, Stephant E, et al. Relation between right-to-left shunts and spinal cord decompression sickness in divers. Int J Sports Med 2009;30:150-3.
- Schwerzmann M, Seiler C, LippE, et al. Relation between directly detected patent foramen ovale and ischemic brain lesions in sport divers. Ann Intern Med 2001:134:21-4.
- Schuchlenz HW, Weihs W, Hackl E, Rehak P. A large Eustachian valve is a confounder of contrast but not of color Doppler transesophageal echocardiography in detecting a right-to-left shunt across a patent foramen ovale. Int J Cardiol 2006;109:375-80.
- Gin KG, Huckell VF, Pollick C. Femoral vein delivery of contrast medium enhances transthoracic echocardiographic detection of patent foramen ovale. J Am Coll Cardiol 1993;22:1994-2000.
- Klingmann, C, Rathmann N, Hausmann D, et al. Lower risk of decompression sickness after recommendation of conservative decompression practices in divers with and without vascular right-to-left shunt. Diving and Hyperbaric Medicine 2012;42(3):146-150.
- [Swiss Underwater and Hyperbaric Medical Society. Empfehlungen 2007. Der Schwiezerischen Gesellschaft Fur Unterwasser-und Hyperbarmedizin Zum Tauchen Mit Einem Offenen Foramen Ovale][cited 2012 June11]. Available from: http://www.suhms.org/downloads/SUHMS%20PFO%20Flyer%20d.pdf(German)
- Scott P, Wilson N, Veldtman G. Fracture of a GORE HELEX septal occluder following PFO closure in a diver. Catheter Cardiovasc Interv 2009;73:828-31.
- Wahl A, Praz F, Stinimann J, Windecker S, Seiler C, Nedeltchev K, et al. Safety and feasibility of percutaneous closure of patent foramen ovale without intra-procedural echocardiography in 825 patients. Swiss Med Wkly. 2008:138:567-72.
- Saguner AM, Wahl A, Praz F, et al. Figulla PFO occluder versus Amplatzer PFO occluder for percutaneous closure of patent foramen ovale. Catheter Cardiovasc Interv 2011;77:709-14.
- Furlan AJ, Reisman M, Massaro J, et al. Closure or medical therapy for cryptogenic stroke with patent foramen ovale. N Engl J Med. 2012;366:991-9.
- Billinger M, Zbinden R, Mordasini R, et al. Patent foramen ovale closure in recreational divers: effect on decompression illness and ischaemic brain lesions during long-term follow-up. Heart. 2011;97:1932-7.
- Anderson G, Ebersole D, Covington D, Denoble PJ. The effectiveness of risk mitigation interventions in divers with persistent (patent) foramen ovale. Diving Hyperb Med 2019 Jun 30;49(2):80-8
InDepth: No Fault DCI? The Story of My Wife’s PFO (12.2019)
InDepth: Undergoing PFO Surgery as a Team: Deana & Bert’s Excellent Adventure (12.2020)
InDepth: Uncovering the Link Between PFO and Inner Ear DCS (5.2019)
European Heart Journal: European position paper on the management of patients with patent foramen ovale. Part II – Decompression sickness, migraine, arterial deoxygenation syndromes and select high-risk clinical conditions (JAN 2021)
Dr. Douglas Ebersole, MD is a cardiologist specializing in coronary and structural heart interventions at the Watson Clinic LLP in Lakeland, Florida. He is also an avid technical, cave, and rebreather diver and instructor. He can be reached at firstname.lastname@example.org.
Is Oxygen Narcosis A Thing?
There’s been a long running debate as to whether oxygen is a narcotic diving gas. Agencies like CMAS, GUE, PADI and PSAI include O2 in their equivalent narcotic depth (END) calculations. Others like BSAC, IANTD and TDI do not. The problem has been reliably measuring gas narcosis. Enter medical researcher and tech instructor Xavier Vrijdag, who has developed a novel EEG algorithm that can detect the subtle effects of gas narcosis on the brain. His results promise to lead to a deeper understanding of gas narcosis. Hint: Nitrox divers can breathe easy; it’s less narcotic than air!
