Decompression Sickness
Definition and Early Management

Called “bends” by early investigators, it is now classically divided into Type I, Type II and “Type III” (a phrase coined by Bove and Neumann to describe a combination of  DCS and arterial gas embolism). Type I DCS includes cutaneous manifestations and minor joint pain, or “pain only”; Type II includes severe symptoms related to the cardiopulmonary and neurological systems. Type III is a combination of AGE and DCS with neurologic symptoms.

Pain syndromes spot the pain in the limbs-not the central skeleton. It is dull, difficult to characterize and localize and is located in the shoulders, elbows and hands in divers. Compressed air workers have more pain in their lower extremities.

It is caused by bubbles, intravascular and extravascular with large gas stores in the fatty bone marrow. This is a cause of dysbaric osteonecrosis.

Neurologic Syndromes are increasing in sport divers and the spinal cord is the most commonly involved site. Symptoms include abdominal, low back, lower extremity pain, weakness and loss of feeling and function. Cerebral involvement is much more common than previously thought and may account for a portion of the “spinal cord” lesions. Peripheral nerves can also be involved causing numbness, limb pains and weakness.

• Recognition *Symptoms usually appear 15 minutes to 12 hours after surfacing*

Signs

• • • Blotchy rash
    • Paralysis or weakness
    • Coughing spasms
    • Staggering or instability
    • Unconsciousness

Symptoms

• • • Tired feeling
    • Itching
    • Pain, arms, legs or trunk
    • Dizziness
    • Numbness, tingling or paralysis
    • Chest compression or shortness of breath

Early Management

• • • Immediate oxygen breathing, continue even if person improves

    markedly

    • Stabilize patient the same way as for Air Embolism
    • Urgent recompression after stabilization in trauma facility
    • Early recompression treatment for all forms of decompression sickness. There is a lightweight, portable recompression facility that would appear to be ideal for the liveaboard or dive operation far from a fixed-base chamber. This is the ‘SOS Hyperlite Stretcher’. More information can be obtained at http://www.hyperlite.co.uk/ .

======================================================================

Frequently Asked Questions

Nitrogen narcosis and pulse oximetry?

Query:

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?

Answer:

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.

Cause of inert gas narcosis

Query:

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

Answer:

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.

Oxygen

Hypoxia from tank corrosion

Query:

What would happen if a person breathed from a tank that has corrosion, or was in long term storage @ 3000psi?

Answer:

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.

http://snipurl.com/4r3p

Loss of consciousness on rebreather due to hypoxia

Query:

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 .

His symptoms where

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.

Answer:

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.

Oxygen Toxicity Questions

Query:

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.

Answer:

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.

Reference:

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

http://snipurl.com/4r3n

Oxygen Radicals and Diving

Query:

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.

Answer:

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.

Breath hold Diving (Free diving)

Query:

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 ?

Answer:

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 people 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.

http://www.scuba-doc.com/taravana.html

Gas embolism does not occur in the free diver unless he/she breathes compressed air at depth.

Free Diving

Query:

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.

Answer:

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 only to the extent of the small amount of air in the lungs and the time spent at depth. Therefore nitrogen narcosis is not usually a problem. Decompression sickness is not a problem unless the free diver does repetitive dives without off-gassing. (See Taravana on our web site)

http://www.scuba-doc.com/taravana.html

Nitrogen Uptake and free diving

Query:

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.

Answer:

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.

Shallow Water Blackout

Query:

What first procedure is recommended for swb?

Answer:

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

Carbon Monoxide

Carbon Monoxide Scuba Testers

Query:

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?

Answer:

There is a product called CO-Cop (R), produced by “Purification Supplies” and can be purchased at the following web site:

http://www.lawrence-factor.com/

Deep Water Blackout

Query:

Hi

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.

Answer:

Hello Dr.:

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.

Nitrous oxide and diving

Query:

I have a some questions on the use of Nitrous Oxide after a dive or before diving. Any information would be greatly appreciated.

Answer:

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 oxide) must never be used in any condition where air is trapped in the body and expansion would be dangerous. For example, it will exacerbate pneumothorax and increase pressure from any intracranial air. Air in any other cavities such as the sinuses, middle ear and gut may also expand. Problem areas are:-

Head injuries with impaired consciousness.

