narcosis and pulse oximetry?
Is it possible to detect Nitrogen Narcosis through pulse oximetry, or other blood oxygen saturation monitoring techniques? Surely if the quantity of nitrogen in the blood increases, it must displace another absorbed gas, ie oxygen; lack of oxygen in the blood could explain the dizziness etc experienced by 'narked' divers - if this is the case, then I wonder if the drop in blood oxygen is sufficient to be detectable using such methods?
Nitrogen narcosis has everything to do with the partial pressure of nitrogen and has no relationship with the partial pressure of oxygen.
In fact, elevating the pp of nitrogen or any other gas would not impact the ppO2. This follows Dalton's Law.
"The total pressure exerted by a mixture of gasses is equal to the sum of the pressures of each of the different gases making up the mixture--each gas acting as if it alone were present an occupied the total volume" -Dalton
What this means in laymans terms is, each gas within a mixture acts independently of the others. The individual pressure exerted by a particular component of the gas mixture in proportional to the number of molecules of that particular gas within the mixture. This individual pressure exerted by a component gas in referred to as a partial pressure.
I'm currently involved in a normoxic trimix course and we've had a very interesting discussion regarding the cause of inert gas narcosis. There seems to be several theories, one including increased levels of GABA but that seems odd when taking into account that GABA decreases with elevated PO2 levels. We've been discussiong the "ice-berg" theory as well, but we couldn't really put all the peaces together.
What is the current theory about the
cause and physiology of inert gas narcosis? Are there any good links??
Physician from Sweden
Most people feel that the cause of IGN is the same as that causing gas anesthesia - "The Meyer-Overton Theory" which states roughly that the degree of anesthetic action is directly related to the solubility of the agent in lipids.
There is a nice discussion of this in Edmonds text, Diving and Subaquatic Medicine, 4rd Edition., p.183.
What would happen if a person breathed from a tank that has corrosion, or was in long term storage @ 3000psi?
It's possible to breathe air from old tanks with corrosion that have been reduced in the percentage of oxygen. O2 is depleted by the oxidation process and hypoxia with unconsciousness as the result. If this should occur underwater, drowning would ensue.
Here is a site that discusses the inspection of tanks.
Our question relates to the cause of a person becoming unconscious in a pool at a depth of between 2.5 - 3.5 metres, whist using an oxygen rebreather .
Feeling of light headiness
Shortness of breathe
And he became unconscious.
He was removed from the water with signs of blueness around face and extremities.
I have not been able to find any information on signs, symptons or causes of Nitrogen poisoning caused by not flushing his system, on water entry. He would have been in and out of the water about 10 -15 times over 2 hours. Total time in the water was about 15 minutes prior to collapsing. His equipment was found to be functioning correctly and he still had oxygen in his cylinder. He is 50 yrs old.
The shallow diving that you describe pretty much rules out unconsciousness from the effects of nitrogen (decompression accident and narcosis).
Other things that can cause unconsciousness in a diver using a rebreather include the following:
---Central nervous system oxygen toxicity. This can cause convulsions and loss of consciousness underwater with drowning. The likelihood of this occurring increases with the time of exposure and partial pressure of the oxygen. Again the shallow dive and short time would militate against this as a cause of your diver's problem.
---Hypoxia. Low oxygen relates to procedural difficulties of purging and having lowered O2 in the breathing loop or accidentally exhaling into the breathing bag during the procedure. Hypoxia can also be caused by equipment malfunctions, such as battery flooding or microprocessor failure. The blue color of the diver would indicate that there was a low O2 problem.
---Hypercarbia. A high CO2 level usually gives ample physical warning signs of deep and rapid breathing, shortness of breath, rapid breathing, severe headache and finally confusion with loss of consciousness. The skin is usually red in color.
Nitrogen narcosis would only occur with the use of gases containing nitrogen on deep dives.
As an instructor I am well aware of the 1.6 limit and 1.4 for effort dives and etc. I was looking for some documentation on O2 toxicity within the 1.6 limit in order to convince a skeptic student about this limit. If you can direct me to such documents I'd appreciate it.
It would not seem that there should be any debate about this subject - as the US Navy in their Diving Manuals have stated that research has shown that the 1.6 bar limits should apply for managed diving situations and not for untethered divers breathing by a mouthpiece (a maximum of 1.4 bar is preferred).