By Xavier Vrijdag PhD. Header image: Drs. Vrijdag and Hanna van Wart preparing participant in front of the hyperbaric chamber. The EEG electrodes are placed inside the cap and two more electrodes are placed under the eyes. Photo by Payal Razdan.
🎶🎶 Predive Clicklist: Love Is Like Oxygen by Sweet (1978)
🎶 Love is Like Oxygen,
You get too much, you get too high,
Not enough and you’re gonna die.
Love gets you high 🎶
To sustain life, every breathing gas mixture for divers must include oxygen. As we descend, invariably, we will breathe oxygen at higher partial pressures than air at the surface. Oxygen is mixed with other gasses, like nitrogen and helium, to create suitable mixes for specific depths. One of the boundaries of going deeper is the experience of gas narcosis.
The effects of gas narcosis increase with a diver’s depth because the ambient pressure and the partial pressure of the individual gasses in the breathing mix increase. Gas narcosis has traditionally been linked to nitrogen when breathing air. Narcosis causes behavioral changes and impaired cognitive abilities. Substituting helium wholly or partly for nitrogen ameliorates the narcosis effects. Similarly, it has been argued that replacing some nitrogen with oxygen reduces a gas mixture’s narcotic potency.
One tool to quantify gas narcosis in different breathing mixtures is equivalent narcotic depth (END). In this method, the narcotic effect of a certain breathing gas mixture, like trimix, is compared to breathing air. With the partial pressures for oxygen, nitrogen, and helium in the gas mixture and the intended dive depth, one can calculate the depth at which air would produce a similar narcotic effect. A long-standing debate within the dive industry is whether oxygen should be included in the ‘is narcotic’ or ‘is not narcotic’ portion of this calculation (See: Calculated Confusion: Can O2 Get You High? by Reilly Fogarty)
One of the most used approximations of the narcotic potency of gasses is the Meyer-Overton correlation. The Meyer-Overton correlation describes a relationship between the narcotic potency of a gas and its solubility in oil; the more soluble, the more narcotic. Oxygen has a higher solubility in oil than nitrogen. Therefore one could argue it is more narcotic than nitrogen. However, oxygen is special since we metabolize it.
Nitrogen is a non-metabolic gas, meaning that the inhaled partial pressure of nitrogen equilibrates with the partial pressure of nitrogen in brain tissue after a short wash-in period. In contrast, oxygen is metabolically consumed, thus lowering the partial pressure of oxygen considerably below the inspired pressure. Therefore, despite its greater solubility in oil, one could argue it might be less narcotic than nitrogen.
In addition, exceptions to the Meyer-Overton correlation exist; some gases that are very soluble in oil should be highly narcotic but turn out not to be. In anesthetic research, we have since learned that for a gas to be narcotic, its molecule needs to be able to bind to receptors on the neurons to cause its narcotic effect. Certain molecules have a shape that does not allow them to bind to these receptors. For oxygen, it is unknown if and how it binds to neuronal receptors. The point here is that just because oxygen is more oil-soluble than nitrogen, that does not automatically mean it is more narcotic than nitrogen.
Measuring the cognitive effects of nitrogen narcosis is most often done with psychometric tests, like math questions, motor tasks or memory queries. Each of these skills is affected at different partial pressures of nitrogen and is impaired at different depths breathing air. The book, Psychological and Behavioral Aspects of Diving by Nevo and Breitstein summarizes the scientific literature quite well. Higher cognitive functions, like reasoning and memory are impaired in the shallow range (~ 5% at 3 ATA (20 m/66 ft), 30% at 6 ATA (50m/164 ft)).
In contrast, more basic skills like gross motor tasks are only impaired at far higher pressure. Quantification of the subtle effects of inert gas narcosis is challenging. Psychometric tests can be affected by learning effects, participant motivation or boredom. Objective neurophysiological measurements like the critical flicker fusion frequency (CFFF) and quantitative electroencephalogram (qEEG) analysis could, in principle, be used to overcome these issues.
