Recreational scuba diving, patent foramen ovale and their associated risks

http://www.frogkick.dk/library/medicine/smw-09706.pdf

The Impacts Of Smoking On Diving By Art Ranz, DDS

Cigarette smoking is one of the largest preventable health and death risks in the United States. It receives enormous amounts of negative media attention and yet millions of people start smoking every year. Unfortunately, it is frequently difficult to have a prudent, scientific discussion about the risks of smoking with someone who is addicted to nicotine. The addiction leads smokers to rationalize or deny the risks of smoking. However, this `head in the sand` response allows them to ignore the obvious impact that smoking has upon their bodies and the more subtle ways it effects many aspects of their lives, such as scuba diving.
The effects of smoking are especially significant for persons who participate in scuba diving. A review of scientific literature about the body's reaction to smoking and nicotine addiction illustrates how smoking can effect diving performance. While the diving and health limitations imposed by tobacco use vary according to the degree of use, tobacco always has some impact on individual health.
The most extensive, long-term, prospective study on smoking and other health issues is the Framingham study. This ongoing study has followed 5,000 people for more than 34 years, providing a wide range of statistical information. For instance, the 30-year-old who smokes 15 cigarettes a day - or less than one pack - shortens his life by five years. Smokers experience a 20-fold increase in lung cancer and greatly increased cancer rates in other organs, including skin, bladder, pancreas, mouth and throat. Smokers have twice the risk of cardiovascular disease, 2.2 times the number of strokes and 3.5 times more intermittent claudication expressed as leg cramping due to a lack of circulation. At any given age, the risk of dying for any reason is twice that of a non-smoker. Smokers have seven times the normal incidence of airway damage and respiratory distress. Children who smoke beginning at age 14 only develop 92 percent of the lung function, on average, that a non-smoking child does. This loss of function is permanent. Obviously, efficient lung function is essential to managing stressful situations and promoting efficient inert gas removal from a diver's blood. Poor circulatory efficiency can have dangerous impacts on inert gas elimination and oxygen delivery to needy muscles, greatly effecting a diver's personal safety. Atherosclerotic plaques in blood vessels form twice as fast when smoking is added to a high fat diet.
There are great increases in the LDL (`bad cholesterol`) that reduces circulatory efficiency and complicates inert gas removal. Inert gas (especially nitrogen) appears to lodge in fatty deposits, creating likely sites for bubble congregation and growth. Furthermore, 90 percent of patients with infections after spinal surgery are smokers and bone marrow density in men is decreased almost 20 percent and in women 25-30 percent, while the incidence of back pain from a work related injury increases from one in five to one in two for smokers. Hyperbaric bone damage (osteonecrosis) has gained increasing concern among medical professionals as researchers strive to demonstrate the cause of occasional bone degradation. To be sure, reduced bone density due to smoking aggravates the problem and some researchers are suggesting a more careful analysis of the relationship between hyperbaric damage and tobacco smoking.

How does tobacco cause such dangerous repercussions?

There are four groups of dangerous substances present in cigarette smoke:

1. Carcinogens and co-carcinogens are mostly polycyclic aromatic alcohols that directly initiate cancer formation. These affect areas in direct contact with the smoke and also distant organs through absorption into the bloodstream.
2. Irritants cause immediate coughing and broncoconstriction, inhibit cilliary action in the lung and stimulate mucus secretion.
3. Chronic exposure to nicotine induces an increase in the number of nicotinic cholinergic receptors in the brain, causing structural and functional changes in the brain and nervous system. It induces tolerance and physical and psychological changes upon withdrawal. These are classic developments from an addictive drug.
4. Toxic gases are inhaled, including carbon monoxide, hydrogen sulfide and hydrogen cyanide.

Smoking related cancer is tragic, costly and largely preventable, but the direct impact to diving is often less obvious. By way of illustration, the irritants present within smoke induce a chronic inflammation of the alveoli causing the body to produce proteolytic enzymes that eat away at the alveolar wall. Cilia are microscopic hairs that fan and carry harmful particles out of the lung. The irritants present in smoke impede these cilliary actions. With the addition of increased secretions, the lung has now lost a significant part of its defenses from outside agents. Chronic bronchitis develops, making smokers more susceptible to emphysema, viral and bacterial infections. As this process continues over the years and more alveolar damage occurs, there is a loss of capillaries in the walls which causes `ventilation-perfusion abnormalities.`
This damaging chain of events leads to a reduction in the area of alveolar membrane available for gas exchange and also to perfusion of unventilated areas and ventilation of unperfused areas. In simple terms, gas exchange is compromised and air (or other gases) is not reaching the blood for exchange. General lung function is often severely compromised in the smoking population as is evidenced by several clinical measurements in the lung. The standard measure of lung function is the forced expiratory volume in one second or FEV1. This is the amount of air that can be exhaled in one second.
The Framingham study showed the FEV1 to be decreased to 80 percent of expected values in smokers. This decrement in lung function creates less efficient ventilation on exertion and decreases the force of the cough (a vital protective mechanism for the lung) and may indicate a general degradation of lung health. The forced vital capacity (FVC) is another common measure of lung function and measures the amount of air one can expel from a full inhale to a full exhale. On average, smoking reduces FVC by 10 percent in moderate smokers. A 10 percent reduction in vital capacity is a significant indication of lung dysfunction and an obvious deterrent to pulmonary exchange in decompression.
Nicotine is not only a powerfully addictive drug, but a potent pharmacological agent. Nicotine promotes platelet aggregation and fibrinogen formation, which are precursors to the clots that obstruct small blood vessels. An obstruction initiates negative repercussions that increases the risk of diving and decompression. The heart rate increases, elevating oxygen consumption and the shrinking of small blood vessels increases total peripheral resistance. The resistance, in turn, causes more problems such as increased blood pressure and poor circulation in the periphery of the body. Peripheral circulation involves the miles of very small blood vessels all over the body. The vessels are problematic in efficient inert gas elimination. For example, the extremities contain numerous areas of reduced circulatory efficiency such as the joints (responsible for the majority of decompression sickness). When divers begin to get chilled, a natural reduction in blood circulation to the peripheral system occurs to maintain a reasonable core temperature. Smoking exacerbates this problem as studies show that the circulation in small blood vessels is reduced 19 percent after just two cigarettes. Poor gas exchange and increased risk of decompression sickness results.