Artificial, traumatic or spontaneous pneumothorax.

Air embolism.

decompression sickness.

Abdominal distension.

Maxillofacial injuries.

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:

1.) BOC Gases. (1995). Entonox. Suggested Protocol

Document BOC: Guildford.

2.) 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.

3.) Gudmarsson, A. N. (1994) “Nitrous oxide as analgesic for painful

procedures outside the operating theatre.” British Journal of Anaesthesia,

72: Supp 1:A241:125.

4.) United Kingdom Central Council for Nursing, Midwifery and Health

Visiting. (1992). The Scope of Professional Practice. UKCC: London.

5.) Acott CJ, et al. Decompression illness and nitrous oxide anaesthesia in

a sports diver.

Anaesth Intensive Care. 1992 May;20(2):249-50.

6.) McIver RG, et al. Experimental decompression sickness from hyperbaric

nitrous oxide anesthesia. SAM-TR-65-47. Tech Rep

SAM-TR. 1965 Aug;:1-12.

7.) Eger EI II, Saidman LJ: Hazards of nitrous oxide

anesthesia in bowel obstruction and pneumothorax. Anesthesiology 26:61,

1965

SAC (Surface Air Consumption)

Nitrogen consumed, nitrogen absorbed

Query:

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.

Answer:

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 consumption (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 supersatured. Thus, if a diver had an inherently lower SAC rate, say less than the average of 0.5 cfm, the result would be that the chances of getting DCS are lower 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 observations to substantiate this theory. DCS relates to the decrease in ambient pressure in fast and slow tissues as the diver ascends, allowing bubble formation to occur as the nitrogen comes out of saturation independent of the previous 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 .

=======================================================================

Decompression Illness and Arterial Gas Embolism are discussed in another book. “The Bends and Gas Embolism 101″.

High Pressure Nervous Syndrome

Helium

During the 1930’s the U.S. Navy tested other gases as a substitute for nitrogen. Their scientists conducted experiments using rare gases such as helium, neon, and argon. After numerous trials, helium was selected as the most suitable gas to dilute oxygen for deep diving.

Helium is the second lightest element known to man; in fact, only hydrogen is lighter. Helium is one seventh as light as air and our atmosphere only contains 5 part per million of helium. Certain natural sources in the U.S. and Canada contain as much as 2% helium and this is where much of this gas is

collected.

Helium is chemically inert; it has no color, taste, or odor. These characteristics make it an almost perfect gas for diving. However, helium has two disadvantages. First, helium is extremely expensive due to its rarity. Secondly, helium has high heat conductivity and will rob body heat from a diver at a rapid rate. There are also other major disadvantages to diving with helium mixes; it is more difficult to decompress, i.e., deeper and longer stops are required as compared to air; and there is a greater risk of a serious case of decompression sickness if stops are not done per plan.

In deep saturation diving, under rapid compression rates, divers sometimes suffer from a phenomenon known as the High Pressure Nervous Syndrome (HPNS).

HPNS

NOAA has the following to say about HPNS:

“At diving depths greater than 600 fsw (183 msw), signs and symptoms of a condition known as the high pressure nervous syndrome (HPNS) appear and become worse the faster the rate of compression used and the greater the depth or pressure attained. HPNS is characterized in humans by dizziness, nausea, vomiting, postural and intention tremors, fatigue and somnolence, myoclonic jerking, stomach cramps, decrements in intellectual and psychomotor performance, poor sleep with nightmares, and increased slow wave and decreased fast wave activity of the brain as measured by an electroencephalogram (Bennett et al. 1986).

First noted in the 1960’s, HPNS was referred to initially as helium tremors. Since that time, numerous studies have been conducted that were designed to determine the causes of HPNS and to develop means of preventing it (Bennett 1982).

Methods of preventing or ameliorating HPNS include using a slow and steady rate of compression to depth, using a stage compression with long pauses at selected intervals, employing exponential compression rates, adding other inert gases such as nitrogen to helium/oxygen mixtures, and selecting personnel carefully. At present, the data suggest that adding 10 percent nitrogen to a helium/oxygen mixture, combined with the use of a proper compression rate, ameliorates many of the serious symptoms of HPNS (Bennett 1982).”