During the CFFF test, the participant looks at a small light oscillating rapidly on and off (flickering). The fusion frequency is obtained by increasing the flicker frequency until the participant perceives a change from flicker to fusion (no further flickering) or the other way around. An increase in CFFF equates to an increase in alertness, whereas a decrease in CFFF is associated with a decrease in alertness, for instance, caused by gas narcosis. Some studies have shown a decrease in CFFF during air-breathing dives at 4 ATA.
Hyperbaric inert gas narcosis is generally considered a manifestation of depressed brain activity when measured with EEG at large depths. Continuous measurement of the EEG results in a considerable amount of data, and analysis is usually performed afterward. This requires much training and time. qEEG has the potential for real-time analysis of the continuous EEG, giving the user an easy-to-interpret result about the narcotic effect. The subtle changes of gas narcosis at typical sport diving depths would otherwise be hard to detect in the EEG. Such analyses would allow comparison between divers and successive dives.
Measuring hyperbaric oxygen and nitrogen’s comparative effects on the brain is difficult. Ideally, the comparison should occur at equivalent inspired pressures of the two gasses. However, nitrogen narcosis symptoms typically present at depths greater than 30m/100 ft (4 ATA); a pressure at which oxygen-breathing would carry the risk of cerebral oxygen toxicity. A pressure of 18 m/60 ft (2.8 ATA) is considered the maximum safe inspired oxygen pressure in hyperbaric oxygen treatments with resting patients in a dry hyperbaric chamber. [WARNING: A PO2 of 2.8 ATA is incompatible with diving!] It follows that the measurement method to detect gas narcosis needs to be sensitive enough to catch the subtle effects of gas narcosis in the more limited and safe inspired pressure range of oxygen.
In a research program funded by the US Navy Office of Naval Research, I studied the subtle narcotic effects of nitrogen and oxygen together with Dr. Hanna van Waart, Professor Jamie Sleigh, and Professor Simon Mitchell.
Measuring The Subtle Effects Of Nitrogen Narcosis
In the nitrogen narcosis study, twelve technical divers breathed air and 21% / 79% oxygen-helium (‘heliox’) at 18 m/60 ft and 50 m/164 ft (2.8 and 6 ATA, respectively) inside a hyperbaric chamber while we recorded the electrical signals of the brain (EEG), performance on a mathematics test and the CFFF. Breathing air at 50m/164 ft (6 ATA) is typically cited as causing sleepiness, euphoria, overconfidence, idea fixation, and impaired reasoning, memory, calculus, and judgment. However, these symptoms may be alleviated by enhanced concentration in motivated divers.
The CFFF did not change during the air-breathing hyperbaric exposure to 6 ATA compared to surface recordings. Hence, the CFFF did not detect the nitrogen narcosis effect at this depth. We also reviewed the CFFF diving literature and found a complicated and often contradictory picture. Various studies during air breathing conducted at 4 ATA have suggested that nitrogen narcosis is the cause of a reduction in CFFF at this depth. However, this result does not extrapolate to greater depth, even though it is known that cognitive performance is further reduced with increased depth. Several studies—including our experiments—performed at 6 ATA while breathing air did not show impairment, but instead showed either no change or an increase in CFFF. Hence, in our study, CFFF failed to detect or quantify a narcotic effect known to be present at 6 ATA.
On the contrary, we successfully developed a quantitative EEG metric to measure narcosis produced by nitrogen at hyperbaric pressures. The functional connectivity metric is based on the so-called mutual information analysis, and was summarized using the global efficiency network measure. Mutual information measures the information that is similar between two signals, calculated between all EEG channels. Higher mutual information means that the signals are more alike.
Global efficiency measures how well connected a network of channels is. High global efficiency based on mutual information means that more signals are similar. Normal cognitive function requires regional specificity, which might be lost (that is, signals become more similar) during impairment.