The Problem with Carbon Monoxide

It is important to understand the Oxygen Dissociation Curve when reviewing the impact of smoking on oxygen transport mechanisms. This curve illustrates the assimilation of oxygen in large amounts even with low oxygen pressures in the lungs. Hemoglobin picks up the oxygen from the lungs and transports it to the tissues where it is released. Several factors control how easily the oxygen is released from its hemoglobin carrier. Higher concentrations of carbon dioxide in the blood cause the body to react as if there is poor ventilation and a greater need for oxygen. This environment initiates the release of more oxygen to the tissues. Under these conditions the hemoglobin affinity for oxygen is reduced, making it easier for oxygen to be released. In reference to the Dissociation Curve, this condition is sometimes referred to as a `shift to the right` and results in a greater supply of oxygen to the tissues. However, a `shift to the left` prevents oxygen from being released to the tissues. This condition is prominent with the carbon monoxide accumulation that results from smoking.
The primary mechanism behind the risk of carbon monoxide impact is twofold. First it binds to hemoglobin 250 times better than oxygen, making a compound called carboxyhemoglobin. This compound replaces the oxygen in the hemoglobin molecule and prevents the leftward shift of the Oxyhemoglobin Dissociation Curve. The increased affinity of hemoglobin for oxygen results in a decrease in oxygen carrying capacity and impaired release of the oxygen once it reaches the tissues. Non-smokers have about one percent carboxyhemoglobin while smokers have close to 15 percent. To illustrate the severely harmful effects of CO in the blood, imagine that an individual has 50 percent of their hemoglobin bound to CO. Compare this individual with another person who has lost half of their hemoglobin (due to severely bleeding ulcers, chronic gastrointestinal bleeding or massive injuries, for instance).The individual who has 50 percent of their hemoglobin bound with CO will die. But, the person who has a 50 percent loss of hemoglobin will still not experience hypoxia while in a resting state.
Furthermore, chronic hypoxia (reduced oxygen) results from the smoking induced impairment of oxygen transport and causes the production of more red blood cells. The red blood cells are the containing mechanism for oxygen transport in the hemoglobin. The Framingham study has shown that smokers have a significant increase in the percentage of red blood cells in the blood (increased hematocrit). Normally the red blood cells are about 35-40 percent of the blood by volume. Smoking can cause this to increase by 20 percent, making the blood much more viscous, inducing obvious complications to efficient circulation. This problem is further aggravated by the pressures found below the surface and causes sludging of the red blood cells in the small capillaries, damaging the cells lining the blood vessels (endothelium).
The transport of hydrogen cyanide to the lungs during smoking creates additional decrements to health and diving safety. This noxious gas directly prevents use of oxygen by the cells by interfering with the cellular engine- the mitochondria. Even small amounts of hydrogen cyanide are deadly. The presence of this toxic substance causes direct injury to the lung by interfering with the alveolar enzymes normally responsible for maintaining the integrity of the alveolar membranes. Hydrogen sulfide is another dangerous substance in cigarette smoke and is a direct toxin to most all cell life, especially to tissues it directly contacts such as the lungs. The numerous impediments to a healthy circulatory and respiratory system establish an insidious cycle of unacceptable risk to safe diving practices.
For instance, when increasing environmental demands require the delivery of more oxygen, the smoker is at a serious disadvantage. An increased supply of oxygen in the inspired air does not help delivery of more oxygen to the tissues where it is needed. There are two ways to increase oxygen delivery with increased demand: increasing blood flow through the tissue and raising the coefficient of oxygen usage. The former is compromised by the inferior cardiovascular condition of the smoker (consider the number of serious atheletes who smoke). The latter is increased by two things that happen automatically: greater partial pressure of oxygen between blood and tissue (resulting from the increase in oxygen consumption in the tissues) and the rise in carbon dioxide as a byproduct of increased metabolism. This increase in carbon dioxide causes the hemoglobin curve to shift to the right and allow more release of oxygen. This typically beneficial reaction is countered by the smoker's CO poisoning and the shift back to the left. The really adverse effect of smoking is the 20-30 percent rise in peripheral resistance (closing or restriction of small blood vessels) caused by the presence of nicotine. Small blood vessels are where the exchange of gases takes place and a reduction of circulatory efficiency in this area may be significant. Reduced blood flow and impeded oxygen release prevent efficient oxygenation especially when it is needed most. Therefore, the simple act of smoking initiates circulatory reactions that place divers in harm's way. Whether from decompression illness risk or ineffectual response to stressful environments, the smoker intentionally places himself and his team at greater risk.

Understanding Smoking's Short Term Impact on Diving

Smokers and those who choose to dive with them should consider not only the long-term health impacts, but the immediate implications of smoking and diving. Consider the increase in sudden cardiac death, the reduced ability to absorb and deliver oxygen to the cells, the obvious cognitive impairment, the likely increased risks of decompression illness, the increased likelihood of lung overpressurization injuries and the many other dangerous effects of smoking and diving. With all of the damage and risk associated with smoking and diving, what possible justification (save addiction) can there be to continue? Individuals with drug addictions, which is clearly what smoking is, must be encouraged to seek assistance and be freed from this damaging habit.
Consider that many `diving deaths` are thought to be cardiovascular in nature: cardiac arrhythmias, myocardial infarcts and strokes just to name a few. The smoker's incidence of these maladies is much higher. With this in mind, can a smoker be a responsible diving buddy? Can they help other divers out of trouble or are they merely likely to create problems? With increased anxiety, the heart beats faster and the breathing rate increases. Increased heart rate is the number one cause of increased oxygen use by the heart muscle and the heart of a smoker has a reduced ability to deal with the increased demand for oxygen. As a result, pulmonary exchange is poorer and utilization of breathed gases is compromised, leading to greater gas consumption and reduced ability to assist other divers. All dives are decompression dives. The list is long on how smoking causes decreased gas exchange and potential for decompression sickness. The ability of the lungs to filter bubbles is a major reason that every dive does not result in clinical decompression injury. The lungs are directly damaged by smoking. Ventilation, monitored by FEV1, is decreased, and the Forced Vital Capacity, or FVC, is decrease by at least 10%. With decreased pulmonary function, the lungs' function as a big bubble trap is compromised and the risk of decompression illness is increased.
Nicotine causes significant peripheral constriction, further compromising elimination of gas in the areas most difficult to get the inert gases out the small vessels and the area they perfuse. It causes increased platelet aggregation and fibrinogen production which only gives the body a head start on the same process that bubbles produce in occluding vessels and damaging vessel walls. One prominent theory of decompression illness suggests that bubbles in the bloodstream cause damage to the endothelium, the lining of the blood vessel walls, setting off a cascade of body reactions to repair itself. With nicotine in the body this process is aggravated and accelerated, causing platelets and blood clots to clog the small blood vessels. This reduces the body's ability to get rid of inert gasses. Nicotine gives the body a head start on the bad things that happen with bubble formation. The smoker has increased numbers of red blood cells per volume, or increased hematocrit, which sounds good, but actually makes the blood `thicker.` Increased atmospheric pressure from diving causes sludging of red blood cells in small vessels and the clogging of these vessels is aggravated by the increased hematocrit of the smoker. This is more bad news for perfusing the small vessels in the decompression part of the dive. Increased hematocrit may be directly involved with the endothelial damage which has been implicated in DCS. Carbon monoxide inhibits the transportation of oxygen mostly in its effect upon the hemoglobin and the hemoglobin disassociation curve. Smoking directly reduces pulmonary blood volume and the number of open capillaries in the lung, causing a ventilation to perfusion impairment with the obvious impairment of gas transfer at a time when every little bit is vital.
Acute nicotine withdrawal causes severe performance degradation, memory impairment, confusion, impulsiveness and slowed reaction time, just to name a few. Any of these are serious problems when simple decisions become life or death decisions under water. In a recent study of `undeserved hits` (a dive where supposedly all decompression limits are met and ascent rates are appropriate, but the diver still suffers from decompression illness), smoking and lung damage from smoking seemed to play a key role. Two groups emerged, those with intra-cardiac shunts and those without. Those with shunts had more brain symptoms and none smoked, while those without shunts, 50 percent smoked, a remarkable number. These divers experienced mostly spinal neurological sequelae and had deficits identical to divers with rapid ascents and pulmonary barotrauma. This implies that the smokers had occult lung disease that precipitated the pulmonary barotrauma giving more evidence of hindrance on the body's bubble filter. This makes perfect sense when considering the damage caused by smoking on the small airways and the alveolar walls which allow bubble to pass though the system instead of being filtered. Please think about these facts before picking up that next cigarette or diving with someone who smokes. If you smoke, see your doctor for help with overcoming the addiction. Make your diving safe and fun.