NOAA, in their Diving Manual (Table 15-2), provide guidance for technical divers to use to manage oxygen toxicity. The upper range of these limits (1.6 bar PO2 for 45 minutes) entail too much risk for untethered divers breathing through a mouthpiece. A maximum of 1.5 bar, or even better 1.4 bar is generally used by these divers. There would be only a few minutes decompression advantage by using 1.6 rather than 1.4.
1. Office of Undersea Research: NOAA Diving Manual: Diving for Science and Technology, 4th Edition, Silver Spring, MD, NOAA 2001.
2. There are numerous references in the sections on oxygen toxicity in Bove's 'Diving Medicine' and Edmonds' Diving and Subaquatic Medicine', 4th Edition.
3. Search Medline for Oxygen Toxicity
I am a diving medical officer of the Dutch army. One of the methods of professional diving is with surface decompression, using oxygen for a faster decompression. The divers using this method tell me that they feel more tired after using this technique then after just air diving. My theory is that this might be caused by a higher production of oxygen radicals. Can some one tell me if there is already experience with the production of oxygen radicals during diving and with method they are measured.
This is an interesting subject and is called whole body toxicity by some. In Bove's text, Hamilton states that when an exposure to hyperoxia (PO2 level greater than 50 kPa or 0.5 bar) is low enough not to cause convulsions, the exposed person will in time develop a variety of symptoms, mainly in the lungs, and this is called pulmonary oxygen toxicity. Other symptoms include a syndrome of vague conditions including headache, nausea, general malaise, paresthesias and general loss of aerobic capacity. The reduction in vital capacity is the real culprit.
The effect of O2 on the central nervous system ( the Paul Bert effect), results in: muscle twitching and spasm, nausea and vomiting, dizziness, vision (tunnel vision) and hearing difficulties (tinnitus), twitching of facial muscles,irritability, confusion and a sense of impending doom, trouble breathing, anxiety, unusual fatigue, incoordination and convulsion.
The production of superoxide (O2-) under hyperoxic conditions is markedly accentuated leading to the generation of potent oxidants such as hydrogen peroxide (H2O2), hydroxyl radical (HO.), and peroxynitrite (ONOO-). Superoxide dismutase (SOD), by rapidly removing O2-, reduces the tissue concentration of O2- and prevents the production of HO. and ONOO-. Three forms of SOD exist in the lung: CuZnSOD, MnSOD, and extracellular SOD. Considerable supportive, though not all conclusive, evidence suggests that all three forms of SOD are essential for the pulmonary defense against oxygen toxicity, and that enhancement of pulmonary SOD has the potential of protecting against oxygen toxicity.
During its reduction to water, O2 readily gives rise to dangerously reactive intermediates. This threat is diminished by families of defensive enzymes which include the superoxide dismutases, catalases and peroxidases. Free radical chain reactions are controlled by antioxidants, such as ascorbate and the tocopherols, and oxidative damage, which occurs in spite of these defenses, is largely repaired or is nullified by de novo biosynthesis.
It would not be correct to translate all of this to your divers decompressing with oxygen, but it is interesting. Most of the difficulties noted above occured in saturation divers.
Free diving - how long on average do the divers hold their breath for and can they get the bends when they are ascending from those depths ?
Breathholding time for the free diver is highly variable as this is very adaptive. Divers who do this often and train themselves can prolong their dive times considerably.
Decompression sickness (bends) is a
rare event with sport divers who free dive. However, it can occur in
who make many dives in a short period of time, such as the pearl divers
of the Orient and the ama. 'Taravana' is the name of the condition that
natives get from this activity.
Gas embolism does not occur in the free diver unless he/she breathes compressed air at depth.
Can you tell me what happens with the body (when freediving) as the pressure increases. I do know all the physical things that occur, but I'm asking because I recently reached over a hundred feet. My body did the expected things, but my head felt like I was "high". Can you explain this? Can
you also tell me what to expect at the deeper depths.
