fisiologia edi

ADVANCED DIVING PHYSIOLOGY “Exploring the Physiology of Breathing Air and Mixed-Gases Under Pressure!”

Lee H. Somers, Ph.D.

The human's normal atmosphere, oxygen and nitrogen, produces both toxic and narcotic effects when breathed at high pressure. In addition, the inert gas is absorbed and must be eliminated from the body at a controlled rate to avoid serious complications. Carbon dioxide has significant implications at the higher pressures encountered while diving and may alter the human’s sensitivity to both oxygen and nitrogen. The effects of high pressure on the human body and breathing media must be well understood and respected by all divers. Failure to do so can lead to serious injury or, even, death. The material information in this paper is intended to provide a general overview of specific physiological factors associated with breathing nitrogen-oxygen mixtures at shallow depths, compressed air at intermediate depths, and oxygen-helium-nitrogen mixtures at deeper depths as well as use of high-oxygen EANx or 100% oxygen during decompression. It is assumed that the reader has a working knowledge of basic diving physics and physiology.

GASES FOR DIVING Recreational divers are traditionally trained for use of compressed air only. On the other hand, commercial and military divers have recognized the advantages of alternative gas mixtures for decades. Today, recreational divers are discovering these advantages (and risk) of breathing oxygen, enriched air nitrox, and trimix. The following is a summary of the gases commonly used in diving today. Oxygen Oxygen, one of the most abundant chemical elements on earth, is essential for life. Living organisms use chemical reactions based on oxygen to generate heat and chemical energy, a process known as metabolism. The human body normally functions within a relatively narrow oxygen partial pressure range -- 0.16 ata to 1.6 ata. If the partial pressure of oxygen is too low, a diver will experience hypoxia and may lose consciousness. On the other hand, at significantly elevated pressure oxygen becomes toxic to the central nervous system. Oxygen has considerable value as first aid gas for decompression illness (i.e., decompression sickness and

arterial gas embolism). It is also the principal gas in medical treatment of divers who have experienced decompression illness, carbon monoxide poisoning, and near drowning. Today, there is considerable concern regarding safe handling and use of oxygen rich gas mixture by recreational divers. How dangerous is oxygen? Contrary to popular belief, oxygen itself is not a flammable gas. Rather it is a very strong oxidizer that combines chemically with other compounds and fuels producing an exothermic [heat producing] reaction. The rate at which this chemical reaction [oxidation] occurs is a critical factor. Examples of slow rates of oxidation include deterioration of synthetic rubber components and corrosion of metals. Fire represents a moderately fast rate of oxidation and an explosion is an excellent example of high-speed oxidation. Oxygen coming into contact with hydrocarbons under the right conditions can result in violent oxidization. We must take into consideration the fact that anything will burn [oxidize] when heated to a sufficient temperature in the presence of oxygen. With proper training and precaution, you can handle oxygen and oxygen-rich gas mixtures as safely as compressed air.

Inert Gases Nitrogen, the main component of the earth's atmosphere, is colorless, odorless, tasteless, and inert (in its free state). However, when breathed at elevated pressures, it is selectively soluble in various body tissues and acts as an intoxicant or anesthetic on the central nervous system. Helium is colorless, odorless, tasteless, inert, non-toxic, and nonexplosive. It is also the second lightest known element. Helium is a rare element found in only trace quantities in atmospheric air (about 5 ppm). However, it does coexist with natural gas in some geographic locations and may be separated as a single element. Helium has become the major inert gas substituted for nitrogen in deep-diving breathing media. The narcotic effects of helium are relatively limited and breathing resistance is significantly reduced due to lower density. During rapid descent to extreme depths (beyond 600 fsw) while breathing helium-oxygen, divers often experience muscle tremors and other central nervous system effects, a condition known as High Pressure Nervous Syndrome (HPNS). Helium has very high thermal conductivity, which can cause rapid

© 1997 by Lee H. Somers, Ph.D.

Advanced Diving Physiology

heat loss in a helium rich environment. However, contrary to popular belief, divers breathing helium rich mixtures at shallower technical diver depths do not experience significant respiratory heat loss. Hydrogen, the lightest of all elements, is also colorless, odorless, and tasteless. Rarely found in a free state on earth, it is the most abundant element in the rest of the universe; the sun is nearly pure hydrogen. Hydrogen is violently explosive when mixed with gases containing greater than 5.3% oxygen. However, it has been combined with helium and oxygen (hydreliox) to demonstrate superior performance characteristic for deep saturation dives at depths exceeding 1,800 fsw. Argon, a colorless and odorless inert gas, is about twice as narcotic as nitrogen. Although it has been used in decompression gas mixtures, narcotic potency and high density make it unattractive for standard breathing gas mixtures. Because of its thermal properties, argon has experienced increased popularity as a dry suit inflation gas. The thermal conductivity of argon is about 20 percent less that air and only 1/9 that of helium. Argon comprises about 0.94 percent of atmospheric air and is produced by fractionation of liquid air.

Other Important Gases Carbon dioxide, a natural waste product of metabolism, is colorless, odorless, and tasteless (in normal concentration). However, when it reacts with water it forms carbonic acid that produces a distinctive acrid taste and smell. Carbon dioxide is the principal respiratory process stimulant. High carbon dioxide production and retention by the body can enhance the onset of nitrogen narcosis, oxygen toxicity, and decompression sickness. High concentrations are toxic to the human body and may produce unconsciousness with subsequent death. Carbon monoxide, the product of incomplete combustion of fossil fuels, is highly poisonous, and all possible measures must be taken to prevent its contaminating the diver's gas supply.

Breathing Mixtures Breathing gas mixtures consist of oxygen and one or more diluent gases. In selecting a breathing gas or gas mixture for diving, one must consider metabolic needs, oxygen partial pressure and dose limitations, narcotic potency, density, thermal properties, decompression, cost, equipment compatibility, supply logistics, and fire or explosion risks. Atmospheric air, the most common diver breathing gas, is composed of nitrogen (78.1 percent), oxygen (20.9 percent), carbon dioxide (0.033 percent), and various inert and rare or trace gases. It may also contain

varying amounts of water vapor and suspended or dissolved solids. In spite of its universal use, air has significant limitations as a diving gas. Pure breathing grade oxygen is used with closed-circuit oxygen rebreathers by military and scientific divers. Carbon dioxide is chemically removed from the diver's expired oxygen and the remainder is recirculated through the breathing circuit. Pure oxygen is also used in technical diving with open-circuit scuba as a decompression gas. Rigid time exposure and depth limits must be observed when breathing pure oxygen. Nitrogen-oxygen mixtures (nitrox) were introduced to diving in 1789. By reducing the amount of nitrogen in the mixture, a diver can gain significant dive time and decompression advantages. Today, standard mixtures of enriched air nitrox (EAN 32 and EAN 36), are used extensively in both recreational and professional diving. The term enriched air nitrox is more reflective of the production techniques than the actual gas composition. Technical divers use mixtures with oxygen content ranging from 25 to 80 percent. Enriched air nitrox is used widely as a decompression gas for ascent from both air and trimix dives. Helium-oxygen mixtures (heliox) are substituted for air in order to counteract narcotic potency and density-induced breathing resistance at deeper depth. This mixture has seen wide use in commercial and military diving. However, the high cost of helium and extensive decompression times makes it less attractive as a technical diver gas. Trimix refers to a gas mixture of oxygen and two inert diluent gases. Today, technical divers routinely use varying mixtures of oxygen-helium-nitrogen to depths in excess of 300 fsw. By blending a depth specific gas mixture, the diver can control both hyperoxia and the narcotic level of the mixture. Technical diver trimix is commonly produced by blending specific amounts of helium with oxygen and adding air to achieve final cylinder pressure. Low nitrogen trimix (5 percent nitrogen) was used to eliminate the onset of High Pressure Nervous Syndrome in extremely deep heliox saturation dives and a mixture of oxygen-helium-hydrogen appears best suited for working dives in the 2,000 fsw depth range. Neon-oxygen has seen limit use in experimental diving. Expense is the primary limitation. Although neon is denser than helium, it appears to be free of narcotic properties. Argon-oxygen has been used as an experimental decompression gas. Argon is denser and more narcotic than nitrogen. However, at shallower decompression depths it can accelerate the removal of nitrogen or helium from body tissues during the last stages of decompression. Argon saturates the body tissues more

- 2 -


slowly than nitrogen or helium, therefore it can reduce the total inert gas pressure in the tissue.

INERT GAS ABSORPTION & ELIMINATION On the earth’s surface, we breathe a mixture of oxygen and nitrogen along with minute amounts of other gases at a pressure of one atmosphere. The oxygen tension (pressure) in the freshly inhaled air is slightly higher than that in the blood filled capillaries of the lungs. Therefore, oxygen passes (diffuses) from the lungs into the blood stream and is carried to tissues throughout the body where it is used to support metabolism. At the same time, the carbon dioxide tension (pressure), a by-product of our body’s metabolism, is higher in the blood returning to the lungs than in the lungs themselves. Consequently, it diffuses into the lungs and is exhaled to the atmosphere. However, the major component of the air we breathe is nitrogen, an inert gas, which remains inactive in the metabolic process. The nitrogen pressure in our body is equal to the nitrogen pressure in the atmosphere (or is in equilibrium with the atmosphere).

Breathing Gas at Depth What happens if we change the pressure of the breathing gas? Remember that the pressure of the gas breathed from scuba increases during descend to depth. At 33 feet (10 meters), the inspired gas pressure has doubled. There is now a much greater pressure or driving force pushing the gases into our blood stream. Gases readily pass from an area of higher pressure to one of lower pressure. The metabolic processes still use oxygen and produce carbon dioxide. However, the inert gas (nitrogen and/or helium, depending on breathing mixture) simply dissolves in the blood and is carried to capillaries throughout the body where it diffuses into the tissues. This diffusion process is rapid during the initial portion of the dive as depth increases. Inert gas quickly diffuses into the spinal cord and brain where there are many closely spaced capillaries. These organs are well perfused with blood. Such tissues are often referred to as fast tissues where blood flow is the primary controller of inert gas exchange. By comparison, the tissues found in the joints of the body are less well-perfused slow tissues. In slow tissues, the uptake (and subsequent elimination) of nitrogen is less rapid. Gas exchange in skeletal muscle tissues varies significantly with temperature and exercise levels.1 Throughout a dive, we continue to absorb inert gas. The amount of inert gas absorbed can be predicted based on mathematical models. These

mathematical predictions relate primarily to pressure (depth) and exposure time and serve as the basis for developing dive tables or programming dive computers. However, they do not generally take into account the fact that inert gas exchange can be quite variable depending on factors such as exercise, thermal stress, circulatory efficiency (often age-related), amount of body-fat, and hydration level. The presence of some drugs and alcohol (or post-consumption physiological changes) is also a factor.