References

1. Freund Karen MD et al. The health risks of smoking, The Framingham study: 34 years of follow-up AEP Vol. 3, No. 4 July 1993 417-424
2. American Heart Association. Environmental Tobacco Smoke, Heart and Stoke Guide 1998
3. American Lung Association. Smoking Fact Sheet 1998
4. Sorle Paul. Influence of cigarette smoking on lung function at baseline and follow-up in 14 years: The Framingham study J. Chron Dis Vol. 40, No. 9 pp. 849-856 1987
5. Olofson J. Mortality related to smoking habits, respiratory symptoms and lung function. Eur J Respir Dis (1987) 71, 69-76
6. Wolf Philip MD. Cigarette smoking as a risk factor for stroke: The Framingham Study. JAMA Feb. 19, 1988-Vol 259, No. 7
7. Tager Ira B. Effect of cigarette smoking on the pulmonary function of children and adolescents. Am Rev Respir Dis 1985 131:752-759
8. Beck Gerald Smoking and lung function Am Rev Respir Dis. 1981 Feb;123(2):149-55.
9. Castelli William P. MD Diet, smoking, and alcohol: Influence on coronary heart disease risk. American Journal of Kidney Diseases, Vol. XVI, No. 4 Suppl 1 (October) 1990: pp 41-46
10. Kwiathkowski, Timothy C. Cigarette smoking and its orthopedic consequences. Amer J Orthop 1996 Sept 25(9) 590-
11. Slolnick, ET Exposure to environmental tobacco smoke and the risk of adverse respiratory events in children receiving general anesthesia. Anesthesiology 1998 May:88(5):1144-53
12. Anderson HR Passive smoking and sudden infant death syndrome: review of the epidemiological evidence. Thorax 1997 Nov;52(11):1003-9
13. Valkonen M, Passice smoking induces atherogenic changes in low-density lipoprotein. Circulation 1998 May 26;97(20):2012-6
14. Chan D Cigarette smoking and age related macular degeneration Optom Vis Sci 1998 July;75(7):476-84
15. Solberg Y The association between cigarette smoking and ocular diseases. Surv Opthalmol 1998 May-Jun;42960:535-47
16. American Lung Association Fact Sheet: Second Hand Smoke 1998
17. Hackshaw AK Lung cancer and passive smoking Stat Methods Med Res 1998 Jun;7(20):119-36
18. Armin Ernst, MD Carbon Monoxide Poisoning NEJM Vol. 339, No. 22, Nov. 26, 1998 pp. 1603-8
19. Timisjarvi J et. al. Effect of smoking on the central circulation at rest and during exercise as studied by radiocardiograpy. Mukliarmedizin 1980;19(50:239-43
20. Sommese Teresa MD et al. Acute effects of cigarette smoking withdrawal: Review of the literature. Aviation, space and Environmental Medicine Feb. 1995 pp. 164-7
21. West Robert Ph.D. What happened to anxiety levels on giving up smoking? Am J Psychiatry 154:11 Nov. 1997 1589-92
22. Wilmshurst P Role of cardio-respiratory abnormalities, smoking and dive characteristics on the manifestations of neurological decompression illness. Clin Sci 1994 Mar;86(3):297-303
23. Brodbeck John R. et al. Best and Taylor's Physiological Basic of Medical Practice Ninth Edition Williams and Wilkins Company. 1973

The Quarter Turn That Kills

At least one diver won’t be spending the holidays with family and friends this year, thanks to the dangerous practice of opening a scuba tank valve all the way, only to close it back a quarter turn. According to an article in the Daytona Beach News-Journal, an Edgewater, Florida, diver perished October 9 with more than 140 bar/2,000 psi remaining in his tank. His valve, however, was only open one-quarter turn.

The same thing happened to cave-diving pioneer Sheck Exley over four decades ago. Exley was descending, head-first, into a narrow crack in what is now Wes Skiles Peacock Springs State Park. Exley had accidentally closed his tank valve all the way, then opened it a partial turn, as he was taught. His regulator still breathed fine at the surface but, upside down at 20 m/65 ft, Exley found himself starved for air.

Exley ended up surviving what had been a very close call, and made it a standard of practice in cave diver training to either open valves all the way or fully close them. This has become a standard of practice in tech diver training as well. For reasons passing understanding, however, it has not become a standard of practice in recreational diving.

Where Does This Come From?

It’s common in industries ranging from welding to HVAC to never fully open a cylinder valve. The concern is that, if you try to force open a valve that is already open, you may damage the valve. Well, guess what? If your acetylene valve is only partially open, you may not be able to weld. If your scuba tank is only partially open, you may very well die.

In shallow water, a partially open valve may still be capable of delivering sufficient gas. At depth, however, the same valve setting can leave a diver starved for air.

Forcing a tank valve past its normal stopping point in either direction is a bad idea — even though modern scuba valves are a lot harder to damage than people realize. Curiously, you never hear dive instructors say, “Close your valve all the way and then open it a partial turn.”

In the final analysis, valve damage beats being dead.

So What Should You be Doing?

So that you live to enjoy another holiday:

• Open and close scuba tank valves only by turning them very gently. Stop as soon as you feel resistance. A valve turnwheel that does not turn easily requires service.

• Make sure your valves are either all the way open, or all the way closed.

• Be wary of well-meaning buddies and even dive boat crew checking your valve position for you. Even divemasters have been known to accidentally close a valve all the way, then open it a partial turn. Because this can work in shallow water, divers may not realize they are at risk until it is too late.

• To help ensure your valve is open all the way, take several deep breaths from your regulator while looking at your pressure gauge. The needle or reading should hold rock steady. If it drops with each breath, your valve is closed. If it fluctuates with each breath, your valve is only partially open. Do not dive until the valve is open all the way.

The next time you run into an instructor teaching this archaic and dangerous practice, set him straight. Better to ruffle some feathers than to bury a dead student.

Apeks TX50. Diver deaths result in changes to Navy Dive Manual, equipment.

Norfolk. Va. -Navy divers James Reyher and Ryan Harris both went down together, to a rare scuba diving depth of 150 feet, to finish a training mission needed for a deployment–but they didn’t return to the surface alive.