HPNS can result from diving mixtures that contain helium. Here are three actions that you can take to avoid HPNS. They are:

-Don’t dive Heliox (O2/He) deeper than 400 FSW.

-Don’t dive Trimix (O2/He/N2) deeper than 600 FSW.

-Note: Adding as little as 10% Nitrogen to He/O2 mixes buffers the mix to the point that it can be used to 600 FSW without experiencing HPNS.

-Use (very) slow descent rates. Descending slower than one FSW per minute beyond 400 FSW on Heliox and 600 FSW on Trimix keeps HPNS at bay. Unfortunately, this slow rate of decent is only practical in commercial diving and is of no use in tech diving.

References

Bennett, P.B. 1982b. The high pressure nervous syndrome in man. In: The Physiology and Medicine of Diving and Compressed Air Work. (P.B. Bennett and D.H. Elliot, eds), Balliere-Tindall, London. pp. 262-296.

Bennett, P.B. 1990. Inert gas narcosis and HPNS. In: Diving Medicine, Second Edition (A.A. Bove and J.C. Davis, eds.).W.B. Saunders Company, Philadelphia. pp. 69-81.

Bennett, P.B, R. Coggin, and J. Roby. 1981. Control of HPNS in humans during rapid compression with trimix to 650 m (2132 ft). Undersea Biomed. Res., 8(2): 85-100.

=======================================================================

Breath-hold Diving: Taravana

Taravana, What is it?

Taravana, a condition first observed by E.R. Cross in 1958, and reported in 1958- is a diving syndrome seen in working Tuamotu Island natives diving the Takatopo Lagoon. The word apparently means ‘to fall crazily’ and is thought to represent decompression illness in these divers. P. Paulev, a Danish naval officer described his own personal experiences with DCS from breath-hold diving in 1965.

More recently, Dr. Robert Wong, in an excellent article in the Journal of the SPUMS, (September 1999) summarizes the information known about the condition and reports two more Australian cases. Decompression illness from breath-hold diving is quite rare but can occur. This is usually seen in divers who are making many deep dives in a short period of time with little surface interval. The symptoms are usually vertigo, nausea and lethargy, paralysis and death. Recompression is the recommended treatment.

Significance to Scuba Divers

Of particular relevance to the sport diver is what happens to the snorkeling breathhold diver who dives during the surface interval between scuba dives. Of particular relevance to the sport diver is what happens to the snorkeling breathhold diver who repeatedly dives during the surface interval between scuba dives. Very little nitrogen is transferred from the alveoli to the blood during one breathhold dive. (Hong in Bove’s Diving Medicine, 1997, p. 67).

Repeated dives alter the off-gassing process as well as taking on more gas and would completely change the dive profiles. Free diving onloads N2, to a small degree, more or less depending upon the depth and time at depth of the dives and this time should be taken into consideration when calculating residual nitrogen. Snorkelers between scuba dives should stay on the surface.

Reference: http://www.scubamed.com/divess.htm#anchor447923

Of Historical Interest

Here is interesting information from Glen Egstrom, Ph.D that I thought very interesting:

“I spent some time in the Tuamotus and worked with some French doctors who studied this problem. The free divers work to depths 150 fsw or more. During the “season” there are incidents of Taravana, which I believe means ‘crazy’. There is a detailed discussion by E.R.Cross in the book ‘Breath-hold Diving’ a proceedings of a workshop in Japan that I had the pleasure to attend in 1965. It is publication 1341 National Academy of Sciences, National Research Council Wash. D.C. 1965. It was not unusual for the natives to hyperventilate for 2 – 10 minutes before descending to depth and staying 30 – 60 seconds up to 2 min. on shell collecting dives. They go down with a lead weight between their feet and leave the weight near the bottom. I dove with a couple of them for nearly a month and even got my depth down to 100. Those were the days, we went on scuba and watched them work in shark infested waters with little of no concern. Paulev, a Danish M.D., also has his paper on DCS following repeated breath-hold dives in a Norwegian submarine escape tank. He bent himself quite badly and made the lecture circuit discussing his exploits. He and I spent quite a bit of time together at the conference and I was struck by his story. Bottom line- there is little doubt that one can sustain serious DCS while breath hold diving but you really must work pretty hard at it.”