Decompression: A Normal Ascent Now it is time to ascend back to the surface decompress. Our body tissues now contains a significant amount of excess inert gas. As we ascend, the ambient pressure and the gas pressure in our lungs is reduced. The pressure of the dissolved gases in our tissues now exceed the ambient pressure. Tissues may approach a state of supersaturation. Fortunately, our body will tolerate a certain level of excess tissue gas pressure. This is why dive tables and computers indicate that we can ascend directly back to surface pressure provided that dive depth and time remain within specific limits. The gas diffuses from our tissues to the blood stream and is carried to the lungs where it is exhaled. It appears that we can complement this off-gassing process through good diving practices. For example, research has shown that a slow or interrupted ascent may be a significant safety factor in deterring problems related to off-gassing. [Note: An ascent rate of 30 feet/minute (9 meters/minute) and a safety stop (at the end of a dive not requiring mandatory decompression stops) for a few minutes at 10 to 20 feet (3 to 6 meters) appears to be very beneficial for recreational scuba divers.] These procedures appear to allow rapid gas exchanging neurological tissues, such as the brain and spinal cord, sufficient time to eliminate excess nitrogen and reduce the degree of supersaturation. Once we have returned to the surface, our body will continue to eliminate excess inert gas for some time, depending on the time and depth of the dive. This residual inert gas must be considered when planning repetitive dives. Also, post-dive activity can also influence tissue off-gassing process. Vigorous exercise, immersion in hot water, and alcohol consumption is discouraged. Hydration with water or juices is encouraged. The relevance of these recommendations will be evident in the following discussion.

Decompression Sickness Decompression sickness (DCS) results from the formation of bubbles within tissues. When the

- 3 -


pressure of the dissolved gases reach supersaturation levels during ascent, bubbles can form within body tissues and the blood stream. Some researchers suggest that bubbles do not actually form in the blood itself. Rather, residual extravascular (outside of the blood-carrying system) gas may actually rupture tiny capillaries and pass seed bubbles into the blood. It is interesting to note that researchers using ultrasonic detection devices commonly find bubbles in the venous system, right ventricle of the heart, and pulmonary artery of divers immediately after they surface. Under normal conditions, these venous bubbles are considered harmless since they are filtered by the pulmonary capillary system and exhaled. Two ways that these bubbles can play a role in symptomatic decompression sickness will be discussed later. X-rays have revealed pockets of gas in joints and in and around the spinal cord, even without a decompression event. These pockets apparently form as a result of viscous adhesion between moving tissues surfaces. It is likely that residual gas from these pockets is the source of bubble nuclei from which the actual bubbles that cause decompression sickness form. As previously stated, these extravascular bubbles may actually rupture tiny capillaries as they expand and enter circulating blood as seed bubbles. Symptoms of decompression sickness relate to both extravascular and intravascular bubbles. One of the most common symptoms, limb or joint pain, probably occurs a bubbles stretch tissue and stimulate nerve endings around the joint. Neurological symptoms such as numbness, tingling, and paralysis are caused by the presence of bubbles in the spinal cord. These bubbles physically disrupt nerve cells and circulation. Other symptoms of spinal cord involvement can include bladder, bowel, and sexual dysfunction. A large aggression of bubbles in the capillaries of the lungs can cause shortness of breath and coughing (cardiorespiratory decompression sickness or “chokes”). The condition is further complicated by secondary effects. Being foreign bodies in the vascular system, bubbles can activate the coagulation system, causing reduction in blood flow. Now, let’s return to the bubbles found in venous circulation discussed previously. Under normal conditions, the gas from these bubbles exits the body through respiration and they do not lead to symptoms of decompression sickness. However, large numbers of bubbles entering the lungs can exceed the filtering capacity of the pulmonary capillary system and allow bubbles to enter the arterial system. Ultimately, these bubbles can reach the brain.

Another method by which bubbles can enter arterial circulation is through a patent foramen ovale, a tiny opening between the right and left atria of the heart. This opening exist in the heart of all fetus and shortly after birth, the opening normally closes. However, it is estimated that this closure is not complete in 10 to 20 percent of the population. Thus, bubbles being carried in venous circulation can bypass circulation to the lungs and directly enter arterial circulation. Preliminary studies of decompression sickness patients reveal that a patent foramen ovale can be detected in about 50 percent of divers experiencing serious neurological symptoms. Individuals with this condition are possibly five times more likely to suffer serious decompression problems. This condition can be detected by medical tests. A rarer condition known as atrial septal defect could have much the same effect. Bubbles reaching the brain can disrupt vision, speech, thought processes, personality, or consciousness as well as cause hemiplegia (paralysis of one side of the body) or convulsions. Spinal Cord Involvement: Why? Neurological decompression sickness occurs much more frequently in the spinal cord than the brain. Why? Spinal cord decompression sickness is most likely caused by bubbles that form with in substance of the cord itself. One supportive hypothesis is that the spinal cord is subject to continuous movement which, as in joints, may generate bubble nuclei by viscous adhesion. Furthermore, the spinal cord is completely enclosed in inelastic connective tissue membrane. Consequently, bubbles can increase pressure within the spinal cord. This can result in reduction of blood flow and further compound the damage caused by bubbles. Like many human endeavors, diving has risks that can be reduced but never completely eliminated. We accept risk every time we drive or ride in an automobile. Statistically, the risks associated with a hike in the mountains appears to be greater than those associated with a recreational scuba dive. Avoidance of decompression sickness is now considered to be a matter of probability rather than a clear demarcation between safe and unsafe. What level of risk are divers willing to accept? Based on the best data available, the risk of developing decompression sickness appears to be relatively low. However, we must remember that there is no dive table or computer that can provide absolute protection. The mathematical models used for dive tables and computers today do not take into account individual variability and the day

- 4 -


to day factors that might influence susceptibility to decompression sickness. They are developed for the “average” diver. As physiologists learn more about decompression sickness, acquire large databases, and develop probabilistic models, it is likely that improved tables and computers will more realistically complement a wider range of human physiological variability. Future computers may allow a diver to declare the probability with which they are comfortable. Until that time, the burden of risk reduction rest with intelligent use of current tables and computers. A knowledgeable diver can and must make judgments on conservative use of tables and computers based on personal and environmental factors. (Note: First aid for decompression illness will be discussed future papers.)

Predisposition to Decompression Sickness Alcohol has no place in diving. The human body is compromised for many hours, possibly days, after excessive consumption. Not only are mental processes impaired but also circulatory efficiency. Some researchers also suggest that changes in blood flow caused by drinking alcohol after diving might accelerate release of inert gas and indirectly enhance bubble formation. Others suggest that alcohol can directly contribute to bubble formation by reducing bubble surface tension and therefore, enhancing growth. Alcohol consumption following a dive could potentially push silent (asymptomatic) bubbles into the realm of symptomatic bubbles. A prudent diver will not drink alcoholic beverages between or for a reasonable period of time after diving. Alcohol appears to have a significant influence on bubble development and may play a notable role in your susceptibility to decompression sickness. Increased age and obesity alter circulation efficiency and can also increase susceptibility to decompression sickness. Excessive physical exertion increases the respiration rate and the rate of circulation of the total blood volume. Consequently, during excessive exertion under pressure, larger than normal amounts of nitrogen are transported to the tissue per unit of time. Consider a diver working hard underwater, e.g., moving heavy objects, swimming against a strong current, etc. This diver's tissues may absorb nitrogen equivalent to 10-20 minutes of extra diving time under normal conditions, and even if the diver is on a no-stop dive schedule, decompression sickness can develop. There is also evidence that heavy exercise before a dive can also alter the way nitrogen is released from the body at the end of the dive. Poor

physical condition further augments the risk of decompression sickness. Forceful movement of muscles and joints pre-dive, post-dive, or under increased ambient pressure can result in an increase in bubble formation. Keep in mind that “decompression” continues for a period of time after a diver leaves the water. Most authorities caution against vigorous post-dive exercise because it changes bubble formation and circulation dynamics as well as offgassing rates. It is also possible that the continuous ascent-descent procedure associated with post scuba dive skin diving can complicate the off-gassing process. Excessive carbon dioxide buildup in tissue has also been empirically and experimentally observed to lower the threshold for bubble formation during ascent. Loss of fluid from the body through diuresis, combined with fluid loss associated with breathing dry gas, causes a degree of dehydration that may well reduce the efficiency of the circulatory system. Alcohol also produces a diuretic effect thereby causing dehydration. Reduced circulatory efficiency may in turn modify the normal nitrogen absorption-elimination rates and contribute to the formation of extravascular bubbles (i.e., decompression sickness). Consequently, it is possible that drinking large quantities of liquid (such as diluted fruit juice and water) before and between dives could be significant in avoiding decompression sickness. Plain water is considered to be one of the best liquids for divers. Predisposing factors cannot be overlooked in operational diving. If all of these factors were accounted for in standard dive tables, the tables would be impractical for normal diving and divers. Consequently, the discretion of the individual diver must be relied upon to take these factors into account when planning a dive. Slightly reduced dive time and a more conservative decompression schedule is a small price to pay when one considers the possibility of serious injury, lifelong physical impairment, and the many hours in a hyperbaric chamber required to treat decompression sickness.