The dive that killed the two sailors was unprecedented according to the Command Master Diver of EOD Group 2, more than 31,000 dives have been performed by their command . Never before had there been a training dive done at that depth in the last five years.
The question now is whether the decision to take the risk and do the deep dive is enough to charge the 2 senior leaders of Company 2-3, Mobile Diving and Salvage Unit 2 with involuntary manslaughter.
The unit’s master diver, Senior Chief James Burger, and the officer-in-charge, Chief Warrant Officer Mark Smith, are facing a possible court-martial for their role in the decision-making process that led to the deaths.
After two days of testimony, the Article 32 hearing for both men was formally closed Thursday afternoon.
New details emerged during questioning from Navy investigators, who say there are two possible theories for why Reyher and Harris died.
Their connecting rope to the boat above could have gotten tangled around something inside the Superpond at Aberdeen Proving Ground. A survey of the bottom by NCIS agents found metal beams, copper wire, and other hazardous obstacles that divers could get stuck on.
Investigators also think both of Reyher’s breathing regulators weren’t working when they got to the deeper depths. That regulator is the Apeks TX-50.
During the hearing, it came to light that several of Reyher and Harris’s rescuers also had problems using the same type of regulator, either not giving enough air or freezing over while trying to get down to save them.
The Navy has since barred the use of that regulator in cold water diving.
According to witness testimony, though, the equipment failures still came after “deficiencies in decision-making” by Smith and Burger.
When the preferred method of using the MK-16 diving system was no longer an option due to electronic failure, Navy evaluators say they had other options to finish the mission besides scuba.
The Navy’s normal diving limits for scuba are 130 feet, unless a commander can prove operational necessity–but Smith and Burger still went ahead with what many witnesses called “a dangerous dive.”
After the February deaths, the Navy diving manual was actually changed, to specifically state that “there is no such thing as an operational necessity in training,” to make sure this never happens again.
The investigating officer of the Article 32 hearing will take about two weeks to make his recommendation on whether the involuntary manslaughter or dereliction of duty charges are proper in this case.

Then, it will be up to the commanding officer of Naval Expeditionary Combat Command at Little Creek whether to actually convene a court-martial.

“Always analyse your gas” – Statement from the NACD - August 13, 2013

Following a recent fatality at Ginnie Springs, the National Association for Cave Diving has issued the following statement.

NACD Gas Analysis Advisory

The recent death of a cave diver highlights the necessity to review some critical procedures that we should be doing before all dives – gas analysis. A couple of years ago there was a cave diver death in Cozumel that resulted from breathing high carbon monoxide content in a cylinder. This created quite a commotion that caused the sales of CO analyzers to jump quite a bit. These days it’s not uncommon to see divers analyzing their cylinders for CO during the pre-dive process. However, even with that awareness it is a bit surprising that there are still divers that do not analyze all cylinders for oxygen content. While the NACD does not have courses for mixed gas procedures diving at this time, all NACD instructors should be emphasizing the need for gas analysis during the pre-dive process.

It is always worth having everything you need to hand when analysing and labelling diving gas. 990 Magazine

Divers should re-analyze all cylinders to be used on a dive at the site during the pre-dive process and make sure the cylinders are properly labeled with oxygen content, helium content (if any helium in the blend), and MOD. This should occur even if the cylinders were personally filled by the diver. Each and every cylinder should be analyzed and clearly labeled, even if there is an isolator connecting the cylinders, and regardless what gas is believed to be in the cylinder.

While it is understood that not everyone may own enough cylinders to permanently mark them with content and MOD, cylinders being used for 100% oxygen should be permanently marked and only used for 100% oxygen. However, permanent markings do not substitute for additional labeling. Even permanently marked cylinders need to be analyzed and labeled with content and MOD to show confirmation of the contents. There should never be any confusion about labeling. It should be clear and concise to anyone who looks at it.

Finally, there is some controversy over whether gas analysis should be an individual responsibility or a team responsibility. All divers with mixed gas training of any kind have been instructed that all gas should personally be analyzed prior to every dive. Almost every dive training class emphasizes gas sharing with teammates. With that, there is always the potential for a diver to be breathing from a teammate’s cylinders. Gas analysis and confirmation should be a team project during the pre-dive process.

Rosemary E Lunn analysing a Nitrox stage prior to diving Scapa Flow / 990 Magazine

The lessons to take away from this:

1. Analyze every cylinder, whether you think it is filled with air, Nitrox, Trimix, or Oxygen,
2. Label every cylinder with gas content and MOD
3. Remove all old, Oxygen, Nitrox, and Custom Mix labels if the cylinder is to be repurposed.
4. Make gas analysis a team project.

If you are unfamiliar with or out of practice with analyzing gas contact any NACD instructor and request a gas analysis refresher. If you do not have an NACD instructor nearby contact the training committee and we will provide you with an instructor who can help you.

Gas analysis is not an optional activity. Your life depends upon it.

Rob Neto
NACD International Training Director
NACD International Safety Officer

Source: NACD

Sualtı Dünyası Dergisinin 128'inci sayısı yayında

Sn. Ateş Evirgen, Sualtı Dünyası (Marine Photo) dergisinin 128'inci sayısında, benim  beşinci makaleme de yer verdi.

Derginin web sayfasından (http://www.sualtidunyasi.com.tr) ücretsiz üye olarak, bu ve bundan önceki sayıları online okuyabilirsiniz. (isterseniz acrobat reader formatında kayıtta edebiliyorsunuz)

OXTOX from DAN website http://www.diversalertnetwork.org

OXTOX: If You Dive Nitrox You Should Know About OXTOX

DAN discusses the dangers of oxygen toxicity when using nitrox as a breathing gas

By Dr. E.D. Thalmann, DAN Assistant Medical Director; Captain, Medical Corps, U.S. Navy (retired)

It's a fact: we need oxygen to live. It's because of the way our cells use oxygen that we are able to breathe, exercise, and even think. In each of our cells, structures called mitochondria take the oxygen which diffuses in from our blood, disassemble it into its two component atoms (remember, oxygen - O2 - is composed of two oxygen atoms), and then hook some available hydrogen nuclei to them to form water.

The process releases energy, which is used for all functions of life. The problem is that in disassembling the oxygen molecule, it involves a step in which an extra electron is hooked on. This forms an intermediate called a superoxide anion, and this is a bad actor. It is highly reactive, and it will make mincemeat out of most other molecules it comes in contact with.

These anions are like coals in a furnace: as long as they are contained, we get lots of safe chemical energy; if they get out we get a great deal of damage. The mitochondria are designed to contain these superoxide anions, but just in case some get loose, there are a host of protective chemical reactions designed to sop them up and prevent them from doing any damage.

Besides producing excessive amounts of the superoxide anion, elevated tissue oxygen levels also affect a variety of other biochemical reactions which may affect oxygen toxicity in ways that are only beginning to be understood. Tissue-protective mechanisms and biochemical reactions are tuned to life in an atmosphere containing 21 percent oxygen, or 0.21 atmospheres absolute (ata) oxygen partial pressure. (See sidebar: "Remember Partial Pressure?", page 34.) As the partial pressure increases above this comfortable 0.21 ata, protective mechanisms are slowly overwhelmed and biochemical reactions are affected. This may eventually result in "oxtox," or oxygen toxicity.

Oxtox - What Is It?

Oxygen toxicity is a time duration phenomenon: that is, both time and partial pressure play a role. If an oxygen partial pressure of 2 ata is breathed for a few minutes, there would probably not be any problem. But, breathing it for an hour, might cause problems. This is why oxygen exposure limits are given as partial pressure/time limits. As the partial pressure gets higher, the recommended exposure time gets shorter.