The same things happen to the free diver that happens to the scuba diver or any other person at depth. There are physical laws that cause changes in the partial pressures of gases and the effect does not occur to any great degree because of the rapidity of the descent and ascent and the small amount of nitrogen in the lungs. Boyle's Law is operative but since the free diver is not breathing, the lungs just compress on descent and expand on ascent without the danger of 'burst' lung or pulmonary barotrauma.
So - you get nitrogen saturation
to the extent of the small amount of air in the lungs and the time
at depth. Therefore nitrogen narcosis is not usually a problem.
sickness is not a problem unless the free diver does repetitive dives
off-gassing. (See Taravana on our web site)
Last week after an hour scuba-diving in the Mediterranean, while we were waiting for everybody to finish their inmersion, I took off my wet suit and enjoy the warm clear water free of diving equipment. As the water was so transparent I decided to put on my mask and do some snorkeling. I only went down three or four times and not very deep, it was just 4 or 5 meters deep. I helped to release the anchor and the instructor saw me and told me that I shouldn't do that because of all the nitrogen I had in my body and I was going down to a pressure of 1.4 atm.
I wonder if that is correct considering that I wasn't breathing air at that pressure or doing any hard exercise.
I'm afraid that the dive master was correct on several counts.
*The surface interval should be spent without exercise. NASA scientists have shown unequivocally that exercise should not be taken after or between dives due to the nucleation of bubbles.
*Returning to depth, even if you are not breathing, completely changes your residual nitrogen and thus your situation on the tables.
*There is some nitrogen taken up on even a single shallow dive. This is not enough to worry about if you are simply snorkeling - but does alter your table and computer configuration for subsequent dives.
*Multiple shallow dives can and do lead to decompression illness. See http://www.scuba-doc.com/gasesprbs.html#Taravana
What first procedure is recommended for swb?
1. Get the person out of the water
2. Establish and maintain respiration and circulation
3. Administer 100% oxygen
4. Positive pressure breathing if respiration is not spontaneous
5. External cardiac massage if necessary.
6. If DCS or CAGE is suspected - rapid recompression in a chamber
There is a small CO detector that can be used to test the air in a scuba tank for carbon monoxide.
There are some Swiss doctors would like to get some testers but a problem is that the Swiss dive shops cannot locate a supplier. Could you find out about this and relay the information?
There is a product called CO-Cop (R), produced by "Purification Supplies" and can be purchased at the following web site:
I'm a diving doc from Calgary, Alberta, Canada. I recently heard about a condition called "deep water blackout". Supposedly, divers have lost consciousness for no apparent reason usually at depths of about 300ft. This was presented as despite the use of appropriate bottom mix (eg trimix). An explanation given was a nitrogen narcotic affect.
Can you give me more information? I can't believe you could get a nitrogen effect diving the correct mix of trimix.
Dr. David Elliott describes deep water blackout as unconsciousness in deep air scuba diving and appears to be a hazard only in those compressed air divers who swim deeper than the limits imposed by the several training agencies. ("Extreme Air divers").
Of the many causes of impaired consciousness at depth, the concept of "Deep Water Blackout" is distinct from the more obvious possibilities such as CO poisoning and MI. It is part of an ill-defined and rare group of incidents which should probably be best called "Loss of Consciousness of Unknown Etiology".
Exercise appears to exacerbate the condition and the other possible factors for Deep Water Blackout appear to be increased CO2, associated with a short burst of motivated hard exercise; oxygen greater than pO2 of 1.6 bar; and nitrogen narcotic at rest and potentiated by elevated CO2.
I have a some questions on the use of Nitrous Oxide after a dive or before diving. Any information would be greatly appreciated.
This topic came up during a discussion on paramedic 'routine' treatments where it was said by the paramedics that Entonox was a routine treatment for accident victims and that being a diver was 'not' a contra-indication. There was general agreement that the 50% O2 (while less good than 100% O2) was not bad there were some very strong statements made by some
divers about the undesirability of the N2O. I can understand that in cases of marginal DCS one might not wish to mask symptoms with a general pain killer but there were also claims that the N2O would actively be dangerous as promoting bubble formation.
As this is potentially serious to any diver who requires post dive paramedic treatment, do you have any advice or (preferably simple) references please? I cannot currently find an authorative answer, some of the divers concerned were adamant that they were right and the paramedics freely admitted that being non-divers it was not something they knew about.
