It is a review of your OW class. Very little additional information is present. You'll do fine.
Nitrox vs Air
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Spectre
Contributor
dc4bs once bubbled...
1 ATM above surface level? in space?
I'm guessing you meant .5 ATM above surface level.
Yea yea yea.. can you tell I'm not an air guy?
I would have just said 18,000 feet if I knew the number [Thanks walter!]...
But'cha all get the point
So... if I'm playing the numbers correctly, Air becomes hypoxic @ 12,000 feet?
Not quite that far up. At 12,000 ft the pressure is .636 atm resulting in a PO2 of .13 atm. At 11,000 ft the pressure is .662 atm resulting in a PO2 of .139 atm which is still hypoxic.
nothing to offer as far as the mathematical calcs...but the course as soemone else has mentioned is worth it if youare diveing deeper than 60 fsw and doing repetive dives. As Stone mentioned I too find I feel less tired after diving nitrox mixes as opposed to air. I don't believe that there is any written evidence that this is a positive effect, but my own personal experiences. :boom:
notabob
Contributor
Hypoxia depends less on altitude than on a person's physiology. Typically, the effects start becoming obvious above 10-12kft. However, factors such as fatigue, lung condition, etc. will vary from person to person and even from one day to another. At night, for example, under strenuous conditions a task-loaded tired smoker can start feeling its effects and start losing concentration even below 10k. With all this said, a human body is very adaptable, and you can acclimate yourself to higher altitudes and lower o2 pP. Mountain climbers, astronomers that live at high-mountain telescopes for an extended period of time, and even astronauts (pressure levels inside spacecraft are lowered significantly prior to spacewalks in order to allow the spacewalking astronauts to acclimate to the lower pressures inside the space suits. don't have the specific numbers, though).
-Roman.
-Roman.
The Iceni
Medical Moderator
... This a is a copy of an earlier post of mine.
Walter, In that thread I think I very effectively destroy any theories that oxygen causes ANY narcosis at all in life because it is a stimulant.
The Iceni
Medical Moderator
The Meyer-Overton principle can be used to predict the anaesthetic properties of gasses and predicts that oxygen should be approximately six times as narcotic as nitrogen, I believe. However this is not seen in practice. Why?
There are two good reasons.
Firstly, unlike nitrogen, oxygen is not inert and there is a gradient between the blood and the tissues because it is used up by the body's metabolism, while nitrogen is not and its partial pressure is the very much the same throughout the body as in the inspired gas.
Secondly, oxygen is a stimulant countering the depressant - narcotic - effects of the other (inert) inhaled gasses.
i) The pressure gradient;
The partial pressure of oxygen in normal breathing air of 0.21 bar is 158.8 torr. On inspiration the breathing gas is diluted with saturated water vapour with a partial pressure of 47 torr so its pp in the bronchi is 112 torr (0.15 bar). Because air in the lung is affected by dead space and by venous return of carbon diaoxide when it reaches the alveolus the ppO2 is 105 torr (0.14 bar). In the arterial system it is about 97 torr (0.13 bar). Across the capillary bed it is considerably further reduced to about 35 torr (0.05 bar).
But it does not stop there! In the tissue fluid the partial pressure of oxygen is further reduced to about 20 torr (0.026 bar). The oxygen then arrives at, and crosses, the cell membrane. In the cytosol it is about 10 torr (0.013 bar) whereas within the mitochondria, which is where all the energy producing reactions (cellular respiration) takes place it is only in the region of 6 torr or 0.008 bar in normal healthy tissues. YES 0.008 bar! Clearly oxygen is so powerful the body needs it in only very small amounts to generate all the energy it needs. (See McGilvery, Bichemistry a Functional Approach.)
If the partial pressure of oxygen in the tissues varies from this low level the normal chemical reactions producing the body's energy either cease or go out of control. Consequently an hypoxic inspired ppO2 of less than 75 mmHg or 0.1 bar is unable to support life and partial pressures above 1.8 bar are toxic.
ii) Oxygen as a stimulant.
This is the realm of the biochemist and is extremely complex but suffice it to say that there are many stages in cellular respiration resulting in oxidative phosphorylation and generation of the energy molecule ATP. This battery of enzymes acts like the controls of a car but can be damaged by poisons, temperature and biochemical changes within the cell, such as changes in acidity (H+ concentration).
Cyanide kills by blocking the mitochondrial enzyme at the very end of this long biochemical chain, which is the only biochemical reaction that uses molecular Oxygen itself. Cyanide poisoning produces a fatal tissue hypoxia through starving it of energy even though Oxygen may be present and freely available in higher than normal quantities.
So how can we explain oxygen toxicity? Too much oxygen causes damage to the lungs and mucous membranes after prolonged periods of exposure (whole body or pulmonary toxicity). This can easily be explained as a chronic inflammation, whatever the biochemical mechanisms. (Although these are likely to be the same as those producing CNS toxicity and related to the hydrogen ion). It is easy to speculate that it does not take much to raise the intra-mitochondrial oxygen partial pressure above the normally low value of 0.008 bar when breathing any enriched nitrox mix as oxygen is being supplied to the tissues in quantities far in excess of the body's metabolic needs.
In general if the inspired partial pressure of Oxygen exceeds 1.8 bar CNS toxicity will eventually be produced in all subjects leading to grand-mal convulsions, which must be avoided in divers at all costs.
Possible explanations of CNS oxygen toxicity.