What kind of problems might breathing a high oxygen partial pressure cause? It is the lungs and the brain which are the target organs of major concern in diving oxygen toxicity. Oxygen toxicity in the lungs (pulmonary oxygen toxicity) is like getting a bad case of the flu, but it will rarely cause permanent damage. The most common situation in which pulmonary oxygen toxicity might occur is during very long recompression treatments.

Oxygen toxicity of the brain, commonly referred to as central nervous system (CNS) oxygen toxicity, is different. It can occur during actual diving, and when it does, it can ruin your day - and possibly more. Some symptoms of CNS oxygen toxicity include flashing lights in front of the eyes, tunnel vision, loud ringing or roaring in the ear (tinnitus), confusion, lethargy, a feeling of nausea or vertigo, areas of numbness or tingling, and muscular twitching, especially of the lips.

These CNS symptoms are inconvenient, and a warning to change to a breathing gas with a lower oxygen partial pressure as soon as possible, but do not put the diver at risk of injury at this point. The big daddy of CNS symptoms does, however. It is the full-blown grand mal convulsion. During a convulsion, a diver will thrash about, perhaps bang his head into something hard, or if underwater, may lose his mouthpiece. The result can be trauma or drowning.

The good news is that convulsions are rare; the bad news is that all the inconvenient CNS symptoms noted above do not always provide warning of an impending convulsion. In some cases, a convulsion may occur without any warning at all. One more piece of good news: the convulsion in and of itself is not harmful, so if you don't crack your head or drown, you should have no permanent damage.

By now you're probably asking where these dire descriptions are leading.

To a better understanding, we hope, of diving on nitrox. As air-breathing sport divers need to know about decompression sickness (DCS), divers using high oxygen in nitrogen mixtures (nitrox) need to know about oxygen toxicity. (To read more about nitrox, see Alert Diver, January/February 1996, p.32.)

Both decompression sickness and oxygen toxicity are rare occurrences; they can be made rarer with good diving practices. With DCS, it's using your table or computer conservatively and keeping the ascent rate down. With oxtox, it's paying attention to the partial pressure and the amount of exposure time.

The main thing we're discussing here is CNS oxygen toxicity, because this is the most dangerous kind. Lung oxygen toxicity is unlikely to be a problem for recreational divers, so it will be mentioned only in passing.

Remember Partial Pressure?

The partial pressure of a gas is a measure of the number of molecules in a given volume - the molecular concentration. The physiological effects of a gas are due mainly to its partial pressure, no matter what the total pressure is.

If a gas has only one component, say 100-percent oxygen, the partial pressure and the pressure are the same. If there is a gas mix, then the partial pressure is the gas fraction times the total pressure. A 50 percent oxygen-in-nitrogen mix has an oxygen partial pressure (pO2) of 1.0 atmosphere absolute (ata) at a depth of 33 feet / 10 meters where the total pressure is 2 ata.

At this depth the 50 percent oxygen would have the same physiological effect as 100 percent oxygen at the surface. Breathing a 100 percent oxygen mix at a depth of 33 feet / 10 meters (2 ata total pressure) would be equivalent to breathing the 50 percent mix at 132 feet / 40 meters (5 ata total pressure).

Royal Navy Studies

The grand old man of CNS oxygen toxicity is Professor Kenneth Donald, who cut his teeth on the problem during World War II in Great Britain. (Want to know more? Read Reference 1, page 40.) At that time the Royal Navy was under pressure to develop the technology used by the Italians to severely damage the battleships HMS Queen Elizabeth and HMS Valiant in the harbor of the port city of Alexandria, Egypt, in 1941.

Italian divers wearing 100 percent oxygen rebreathers, drove a torpedo close into a ship. While submerged to avoid detection, they detached its warhead under the ship's hull, and beat a hasty retreat after a timer was set.

The Royal Navy soon began developing its own band of underwater divers called "Charioteers" to carry out similar missions. Dr. Donald was assigned as a Surgeon Lieutenant to provide medical care during training of the divers using the British 100 percent oxygen rebreathers. The accepted safe limits for breathing 100 percent oxygen at the time (2 hours at 50 feet / 15 meters, 30 minutes at 90 feet / 27 meters) produced enough convulsions that the British Admiralty decided some sort of studies were needed to define the scope of the problem and, hopefully, find a solution.

About to be transferred to the Shetland Islands, Dr. Donald had a change of fortune and proceeded instead to a facility just outside of London, where he found himself heading up a major research effort to get a handle on the problem of CNS oxygen toxicity.

Royal Navy Discoveries

Over the next three years, Dr. Donald's team conducted literally hundreds of exposures on human volunteers (remember, there was a war on). This series of studies formed the basis of what we know about CNS oxygen toxicity, namely:

There is a large individual variation in susceptibility and time of onset to symptoms. This is what is referred to as "oxygen tolerance."

Compared to dry exposures, immersion decreases oxygen tolerance a great deal, decreasing exposure times up to a factor of four or five.

Exercise decreases oxygen tolerance a lot, compared to rest.

Diving in very cold (<49°F / 9°C) or very warm (>88°F / 31°C) water seems to decrease oxygen tolerance.

The goal of the research was to develop a set of oxygen exposure limits - that is, a table that indicated how long a diver could safely breathe 100 percent oxygen at various depths. The main obstacle toward developing a good set of exposure limits was the large individual variation in oxygen tolerance. Not only did the time of onset and severity of CNS symptoms vary considerably between divers, but in a given diver there was a large day-to-day variation. One stalwart individual made dives twice a week for over three months on exactly the same dive profile (70 feet / 21 meters, 65°F / 18°C, at rest, 100-percent oxygen) until signs of oxygen toxicity developed (again, a notable contribution to the war effort!). His symptom onset time was random and ranged from seven minutes to 148 minutes!

As a result of these studies, the Royal Navy considered it unsafe to breathe 100 percent oxygen below a depth of 25 feet / 7.6 meters (an oxygen partial pressure of 1.76 ata). In fact 25 feet / 7.6 meters was the shallowest depth tested. No particular time limit was given for this exposure, but the longest time tested was two hours. The carbon dioxide absorbent canisters of the diving rigs of the day rarely lasted more than 90 minutes.

The Royal Navy made deeper dives by using nitrogen-oxygen mixtures in the newly developed semi-closed circuit rebreathers. This was the beginning of so-called "mixed-gas diving," where the breathing gas is mixed from oxygen and nitrogen rather than simply being compressed from atmospheric air.

U.S. Navy Studies

In the 1950s, Dr. E.H. Lanphier, then a Lieutenant in the U.S. Navy Medical Corps, undertook a series of studies at the Navy Experimental Diving Unit (NEDU), located at that time in Washington, D.C., to investigate whether oxygen exposure limits could be developed for 100 percent oxygen dives deeper than 25 feet / 7.6 meters. Table 1 (below) shows the limits that he recommended. The 100 percent oxygen exposure limits in Table 1 remained in use up to 1970 and with only slight modifications were used through 1991 when they were again changed.

Dr. Lanphier was also charged with investigating how these limits should be applied to the oxygen partial pressures encountered in mixed-gas nitrox diving. During nitrox diving, oxygen partial pressures similar to those used in 100 percent oxygen diving may be encountered, but since nitrogen has been added, these partial pressures are reached at a greater depth and, therefore, at a greater breathing gas density.