Neurological Damage and Aseptic Bone Necrosis2 What are the potential long-term consequences of diving, if any? Recently, there has been concern with regard to possible long-term neurological effects from recreational diving. It is true that several studies have identified abnormalities in divers. However, the true significance for recreational divers is unclear. With regard to traditional recreational diving, Dr. Stone states, “If a recreational diver hasn’t had an acute injury from diving, there is no reason to suspect that

- 5 -


he or she will develop any long-term damage related to diving.” There appears to be two key issues relative to long-term consequences of diving. First, such consequences seem to be most significant in the commercial diver population and apparently of limited significance in the recreational dive population. However, it is important to note that recreational diving implies a depth limit of 130 feet (40 meters), no-decompression, and use of compressed air. Today, many recreational dives are diving to depths in excess of 130 feet (40 meters) breathing air and to depths greater than 300 feet (91 meters) breathing mixed gases. The depth and gas exposures now approximate that of a commercial diver for small select population of technical divers. Second, the potential for long term consequences appears to be linked to prior diving injury (i.e., decompression sickness). Subjectively, it is likely than far more recreational divers than we are aware of experience symptoms of decompression sickness and do not submit to treatment. Is there an increasing reason for concern as more and more individuals enter into technical recreational diving? There is no answer to this question at the present time. The following excerpt on potential for long-term neurological damage was taken from an article by Dr. Tabby Stone published in Discover Diving.

The Lancet [a British medical journal] article dealt primarily with differences between the MRI scans of 52 divers compared with 50 control subjects who engaged in other sports. MRI scanning is a technique used to make images of various parts of the body. The researchers found a higher incidence of "focal hyperintensities" in the divers than in the controls. The number of these lesions in the divers did not correlate with number of dives or years of diving experience. One diver in the series had a history of DCS, and two others reported "dangerous situations which almost caused decompression sickness". The significance of this was discussed during a question and answer session at the Undersea and Hyperbaric Medical Society, Pacific Chapter meetings in October 1995. It was pointed out that focal hyperintensities are also called Unidentified Bright Objects (UBOs) and that they are a common finding and increase with age. Since UBOs are, by definition, unidentified, they have not been directly related to any problem. The number of UBOs found also varies somewhat with the technique used when the MRI is performed. (Since all the exams in the study were done in the same manner, this would make no difference between subjects and controls.) Some criticisms of the study have been printed since it came out. It's been Pointed out that the selection

process for the divers was not random. There may have been a bias toward selecting divers who thought something might be wrong, such as the diver with a history of DCS and those with the "dangerous situations." Also, the findings in this report conflict with previous studies of professional divers' which did not show any increased incidence of these lesions. The secondary finding of the report was the presence of injuries to the disks in the neck. The disks are the cushions between the bones of the spine. The authors felt they also could have been damaged by bubbles. Others have suggested the damage is more likely a response to the divers neck position in the water or trauma from things like carrying tanks on the back. The Lancet study is not the only one to question whether there are long-term neurological effects from diving. In a Scottish/English study using a type of scanning called HMPAO-SPECT, which measures brain function based on blood flow, recreational divers were part of one of three groups studied. In this case, the professional divers who had a history of DCI showed 58% abnormal scans. The mix of recreational and professional divers without any history of DCI showed 35% abnormal scans and non-divers had no abnormal scans. This is a relatively new technique and the meaning of the variations in blood flow are not well defined. And, once again, there was no correlation between the abnormalities found and any symptoms in the divers. Two English physicians, Drs. Palmer and Calder, have examined the brains and spinal cords of divers who have died either following decompression illness, or from other causes. As would be expected, they found evidence of damage when there was a history of decompression problems. But, in a small number of cases, they have reported lesions when there was no known history of decompression illness, or any evidence neurological damage before death. At one time, there was belief in dementia (a loss of mental function) sometimes called the "punch-drunk diver " or "diver's dumbness." But, studies have shown that unless there is a history of diving accidents, there isn't any difference in mental function between divers and non-divers.

Aseptic bone necrosis has be evident in the commercial diving population for a many years. Bone necrosis incidence increased as deeper and longer dives became more common. However, British studies have apparently not identified cases in professional divers who were diving only at the usual sport diving depths. The following is an excerpt for Dr. Tabby’s article:

In 1911, not long after x-rays became available as a diagnostic tool, a late form of bone damage in caisson workers and divers was described. The general type of condition is called "aseptic bone necrosis." Necrosis is the death of cells, and aseptic means it happens without evidence of infection. When it occurs in divers, the

- 6 -


more specific term "dysbaric osteonecrosis," meaning bone death from pressure effects, is often used. Presumably, bubbles block critical circulation, causing the death of bone cells, leading to destruction of part of the bone. The bone lesions tend to occur in the long bones of the legs and upper arms, with the majority of them in the lower part of the femur (the upper leg bone). They are usually detected on x-rays as areas where calcium has been deposited in a bone following injury. With enough bone destruction, there can be pain and significant disability, especially if the bone near a joint is destroyed. Joint damage in divers is more common in the shoulder, and at the hips in caisson workers. British occupational health reports from the 1970s showed that bone necrosis incidence rose from around 1% to nearly 5% of divers as deeper and longer dives became more common. Bone lesions are more common when there is a history of decompression sickness. The site of bone lesions is often, but not always, in the same limb where bends pain has occurred. It's important for recreational divers to note that no bone lesions were found in divers who never exceeded a depth of 30 meters (about 99 fsw). While there are lots of cases of bone necrosis in professional divers, there are only sporadic reports of it occurring in sport divers.

NITROGEN NARCOSIS In 1835, a Frenchman named Junod described human response to breathing compressed air under pressure as “the functions of the brain are activated, imagination is lively, thoughts have a peculiar charm and in some persons, symptoms of intoxication are present.”3 One hundred years later (1935) Behnke and co-workers clearly attributed this narcotic response to the elevated partial pressure of nitrogen in compressed air characterized by “euphoria, retardment of the higher mental processes and impaired neuromuscular coordination.”4 Although the nitrogen in air is physiologically inert under normal conditions, it has distinct anesthetic properties when the partial pressure is sufficiently high. The problem of compressed air intoxication has long been recognized by both divers and researchers.5 A critical review of the effects of inert gas narcosis can be found in Undersea Biomedical Research. 6 Modern diver education materials universally affirm that divers become impaired by the effects of nitrogen narcosis as they descend below 100 feet (30 meters) and that the severity of this impairment increases with depth. Dr. Peter Bennett writes, "At depths greater than 180 fsw (6.5 ata), no trust should be placed in human performance or efficiency in breathing compressed air."3 Today, we realize that there is also considerable individual variability regarding symptomatic narcosis.

The classic view of nitrogen narcosis present in most modern textbooks emphasized escalating degrees of physical and mental compromise eventually progressing to stupefaction and, even, unconsciousness. At depths of 100 feet (30 meters) a diver may mild euphoria and slowed response. As the diver descends deeper the diver experiences hallucinations and impaired judgment. This is followed by severe impairment of intellectual performance. As the diver approaches 300 feet (92 meters) stupefaction and mental abnormalities prevail with almost total loss of intellectual faculties. The diver may lose consciousness. The bulk of research data on nitrogen narcosis appears to be based on studies conducted in a dry hyperbaric environment (chamber). These studies often involved groups of subjects being pressurized together. The classic euphoric character of nitrogen narcosis or “rapture of the deep,” may have evolved, in part, from observations of uncontrolled laughter and loquacity (excessive talkativeness) associated with the jovial group atmosphere. From a practice point of view, diver performance in a hyperbaric chamber as compared to underwater reflects some inconsistencies. Underwater, euphoria does not appear to manifest as episodes of laughter nor do divers appear to have the uncontrollable urge to pass their mouthpiece to a passing fish. The forbidding classical views of nitrogen narcosis have prompted experts and instructors to advice diver to avoid narcosis by not descending too deep and to ascend immediately if symptoms appear. This is actually excellent advise. Nitrogen narcosis should be avoided if possible. However, this view has also stifled most discussion on how to manage the effects of narcosis and improve efficiency and safety for those who must or elect to dive under the influence of narcosis. Classical views of nitrogen narcosis have been subject to review.3,7 Some of the following information will differ from more classical views presented in many modern textbooks. A theory called the slowed processing model has been proposed. This theory suggests that, before unconsciousness, the primary effect of narcosis on performance arises from a single fundamental defect in the central nervous system -- a decrease in arousal. This defect slows response, but apparently does not cause perception distortions of either vision or audition. Test subjects at a depth of 295 fsw [in a hyperbaric chamber] show an increase in reaction time and errors on a Serial Choice Reaction Timer. However, when the test subjects were trained to simply slow down, the errors were eliminated. The slowed processing model holds

- 7 -


that decreased accuracy on many tasks is due to untrained individuals working too rapidly and willingness to take more risks than usual. Some research further suggests that disorganized behavior is not necessarily a part of narcosis and can be overcome by training. In training, divers must learn to prioritize. The potential cost of errors must be weighed against work or time efficiency and safety. A hurried and incorrect decision on critical safety issues such as orientation could lead to dire consequences. The slowed processing model is unsuccessful in explaining memory loss and learning recall. Inability to recall events that occurred at depth was document in early diving research. More recently it has been shown that material learned before a dive [i.e., instructions and dive plan information] may not be recalled during a dive. Furthermore, learning of new material during the dive will also be impaired. This can contribute to difficulty in solving problems which may be encountered during the dive. As dive depth increases, a diver should rely on memory as little as possible. Whenever a diver must rely on memory, the material and skills must be highly over-learned and memory cues used to minimize forgetting. For example, divers must over learn any emergency procedure that must be executed quickly in a precise sequence. Over learning a skill involves repetition of performance sequences numerous times throughout training. Memory clues may be in the form of a check-off list or obtrusive signal system [i.e., alarm to denote bottom departure time]. Subjective sensations influenced by narcosis include euphoria, state of consciousness, work capability, and inhibitory state. Emphasis on euphoria may have obscure other sensations. Apart from rash behavior, subjective sensations can potentially distract the divers attention from the environment and task. For example, diver under the influence may pay more attention to the sensations of narcosis rather than concentrating on the environment and task. There also appears to be a fairly strong relationship between the severity of narcosis and performance impairment. Divers must also recognize that a variety of other sensations related to cold, anxiety, and fatigue may mask narcosis. As previously stated, narcosis can be avoided by not descending too deep and ascending immediately when symptoms occur. This is excellent advice! Narcosis should be avoided if possible. However, the adventurous divers who elect to venture into the narcosis depth range are well advised to better prepare themselves for the narcosis experience through over learning, use of memory clues, and becoming familiar [and comfortable] with the sensations of narcosis.