Answer: The divers were absolutely right!! Entonox is the trade name for the mixture of 50% nitrous oxide and 50% oxygen, recognised by some patients as "gas and air." Its low fat solubility causes rapid onset of analgesia. Rapid elimination upon cessation of inhalation makes it ideal for procedural pain. Nitrous oxide is eliminated unchanged from the body, mostly by the lungs.
However -- Entonox (50% nitrous
must never be used in any condition where air is trapped in the body
expansion would be dangerous. For example, it will exacerbate
and increase pressure from any intracranial air. Air in any other
such as the sinuses, middle ear and gut may also expand. Problem areas
Head injuries with impaired consciousness.
Artificial, traumatic or spontaneous pneumothorax.
In addition, inappropriate, unwitting or deliberate inhalation of Entonox will ultimately result in unconconciousness, passing through stages of increasing light headedness and intoxication, a very dangerous thing with a diver with a decompression accident.
Here are some references which might be helpful:
BOC Gases. (1995). Entonox. Suggested Protocol
Document BOC: Guildford.
Report of the Working Party of the Commission on the Provision of
Surgical Services. Pain after Surgery. London: Royal College of Surgeons
of England and College of Anaesthetists, 1990.
Gudmarsson, A. N. (1994) "Nitrous oxide as analgesic for painful
procedures outside the operating theatre." British Journal of Anaesthesia,
72: Supp 1:A241:125.
United Kingdom Central Council for Nursing, Midwifery and Health
Visiting. (1992). The Scope of Professional Practice. UKCC: London.
Acott CJ, et al. Decompression illness and nitrous oxide
a sports diver.
Anaesth Intensive Care. 1992 May;20(2):249-50.
McIver RG, et al. Experimental decompression sickness from
nitrous oxide anesthesia. SAM-TR-65-47. Tech Rep
SAM-TR. 1965 Aug;:1-12.
Eger EI II, Saidman LJ: Hazards of nitrous oxide
anesthesia in bowel obstruction and pneumothorax. Anesthesiology 26:61,
If two divers had exactly the same dive profile (same depth and length of time underwater) but one consumed more air than the other then shouldn't the one with more air consumed have also more
nitrogen in his body? I was surprised to notice that air consumed is not used as a factor for nitrogen absorbed when the type of air mixture( nitrox or heliox) is.
There is a hypothesis that attempts to relate the surface air consumption (amount of nitrogen breathed) with the amount absorbed and thus to the risk of a decompression accident. Although surface air consumption is quite important in developing a dive plan and decompression tables, it has little to do with nitrogen absorption at depth - a function of depth/time and partial pressures. (CO2 and exercise might have some part to play in this situation).
In this hypothesis, nitrogen, as the
inert air component, is not a driving factor for surface air
(SAC), rather 02 and increased CO2 are; conditions that increase demand
for 02 or production of C02 increase air, or gas, consumption and thus,
nitrogen uptake is faster at depth until the tissues are
Thus, if a diver had an inherently lower SAC rate, say less than the
of 0.5 cfm, the result would be that the chances of getting DCS are
than someone with the average SAC, which is assumed to be the SAC rate
operant when dive tables were tested and
designed. Conversely, for those with SAC above the average, the likelihood of getting DCS is greater even if dive times are substantially lower than the dive table values, as these divers supersaturate sooner.
In many of the qualitative risk factors for DCS it is hypothesized these situations increase 02 consumption or C02 generation and thus increase their DCS risk. http://www.scuba-doc.com/prvndcs.htm
I can find no studies or
to substantiate this theory. DCS relates to the decrease in ambient
in fast and slow tissues as the diver ascends, allowing bubble
to occur as the nitrogen comes out of saturation independent of the
breathing rate. As the diver
descends, blood is saturated rapidly with nitrogen (independent of the breathing rate) and thus the rest of the body is saturated at the rate of the tissues (some fast tissues, such as the spinal cord - some slow, such as connective tissue). All of our decompression tables are based more or less
on this Haldanian model. There are good discussions of this in Bove's 'Diving Medicine' and Edmonds 'Diving and Subaquatic Medicine', both of which can be bought online at http://www.scuba-doc.com/DMbkstr.htm .
Ernest Campbell, MD, FACS All Rights Reserved.