Observations often inaccurate

Likely to make incorrect decision about what to do

Diver may not care about job or safety

Figure 3-16. Nitrogen Narcosis.

Figure 3-16. Nitrogen Narcosis.

3-10.2.1 Pulmonary Oxygen Toxicity. Low pressure oxygen poisoning, or pulmonary oxygen toxicity, can begin to occur if more than 60 percent oxygen is breathed at one atmosphere for 24 hours or more. While diving, this can occur after a 24-hour exposure to ppO2 of 0.6 ata (e.g., 60 fsw breathing air). Long exposures to higher levels of oxygen, such as administered during Recompression Treatment Tables 4, 7, and 8, may quickly lead to pulmonary oxygen toxicity. The symptoms of pulmonary oxygen toxicity may begin with a burning sensation on inspiration and progress to pain on inspiration. During recompression treatments, pulmonary oxygen toxicity may have to be tolerated in patients with severe neurological symptoms to effect adequate treatment. In conscious patients, the pain and coughing experienced with inspiration eventually limit further exposure to oxygen. Return to normal pulmonary function gradually occurs after the exposure is terminated. Unconscious patients who receive oxygen treatments do not feel pain and it is possible to subject them to exposures resulting in permanent lung damage or pneumonia. For this reason, care must be taken when administering 100 percent oxygen to unconscious patients even at surface pressure.

3-10.2.2 Central Nervous System (CNS) Oxygen Toxicity. High pressure oxygen poisoning, or central nervous system (CNS) oxygen toxicity, is most likely to occur when divers are exposed to more than 1.6 atmospheres of oxygen.

Susceptibility to central nervous system oxygen toxicity varies from person to person. Individual susceptibility varies from time to time and for this reason divers may experience CNS oxygen toxicity at exposure times and pressures previously tolerated. Because it is the partial pressure of oxygen itself that causes toxicity, the problem can occur when mixtures of oxygen with nitrogen or helium are breathed at depth. Oxygen toxicity is influenced by the density of the breathing gas and the characteristics of the diving system used. Thus, allowable limits for oxygen partial pressures differ to some degree for specific diving systems (which are discussed in later chapters). In general, oxygen partial pressures at or below 1.4 ata are unlikely to produce CNS toxicity. Closed-system oxygen rebreathing systems require the lowest partial pressure limits, whereas surface-supplied helium-oxygen systems permit slightly higher limits.

3- Factors Contributing to CNS Oxygen Toxicity. Three major external factors contributing to the development of oxygen toxicity are the presence of a high level of carbon dioxide in the breathing mixture resulting from CO2 absorbent failure, carbon dioxide in the helmet supply gas, or inadequate ventilation during heavy exertion.

3- Symptoms of CNS Oxygen Toxicity. The most serious direct consequence of oxygen toxicity is convulsions. Sometimes recognition of early symptoms may provide sufficient warning to permit reduction in oxygen partial pressure and prevent the onset of more serious symptoms. The warning symptoms most often encountered also may be remembered by the mnemonic VENTIDC:

V: Visual symptoms: Tunnel vision, a decrease in diver's peripheral vision, and other symptoms, such as blurred vision, may occur.

E: Ear symptoms. Tinnitus, any sound perceived by the ears but not resulting from an external stimulus, may resemble bells ringing, roaring, or a machinery-like pulsing sound.

N: Nausea or spasmodic vomiting. These symptoms may be intermittent.

T: Twitching and tingling symptoms. Any of the small facial muscles, lips, or muscles of the extremities may be affected. These are the most frequent and clearest symptoms.

I: Irritability: Any change in the diver's mental status including confusion, agitation, and anxiety.

D: Dizziness. Symptoms include clumsiness, incoordination, and unusual fatigue.

C: Convulsions. The first sign of CNS oxygen toxicity may be a convulsion that occurs with little or no warning.

Symptoms may not always appear and most are not exclusively symptoms of oxygen toxicity. Twitching is perhaps the clearest warning of oxygen toxicity, but it may occur late, if at all. The appearance of any one of these symptoms usually represents a bodily signal of distress of some kind and should be heeded.