They must learn to allocate attention between a task and narcosis sensations. Symptoms cannot be entirely ignored, however, the diver can decrease performance deficit my not allowing these sensations to dominate their attention. Divers must learn to use the intensity and types of sensations to estimate performance capability. Subjective sensations may be the first warning of a potentially life-threatening situation. There is general agreement that acclimatization or adaptation may also play a role in narcosis tolerance. Diver have reported subjective short-term acclimatization following frequent and repeated deep dives. However, at this time it is unclear as to the kind of adaptation that takes place. Is it true adaptation or non-specific learning? Do divers actually “acclimatize” or simply “learn to cope” with the sensations of narcosis. True adaptation may only relate to specific circumstances not presently understood. Furthermore, divers may mistake non-specific learning for true adaptation. It is also unclear as to the adaptation relationship between subjective symptoms and objective performance. Divers may be basing their opinions about adaptation primarily on subjective symptoms. Obviously, considerably more research is needed. What does all of this mean to the diver? The forgoing must be considered as a over-simplification of performance prediction in the underwater environment. It is evident that a variety of stressors coexist with narcosis -- hypercapnia, cold, anxiety, perceptual distortions, and weightlessness. All can place severe limits on performance. Over the years both divers and researchers have expressed many opinions with regard to factor that influence a divers sensitivity to nitrogen narcosis. It has been suggested that anxiety may have an additive or synergistic interaction with narcosis. Although some studies have lead to the conclusion that anxiety may interact with narcosis, the co-existence of other stressors complicate isolating and measuring the possible relationships. Can the same be said about apprehension? Anticipation? Some observations apparently suggest that if a diver, especially an inexperienced diver, is preconditioned before a dive to believe that narcosis sensations will appear at a shallow depth, the experience is likely to occur. It has been widely held for many years that elevated levels of carbon dioxide potentiates (increases) narcosis synergistically. Other evidence favors the view that carbon dioxide has additive, not synergistic, effects in combination with hyperbaric air. Regardless, the potential influence of carbon dioxide on a diver cannot be minimized. Carbon dioxide retention appears to be enhanced by exercise and cold

- 8 -


stress. Carbon dioxide retention is not uncommon in trained divers who hypoventilate. Decrements in performance has been demonstrated in divers with elevated levels of carbon dioxide. It should be noted that some symptoms, such a dizziness, are common to both narcosis and hypercapnia. What is causing dizziness? Narcosis? Carbon dioxide? Both? It is widely believed by divers that there is a synergistic relationship between oxygen and narcosis. It has been proposed that oxygen potentiate the effects of narcosis by interfering with the elimination of carbon dioxide. However, a review by Fowler and associates suggest that the evidence is too contradictory to draw any conclusion. Research evidence does favor the long standing conclusion that ethanol (alcohol) exacerbates narcosis. The implications are obvious. Diving following consumption of alcoholic beverages is, at best, unwise and, at worst, life-threatening. The effects of prescription medications on narcosis is more difficult to assess. In general, it is any drug with an anesthetic or intoxicating effect may reduce the narcosis threshold. Some seasickness remedies and antihistamines may potentiate narcosis. Unfortunately, response or reaction to drugs observed at the surface is not a reliable indictor of their effects under pressure. However, many prescription and non-prescription drugs carry warnings of behavioral toxicity such as “may cause drowsiness” or “caution against engaging in operation requiring alertness.” At depth, whether or not a drug potentiates narcosis, reactions such as drowsiness or lack of alertness can be life-threatening. Illicit drugs can have varying effects. Marijuana affects the sense of timing as exacerbating cold stress. Cocaine, among other effects, has a marked effect on behavioral functions such as judgment. Again, the implications are obvious. Illicit drugs are highly contraindicated in diving, shallow or deep. The effects illicit drugs are in themselves inconsistent with prudent diving practices. Subjectively, it is likely that many of these drugs potentiate narcosis. Further information on the relationship of drugs and narcosis can be found in selected references. 8,9 Nitrogen narcosis is a well-documented response to breathing hyperbaric air. As previously states, narcosis should be avoided if possible. However, if extended range compressed air diving is to be carried out with some degree of risk management and efficiency, training procedures must address both the effects of narcosis and the effects of the many stressors which may co-exist with narcosis underwater. To this end, Dr. Fowler offers the following suggestions:

• Disorganized behavior is not a necessary part of

narcosis and can be overcome by training. Errors can be avoided by slowing down.

• Divers should rely on memory as little as possible when memory must be relied on. The material should be highly over-learned and memory cues used to minimize forgetting.

• Divers must become familiar and comfortable with the sensations of narcosis, and learn to al locate attention between the task and the symptoms in a manner appropriate to the situation. Divers can learn to use the intensity and type of symptoms to estimate performance capability.

• Divers should practice as much as possible prior to the dive on the tasks to be performed underwater.

It has been suggested that diving under the influence of narcosis can be likened to driving under the influence of alcohol. Driving under the influence is unsafe and ill-advised. National educational campaigns constantly inform the public of the risks, and legal consequences can be severe. Yet, millions of people drive daily under varying degrees of alcohol and drug induced impairment and arrive at their destination without serious incident. However, drunk driving is one of the leading causes of fatal driving accidents. Similarly, many divers complete deep dives under varying levels of nitrogen-induced impairment and arrive back at the surface without serious incident. What is the role of nitrogen narcosis in diving accidents? The answer to this question may be obvious to some and unclear to others. Helium is commonly substituted for nitrogen as a means of reducing both narcosis and breathing resistance. Equivalent Narcosis Depth (END) can be calculated using the formula,

( )( )EAD

FN D=

+

−2 330 79

33.

where FN2 is the decimal fraction of nitrogen in the mixture and D is the depth in feet of sea water (fsw). What is the END for diver breathing Trimix 14/50 at a depth of 300 fsw? If the mixture contains 14% oxygen and 50% helium, the balance is 36% nitrogen. Substituting these values into the END formula,

- 9 -


( )( )EAD =

+

−.

.36 300 33

0 7933,

the equivalent air depth is 119 fsw.

HYPOXIA Oxygen is essential to life -- without it the human cannot survive. In its free state, oxygen is colorless, odorless, and tasteless. It is the partial pressure of oxygen that determines if the amount of oxygen in the breathing medium is adequate to sustain normal physiological functions. Atmospheric air contains about 21% oxygen and thus provides an oxygen partial pressure of about 0.21 ata [0.21 x 1 ata = 0.21 ata] at sea level pressure. This is ample for human life support. However, if oxygen levels drop below 0.16 % [or 16 ata at sea level] humans will experience the onset of hypoxia. Initially, pulse rate and blood pressure will increase as the body attempts to offset the hypoxia by increasing blood flow. A small increase in respiration rate may also occur. If some level of oxygen is present and/or hypoxia develops gradually, symptoms typical of brain function impairment will appear. The abilities to concentrate, think clearly, have fine control of muscles, and perform delicate tasks are typical early impairments. Confusion, faulty judgment, emotional instability and muscle function impairment soon follow. Unfortunately, these responses may be insignificant to serve as warnings. The victim of hypoxia is usually unable to understand that s/he is in trouble. In fact, s/he may experience a sensation of euphoria [feeling better] while drowsiness and weakness increase and consciousness is lost. Few individuals will recognize hypoxia symptoms in time to take effective action. If the oxygen partial pressure drops to 0.12 ata [12% at sea level], most individuals will lose their ability to function. Hypoxia will stop the normal function of any body tissue cell and eventually kill the cell. Brain tissue cells are by far the most susceptible to its effects. Unconsciousness usually occurs at about 0.10 ata [10% at sea level] and permanent brain damage and death will probably result below 0.10 ata. Unconsciousness occurs almost immediately in the complete absence of oxygen. Hypoxic individuals must be returned to an environment with sufficient oxygen immediately. If respiration has ceased, but heart action continues, artificial respiration must be started without delay. If heart action has ceased, cardiopulmonary resuscitation must be performed. There are several possible causes of hypoxia in divers. First, breath-hold divers most commonly lose

consciousness for oxygen deficiency (hypoxia) rather than carbon dioxide excess. Second, the oxygen in compressed air can be consumed by oxidization of a steel-alloy scuba cylinder if moisture is present in the cylinder. Although a rare occurrence, fatalities have been attributed to this process. In one case, the oxygen level was reduced to 2 percent. Third, in mixed gas diving the divers breathing mixture may simply have too little oxygen to support normal body processes. In order to prevent oxygen toxicity (discussed later) when breathing a gas mixture at great depths, it may be necessary to reduce the amount of oxygen in the “bottom mix” to 10% or less. Such mixtures can cause hypoxia when breathed at shallow depths. Divers descending to very deep depths often use a “travel-mix.” Fourth, it is possible for a gas blender to make a mistake and prepare a cylinder of mixed-gases with too little oxygen. The consequences are obvious. Finally, the percentage of oxygen in the inspired breathing gas can vary with flow rate or oxygen sensor function in recirculating scuba. The cause of oxygen deficiency depends on the type of recirculating scuba. Even closed-circuit oxygen scuba (using 100% oxygen) can lead to hypoxia if the system is not purged and properly prepared for diving.

HYPEROXIA The human body has evolved to function in an environment when the oxygen percentage is about 21% and partial pressure is about 0.21 atmospheres absolute (ata) at sea level. If partial pressure of oxygen is reduced below 0.16 ata the diver will experience hypoxia or oxygen deficiency. On the other hand, oxygen partial pressures of 1.3 ata or higher induce hyperoxia or a condition of abnormally high oxygen. Extended range air diving presents three possible areas of hyperoxia risk. The greatest concern is the possibility of a diver experience oxygen toxicity while breathing high-oxygen EANx or 100% oxygen during decompression. Next, what if a diver mistakenly oxygen or a high-oxygen EANx at depth? It has happen! The following is an account of such an incident: 10

An experienced 47 year old spear-fisherman apparently switched to his oxygen regulator by mistake while chasing down a grouper at about 220 fsw/36 msw)during a deep air dive, convulsed and drowned. He was found on the railing of the RB Johnson with his regulator out of his mouth by his partner, who was reportedly diving trimix. The body was later recovered by the charter boat captain.