References:

Suk-Ki Hong in Breath-hold Diving section of Bove’s ‘Diving Medicine’, p. 69. 1997.

Paulev, P. “DCS following repeated breath-hold dives”. J.Appl. Physiol. 20(5): 1028-1031. 1965.

Edmonds, C. “Diving & Subaquatic Medicine”. 1981.

Cross E.R., Taravana – Diving Syndrome in the Tuamotu diver. In ‘Physiology of breath-hold diving and the ama of Japan.’ National Academy of Science – National Research Council Publication 1341. 1965; 207-219.

Bove, A.A., ‘Diving Medicine’, Taravana

Wong, RM, Taravana Revisited: Decompression Illness After Breath-hold Diving,

SPUMS Journal, Volume 29, No.3, September, 1999

Free Diving and Shallow Water Blackout

SHALLOW WATER BLACKOUT (Latent hypoxia)

Shallow water blackout (SWB) is the sudden loss of consciousness caused by oxygen starvation following a breath holding dive. This was first described by S. Miles as “latent hypoxia”, shallow water blackout is the term he ascribed to unexplained loss of consciousness in divers using closed-circuit oxygen breathing apparatus at shallow depths. Unconsciousness strikes most commonly within 15 feet (five meters) of the surface, where expanding, oxygen-hungry lungs literally suck oxygen from the divers blood. Once you lose consciousness you are likely to drown. The blackout occurs quickly, insidiously and without warning. The victims of this condition die without any idea of their impending death.

There are about 7000 drownings in the U.S. annually – many of whom are good swimmers. Craig, in 1976 reported interviews of survivors of near drowning. All had hyperventilated prior to the swim, had the urge to breathe, and had no warning of the impending unconsciousness. Hyperventilation is used by free divers to reduce the concentration of CO2 and extend the length of breath-holding.

Beginning breath-hold divers, because of their lack of adaptation, are not generally subject to this condition. It is the intermediate diver who is most at risk. He is in an accelerated phase of training, and his physical and mental adaptations allow him to dive deeper and longer with each new diving day- sometimes too deep or too long. Advanced divers are not immune.

Conditions that produce latent hypoxia (Shallow water blackout)

Hyperventilation

Hyperventilation is the practice of excessive breathing with an increase in the rate of respiration or an increase in the depth of respiration, or both. This will not store extra oxygen. On the contrary, if practiced too vigorously, it will actually rob the body of oxygen. The magical benefit of hyperventilation is what it does to carbon dioxide levels in the blood. Rapid or deep breathing reduces carbon dioxide levels rapidly. It is high levels of carbon dioxide, not low levels of oxygen, that stimulate the need to breathe.

The beginning diver is very sensitive to carbon dioxide levels. These levels build even with a breath-hold of 15 seconds, causing the lungs to feel on fire. The trained diver has blown off massive amounts of carbon dioxide with hyperventilation, thus outsmarting the brain’s breathing center. Normally metabolizing body tissues, producing carbon dioxide at a regular rate, do not replace enough carbon dioxide to stimulate this breathing center until the body is seriously short of oxygen.

Hyperventilation causes some central nervous system changes as well. Practiced to excess, it causes decreased cerebral blood flow, dizziness and muscle cramping in the arms and legs. But moderate degrees of hyperventilation can cause a state of euphoria and well-being. This can lead to overconfidence and the dramatic consequence of a body performing too long without a breath: blackout.

Pressure changes in the freediver’s descent-ascent cycle conspire to rob him of oxygen as he nears the surface by the mechanism of partial pressures. Gas levels, namely oxygen and carbon dioxide, are continuously balancing themselves in the body. Gases balance between the lungs and body tissues. The body draws oxygen from the lungs as it requires. The oxygen concentration in the lungs of a descending diver increases because of the increasing water pressure.

