O2 toxicity liklihood below pp 1.4

[IWantToBeAFish]

Hi all,

A discussion arose today over the details surrounding O2 toxicity occurrence below partial pressure of 1.4. My view is that while very unlikely (more unlikely than DCS occurrence within NDL), it is still possible. Does anyone have any good references for studies that discuss this? I'm interested just how low a partial pressure has been observed to cause toxicity.

Thanks!

Adam

 

[tphelps]

I somewhat agree that it is possible due to different physiology but also very unlikely. There is a reason why we set the pp02 for 1.4 as a conservative max and use 1.6 pp02 for tec diving. However I dont know of any studies that supports this theory. I just think that different people will react differently to the pp02.

 

[DocVikingo]

Hi Adam,

CNS ox-tox is a random occurrence whose time-to-event becomes briefer as ppO2 elevates. There is solid evidence to support your contention of inter-individual (as well as intra-individual) variability in response to a given ppO2 across time & situation. This obviously complicates matters immensely.

The exact threshold for CNS ox-tox is no doubt multifactorial and very likely includes temperature, activity level & stress exposure, but we simply have not as yet quantified all possible contributors in the individual case, and perhaps never will. For >2 decades, the Naval Safety/Special Warfare Center conducted a test of individual sensitivity to HBO2 for combat swimmer ops, but dropped it in '97 because it really wasn't doing a good job of predicting individual candidate thresholds.

I am not aware of any published research that pointedly & specifically addresses your inquiry, but there are plenty of research findings that offer general support for the quite conservative proposed ppO2s of 1.4 for rec & 1.6 for tech, and for the extremely tiny likelihood of sustaining CNS ox-tox during recreational diving where ppO2 is kept at or below 1.4.

E.g.:

- Undersea Hyperb Med. 2004 Summer; 31(2):199-202.

Incidence of oxygen toxicity during the treatment of dysbarism.

Smerz RW.

SourceHyperbaric Treatment Center, University of Hawaii, John A. Burns School of Medicine, Honolulu, Hawaii, USA.

Abstract

Oxygen (O2) toxicity may result from exposure to partial pressures of O2 above 0.6ATA. Potential toxic exposure for divers occurs during the treatment of dysbarism. In the recompression chamber, PO2 may range from 0.9ATA to 3.3ATA depending upon the treatment table employed. This retrospective study examines the nature and incidence of O2 toxicity in 998 patients who underwent recompression treatment at our facility from 1983 through 2001. Only patients evaluated for diving related injury were considered for this study. Of 1189 charts reviewed, 998 patients received recompression and were entered into this study. The total number of treatment exposures was determined as was the total number of O2 toxicity events characterized as either pulmonary or CNS, and patients were divided into male/female analysis. Overall incidence as well as the incidence for both toxicity types was determined, and their occurrence in both male and female patients was ascertained. 2166 recompressions were undertaken, 449 female and 1717 male. The peak PO2 for these treatments ranged from 2.6ATA to 2.9ATA. 155 O2 toxicity events occurred in 152 patients, 49 females and 103 males. Three patients, 2 females and 1 male, had mixed events. Incidence of an O2 toxic event = 7.0 per 100 recompressions. Incidence of pulmonary toxicity overall = 5.0 per 100 recompressions, while CNS events = 2.0 per 100 recompressions with overall seizure rate = 0.6 per 100 recompressions. In females, pulmonary toxicity rate = 6.9 per 100 recompressions, CNS toxicity rate = 4.4 per 100 recompressions with seizures occurring at 1.3 per 100 recompressions. In males, pulmonary toxicity rate = 4.6 per 100 recompressions, CNS toxicity rate = 1.4 per 100 recompressions, and seizures at 0.4 per 100 recompressions.


- Seizure incidence in 80,000 patient treatments with hyperbaric oxygen.

Yildiz S, Aktas S, Cimsit M, Ay H, Toğrol E.

Source: Gülhane Military Medical Academy, Haydarpaşa Training Hospital, Department of Underwater and Hyperbaric Medicine, 81100 Kadiköy-Istanbul, Turkey. syildiz@gata.edu.tr

Abstract

INTRODUCTION: Hyperbaric oxygen treatment (HBOT) involves some risk of central nervous system (CNS) oxygen toxicity, which may be revealed by various signs and symptoms including seizures in patients breathing O2 at pressures of 2 ATA or higher. The aim of this study was to determine the incidence of such seizures in the Underwater and Hyperbaric Medicine Departments of two university hospitals.

METHODS: We retrospectively evaluated 80,679 patient-treatments for 9 clinical indications to determine the incidence of seizures attributable to CNS O2 toxicity. Because different protocols were used for HBOT, the treatments were studied in four groups according to the chamber type used and the medical facility at which it was located.

RESULTS: Only 2 seizures were documented, yielding an incidence of 2.4 per 100,000 patient-treatments. Both cases occurred in a multiplace chamber pressurized to 2.4 ATA with O2 delivered by mask for three x 30 min with 5-min air breaks.