- 10 -


The diver was wearing twin "independently configured" 100 cubic foot cylinders, and an E-cylinder oxygen pony for decompression. Using this configuration, a diver must repeatedly switch regulators during the dive in order to balance the gas supplies. Though the diver used a distinct oxygen regulator which was labeled in green, his primary, secondary and oxygen regulators were banded together and mounted over his right shoulder. It is believed he mistakenly switched to his oxygen regulator in the heat of the chase (A P02 of 7-8 atm), having speared his first grouper at 240 fsw (74 msw) earlier in the dive. He convulsed, spitting the regulator out of h s mouth and drowned. Vomit and blood were found in his mask.

Finally, oxygen toxicity has been documented in divers breathing compressed air at too deep of depth where the oxygen partial pressure can reach toxic levels. It should be noted that the partial pressure of oxygen in compressed air reaches 1.6 ata a depth of 218 feet (67 meters). The following is an account of an incident involving an oxygen convulsion at depth:

11

A full cave and nitrox instructor suffered an oxygen convulsion during a deep air dive in a sink hole in Mexico and drowned in March 1993. His partner who experienced CNS toxicity warning signs during the dive and a safety diver survived. The two later recovered the body. The team had planned a 20 minute air dive in excess of 230 fsw (71 msw) -- the depth of the saltwater halocline -- in a cavernous open-water sinkhole near Merida on the Yucatan Peninsula Because of the difficulty in obtaining helium mixes in Mexico, the team decided to conduct the dive on air followed by oxygen for decompression. Both were experienced deep divers. A weighted descent line was rigged for navigation and for staging oxygen and extra air cylinders. The safety diver was to descend with the team to 220 fsw, ascend to a shallower depth and wait for the dive team. After a long slow descent past the halocline, the team tied into the descent line to explore the well at a leisurely pace. Informed sources estimated their maximum depth to be close to 300 fsw (92 msw) (A P02 in excess of 2.0 atm - ed.). The surviving partner experienced a tingling in his lower lip and turned back to “call the dive” only to see the (other) diver headed back as well. When he reached the line, he sensed that the diver was in trouble. The diver grabbed the line and began a hurried hand-over-hand ascent. The partner reached the diver, gained control and they began to ascend together. The diver continued to pull on the line creating slack and getting himself tangled. His partner cut him free. The diver then darted got tangled again and apparently convulsed. By the time his partner reached him the diver's regulator was out of his mouth. At that point they were still deeper than 230

fsw (71 msw). After repeated attempts to force the regulator back into the diver's mouth with no success, the surviving partner realized the diver "was gone” and leaving the body entangled in the line, ascended to complete his decompression. Following decompression, the partner and safety diver were able to pull up the line and recover the body.

Divers breathing oxygen-nitrogen mixtures (nitrox) and oxygen-helium-nitrogen mixtures (trimix) must take great care to not exceed a given partial pressure of oxygen depending on the conditions of the dive.

Central Nervous System Oxygen Toxicity As the oxygen partial pressure increases, physiological changes begin to take place that can ultimately affect the central nervous system. If the partial pressure is increased to sufficient levels symptoms of oxygen toxicity will occur. Oxygen toxicity is a complicated series of interrelated physiological processes that are still not fully understood. Development of oxygen toxicity relates to the partial pressure of oxygen in the inspired breathing gas and the amount of time the diver is exposed to elevated oxygen pressure. In addition, a diver’s susceptibility to oxygen toxicity can be significantly influenced (increased) by immersion, physical exertion, carbon dioxide retention, and thermal stress (heat and cold). Furthermore, some individuals appear to be more sensitive to elevated oxygen levels than others and certain drugs may also influence sensitivity. Finally, susceptibility can also vary from day to day for a given individual. Depending on the level of activity, diving conditions, and exposure time, a diver enters the zone of hyperoxia between 1.3 and 1.6 ata oxygen partial pressure. Why is there so much concern about oxygen limits and oxygen toxicity? As the diver enters the hyperoxia range, serious, even life-threatening, symptoms of central nervous system (CNS) oxygen toxicity can develop. The diver may experience visual and hearing disturbances, nausea, vomiting, muscle twitching, dizziness, and/or irritability. Any of these can be disillusioning to very serious events underwater. However, the most serious consequence of oxygen toxicity is the onset of convulsions. If the diver convulses, death by drowning is a near certainty. Another sobering reality is that the convulsions may not be preceded by any of the less serious symptoms. Even if the diver experiences one of the lesser symptoms, there may not be time to take corrective measures before the onset of convulsions. The

- 11 -


symptoms of oxygen toxicity can be remembered using the acronym ConVENTID.

Convulsions12 Convulsions are the most serious consequence of poisoning with excess oxygen and may occur suddenly without being preceded by any other symptoms. During a convulsion, the individual loses consciousness and his brain sends out uncontrolled nerve impulses to his muscles. At the height of the seizure, all of the muscles are stimulated at once and lock the body into stiffness. The brain soon fatigues and the number of impulses slows. In this phase, the random impulses to various muscles may cause violent thrashing and jerking for a minute or so. Sometimes involuntary urination and defecation, and occasionally erection and ejaculation, take place during convulsion. After the convulsive phase, the brain is completely tired, and post-convulsive (postictal) depression follows. During this phase, the patient is usually unconscious and quiet for a while, then semi-consciousness and very restless. The victim will then usually sleep on and off, waking up occasionally though still not fully rational. The phase of depression sometimes lasts as little as 15 minutes, but an hour or more is not uncommon. At the end of it, the individual will often become suddenly alert and complain of no more than fatigue, muscular soreness, and possibly a headache. After an oxygen convulsion, the diver will usually remember clearly the events up to the moment when consciousness was lost, but will remember nothing of the convulsion itself, and little of the postictal phase. Despite its rather alarming appearance, the convulsion itself is usually not much more than a strenuous muscular workout for the victim. In an oxygen convulsion, the possible danger of hypoxia during breath-holding in the stiff phase is eliminated. The tongue may be chewed when the jaw takes part in the jerking phase, and once in a great while a bone will give way under the strain of the contracting muscles. If convulsion occurs in a hyperbaric chamber, one tender should be able to keep the man from thrashing against hard objects and hurting himself. Complete restraint of his movements is neither necessary nor desirable. The oxygen mask should be removed immediately. It is not necessary to force the mouth open to insert a bite block while a convulsion is taking place. After the convulsion subsides and the mouth relaxes, keep the jaw up and forward to maintain a clear airway until the diver regains consciousness. Breathing almost invariably resumes spontaneously.

Bringing a diver up rapidly during the height of convulsion could possibly lead to gas embolism. In the use of SCUBA, the consequences of convulsions are likely to be more serious, with drowning the main danger. This is a situation where using the buddy system in self-contained diving can mean the difference between life and death. Even if a diver with oxygen toxicity continues to breathe oxygen, the convulsion will almost always cease in a few minutes and be followed by a quiet interval of several minutes. If the oxygen partial pressure is then lowered, there will seldom be a further seizure. Usually, the convulsive phase is over before any drug could be injected to stop the seizure, and such treatment is necessary only in the extremely rare cases where convulsion continues after lowering the oxygen pressure. If one of the early symptoms of oxygen toxicity occurs, the diver may still convulse up to a minute or two after being removed from the high oxygen breathing gas. This is known as the “Off-Effect.” One should not assume that an oxygen convulsion will not occur unless the diver has been off oxygen for two to three minutes.

SYMPTOMS OF OXYGEN

TOXICITY Con Convulsions V Visual disturbances E Ear (hearing) disturbances N Nausea and vomiting T Twitching muscles I Irritability D Dizziness

If a diver with oxygen convulsions is prevented from drowning or other injury, full recovery can be expect within 24 hours with no lasting effects. Nor will the diver be any more or less susceptible to oxygen toxicity in the future. Following convulsive experiences a diver may be more inclined to perceive warning symptoms during subsequent exposures to oxygen, but this is most likely a psychological matter. The actual mechanism of CNS oxygen toxicity remains unclear in spite of many theories and much research. From the diver's standpoint, prevention of oxygen toxicity is the most important thing. When the use of high-oxygen mixtures is advantageous or necessary, divers must apply sensible precautions such as being sure the breathing apparatus is in good order, observing the depth-time limits, avoiding excessive exertion, and heeding abnormal symptoms if they appear.

Convulsive Symptoms The most serious symptom of CNS oxygen toxicity is convulsion. The following factors should be noted regarding an oxygen convulsion:

- 12 -


1. The diver is unable to carry on any effective breathing during the convulsion.

2. After the diver is brought to surface, there will be a period unconsciousness or neurological impairment following the convulsion; these symptoms are distinguishable from those arterial gas embolism.

3. No attempt should be made insert any object between clenched teeth of a convulsing diver. Although a convulsive diver may suffer a lacerated tongue, this trauma is prefer; to the trauma that may be cause during the insertion of a foreign object. In addition, the person providing first aid may incur significant hand injury should person be bitten by the convulsing diver.

4. There may be no warning of impending convulsion to provide the diver the opportunity to turn to the surface. Therefore buddy lines are essential to closed-circuit oxygen diving. (Author Note: Buddy lines are apparently commonly used in U.S. Navy diver training involving use of high oxygen gas mixtures or pure oxygen with scuba. However, they appear to be used in relation to limited visibility conditions in recreational scuba diving.)

Management of Underwater Convulsion The following steps should be taken when dealing with a convulsing diver:13 1. Assume a position behind the convulsing diver.

Release the victim's weight belt unless the diver is wearing a dry suit, in which case the weight belt should be left in place to prevent the diver from assuming a face down position on the surface.

2. Leave the victim's mouthpiece in his/her mouth. If it is not in the mouth, do not attempt to replace it.

3. Grasp the victim around the chest. 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 buoyancy control device (BCD) may be grasped if necessary.

4. Make a controlled ascent to the surface, maintaining a slight pressure on the diver's chest to assist exhalation.

5. If additional buoyancy is required, activate the victim's BCD. The rescuer should not release weight belt or inflate BCD unless necessary.