The novel EEG method successfully differentiated between breathing air at the surface and air at 50m/164 ft (6 ATA) with a 35% increase in the functional connectivity metric. To our surprise, we could even detect a trend of a 19% increase at the much lower pressure of 18 m/60 ft (2.8 ATA). This indicates a dose-response between EEG functional connectivity and nitrogen narcosis. No significant change in the metric was found during the hyperbaric heliox exposures, which was expected because helium is known to be a non-narcotic gas. This lack of an effect of heliox confirmed that nitrogen exposure and not the environmental pressure change was responsible for the changes we saw in EEG functional connectivity.
Another implication of the increased functional connectivity metric during air breathing at 18 m/60 ft (2.8 ATA) is that it should be sensitive enough to measure the narcotic effects of oxygen at 18m/60 ft inside a hyperbaric chamber, if such effects exist. As stated above, we can safely breathe oxygen at 18 m/60 ft inside the safety of a hyperbaric chamber, where there is no risk of drowning, compared to being submerged. If oxygen were to have similar narcotic effects as nitrogen, we expect that functional connectivity would change in a similar way during oxygen exposure as it did in the air-breathing experiment at 18 m/60 ft.
Measuring Oxygen Narcosis
In the oxygen narcosis study, twelve technical divers breathed 100% oxygen at the surface, 4 m/13 ft and 18 m/60 ft (1, 1.4, and 2.8 ATA, respectively) inside a hyperbaric chamber while we recorded the EEG. Four meters/13 ft (1.4 ATA) was chosen as it approximates the upper limit of oxygen exposures accepted in diving, while 18m/60 ft (2.8 ATA) is the maximum exposure to oxygen inside a hyperbaric chamber with a minimal risk of oxygen toxicity.
The EEG functional connectivity metric did not increase while breathing hyperbaric oxygen. This contrasts with the 19% increase we reported above in participants breathing air at 18m/60 ft (2.8 ATA). This suggests that oxygen is not producing the same changes in brain electrical activity seen during hyperbaric air breathing.
It is only now, with the development of this novel EEG analysis algorithm, that we have been able to investigate the subtle effects of hyperbaric oxygen in more detail, and based on our results we hypothesize that oxygen probably does not bind to the same neuronal receptors and hence does not cause similar narcotic effects to those induced by nitrogen. For nitrox divers, this probably means that the increased oxygen slightly reduces the narcotic potency of the breathing gas.
OzTek presentation: Measuring gas narcosis in divers
British Journal of Sports Medicine: Towards gas narcosis monitoring in compressed gas diving (PhD Academy Award). (2022)
Scientific Reports: EEG functional connectivity is sensitive for nitrogen narcosis at 608 kPa. (2022)
Physiological Reports: Does hyperbaric oxygen cause narcosis or hyperexcitability? A quantitative EEG analysis. (2022)
Diving and Hyperbaric Medicine Journal: Investigating critical flicker fusion frequency for monitoring gas narcosis in divers. (2020)
InDEPTH: Calculated Confusion: Can O2 Get You High? by Reilly Fogarty (2019)
Alert Diver.Eu: Rapture of the Tech: Depth, Narcosis and Training Agencies by Michael Menduno (2020)
Alert Diver.Eu: Measuring Inert Gas Narcosis by Michael Menduno (2020)
Xavier Vrijdag is a diving medical researcher at the University of Auckland investigating the effects of gas narcosis in divers on the brain. He has a master’s degree in Technical Medicine for the University of Twente, the Netherlands, where he developed an algorithm to quantify cerebral arterial gas embolism in the hyperbaric environment. In 2022, he completed his doctoral thesis on the effects of nitrogen, oxygen, helium and carbon dioxide under pressure.
Xavier has worked as a researcher and technical physician at the department of Diving and Hyperbaric Medicine of the Academic Medical Centre, Amsterdam, the Netherlands. Before coming to New Zealand, he worked as a hyperbaric technician and researcher at Deep Dive Dubai. He is an instructor for medical courses of DAN Europe, holds certifications from seven training agencies, and is an SSI divemaster instructor, normoxic trimix instructor, cave instructor and freediving level 2 instructor, and is a GUE fundamentals instructor.
Besides work, Xavier is an avid cave and wreck diver and photographer, as well as being part of a CaveSAR/LandSAR cave rescue team in New Zealand.