3-10.2.3 CNS Convulsions. Convulsions, the most serious direct consequence of CNS oxygen toxicity, may occur suddenly without being preceded by any other symptom. 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 a state of rigidity.

This is referred to as the tonic phase of the convulsion. The brain soon fatigues and the number of impulses slows. This is the clonic phase and the random impulses to various muscles may cause violent thrashing and jerking for a minute or so.

After the convulsive phase, brain activity is depressed and a postconvulsive (postictal) depression follows. During this phase, the patient is usually unconscious and quiet for a while, then semiconscious and very restless. He will then usually sleep on and off, waking up occasionally though still not fully rational. The depression phase sometimes lasts as little as 15 minutes, but an hour or more is not uncommon. At the end of this phase, the patient often becomes suddenly alert and complains of no more than fatigue, muscular soreness, and possibly a headache. After an oxygen-toxicity convulsion, the diver usually remembers clearly the events up to the moment when consciousness was lost, but remembers nothing of the convulsion itself and little of the postictal phase.

3- Recommended Actions. 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 breathholding in the tonic phase is greatly reduced because of the high partial pressure of oxygen in the tissues and brain. If a convulsion occurs in a recompression chamber, it is important to keep the individual from thrashing against hard objects and being injured. Complete restraint of the individual's movements is neither necessary nor desirable. The oxygen mask shall 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.

Convulsions may lead to squeeze while surface-supplied helmet diving if the diver falls to a greater depth, but bruises and a chewed tongue are more likely the only consequences. Bringing a diver up rapidly during the height of a convulsion could possibly lead to gas embolism. When using scuba, the most serious consequence of convulsions is drowning. In this situation, using the buddy system can mean the difference between life and death.

The biochemical changes in the central nervous system caused by high oxygen partial pressures are not instantaneously reversed by reducing the oxygen partial 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. One should not assume that an oxygen convulsion will not occur unless the diver has been off oxygen for 2 or 3 minutes.

If a diver with oxygen convulsions is prevented from drowning or causing other injury to himself, full recovery with no lasting effects occurs within 24 hours. Susceptibility to oxygen toxicity does not increase, although divers may be more inclined to notice warning symptoms during subsequent exposures to oxygen. However, this is most likely a psychological matter.

3- Prevention. The actual mechanism of CNS oxygen toxicity remains unknown in spite of many theories and much research. Preventing oxygen toxicity is important to divers. When use of high pressures of oxygen is advantageous or necessary, divers should take sensible precautions, such as being sure the breathing apparatus is in good order, observing depth-time limits, avoiding excessive exertion, and heeding abnormal symptoms that may appear.

3-10.3 Absorption of Inert Gases. The average human body at sea level contains about one liter of dissolved nitrogen. All of the body tissues are saturated with nitrogen at a partial pressure equal to the partial pressure in the alveoli, about 570 mmHg (0.75 ata). If the partial pressure of nitrogen changes because of a change in the pressure of the composition of the breathing mixture, the pressure of the nitrogen dissolved in the body gradually attains a matching level. Additional quantities are absorbed or some of the gas is eliminated, depending on the partial pressure gradient, until the nitrogen partial pressures in the lungs and in the tissues are in balance.

As described in Henry's law, the amount of gas that dissolves in a liquid is almost directly proportional to the partial pressure of that gas. If one liter of inert gas is absorbed at a pressure of one atmosphere, then two liters are absorbed at two atmospheres and three liters at three atmospheres, etc.

The process of taking up more nitrogen is called absorption or saturation. The process of giving up nitrogen is called elimination or desaturation. The chain of events is essentially the same in both of these processes even though the direction of exchange is opposite. In diving, both saturation (when the diver is exposed to an increased partial pressure of nitrogen at depth) and desaturation (when he returns to the surface) are important. The same processes occur with helium and other inert gases.