6. Upon reaching the surface, inflate the victim's BCD if not previously done.

7. Remove the victim's mouthpiece. 8. Signal for emergency assistance. 9. Once the convulsion has subsided, open the

victim's airway by tilting his head back slightly. 10. Ensure the victim is breathing. Mouth-to-mouth

breathing may be initiated if necessary.

11. If an upward excursion occurred during the actual convulsion, transport to the nearest medical facility (chamber, if nearby) and have the victim evaluated by an individual trained to recognize and treat diving-related illness.

Management of Nonconvulsive Symptoms A diver may experience one or more of the noncovulsive symptoms of oxygen toxicity such as dizziness, muscle twitching, visual disturbances, ear ringing, nausea, etc. Keep in mind that noncovulsive symptoms may or may not preceded the onset of a convulsion. The stricken diver should immediately alert the 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 closely for progression of symptoms.

Oxygen Sensitivity Variables In addition to the depth (oxygen partial pressure)-time relationship, there are many potential physiological and operational variables that can alter your susceptibility to oxygen toxicity. Consider the following: • All authorities recommend that the oxygen limit be

reduced for dives when physical or thermal stress is anticipated. However, there are no specific guidelines for quantifying either physical or thermal stress. Such decisions rely on the subjective judgment of the individual diver. Does the average recreational diver have the knowledge to make such judgments?

• Carbon dioxide retention is well-document as

increasing an individual’s sensitivity to oxygen. CO2 retention can be associated with abnormal breathing patterns brought about by exertion, emotional distress, cold, and intentional gas conservation techniques. For some individuals there is a fine line between “controlled breathing” and “skip-breathing.” Furthermore, some individuals are simply “under-ventilators” or “CO2 retainers.” Such individual are considered poor candidates for diving.

• There is considerable individual variability in

susceptibility to oxygen toxicity. In controlled oxygen tolerance tests, some subjects have convulsed after an exposure of only a few minutes where as other subjects have tolerated more than two hours at the same oxygen exposure level. No specific reason has been identified to account for this variability. Furthermore, susceptibility may

- 13 -


vary within the same individual from day to day. What is the true risk for a widely varied population of recreational dives?

• Systemic diseases which increase oxygen consumption can also influence susceptibility to oxygen toxicity. Conditions associated with increased metabolic rates (such as certain thyroid or adrenal disorders) tend to cause an increase in oxygen sensitivity. The U.S. Navy recommends that divers with these diseases should be excluded from oxygen diving. How many physicians who examine recreational divers are familiar with ramifications of disease and high-oxygen partial pressure diving?

• Some drugs appear to increase oxygen sensitivity. This is an area of medicine that is still not well understood. Many recreational divers use various medications to control medical problems. How many physicians who examine recreational divers are familiar with ramifications of drugs and high-oxygen partial pressure diving?

• Computer-assisted diving has enabled the recreational scuba diver to operate within a wide depth range with limited pre-dive planning. Many divers do not establish maximum dive depth prior to a dive. They simply use the environment and computer as a guide. Maximum operating depth for a specific nitrox mixture is based on maximum acceptable oxygen partial pressure. Are recreational dives, mentally and operationally conditioned by the latitudes afforded by computer-assisted air diving, prepared to observed the more stringent depth limits associated with liberal oxygen values?

Oxygen Partial Pressure Limits Recommended maximum oxygen partial pressure limit for use of EANx or pure oxygen varies from 1.3 to 1.6 ata depending on the dive parameters and the physical status of the diver. Nitrox and technical diver training agencies currently recognize and teach 1.6 ata as absolute maximum acceptable oxygen partial pressure for diving under optimal conditions. However, they strongly emphasize that that pressure must be reduced for dives where thermal stress and/or exertion is a factor. The U.S. Navy currently specifies a oxygen partial pressure limit of 1.3 ata for mixed-gas surface-supplied.. This is conservative value is based on, operational experience, numerous studies, and analysis of data from many operational diving. The rationale for this conservative value is that, for all

practical purposes, oxygen toxicity have not been a problem at or below this partial pressure. Dr. Ed Thalmann suggest that an oxygen partial pressure of 1.4 ata or less is acceptable for recreational divers. Between 1.4 and 1.6 ata is considered as the caution zone. Even though, under optimal diving conditions, the possibility of oxygen toxicity at 1.6 ata is low, the margin of error is slim. Individual susceptibility variables, unexpected descent to deeper depths, and heavy exertion in an emergency may precipitate oxygen toxicity at pressures greater than 1.4 ata. Levels of 1.5 and 1.6 ata should be reserved for conditions when the diver is at complete rest, such as during decompression.14 Under condition of extended exposure and some closed-circuit mixed gas scuba dives may require that oxygen partial pressure be reduced to 1.3 ata or less. Keep in mind that oxygen values may change as more research and field experience data becomes available. Scuba divers are taught to never push dive tables or computers to their limits in order to reduce the potential risk of decompression sickness. We are already aware of the fact that there are many physiological variables that can increase your risk of decompression sickness. These physiological variables can change minute to minute, hour to hour, day to day. The same is true of oxygen-related physiological variables. A prudent diver will not push oxygen partial pressure to it’s ultimate limit. The Maximum Operating Depth (MOD) in feet of seawater (fsw) for any selected PO2 can be calculated using the formula,

MODPF

g

g=

−

1 33

where Pg is the desired partial pressure of oxygen and Fg is the fraction of oxygen in the gas mixture. For example, you can determine the MOD for breathing EAN 36 without exceeding a PO2 of 1.4 ata as follows,

MOD =

−

140 36

1 33..

MOD = 95 fsw.

Unlike nitrogen narcosis, which appears to manifest itself progressively from mild to more severe impairment, or decompression sickness, which most commonly presents post-dive, oxygen toxicity can be a much greater threat to the nonchalant and overly adventurous diver. The simple fact that the onset of oxygen-induced convulsions with no preceding minor

- 14 -


symptoms is possible adds another unpredictable dimension to scuba diving. Oxygen may prove to be a far less forgiving gas than nitrogen!

Pulmonary and Whole Body Oxygen Toxicity In addition to CNS effects, breathing oxygen at elevated pressures for extremely long duration can induce pulmonary oxygen toxicity. Pulmonary symptoms have been noted in association with saturation dives, hyperoxic decompression from deep or long dives, and during extended exposures in the treatment of injured divers. They are not considered at be a problem for routine enriched air nitrox and trimix diving activities. Exposures of 3 to 6 hours at a pO2 of 2 ata have produced pulmonary oxygen toxicity symptoms. Pulmonary toxicity can cause considerable lung damage including interstitial and alveolar edema and intra-alveolar hemorrhage and cell destruction. It begins insidiously with a mild substernal irritation that intensifies and is paralleled with increasingly frequent cough. There may be a marked decrease in vital capacity. When exposure to hyperoxia is sufficiently prolonged, recovery may be greatly delayed and there may be permanent residual scarring of the lungs. It is now realized that oxygen toxicity is more complex and the term "whole body" oxygen toxicity is now used to denote effects on the entire body as well as pulmonary oxygen toxicity.15 The terms chronic oxygen toxicity and Lorraine Smith Effect are also associated with this type of oxygen toxicity. It is significant to note that the actual occurrence of pulmonary oxygen toxicity in the scientific and recreational EANx diver population has not, to my knowledge, been documented. Unit Pulmonary Toxic Dose (UPTD) is used to estimate and track pulmonary or whole body oxygen effects. The UPTD method of calculating cumulative pulmonary oxygen toxicity was introduced in 1972 as a means of monitoring therapeutic oxygen exposure.16 Today, a new term is used to predict the amount of oxygen exposure for a given dive, the Oxygen Tolerance Unit. For all practical purposes the UPTD and OTU can be used interchangeably. The OTU is used in Hamilton's REPLEX method to predict and plan oxygen exposures in order to retain safe daily dive limits and a contingency for post-dive therapy, if needed. Allowable daily OTU is also dependent on the number of consecutive days of diving.

BREATHING UNDERWATER Breathe in, breathe out! Breathing is so natural that many people view it only in this simple way. However, the art of breathing correctly is far more complex than breathing in and breathing out.17

Ideally, a good diver is a "diaphragm" breather. In diaphragm breathing, inspiration is initiated by contraction of the diaphragm. As the diaphragm relaxes, the gas is expired. Diaphragmatic breathing is more efficient and much of the inspired gas is distribute into the lower portion of the lungs. Unfortunately, many people of the western world are "chest" breathers -- they basically expand the chest to inspire gas. Chest breathing requires more energy and is less efficient in ventilation. Chest breathers tend to breathe more rapidly and circulatory efficiency is reduced because the heart must circulate more blood to the lungs. As a diver, you must learn to inhale slowly and exhale slowly. Each breath must be deep and evenly paced. This allows full ventilation of the lungs with laminar flow of gas in the airways. If you breathe shallow and rapidly, you initiate turbulent gas flow that is inefficient and can lead to respirator distress. Inadequate ventilation yields a sensation of gas starvation and may stimulate a further increase in breathing rate and "gulping" the gas. Unchecked this breathing pattern can stress the diver and ultimately lead to panic with perception of gas supply failure. As you descend deeper, gas density and, subsequently, breathing resistance increases. Slow, deep breathing becomes even more important. As the you increase your physical work load or experience mental stress, there is a reflexive response to increase breathing rate. You must learn to adjust your work low, mental stress, and respiratory rate to a level that allows slow inhalation and exhalation with an adequate volume of gas to fulfill the body's needs. In your earlier training you may have been told to simply submerge and "breathe normally!" This is incorrect. You must strive to learn to breathe correctly. This is important as any other skill that you learn in scuba diving training. Once you have mastered correct breathing techniques, they will become natural. However, in the event your are stressed underwater, you will still have to make a conscious effort to maintain a slow, deep breathing rate.

