There has been some research done on the subject and I will try to summarise some of the keys points. I will also try to dig out some of the references and post them at some point so you can look at the complete documents if you want.
We all know that the site for the narcotic effect is the brain, specifically the cell wall of the cells within the brain. Given the same partial pressure of oxygen or nitrogen at this site they will both be equally narcotic as predicted by the Meyer Overton law relating to fat solubility and to some extent the molecular size and weight to narcotic potency.
This holds true for all substances exerting an anaesthetic effect. The only difference between anaesthesia with an inhaled modern medical agent and nitrogen narcosis is the partial pressure required for the effect. This is about 0.01 of a bar of isoflourane and about 15 bar for N2 to produce the same level of unconsciousness!
However although the brain is very well supplied with O2 it is also a big consumer of O2. The brain uses oxygen at a high rate and so the tissue partial pressure remains low when breathing air at 1 bar. In order to supply the brain with sufficient O2 we have the compound haemoglobin in blood cells which increases the amount of oxygen carried from 0.3 mls per 100mls dissolved in plasma to 20mls/100mls in red cells with haemoglobin. When breathing air the haemoglobin is fully saturated with oxygen in blood going to the brain in healthy individuals.
This means that increasing the PPO2 in the inspired gas has little effect on the amount of O2 delivered to the brain and so the tissue PO2 (our effect site for narcosis) does not rise until quite high PPO2s, probably in the region of 1.5 - 2.0 bar. This is also the region of CNS O2 toxicity and hence not often breathed underwater or if so, not usually for extended periods of time or at great depth.
Thus whilst O2 is narcotic and can be demonstrated to be so under controlled chamber conditions at a PPO2 of around 3.0 bar, the risk of CNS O2 toxicity also limits the narcotic effect in practical terms underwater.
Incidentally, the effect of increased CO2 (from skip breathing, poor breathing patterns or an issue with CO2 removal or component failure in a CCR) increases blood flow to the brain. CO2 is an epileptogenic, i.e. high levels of CO2 lower the threshold at which a seizure may occur. Increased CO2 is a far more effective way of increasing O2 flow to brain tissue and helps explains an increase in narcotic effect and heightened risk of CNS O2 toxicity and convulsions in the ‘borderline’ region of 1.5 - 2. 0 bar inspired PPO2.
So, both points of view are essentially correct in different circumstances.
So, if you want to include O2 in your equivalent narcotic depth (END) calculations, choose your preferred narcotic depth then:-
FN2 = (END/P) - FO2
where FN2 is the fraction of nitrogen you will have in your trimix, the END is the Equivalent Narcotic Depth you have chosen and P is the absolute pressure of the dive depth.
If we follow on from the example used in the previous post where we used a dive PO2 of 1.35 Bar to calculate our FO2 for a 60m dive we had an FO2 of .18 or 18%.
Our chosen EAD for that dive was 30m so for an END of 30m we use:-
END = 33m = 4.3 Bar
P = 60m = 7 Bar
FN2 = (4.3/7) - FO2
FN2 = (4.3/7) - .18
FN2 = .434
In the previous post our mix was calculated to be 18/37 (i.e. .FHe of 37 or 37% HE). Using the formula to include O2 as narcotic gives us a mix of 18/39, so just a little bit more helium in the mix when counting O2 as narcotic.
FHe = 1 - FO2 - FN2
FHe = 1 - .18 - .43 = .39
© Eau2 & Martin Robson 2016