Artículo sobre incidentes de hiperoxia a ppO2 1,6 o menores

[AndresPP]

Viene a decir que para ppO2 menores que 1,6, los ataques hiperóxicos son escasos y están muy relacionados con el nivel de CO2 en el circuito, así que hay que tener cuidado con agotar la capacidad del filtro y con los sobreesfuerzos puntuales:

https://www.shearwater.com/community/ox ... es-at-po2/


Oxygen Seizures at PO2 ≤ 1.6 Bar: How Rare?


Central nervous system (CNS) oxygen toxicity literally means the poisoning of the brain by too much oxygen. CNS oxygen toxicity is very scary, particularly in the water, where any of the signs or symptoms poses a risk. The U.S. Navy Dive Manual1 uses the mnemonic V.E.N.T.I.D.C. for symptoms and signs:



Conventional wisdom is that CNS oxygen toxicity does not occur unless oxygen partial pressure (PO2) exceeds 1.6 bar, but there is a handful of reports of in-water CNS seizures in the “safe” range of PO2.2, 3 Perhaps it isn’t an all-or-nothing limit… Let’s look at accumulated evidence from mildly hyperoxic (PO2 ≤ 1.6 bar) controlled and monitored dives.

No studies directed at CNS oxygen toxicity have been performed since 1993, but mildly hyperoxic experimental exposures with records of CNS oxygen toxicity outcomes have been conducted for other purposes. A review published in 20134 lists the following: CNS oxygen toxicity studies with rapid changes from one known PO2 to another between 1970 and 1993 included 210 dives with change from surface air to elevated PO2 that was less than or equal to 1.6 bar. Dives primarily to investigate pulmonary (lung) oxygen toxicity before 2013 provided a further 929 experimental dives with PO2 ≤ 1.4 bar and 34 dives with PO2 = 1.6 bar. Dives conducted for the development of rebreather decompression tables numbered 2435, mostly at PO2 = 1.3 to 1.6 bar, but with transients to PO2 > 1.7 bar during descent. For these post-1993 dives, carbon dioxide (CO2) in the inspiratory gas was negligible.

The 210 dives for study of CNS oxygen toxicity included 5 dive-stopping incidents that were probably but not definitely CNS oxygen toxicity, and 2 probable CNS incidents that did not cause the divers to surface early. The other 963 square-profile dives had 1 dive-stopping probable CNS event and 7 sets of symptoms that probably indicated CNS oxygen toxicity, but no definite CNS symptoms. The decompression dives had no CNS-type events despite the PO2 overshoots on descent. In other words, in dives like the experimental ones, oxygen toxicity seizures have not occurred -- the upper bound on the probability is less than 9 in 10,000 -- and other symptoms that are probably CNS oxygen toxicity are rare. In 2013 the U.S. Navy Safety Center had records of almost 29,000 uneventful non-experimental mixed-gas rebreather dives with PO2 nominally 1.3 bar, but certainly with PO2 overshoots on descent.

The experimental record since 1970 suggests that CNS oxygen toxicity is at worst very rare with PO2 ≤ 1.6 bar, but other evidence suggests otherwise. Researchers associated with the Israeli Defence Force published a report2 of 2527 oxygen rebreather training dives at depths shallower than 7 m (23 feet). Those dives included 150 episodes thought to be CNS oxygen toxicity, that is, an overall incidence of 6%, and included ten in which divers who lost consciousness either during the dive or just after surfacing. Even with PO2 = 1.2 bar, 3% of divers reported symptoms consistent with CNS oxygen toxicity after 240 minutes of diving.

The most likely factor related to the relatively high incidence of CNS toxicity during those training dives was CO2 inhalation. From another 36 CNS oxygen toxicity accidents (including 13 more cases when divers lost consciousness) in similar Israeli training dives,3 the gas composition in 18 rebreathers was tested after the incident, and in 11 of them the CO2 partial pressure in the inspiratory loop exceeded 25 mbar (2.5 kPa, 2.5 %Surface Equivalent Value [SEV]). The highest measured CO2 partial pressure was 80 mbar (8.0 kPa, 8 %SEV)!

The apparent problem in those dives was inadequate scrubber capacity. Measured breakthrough time in that model of rebreather was less than dive duration when the CO2 test flow was only 1.12 L/min.5 The French Navy has reported6 1) that scrubber failure in rebreathers of the same type caused of 26 of its 153 rebreather-related accidents recorded between 1979 and 2009, and 2) that the incidence of CNS oxygen toxicity seizures decreased after a switch to a rebreather with larger scrubbing capacity. Intriguingly, experiments to study CNS oxygen toxicity before 1970 had many more “hits” than did the later ones. For the few pre-1970 measurements with PO2 ≤ 1.6 bar, those that caused CNS symptoms involved either exhausting exercise with rebreathers in dry chambers7 or rebreathers in which CO2 accumulation was noted.8 Exercise matters because people breathing against even moderate breathing resistance breathe too little and build up CO2 during periods of heavy exercise.9–11

CO2 in the breathing circuit leads to CO2 retention, that is, to elevated levels of CO2 in the body (see CO2 article). CO2 retention has a number of unhealthy effects, effects that include increased blood flow to the brain. When the inspired PO2 is high, increased brain blood flow increases oxygen delivery to brain tissue, mimicking a higher PO2. Note that during a high PO2 dive, any substances that dilate systemic blood vessels may also increase the risk of CNS oxygen toxicity.

So – beware of CO2! If PO2 ≤ 1.6 bar and a diver is breathing easily, the risk of CNS oxygen seizure is extremely low unless the scrubber breaks through. Scrubber breakthrough creates a real danger of CNS oxygen toxicity even at PO2 of 1.2 to 1.3 bar. Heavy exercise with even a reasonable external breathing resistance also bumps up the risk – another reason to slow down and enjoy the dive.

[pira]