04/07/2024
I have seen a few posts regarding the underwater effects of oxygen toxicity and the recent cave diving incident. I will not enter into discussing this tragic event because it is too early, and it would be disrespectful to the individuals involved and their families and friends. Nevertheless, I would like to post some information about oxygen toxicity with the aim of answering some questions that divers may have on this topic. If you have any further questions, please get in touch with me through my webpage, divingsafe.com
While oxygen is vital for our survival, when breathed under pressure, it may cause inflammation and potential damage to our tissues, adversely affecting the CNS.
The so-called “Bert effect” impacts the Central Nervous System. It is named after Paul Bert, the French physiologist of the 19th century, who was credited for the first studies on DCS. Usually, CNS toxicity develops at ambient pressure above 3 ata, but if the exposure is prolonged, it may happen even at lower pressure. Exposure to high-pressure O2 causes various neurological symptoms, including blurred/tunnel vision, tinnitus, and twitching. Convulsions of tonic-clonic type are often associated with CNS oxygen toxicity. Other factors, including high partial pressure of CO2 in the breathing medium, fatigue, cold, reduced visual input, dark environmental conditions, and stress, may facilitate the onset of CNS toxicity.
NOAA has developed tables and algorithms to identify time limits for oxygen exposure based on the PO2. In the NOAA tables, the maximum acceptable PO2 is 1.6 ata with an associated maximum exposure time of 45 minutes. If more than one dive (in a 24-hour interval) has reached or exceeded the limits of a single exposure, then a minimum surface time of 2 hours is required before any further dive. Spending at least 12 hours at normoxic level will reset the series. The suggested limits are for light activity; a more conservative approach is needed in case of heavy work and stressful conditions.
In general, CNS toxicity causes no residual neurological damage once the PO2 has been reduced; however, if the exposure to high-pressure oxygen continues beyond the point of seizure, then irreversible neurological damage and death may occur, following what is called the “John Bean effect.”
CNS toxicity is a severe risk and requires careful assessment. The critical factor for its mitigation is to respect the maximum operative depth (MOD) based on limiting PO2 to 1.6 ata or, even more conservatively, to 1.4 ata. Nitrox divers can reach such limits at relatively moderate depths if breathing highly enriched mixtures; therefore, they should be very careful in monitoring their depth. Mixed gas divers who use high-oxygen mixes for decompression should ensure that the gas switch to such mixtures is done at the correct depth and well within the relative MOD.
Smith effect: This effect impacts the lungs, causing pulmonary toxicity. It is named after J. Lorain Smith, who, in 1899, while studying the Bert effect in rats, noted fatal pneumonia after four days of exposure to 73% O2 at 1 ata, with the first symptoms developing after about 10 hours. This effect is usually not a primary risk for scuba divers, requiring extremely long exposure for the lungs to be severely compromised. However, the effect can be relevant during hyperbaric treatments.