As the brain and tissues use oxygen, more oxygen is available from the lungs while he is still descending. This all works well as long as there is oxygen in the lungs and the diver remains at his descended level. The problem is in ascent. The re-expanding lungs of the ascending diver increase in volume as the water pressure decreases, and this results in a rapid decrease of oxygen in the lungs to critical levels. The balance that forced oxygen into the body is now reversed. It is most pronounced in the last 10 to 15 feet below the surface, where the greatest relative lung expansion occurs. This is where unconsciousness frequently happens. The blackout is instantaneous and without warning. It is the result of a critically low level of oxygen, which in effect, switches off the brain.

Dalton’s Law of partial pressures applies. (Pb – PO2 + PN2 + Pother gases.)

As Pb decreases, the partial pressures of all component gases decrease in the same ratio. The hypoxia of predive hyperventilation is corrected by an increased PO2 during descent.

During descent, the lung volume decreases due to chest compression, resulting in increased lung PO2, PCO2 and PN2.

* In the lung there is an increased breathing rate and a reduced PCO2. Lung volume is reduced to one-half, lung PO2 is increased, lung PCO2 increases initially, but is followed by lowered PCO2 due to reversed gradient.

* The blood reacts by developing a respiratory alkalosis and a right shift of the HbO2 (oxyhemoglobin) curve. The reaction is CO2 + H2O – H+ + HCO3.

* Carotid body chemoreceptors cause a slow-down of the heart and permit longer breath holding.

* There is vasodilatation of the brain vessels with hypoxia (low oxygen). There is rapid O2 usage, the arterial PCO2 is lowered so that respiration is not stimulated until )2 drops s low that the breath hold breakpoint is reached. The breakpoint (PCO2/PO2) in a trained person is less sensitive to increased PCO2 or lowered O2. The act of consuming oxygen rapidly (as in chasing a large fish), delays the breakpoint because of the higher PCO2 and the exercise per se. The diver becomes lightheaded, dizzy, has tingling, air hunger, muscle rigidity and unconsciousness.

* While at depth, increased lung PO2 provides a favorable gradient for O2 transfer from the lung to blood, occurring more rapidly than if the diver were on the surface.

* Because alveolar PCO2 increases with compression, CO2 does not leave the blood to enter the lung. Arterial CO2 rises rapidly (especially with exercise) initially, then the tissues store CO2. Trained divers use a timed bottom time ( 1.5 minute maximum) to avoid unconsciousness on return to the surface.

On Ascent to the Surface:

* The lung re-expands to normal, the PCO2 becomes elevated as more diffuses into the lung and the PO2 drops dramatically.

* In the blood the PCO2 elevates depending on the depth of the dive and the amount of exercise. Deep dives drive more CO2 from the lungs into the tissues and increases the problem. There is a right shift of the HgbO2 curve.

* When the break point is reached , the chemoreceptors are stimulated by CO2, thus stimulation of respiration. Low O2 also stimulates respiration.

* In the brain:

o CO2 stimulates respirations

o Vasodilation encourages O2 consumption

o Latent hypoxia occurs

o Unconsciousness ensues

* On ascent the lungs re-expand reducing the favorable diffusion gradient for oxygen. Shallower depths cause this gradient to approach zero, the diver reaching a critical state of hypoxia.

* Hypoxia causes unconsciousness, possibly before the diver reaches the surface.

* Signs and symptoms of latent hypoxia (Shallow water blackout)

o Extreme weakness, trembling, unconsciousness in the water, amnesia of the event, drowning.

THE PHYSIOLOGY OF SHALLOW-WATER BLACKOUT

In addition to the changes due to the Physics of Dalton’s Law, there are other physiological changes that take effect during shallow water blackout and free diving.

Diving Reflex

The human body is capable of remarkable adaptations to the underwater environment. Even untrained divers will show a dramatic slowing of the heart when immersed. This is commonly referred to as the diving reflex. Immersion of the face in cold water causes the heart to slow automatically. Chest compression can also slow the heart. Untrained divers can experience up to a 40 percent drop in heart rate. Trained divers can produce an even lower heart rate some can slow to an incredible 20 beats per minute.

Spleen Effects

Trained free divers develop several other physiological adaptations that lead to deeper and longer dives. The spleen, acting as a blood reservoir, assists trained divers in increasing their performance. Apparently their spleen shrinks while diving, causing a release of extra blood cells.