1) Build up of toxic chemicals
Most of the enzymes involved in cellular respiration (oxidative phosphorylation) have sulphydryl groups, which are very sensitive to oxygen. If the cellular pp O2 even approaches half a normal atmosphere these enzymes are deactivated by the formation of disulphide bridges and, as with cyanide poisoning, intracellular respiration slows or stops even though more than enough oxygen is present. Unlike cyanide poisoning, however, CNS Oxygen toxicity is not complete and can rapidly be reversed.
Without oxygen, anaerobic respiration takes place and the concentration of harmful chemical bi-products such as lactic acid with its powerful hydrogen ion (H+) increase, damaging all sensitive tissues including the lungs and brain.
2) Destabilisation of nerve cell membranes.
Enzymes located within nerve and muscle cell membranes are responsible for ion transport the most important of which is ATP phosphokinase. The nerve resting potential is generated by the energy dependent active exchange of potassium and sodium ions against an electrical gradient through gated channels. On stimulation by a neurotransmitter such as adrenaline, the nerve action potential is generated by a sudden opening of these gates and the reversal of polarity for a very short period.
Clearly damage to these intracellular enzymes leaves the nerve fibres no longer able to generate a stable "resting potential". In addition the complex mechanisms normally keeping the various gates closed is also damaged. So the leaky membranes tend to cause the nerves of the brain to fire off at-will rather than when instructed to do so, causing an electrical storm;- a grand-mal convulsion.
The warning features of oxygen toxicity, such as facial muscle twitching, represent a generalised instability of all nerve (and muscle) cell membranes; just waiting for that one nerve cell in the brain to fire off and act as a trigger for all the rest.
3) Reduction in stabilising neurotransmitters.
Gamma Amino Butyric Acid (GABA) is an INHIBITOR within the brain and acts against the stimulants such as adrenaline, noradrenaline, serotonin and dare I say it amphetamine!!
It seems that the enzymes responsible for the production of inhibiting neurotransmitters such as GABA are damaged by high levels of oxygen much more than those producing the stimulant neurotransmitters leading to a generalised excitability.
4) The carbaminohaemoglobin buffer and raised CO2.
Excess carbon dioxide is harmful because in solution it produces carbonic acidic, a source of those extremely harmful hydrogen ions;
H20 + CO2 <-> H2C03 <-> H+ + HC03-
In order to prevent this, most of the CO2 in the blood is normally mopped up by the haemoglobin in venous blood to form inert carbaminohaemoglobin.
When the equivalent of 100% Oxygen or more is breathed, I surmise little haemoglobin is involved in oxygen transport as enough is directly transported to the tissues in simple solution. In excess oxygen permanently, and preferentially, occupies the available sites on the haemoglobin molecule which are no longer free to mop up "acidic" CO2 molecules but enough normally do remain to do the job. In the presence of an inspired PO2 over 3 bar, however, the haemoglobin remains 100% saturated with oxygen and the carbaminohaemoglobin buffer is completely deactivated leading to a subsequent rise in acidity in the blood and brain which may be sufficient to trigger the ensuing fit in an already sensitised brain.
This becomes particularly apparent when the inspired pp CO2 exceeds 6%.
As an aside, the carbaminohaemoglobin buffer is normally involved in respiratory control but this mechanism is destroyed by prolonged exposures to high oxygen or carbon dioxide partial pressures. This is why experienced (free) divers are able to breath-hold for much longer than normal subjects.
It is obvious that excessive work and breath holding predispose to fits by increasing the partial pressure of CO2 and acidity, while hyperventilation is protective because it reduces it.
5) Stress
Stress, cold and subsequent adrenaline release predisposes to fits, a warm relaxed diving environment lessens the likelihood of fits.
The way I see it is that oxygen is just as narcotic as all gas molecules at the level of the cell membrane itself but in practice this effect is countered by the low partial pressures seen there together with the fact that it is not inert and acts as a stimulant in several ways, to reverse any narcotic effects it would otherwise produce.
I suspect, in practice these effects are near enough EQUAL AND OPPOSITE at the pressures recommended for normal scuba diving otherwise we could not dive using scuba!
If that didn't confuse I'll have to try harder!
dascubadweeb
Guest
I'm officially an EANB! (Enriched Air Nitrox B@$CH)! Certified!
Alright, here's what I know....1, you shouldn't be dependent on your 'puter...it is really bad practice, and you should always be backing that up in some fashion.
As for Air vs. Nitrox, I think it is worth it. To the original questions,
1. you don't take on as much nitrogen, so less becomes absorbed in your softer tissues, but you don't eliminate the effect of being narced
2. Bottom time...On the tables I have in front of me, say you go to 90 ft....using EANx 32, NDL is 40min...EANx 36, NDL is 50...Air (20.97% O2), NDL is 25 min. This is just for dive one, if you are doing multiple dives, the difference between these numbers increases.
Please note this is for the IANTD tables, and I also used the IANTD air table for the air NDL, I think both NAUI and PADI are a little different. Anyway, one added bonus I can say to diving Nitrox is this, let's say you are making 3 dives in a day.
Let's say they are to depths of 80, 60, and 50 ft respectively. Say your times are 45min, 55min, 50min, and that you've taken safe and intelligent surface intervals. The big difference between Nitrox and air is that physically you feel less drained (or at least that has been my experience). I am not saying it is an earth shattering difference, but it is noticable to me anyway. Is there any truth to that, maybe so, maybe not. Maybe the doc will let me know. Anyway..thought I'd help
-TT
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