U.S. Findings

From his studies, Dr. Lanphier concluded that the increased gas density encountered during mixed-gas nitrox diving required the exposure times at a given oxygen partial pressure to be shorter than for 100 percent oxygen rebreathers, which can be used only at shallow depths, and which result in a lower gas density. The reason for this decreased tolerance during nitrox diving was thought to be due to decreased carbon dioxide elimination at the greater depths, resulting in higher blood carbon dioxide levels. This would make the diver more sensitive to oxygen toxicity.

These U.S. Navy nitrox mixed-gas nitrogen-oxygen exposure limits are shown in Table 2 (page 36). Notice that compared to those for 100 percent oxygen breathing in Table 1, these are quite a bit shorter for the same partial pressure. With the advent of closed-circuit oxygen rebreathers, the U.S. Navy no longer uses nitrox scuba and no longer publishes nitrox exposure limits in their official diving manual.

The Conflict - and Some Good Advice

The British disagreed with Dr. Lanphier's findings, and the Royal Navy set exposure limits for nitrox diving that were no different than for 100 percent oxygen diving. This area remains controversial - Dr. Donald's case for keeping the exposure limits the same for both 100 percent oxygen and nitrox diving has weaknesses and should not be accepted as proven.

Dr. Lanphier's work is certainly compelling enough that divers should be very cautious before extrapolating oxygen exposure limits based on 100 percent oxygen rebreathing directly to nitrox diving at higher gas densities. Ideally, nitrox limits should be tested at the maximum gas density anticipated for their use.

CO2 Retention

Why would carbon dioxide (CO2) retention become a problem at increased gas densities? There have been many studies showing that as depth increases while breathing air, the high oxygen and increased gas density will normally slow the rate at which we breathe and thereby the rate at which we eliminate carbon dioxide. This will raise the blood levels of carbon dioxide. On top of this, however, is the fact that, because of individual variations, not all divers will slow their breathing in the same amounts.

Dr. Lanphier investigated the problem of divers who tended to breathe more slowly during diving than would normally be expected - so-called "carbon dioxide retainers." He felt that these individuals would be at an especially high risk of CNS oxygen toxicity when breathing high oxygen in nitrogen gas mixtures. Should a nitrox diver be concerned about whether he is a carbon dioxide retainer? Unfortunately, there is no good test to reliably identify carbon dioxide retainers. The best strategy at present is to use conservative oxygen exposure limits.

More U.S. Studies - Oxygen Exposure Limits

In the late 1970s and early ?s, the Navy Experimental Diving Unit (NEDU) - now moved to Panama City, Fla.- conducted a series of studies to look at longer exposure times breathing 100 percent oxygen at shallow depths while exercising at levels typically encountered by combat swimmers while swimming long distances underwater. (Remember, exposure times developed using divers at rest may well cause problems for exercising divers, since exercise decreases oxygen tolerance.)

The conclusion of the study was that four-hour exposures at 25 feet / 7.6 meters (1.76 ata) had a low probability of causing CNS symptoms but were not without hazard since a convulsion was reported at this depth after 72 minutes of exercise. Because of this hazard, it was recommended that routine exposures be carried no deeper than 20 feet / 6.1 meters (1.6 ata) for up to four hours, with a single excursion between 21 and 40 feet / 6.4 and 12 meters for 15 minutes, or between 41 and 50 feet / 12 and 15 meters for five minutes.

Even this recommendation does not completely eliminate the possibility of a convulsion. One diver had a convulsion at 20 feet / 6.1 meters approximately 48 minutes after making a 15-minute excursion to 40 feet / 12 meters at the beginning of the dive. These studies had their share of oxygen convulsions and verified their unpredictability as observed by Dr. Donald some 40 years earlier. One feature of these convulsions that deserves mentioning is that they usually occurred with little or no warning.

With the advent of nitrox diving it is wise to consider these studies. Dr. Andrea Harabin, a scientist at the Naval Medical Research Institute (NMRI) in Bethesda, Md., analyzed the human oxygen exposures from the NEDU studies and used a mathematical model to predict the probability of CNS oxygen toxicity symptoms occurring. (See Reference 2, page 40 for details.)

When she considered all symptoms which resulted in the diver stopping his dive, she found that the model had a threshold at 1.3 ata; that is, the probability of a CNS symptom occurring at or below this level should be essentially zero.

Some of the CNS symptoms that caused dives to be halted could have been due to many other reasons besides oxygen toxicity and were classified as "Probable." In contrast, with "Convulsions" and "Definite Symptoms" (see Table 3, page 37), there is usually no question that oxygen toxicity is the culprit. When Dr. Harabin considered just the convulsions and definite symptoms, she found the thresholds to be 1.7 ata. This analysis again reflects the large degree of uncertainty inherent in these types of human exposures.

USN 100 Percent Oxygen Rebreather Exposure Limits (1954)

TABLE 1

Normal Operations
Depth (feet) 10 15 20 25	Time (min) 240 120 90 65

Exceptional Exposure Operations
Depth (feet) 30 35 40 45	Time (min) 45 34 25 15

USN Oxygen Exposure Limits for Nitrogen-Oxygen Mixed-Gas Diving (1956)

TABLE 2

Normal Exposures
Oxygen Partial Pressure (ata) 1.6 1.5 1.4 1.3 1.2 1.1 1.0	Time (min) 30 40 50 60 80 120 240

Exceptional Exposures
Oxygen Partial Pressure (ata) 2.0 1.9 1.8 1.7 1.6 1.5 1.4 1.3	Time (min) 30 40 50 60 80 120 240

What Oxygen Level Is Safe?

So, what levels of oxygen can be breathed safely? Currently, the U.S. Navy is using 1.3 ata as the maximum limit in its closed-circuit rebreathers - the more conservative threshold found by Dr. Harabin for exercising divers. Using these closed-circuit rigs, exposures exceeding eight hours are possible, and at the 1.3 ata level the chance of CNS oxygen toxicity should be very rare.

Very long exposures, however, may put the diver at risk for some lung toxicity symptoms. The National Oceanic and Atmospheric Administration (NOAA) takes a slightly more conservative approach, recommending 180 minutes at 1.3 ata for normal exposures and 240 minutes only for exceptional exposures (see Table 4). This additional conservatism, according to NOAA, "take(s) operational safety considerations into consideration and are sufficient in duration for anticipated NOAA dives."

The NOAA limits shown in Table 4 are based on the results of the NEDU oxygen exposure limit studies done in the ?s, taking the increased gas densities encountered in nitrox diving into account. The "normal exposure limits" are longer than the nitrox limits proposed by Dr. Lanphier in Table 2 (page 36) but are quite a bit shorter than the 240 minutes, 1.6 ata exposure, currently allowed by the U.S. Navy for 100 percent oxygen diving. However, the "exceptional exposure limits" are virtually the same as originally recommended by Dr. Lanphier, showing that there has not been much change in opinion as to what is safe at these higher partial pressures.

PADI, the Professional Association of Diving Instructors, has proposed a limit of 1.4 ata for open-circuit nitrox scuba diving. Because open-circuit scuba diving would not expose divers to this level continuously, in practice it should be as safe, or safer, than the 1.3 ata U.S. Navy limit for continuous exposures. (See sidebar "Continuous vs. Intermittent Exposures," page 40.) In fact, the shallow exposure times in the 1.3- to 1.4-ata range are mainly to avoid lung oxygen toxicity; the likelihood of CNS toxicity at these levels is very low and probably not much different over this range.