According to William E. Hurford M.D., and co-authors writing in The Journal of Applied Physiology, the spleens of the Japanese Ama divers (professional women shellfish free divers) they studied decreased in size by 20 percent when they dove. At the same time their hemoglobin concentration increased by 10 percent (Volume 69, pages 932-936, 1990).

This adaptation, similar to one observed in marine mammals (the Weddell seals’ blood cell concentration increases by up to 65 percent), could increase the divers ability to take up oxygen at the surface. It could also increase oxygen delivery to critical tissues during the dive.

Interestingly, the spleens contraction and the resultant release of red cells is not immediate- it starts taking effect after a quarter-hour of sustained diving. This spleen adaptation, as well as other physiologic changes, probably take a half-hour for full effect. This might account for the increased performance trained free divers notice after their first half-hour of diving, and also may be one of the causes of unexplained heart failure in the diver with a border line heart condition.

Other adaptations

There are other known adaptations: blood vessels in the skin contract under conditions of low oxygen in order to leave more blood available for important organs, namely the heart, brain and muscles. Changes in blood chemistry allow the body to carry and use oxygen more efficiently. These changes, in effect, squeeze the last molecule of available oxygen from nonessential organs. Most importantly, the diver’s mind adapts to longer periods of apnea (no breathing). He can ignore, for longer periods of time, his internal voice that requires him to breathe.

PREVENTION OF SHALLOW-WATER BLACKOUT

Shallow-water blackout was a hot research topic for diving physicians in the 1960s, when they worked out the basic physiology described above. They also studied the case histories of SWB victims, identifying several factors that can contribute to this condition. These include hyperventilation, exercise, a competitive personality, a focused mind-set and youth.

The use of hyperventilation in preparation for freediving is controversial. No one disagrees that prolonged hyperventilation, after minutes of vigorous breathing accompanied by dizziness and tingling in the arms and legs, is dangerous. Some diving physicians believe that any hyperventilation is deadly because of the variation in effects among individuals and on one person, from one time to another. Other physicians, studying professional freedivers such as the Ama divers of Japan, found that they routinely hyperventilated mildly and took a deep breath before descending. Their hyperventilation is very mild; they limit it by pursed lip breathing before a dive.

Probably the best approach can be found in the U.S. Navy Diving Manual (Volume 1, Air Diving), which states: Hyperventilation with air before a skindive is almost standard procedure and is reasonably safe if it is not carried too far. Hyperventilation with air should not be continued beyond three to four breaths, and the diver should start to surface as soon as he notices a definite urge to resume breathing.

Learn the deadly effects of exercise underwater and plan to deal with this situation.

Freedivers learn to prolong their dives by profoundly relaxing their muscles (see the section on deep diving). Most divers make minimal use of their muscles except when they fight a fish or free an anchor. A physician writing in an Australian medical journal found a common scenario for diving deaths in Australia is the experienced diver with weight belt on, speargun fired.

Medical researchers feel that many pool deaths, classified as drownings, are really the result of shallow-water blackout. Most occur in male adolescents and young adults attempting competitive endurance breath-holding, frequently on a dare. Drowning victims, especially children, have been resuscitated from long periods of immersion in cold water 30 minutes or more. The same is not true for victims blacking out in warm-water swimming pools. Warm water hastens death by allowing tissues, especially brain tissues, to continue metabolizing rapidly; without oxygen, irreversible cell damage occurs in minutes.

SUMMARY

* Do not hyperventilate to excess no more than three or four breaths.

* Reduce exercise at depth.

* Recognize the danger of focusing.

* Don’t hesitate to drop your weight belt.

* Avoid endurance dives.

* Adjust your weight belt so that you will float at 15 feet.

* Don’t practice breath-holding in a swimming pool. Always have an observer standing by to assist.

Learn the basics of CPR and think about adapting them to your diving arena, whether diving from shore, board or boat.

Reference: Hong, SK. 1990. Breath-Hold Diving. In: Bove and Davis, Diving Medicine, 2nd ED., Philadelphia, PA: WB Saunders, pp 59-68.