VENTILATION, BREATHING RESISTANCE AND GAS TRANSPORT

The ability of the cardio-vascular system to circulate blood to various parts of the body determines a man's capacity to do heavy work at the surface. At great depth, work capacity is more directly determined by the effectiveness of pulmonary ventilation. The factor tending to limit thorough ventilation at depth is

- 15 -


that the density of the breathing mixture causes increased resistance to gas movement. Experiments have demonstrated that humans can perform moderate work to depths greater than 2,000 feet while breathing helium-oxygen in a dry chamber. The density of the helium-oxygen at 2,000 feet is about 8.6 times that of air at the surface or about the same as air breathed at 220 feet. Maximum voluntary ventilation (MVV) is the maximum gas volume that can be breathed per minute by voluntary effort. The minute respiratory volume measured during maximum exercise is always less than the MVV. The MVV decreases at higher gas density as the depth is increased. Deterioration in pulmonary ventilation is particularly pronounced as the diver descends from the surface to 1,000 feet. Actual measurements have been made to 1,600 feet and greater depths have been simulated with breathing gases denser than helium. Reduction in maximum exercise or work levels that can be expected of divers in dry chambers at these depths. Immersed divers, because of breathing apparatus breathing resistance and the effects of immersion, are further limited. The ultimate hydrostatic pressure levels under which a human may function have not yet been determined. In dry chamber experiments with various breathing mixtures, helium has been successfully tested to 2,000 feet, neon to 1,000 feet, and nitrogen-oxygen below 300 feet. Helium produced no noticeable effects, and presumably, actual saturation diving using helium will eventually prove feasible at least to that test level. Neon seems to impose no mental or physiological limitations, but because it is more dense than helium, problems of pulmonary ventilation may impose a working limit below some depth (estimated to be 700 feet). Saturation exposures with nitrogen have not been conducted below 100 feet, although there is no reason to assume that they are not possible. The limiting factor with nitrogen rather than respiratory functions will be the narcotic effect at increased pressure. The limiting factor with air is the inevitability of lung damage from prolonged exposure to elevated oxygen partial pressures. An additional consideration with both nitrogen-oxygen mixtures and air is the greater density (compared with helium mixtures) which interferes with pulmonary ventilation. At any given depth ventilation will be superior with a less dense gas, and in some operations (such as when using mixed-gas SCUBA that includes the additional factors of equipment-related breathing resistance and dead space) the difference in breathing effectiveness can be significant. The retention of carbon dioxide because of inadequate ventilation will not only limit the diver's

capacity for work but may facilitate the onset of other problems, most notably oxygen poisoning.

CARBON DIOXIDE RETENTION Carbon dioxide (CO2) is a product of metabolism. Carbon dioxide retention is the presence of excessive amounts of carbon dioxide in the blood and body tissues (hypercapnia). Conditions that may enhance retention of CO2 include unusual exertion with inadequate lung ventilation, increased oxygen partial pressure, increased breathing gas density, and excessive breathing apparatus resistance. Increased alveolar oxygen pressure affects the carbon dioxide response. Increased breathing resistance, whether due to apparatus design or gas density, favors CO2 retention and therefore decreases sensitivity to CO2. Increased breathing resistance causes pCO2 and exertion levels to rise in parallel, whereas ventilation response remains constant, or even decreases. Some researches suggest that elevated oxygen partial pressure rather than increased gas density is primarily responsible for carbon dioxide retention. It appears that exercise and acute hypercapnia (CO2 retention) accelerate the onset of oxygen convulsions. Carbon dioxide may have a marked synergistic or additive action. It is suggested that high levels of carbon dioxide can enhance performance degradation related to nitrogen narcosis. It is evident that extended range divers must be aware of the potential consequences of carbon dioxide retention. If divers do not ventilate their lungs sufficiently to eliminate as much CO2 as is produced (hypoventilation), self-poisoning can occur. Incidents in which a diver has lost consciousness for no other apparent reason have been explained on this basis. Deliberate reduction in breathing rate with short intervals of breath holding (i.e., skip breathing) to conserve gas in the use of open-circuit scuba is an extremely dangerous practice. Most authorities consider it better to breathe normally and consume more gas than to practice periods of breath-holding between inspirations and risk the lethal consequences of CO2 buildup. This practice should not be confused with the continuous long, slow inhalation-exhalation techniques encouraged in scuba diving. Carbon dioxide is also a major consideration for a diver using recirculating scuba. Carbon dioxide must me removed from the breathing loop using a chemical absorbent. Ineffective removal resulting for exceeding the capacity of the chemical absorbent, excess moisture, or improper equipment assembly can lead to carbon dioxide induced unconsciousness with or without warning.

- 16 -


DEPTH BLACKOUT Cave diving researchers have documented cases of blackout at depth.18 Victim simply appears to fall asleep with their eyes open and do not move except for breathing. For unknown reasons the sleeping victim apparently retains the scuba mouthpiece and continues to breathe, lying inert on the bottom, until their gas supply is exhausted. Cases of 15 survivors (rescued by other divers) were analyzed. In all cases the incident of blackout occurred on the individuals deepest dive to that time and the shallowest occurrence involved heavy exertion before blackout. Victims do not recall any symptoms before blackout. It has been suggested that depth blackout results from the cumulative and combined effect of nitrogen, oxygen, and carbon dioxide.

GAS CONTAMINATION Although any gas supply can contain impurities, standards for the production of breathing quality oxygen, helium, and nitrogen minimize the possibility of contamination. Contamination is most commonly associated with compressed air. The atmospheric air compressed into scuba cylinders can be contaminated or contamination can occur during the compression process. The quality of air that the diver breathes should comply, at a minimum, with the following standard19: Oxygen: Atmospheric/19 t0 23% by volume Carbon Dioxide: 500 ppm Carbon Monoxide: 20 ppm Condensed hydrocarbons: 5 mg/m3 Solid and liquid particles: None Most suppliers of compressed air for scuba divers are very conscientious. Furthermore, advancement in compressed air technology and purification equipment insure that most commercial air supplies will be of high quality. Possibly, the greatest risk of air supply contamination is associated with portable air compressors used in remote area diving operations. Care and maintenance of these compressors is sometimes substandard and operators may be careless. Carbon dioxide (CO2) is a natural by-product of metabolism. Elevated CO2 levels in scuba diving are most often associated with physical exertion and inadequate ventilation of the lungs rather than contamination of air in scuba cylinders. The 1000 ppm carbon dioxide level also appears to be a relatively conservative value for compressed air standards. This value also appears to be readily

attainable and acceptable within the diving community. Carbon monoxide (CO) is probably the most serious potential breathing media contaminant. Contamination with carbon monoxide can arise from two primary sources: • The gas may be present in the intake air from

having the compressor intake located too close to or downwind from the exhaust of a gasoline-driven engine or other source of exhaust gas. In large cities and industrial areas, CO is a common atmospheric pollutant and may rise, at times, beyond the safe concentration for divers' air. Consequently, the air supplier must be constantly aware of atmospheric pollution levels and/or take measure to remove excessive CO during the air compression process.

• Oil-lubricated compressors, particularly when not

operated or maintained properly, can develop high cylinder temperatures that cause partial combustion (oil flashing - or dieseling) of the lubrication oil. All breathing air compressors must be maintained in accordance with manufacturers' specifications.

Both of the above conditions can cause air contamination when cylinders are filled using an electrically powered compressor. Carbon monoxide readily combines with the blood hemoglobin, forming COHb, and renders the hemoglobin incapable of transporting sufficient oxygen. Hemoglobin, in fact, combines with CO about 200 times as readily as with oxygen. The diffusion capacity for CO also increases progressively with increasing exercise. When this occurs, tissue anoxia develops even though the supply of oxygen to the lungs is ample. At sea level the toxic effect of CO is proportional to the amount of COHb formed. However, at depth, a diver may tolerate a considerably higher ratio of COHb because some of the oxygen transport requirements are met by the oxygen in solution (due to increased pO2 at depth). Since the reconversion of COHb to oxyhemoglobin is relatively slow compared to the time required for COHb to form, the diver may develop symptoms of CO poisoning immediately on ascent. A study by Erickson indicates that the affinity of carbon monoxide for hemoglobin (Hb) remains constant with depth within the entire range of air diving.20 The percentage of carboxyhemoglobin (COHb) does not increase with depth. The toxicity of 20 ppm carbon monoxide in air at 230 feet (70 meters) is no greater than at the surface. A carbon monoxide

- 17 -


level of 30 ppm in air results in a measured equilibrium value of about 5% COHb. This value is, according to Erickson, medically acceptable. A 3.3% (approximate) COHb equilibrium value corresponds to a 20 ppm carbon monoxide level in air; 10 ppm carbon monoxide has a corresponding value of about 1.7% COHb. As a matter of perspective, in the 1970’s 17 U.S. cities have recorded carbon monoxide levels greater than 10 ppm over 50% of the time during a one-year period. Also, the average light cigarette smoker will have a COHb level of about 3.8% and the extremely heavy smoker may have 19% COHb.21 The wide spectrum of symptoms associated with carbon monoxide poisoning include headache, dizziness, nausea, weakness, confusion, and other mental changes. The tender or diving partner may note failure to respond, clumsiness, and bad judgment. Frequently no symptoms are evident; the diver may lose consciousness without warning and breathing may cease. Symptoms parallel those of other forms of anoxia, with one exception -- the victim's coloration is red instead of blue. In spite of the displacement of oxygen, hemoglobin combined with CO has a bright red color. Consequently, a victim who becomes anoxic because of carbon monoxide poisoning often exhibits an unnatural redness of lips, nail beds, and sometimes the skin. When carbon monoxide poisoning is suspected, get the victim into fresh air (or non-contaminated area) as soon as possible. If breathing has stopped, start artificial respiration at once. Even if a non-breathing victim is revived, they should be monitored closely since respiratory arrest may soon reoccur. The victim should be given oxygen as soon as possible; administration of oxygen increases the amount of oxygen reaching the tissue in spite of the inactivity of the hemoglobin and it also accelerates the elimination of CO from the blood. A carbon monoxide victim must be treated under medical supervision. Low level carbon monoxide poisoning has been successfully treated by oxygen breathing at atmospheric pressure. However, the best treatment of carbon monoxide poisoning victims is administering oxygen at 2 to 3 ata pressure in a hyperbaric chamber. Records of rapid and complete recovery are establishing hyperbaric oxygen as a standard method of treatment. At one time oil vapor, from oil-lubricated compressors, was considered a common potential contaminant of scuba air supply. Fortunately, this is no longer the case. Today, oil contamination appears to be quite rare. Oil contamination is fairly easy to detect. Oil fumes give an unpleasant taste and odor to the breathing mixture, and under pressure the