Is it possible to breathe oxygen at a higher oxygen partial pressure (pO2)?

The answer is yes, but! Dr. Harabin's analysis gave a threshold limit of 1.7 ata (23 feet / 7 meters) for an exercising diver when considering only "convulsions" and "definite" symptoms. This is uncomfortably close to the 25-foot / 7.6-meter (1.76 ata) depth where a convulsion was reported, so backing off to 20 feet / 6.1 meters(1.6 ata) gives a little more breathing room.

Currently the U.S. Navy would allow an exercising exposure at this partial pressure for up to four hours, but that assumes breathing 100 percent oxygen at 25 feet / 7.6 meters by trained combat swimmers. A depth excursion of only 5 feet / 1.5 meters would put the diver in an area where convulsions have been reported, and divers who tend to retain carbon dioxide during exercise may be at increased risk.

The NOAA limit for nitrox diving at 1.6 ata is 45 minutes for normal diving and 120 minutes for exceptional exposure diving. Again, some conservatism is built into these limits and consideration given to the fact that this partial pressure may be breathed at higher gas densities than would be encountered by the divers using 100 percent oxygen.

During a nitrox dive done at Duke University's F.G. Hall Hypo/Hyperbaric Center at 100 feet / 30 meters, breathing 1.6 ata pO2 (oxygen partial pressure) during heavy exercise, a convulsion occurred after 40 minutes. Perhaps this would not have occurred had there been a lower level of exercise, but it does seem to indicate that the NOAA limit of 45 minutes for 1.6 ata nitrox diving is not overly conservative.

Breathing 100 percent oxygen during the 20-foot / 6.1-meter decompression stop is common practice, and at this depth, the partial pressure will be about 1.6 ata. At this shallow depth, under conditions of rest, the chance of CNS oxygen toxicity should be very low. But, like most things in life, this is not certain, as evidenced by a recently reported oxygen convulsion at 20 feet / 6.1 meters during decompression by a technical diver after completing a dive on the Lusitania.

TABLE 3

Symptoms of CNS Oxygen Toxicity Encountered in NEDU Studies

Convulsions: the most serious symptom and the one to avoid at all cost.

Definite: muscle twitching, tinnitus (ringing in the ears), blurred or tunnel vision, disorientation, aphasia (inability to express oneself by speaking), nystagmus (rapid side-to-side motions of the eye), or incoordination.

Probable: more equivocal signs which could be due to oxygen toxicity as well as other causes: light headdress apprehension, dysphoria ("just didn't feel right"), lethargy, and transient nausea.

Recommendations

One thing you should be impressed with by now is that oxygen toxicity is fickle; convulsions have occurred at shallow depths under conditions where most experts would not have expected them to occur.

So, as an air sport diver, how should you view nitrox diving? The answer is: carefully.

Experts rationalizing why particular oxygen exposure limits do or do not cause oxygen toxicity are like investment analysts rationalizing movements in the stock market - everyone has a reason, but know one really knows why!

First, whenever a gas is breathed with an oxygen fraction above 21 percent, you should assume that oxygen toxicity is a possibility and have appropriate training. This not only means having a buddy clearly visible at all times but also knowing what action to take should oxygen toxicity occur. (See sidebar: "What do you do if oxygen toxicity or a convulsion happens?" )

Second, using equipment designed to compress high oxygen mixtures can be hazardous in itself and requires special training.

Third, what you get in your tank may not be what you expect. A method of analyzing the amount of oxygen in the tank independent of the filling station must be available.

Fourth, if you are attracted to rebreathers, remember that they are complex pieces of life-support gear, requiring much more care and feeding than the good old scuba regulator. If you get into rebreathers, expect to get hit with good-sized training and maintenance costs.

Finally, there is the matter of keeping the possibility of oxygen toxicity to a minimum.

Moving Ahead

For open-circuit scuba diving, consider the "green light" region any oxygen partial pressure of 1.4 ata or less (this is about 82 feet / 25 meters on a 40-percent oxygen mix.) As long as this level is never exceeded, other limitations of open-circuit scuba diving will limit the exposure time to lengths where CNS oxygen toxicity is unlikely to be encountered, even for exposures approaching four hours.

Proceeding With Caution

Between 1.4 ata and 1.6 ata (this is 99 feet / 30 meters on a 40-percent mix) is the "yellow light" region. The possibility of oxygen toxicity at 1.6 ata is low, but the margin of error is very slim compared to 1.4 ata. Individual variation, the likelihood of an unplanned depth excursion causing an increase in oxygen partial pressure, and the possibility of having to perform heavy exercise in an emergency put the possibility of oxygen toxicity at levels where caution should be exercised. Thus, levels of 1.5 to 1.6 ata should be reserved for conditions where the diver is completely at rest, such as during decompression. Again, as noted previously, the dive team must still be prepared for the possibility of an oxygen convulsion at these levels.

Stop!

Above 1.6 ata is the "red light" area. Just don't do it. Yes, there is evidence that short exposures at higher levels of pO2 (oxygen partial pressure) are possible but so are convulsions. At these levels, oxygen exposure depth/time limits must be adhered to. Even mild exercise may put divers breathing high-density nitrox mixes at increased risk; and even open-circuit scuba divers can achieve durations likely to get them into trouble at these levels. Diving using these high partial pressures of oxygen should be left to the trained professionals who can weigh the risks and benefits and who have the necessary training and support structure in place, if an oxygen convulsion occurs.

Finally...

Nitrox diving may extend bottom times or decrease the possibility of decompression sickness, depending on how it's used, but it adds to the risk of oxygen toxicity. Decompression sickness rarely occurs in the water and is rarely life-threatening. When it happens underwater, however, life support is usually not an issue - instead, attention is focused on getting to a treatment chamber. If an oxygen convulsion occurs, it almost always occurs underwater, greatly complicating treatment. So while the probability of a convulsion may be low, the possibility of severe injury or death is high if it does occur. Taken together this makes it a risky occurrence, and each diver needs to consider that risk whenever nitrox is used. Experience and good training are essential. This is an area that requires team diving, with the whole team full trained in nitrox diving.

What do you do if oxygen toxicity or a convulsion happens?

Editor's note: After reading the article on nitrox in the January/February 1996 Alert Diver, a DAN member asked what the recommended procedure was in the event of an underwater oxygen convulsion. An oxygen convulsion in the water is rare but potentially life-threatening. Like learning CPR, practicing the proper handling of an oxygen convulsion is maintaining a skill you hope you'll never use. The organization with the most experience with 100 percent oxygen diving is the United States Navy. Its recommendations for managing oxygen toxicity is as follows:

According to the USN Dive Manual sections 14.9.1.1 and 14.9.1.2 the suggested procedure for dealing with seizures is:

Management of Nonconvulsive Symptoms. The stricken diver should alert his dive buddy and make a controlled ascent to the surface. The victim's life preserver should be inflated (if necessary) with the dive buddy watching him closely for progression of symptoms.