DISCUSSION: The seizure incidence reported here is lower than other studies published in the literature. The delivery of O2 by mask rather than hood may be a factor. Nevertheless, it appears that the risk of seizures due to CNS O2 toxicity during HBOT is very low as long as appropriate exclusion criteria and treatment profiles are used.


I, personally, have not heard of a case from out in the field (or should I say water?) of CNS ox-tox occurring at a ppO2 of <2.

Hope this proves useful.

Regards,

DocVikingo

 

[Saturation]

You can check archives from SB and TDS regarding these discussions from the early 2000s, there are studies, my pen name is linked to most of those freely available discussions. I've also archived the accidents on divingaccidents at yahoogroups.

I commented and discussed with DAN that the values often taught are not conservative or universal, even from their old reports dated from the mid-1990s. In summary, the P02 limit should be 1.3 for nitrox as backgas, Trimix at 1.2, this is based IIRC on Arieli study on Israeli RB divers and is supported by earlier observations by Vann et.al. from the 1990s.

Above those limits, I've had 3-4 personal experience with caring for survived CNS oxtox aka seizures in water, and 1 fatality regarding exceeding those limits. Full blow oxtox or close calls were not uncommon for technical divers, for those who pushed the limits up to the early 2000s, all I've assisted were on OC, not RB.

CNS toxicity in closed-circuit oxyge... [Aviat Space Environ Med. 2006] - PubMed - NCBI

 

[TSandM]

It is extremely unlikely that oxygen toxicity is a discontinuous function. In other words, it is highly likely that whatever processes eventually lead to seizures are occurring at all levels of increased ppO2, but that the cumulative damage that results in seizures doesn't occur until the ppO2 reaches certain values.

I know there is a recent documented fatality from seizure in a cave diver who spent some time at 1.4. I believe (have read, but have not independently researched) that there are no reported fatalities below 1.4.

 

[Akimbo]

I find it strange that [-]confusion[/-] convulsion is the only symptom widely discussed by recreational divers. Granted, that is one that is totally unmistakable, but most of the others are far more common and often precede convulsions &#8212; especially nausea, twitching, and visual disturbances.

http://www.scubaboard.com/forums/ma...y/440726-oxygen-toxicity-limits-symptoms.html

 

[lamont]

Chief Justice Roberts has had two seizures breathing a ppO2 of 0.21: http://www.nytimes.com/2007/08/01/health/01seizure.html?_r=0

Just pointing out that on a long enough timeline and with enough dives you'll wind up with a certain baseline of seizures occurring in water, no matter what the ppO2 limit is set to.

 

[boulderjohn]

I find it strange that [-]confusion[/-] convulsion is the only symptom widely discussed by recreational divers. Granted, that is one that is totally unmistakable, but most of the others are far more common and often precede convulsions &#8212; especially nausea, twitching, and visual disturbances.

http://www.scubaboard.com/forums/ma...y/440726-oxygen-toxicity-limits-symptoms.html

When I was first certified for nitrox, the VENTID acronym was heavily emphasized. The newest materials do not have nearly as much emphasis upon this, even in Advanced Nitrox materials. My understanding of this is a growing belief that these warning signs are either not as common as once thought, are easily missed, or provide too little warning before the onset of convulsions to be of great value. I do not have a firm conviction in what I just wrote--I am just reporting the way the thinking seems to be going as I see it.

 

[Akimbo]

&#8230; My understanding of this is a growing belief that these warning signs are either not as common as once thought, are easily missed, or provide too little warning before the onset of convulsions to be of great value. I do not have a firm conviction in what I just wrote--I am just reporting the way the thinking seems to be going as I see it.

That is the exact opposite of what I have experienced in the commercial diving arena. We routinely ran O2 at 1.8 to 2.0 ATA in the water (umbilical for gas & communications to a hat or FFM) and 2.8 in the chamber. I have never seen or spoken with a diving supervisor who had a confirmed OxTox hit on the job. However, divers O2 levels were quickly reduced at the least hint of a symptom &#8212; switch gases and tell the diver to purge their umbilical or just remove the O2 mask in the chamber.

About the only symptom we cut a lot of slack on was Irritability, accompanied by foul language&#8230; who could detect the difference???

 

[eponym]

A discussion arose today over the details surrounding O2 toxicity occurrence below partial pressure of 1.4. My view is that while very unlikely (more unlikely than DCS occurrence within NDL), it is still possible. Does anyone have any good references for studies that discuss this? I'm interested just how low a partial pressure has been observed to cause toxicity.

I can't cite any studies. But I have recent EAN training materials which state that "the threshold for CNS oxygen toxicity appears to be 1.1 atmospheres [of inspired Oxygen]." No citations are provided.

This is in concert with other factors, especially exertion. Carbon dioxide is a vasodilator and may lower your ox-tox threshold by increasing perfusion of neural tissues.