concentration may be sufficient to cause pulmonary irritation, cough, and in extreme cases, pneumonia. Obviously, do not use air if oil contaminated is suspected. Compressor lubricating oil and the aerosols formed from the oil can contaminate a diver’s air supply. Today, oil and other vapors or particulates are seldom a problem for scuba divers since they are easily removed by compressor filtration and purification systems. However, in the event of filtration system absence, malfunction, or improper maintenance, sufficient levels of oil aerosols may be inhaled to cause lipoid pneumonitis (oil-mist pneumonia or lipid pneumonia). This condition was often mentioned in early diving literature, but its clinical and physiological manifestations were not well documented in divers. Most modern textbooks omit the condition. An excellent clinical example of lipoid pneumonitis was documented in a commercial abalone diver who used a surface-supplied air source to deliver air to a regulator-mouthpiece assembly at depth (i.e., hookah system).22 The diver’s symptoms included shortness of breath and dyspnea (labored respiration) during exertion. Physiologic evaluation revealed a restrictive ventilatory defect. A lung biopsy showed fibrosis of the alveolar walls and abnormally elevated level of lipid droplets within the macrophages.23 Field inspection revealed that the diver was using a mineral oil lubricated compressor with no external filter. When questioned, the diver recalled incidents of tasting oil and coughing out oil droplets during and after diving. Modern air delivery systems have minimized the risks of divers contracting lipoid pneumonitis. Avoidance of excessive oil vapor in compressed air requires careful and regular compressor maintenance, water and oil vapor condensers, and an effective filtering system. However, disregard for proper use and maintenance of equipment or failure to acknowledge the presence of foreign substances in the air supply can lead to serious and possibly disabling respiratory problems. If an oily odor or taste is present, discontinue the use of the air supply immediately. Not only is there concerned about lung damage, there is also a possibility of other contaminants such as carbon monoxide. Keep in mind that even the best maintained compressor can pump pollutants for ambient air into a scuba cylinder.

OTHER PHYSIOLOGICAL CONCERNS Certain physiological phenomena have been observed in both dry chamber pressure tests and in

- 18 -


actual deep-diving operations that may be linked to a variety of factors: high ambient pressure, high rates of change in pressure, changes in the composition of the breathing mixture or, possibly, to the constituent gases in the breathing mixture. In addition, divers using closed-circuit scuba are at risk of chemical injury to the lungs.

Compression Pains Compression pains may be experienced during compression or may appear at some point in time after arriving at maximum depth. This deep aching pain, similar to decompression sickness, can occur in the knees, shoulders, fingers, back, hips, neck, and ribs. Pain may be accompanied by popping of the joints or a dry gritty feeling in the joint. Symptoms depend on depth, rate of compression, and individual susceptibility. In mixed gas diving, pain generally does not appear at depths shallower than 300 feet. Deeper than 600 feet, pain may occur at even very slow rates of compression. These pains tend to improve after a few hours or days at depth. The pains are not debilitating but may pose a handicap to the normal conduct of operations. Compression pains are thought to result from the sudden increase in tissue gas tension surrounding the joints causing fluid shifts and interfering with joint lubrication.

High Pressure Nervous Syndrome High Pressure Nervous Syndrome (HPNS) is a derangement of central nervous system function that occurs on deep mixed gas dives.24 HPNS was observed in the mid-1960's during rapid helium-oxygen dive compression. The exact cause remains unclear. Clinical manifestations include muscular tremors (sometimes called "Helium Tremor"), imbalance, incoordination, loss of manual dexterity, loss of alertness, dizziness, abdominal cramps, diarrhea, nausea, decreased alertness, confusion, indifference to surroundings, and a desire to sleep. Electroencephalograph (EEG) changes have also been noted. HPNS is first noted between 400 and 500 feet. The severity appears to be depth, gas, and compression rate dependent. Some success in reducing the severity of HPNS is attributed to adding a small percentage of nitrogen to the breathing mixture. Hydrogen-helium-oxygen also appears to decrease HPNS. However, compression rate reduction appears to be the most important deterrent. Compression rates must be reduced to 1 meter/hour or less at very deep depths. HPNS has occurred during rapid trimix scuba diving descents (100 feet/minute) at depths of approximately 800 feet.

Chemical Injury Divers using closed-circuit scuba may experience upper airway irritation or injury by inhaling or ingesting a caustic alkaline solution formed by water coming into contact with the carbon dioxide absorbent. The diver will immediately experience choking, gagging, foul taste, and burring in the mouth and throat. The condition is sometime referred to as a caustic cocktail. The extent of injury depends on the amount and distribution of the solution.

CONCLUSION As we extend into deeper depths, we must understand and respect potential for heighten risks. Emergency ascents from deep depths can be very unforgiving and the diver is most certainly a prime candidate for decompression sickness. Nitrogen narcosis and other physiological factors associated with breathing gases at higher pressures cannot be ignored. All divers become impaired when breathing air at depth. Often persons do not perceive this impairment because nitrogen narcosis also distorts perception. A diver need only dive to the same depth using an alternative gas mixture with less nitrogen to understand the fact that they really were impaired on air. Divers electing to exceed the 130 foot depth limit must take exceptional care. Any diving beyond a depth of about 180 feet (55 meters) is best undertaken using Trimix (nitrogen-helium-oxygen). Breathing an appropriate Trimix blend at 240 feet is basically equivalent to breathing compressed air at about 100 feet. An extended range dive can be conducted with relative safety provided that the divers are well-trained, experienced, and properly equipped. Such dives must be planned meticulously and divers must completely understand the added risk associated with diving to these deeper depths. One thing is for certain, "Risk increases with depth!"

REFERENCES AND NOTES 1 The discussion of decompression is based on an

excellent paper by Moon, R., Vann, R., an Bennett, P., The Physiology of Decompression Illness, Scientific American (August 1995).

2 Excerpts taken directly from Stone, T., “Long-Term Consequences of Diving,” Discover Diving, Vol. 14, No. 2 (March/April 1996).

3 Bennett, P. “Inert Gas Narcosis and High Pressure Nervous Syndrome” in Bove, A., Bove and Davis’ Diving Medicine, 3rd Edition (Philadelphia: W.B. Saunders Company, 1997).

- 19 -


4 Behnke, A., Thomson, R., and Motlet, E., “The

Psychologic Effects From Breathing Air At 4 Atmospheres Pressure,” American Journal of Physiology 112:554-558 (1935).

5 Hamilton, R. and Kizer, K. (eds.), Nitrogen Narcosis (Bethesda, MD: The Undersea Medical Society, 1985).

6 Fowler, B., Ackles, K., and Porlier, G., "Effects of Inert Gas Narcosis on Behavior -- A Critical Review," Undersea Biomed. Res. 12, 369-402 (1985).

7 Fowler, B., Under the Influence: A Performance Guide to Management in Leach, J., Underwater Science, Volume 12: Man Underwater (Kent, U.K.: The Underwater Association for Scientific Research, Ltd.).

8 Walsh, J. (ed.), Interaction of Drugs in the Hyperbaric Environment (Bethesda, MD: Undersea Medical Society, 1980).

9 Bacharch, A. and Egstrom, G., Stress and Performance in Diving (San Pedro, CA: Best Publishing Co., 1987).

10 AquaCorps Journal No. 6 (June 1993). 11 AquaCorps Journal No. 6 (June 1993) 12 This discussion of convulsions and convulsion

management was taken form the U.S. Navy Diving Manual: Volume 1: Air Diving (1985) and Volume 2: Mixed Gas Diving (1991) with some modification for open-circuit scuba diving.

13 Modified for open-circuit scuba diving from the U.S. Navy Diving Manual (Volume 2: Mixed Gas Diving, 1991).

14 Thalmann, E., “If You Dive Nitrox, You Should Know About OXTOX,” Alert Diver (May/June 1997).

15 Hamilton, W., Tolerating Exposures to High Oxygen Levels: Repex and Other Methods, Marine Technology Society Journal 23(4): 9-25 (1989).

16 Wright, W., Use of the University of Pennsylvania , Institute of Environmental Medicine procedure for calculation of cumulative pulmonary oxygen toxicity. U.S. Navy Exp. Diving Unit, Rept. NEDU 2-72, 1972.

17 For a complete discussion of the science and art of breathing the reader is referred to Mount, T. and Gilliam, B., Mixed Gas Diving (San Diego: Watersport Books, 1993).

18 Exley, S., Basic Cave Diving (Jacksonville, Fl: Cave Diving Section of the National Speleological Society, 1979).

19 Compressed Gas Association: Air Grade E Standard. Divers are encouraged to use Grade F in which the carbon monoxide is reduced to 10 ppm.

20 Erickson, P., "The Toxicity of Carbon Monoxide Under Pressure and Considerations for Standard Setting," Paper presented at the Diver's Gas Purity Symposium, Columbus, Ohio (November 1976.)

21 Winter, P. and Miller, J., "Carbon Monoxide Poisoning," JAMA 236(13) (1976).

22 Kizer, K.W. and Golden, J.A., Lipoid pneumonitis in a commercial abalone diver. Undersea Biomed. Res. 14(6): 545-552 (1987).

23 A tissue cell that functions to protect the body against infection and noxious substances.

24 Bennett, P., "Inert Gas Narcosis and HPNS" in Bove, A. and Davis, J., Diving Medicine (Philadelphia: W.B. Saunders Company, 1990).

FURTHER READING Bennett, P. and Elliott, D. (ed), The Physiology and Medicine of Diving, 4th Edition, (Philadelphia: W.B. Saunders, 1993). Bove, A. (ed), Bove and Davis’ Diving Medicine, 3rd Edition (Philadelphia: W.B. Saunders Company, 1997). Brylske, A., Beating the Bends: A Diver’s Guide to Avoiding Decompression Sickness (Parkville, Mo.: Specialized Publishing Company, 1995). Lippmann, J., Deeper into Diving (Carnegie, Victoria, Australia: J.L. Publications, 1990).

- 20 -

fisiologia edi

Documents