Management of Underwater Convulsion. The following steps should be taken when treating a convulsing diver:

a. Assume a position behind the convulsing diver. Release the victim's weight belt unless he is wearing a drysuit, in which case the weight belt should be left in place to prevent the diver from assuming a face-down position on the surface.

b. Leave the victim's mouthpiece in his mouth. If it is not in his mouth, do not attempt to replace it; however, if time permits, ensure that the mouthpiece is switched to the surface position.

c. Grasp the victim around his chest above the underwater breathing apparatus (UBA) or between the UBA and his body. If difficulty is encountered in gaining control of the victim in this manner, the rescuer should use the best method possible to obtain control. The UBA waist or neck strap may be grasped if necessary.

d. Make a controlled ascent to the surface, maintaining a slight pressure on the diver's chest to assist exhalation.(see commentary below)

e. If additional buoyancy is required, activate the victim's life jacket. The rescuer should not release his own weight belt or inflate his own life jacket.

f. Upon reaching the surface, inflate the victim's life jacket if not previously done.

g. Remove the victim's mouthpiece and switch the valve to SURFACE to prevent the possibility of the rig flooding and weighing down the victim.

h. Signal for emergency pick-up.

i. Once the convulsion has subsided, open the victim's airway by tilting his head back slightly.

j. Ensure the victim is breathing. Mouth-to-mouth breathing may be initiated if necessary.

k. If an upward excursion occurred during the actual convulsion, transport to the nearest chamber and have the victim evaluated by an individual trained to recognize and treat diving-related illness.

Deciding whether to ascend with a diver who is convulsing can be tricky. In section 8-2.4 of Volume 1 of the U.S. Navy diving manual it states:

"If a diver convulses, the UBA should be ventilated immediately with a gas of lower oxygen content, if possible. If depth control is possible and gas supply is secure (helmet or full face mask), the diver's depth should be kept constant until the convulsion subsides. If an ascent must take place, it should be done as slowly as possible. If a diver surfaces unconscious because of an oxygen convulsion or to avoid drowning, the diver must be treated as if suffering from arterial gas embolism."

Obviously, a full face mask is the best way to perform diving with high oxygen mixes because the diver can be kept at depth until the convulsion subsides. If the diver is breathing from a mouthpiece and it comes out of his mouth, there is no option but to surface the diver, since when the convulsion stops he will try to take a breath. Training and practice are the only ways to ensure that divers will know how to bring a convulsing diver to the surface, using a slow, controlled ascent, if that becomes necessary.

In the section on the management of underwater convulsions, the reference to switching the mouthpiece to the surface position would refer only to rebreathers where an open mouthpiece which inadvertently becomes submerged can flood the UBA.

Also, step g should be modified if the victim is breathing nitrox using open-circuit scuba. If someone is convulsing, you won't be able to remove the mouthpiece; and this should never be done by force. Once the convulsion subsides, if the mouthpiece is secure (or if the diver is wearing a full face mask) and if the diver is still in the water and breathing, then leave everything in place until you can get the injured diver out of the water. If he is not breathing, then remove the mouthpiece once on the surface and begin rescue breathing.

The main goal while the injured diver is in the water is to keep him from drowning. Next is to ensure that his airway is open after the convulsion stops by keeping the neck extended.

Finally, be on the lookout for foreign bodies in the trachea. It is possible to bite off the parts of the mouthpiece between the teeth during a convulsion, which can find their way into the trachea, blocking the airway. In these cases, the injured diver will begin coughing as he returns to consciousness, or he may try to breathe but not get any air into his lungs. Here you need to institute the standard procedures taught in CPR classes for foreign body obstruction of the trachea.

Continuous vs. Intermittent Oxygen Exposures

Remember that CNS oxygen toxicity symptoms are a time-duration phenomenon. They will not suddenly occur the minute a particular partial pressure is exceeded - it takes time. As you can see from the exposure limits in the tables (Table 4), as the inspired oxygen partial pressure increases, the exposure time decreases.

The U.S. Navy limit of 1.3 ata for continuous exposures reflects their desire to keep the risk of CNS symptoms essentially zero, no matter how long the dive.

In nitrox diving, however, divers breathe from open-circuit scuba with a fixed fraction of oxygen in the breathing mix. PADI has chosen 1.4 ata as the maximum open-circuit scuba limit; the limitations placed on duration by open-circuit scuba will ensure that the likelihood of CNS oxygen toxicity is no greater than would be experienced by the U.S. Navy closed-circuit divers.

When using open-circuit scuba, the 1.4 ata maximum oxygen partial pressure is reached only at the maximum depth, and for the vast majority of recreation divers, the time spent at this maximum depth will be limited to times where CNS oxygen toxicity is unlikely to be encountered. At all shallower depths, the oxygen partial pressure will be lower, and the overall exposure during the entire dive is unlikely to have physiological effects significantly different than a continuous 1.3 ata exposure. Be careful when extending this analogy to higher partial pressures, however. Formulas are available for integrating the exposures at various depths to predict overall exposure times when looking only at lung oxygen toxicity. This concept does have some support research done at Dr. C.J. Lambertsen's laboratory at the Institute of Environmental Medicine in Philadelphia, Pa.

The case for CNS oxygen toxicity is much more complicated. Research done at the Navy Experimental Diving Unit (NEDU) in 1986 specifically looked at how brief exposures to oxygen partial pressures of 2.0 ata or greater would impact the overall exposure time at 20 feet / 6.1 meters of sea water (fsw). The results were not clear, and it was obvious that no formula could be developed which would allow integration of oxygen exposures at various depths into a single indicator which would help the diver avoid CNS oxygen toxicity. The best that could be said is that a single 15-minute excursion to 40 fsw/12 msw, or for five minutes at 50 fsw/15 msw, probably had no significant effect. This formed the basis of the current U.S. Navy recommendations. No such research has yet been carried out for high oxygen nitrox diving, to my knowledge.

Dr. E.D. Thalmann

Oxygen Partial Pressure and Exposure Time Limits for Nitrogen-Oxygen Mixed-Gas Working Dives (from NOAA 1991 Diving Manual)

TABLE 4

Normal Operations
Oxygen Partial Pressure (ata) 1.6 1.5 1.4 1.3 1.2 1.1 1.0 0.9 0.8 0.7 0.6	Maximum Duration for a Single Exposure (min.) 45 120 150 180 210 240 300 360 450 570 720	Maximum Total Duration for any 24-Hour Day (min.) 150 180 180 210 240 270 300 360 450 570 720

Exceptional Exposures
Oxygen Partial Pressure (ata) 2.0 1.9 1.8 1.7 1.6 1.5 1.4 1.3	Time (min) 30 45 60 75 120 150 180 240

REFERENCES

Donald KM. Oxygen and the Diver. England: Images, 1993. Available through Best Publishing Co., Flagstaff, Ariz. (This reference also covers all of the NEDU studies mentioned and gives full citations for them.)

Harabin AL, Survanshi SS. A statistical analysis of recent Navy Experimental Diving Unit (NEDU) single-depth human exposures to 100-percent oxygen at pressure. Bethesda, M.D. Naval Medical Research Institute Report NMRI 93-59, 1993.

Note: Both NEDU and NMRI Reports are available through: National Technical Information Service, 5385 Port Royal Road, Springfield VA 22161.