3-10.4 Saturation of Tissues. The sequence of events in the process of saturation can be illustrated by considering what happens in the body of a diver taken rapidly from the surface to a depth of 100 fsw (Figure 3-17). To simplify matters, we can say that the partial pressure of nitrogen in his blood and tissues on leaving the surface is roughly 0.8 ata. When the diver reaches 100 fsw, the alveolar nitrogen pressure in his lungs will be about 0.8 x 4 ata or 3.2 ata, while the blood and tissues remain temporarily at 0.8 ata.

3-10.4.1 Nitrogen Saturation Process. The partial pressure difference or gradient between the alveolar air and the blood and tissues is thus 3.2 minus 0.8, or 2.4 ata. This gradient is the driving force that makes the molecules of nitrogen move by diffusion from one place to another. Consider the following 10 events and factors in the diver at 100 fsw:

1. As blood passes through the alveolar capillaries, nitrogen molecules move from the alveolar air into the blood. By the time the blood leaves the lungs, it has reached equilibrium with the new alveolar nitrogen pressure. It now has a nitrogen tension (partial pressure) of 3.2 ata and contains about four times as much nitrogen as before. When this blood reaches the tissues, there is a similar

Figure 3-17. Saturation of Tissues. Shading in diagram indicates saturation with nitrogen or helium under increased pressure. Blood becomes saturated on passing through lungs, and tissues are saturated in turn via blood. Those with a large supply (as in A above) are saturated much more rapidly than those with poor blood supply (C) or an unusually large capacity for gas, as fatty tissues have for nitrogen. In very abrupt ascent from depth, bubbles may form in arterial blood or in "fast" tissue (A) even through the body as a whole is far from saturation. If enough time elapses at depth, all tissues will become equally saturated, as shown in lower diagram.

gradient and nitrogen molecules move from the blood into the tissues until equilibrium is reached.

2. The volume of blood in a tissue is relatively small compared to the volume of the tissue and the blood can carry only a limited amount of nitrogen. Because of this, the volume of blood that reaches a tissue over a short period of time loses its excess nitrogen to the tissue without greatly increasing the tissue nitrogen pressure.

3. When the blood leaves the tissue, the venous blood nitrogen pressure is equal to the new tissue nitrogen pressure. When this blood goes through the lungs, it again reaches equilibrium at 3.2 ata.

4. When the blood returns to the tissue, it again loses nitrogen until a new equilibrium is reached.

5. As the tissue nitrogen pressure rises, the blood-tissue gradient decreases, slowing the rate of nitrogen exchange. The rate at which the tissue nitrogen partial pressure increases, therefore, slows as the process proceeds. However, each volume of blood that reaches the tissue gives up some nitrogen which increases the tissue partial pressure until complete saturation, in this case at 3.2 ata of nitrogen, is reached.

6. Tissues that have a large blood supply in proportion to their own volume have more nitrogen delivered to them in a certain amount of time and therefore approach complete saturation more rapidly than tissues that have a poor blood supply.

7. All body tissues are composed of lean and fatty components. If a tissue has an unusually large capacity for nitrogen, it takes the blood longer to deliver enough nitrogen to saturate it completely. Nitrogen is about five times as soluble (capable of being dissolved) in fat as in water. Therefore, fatty tissues require much more nitrogen and much more time to saturate them completely than lean (watery) tissues do, even if the blood supply is ample. Adipose tissue (fat) has a poor blood supply and therefore saturates very slowly.

8. At 100 fsw, the diver's blood continues to take up more nitrogen in the lungs and to deliver more nitrogen to tissues, until all tissues have reached saturation at a pressure of 3.2 ata of nitrogen. A few watery tissues that have an excellent blood supply will be almost completely saturated in a few minutes. Others, like fat with a poor blood supply, may not be completely saturated unless the diver is kept at 100 fsw for 72 hours or longer.

9. If kept at a depth of 100 fsw until saturation is complete, the diver's body contains about four times as much nitrogen as it did at the surface. Divers of average size and fatness have about one liter of dissolved nitrogen at the surface and about four liters at 100 fsw. Because fat holds about five times as much nitrogen as lean tissues, much of a diver's nitrogen content is in his fatty tissue.

10. An important fact about nitrogen saturation is that the process requires the same length of time regardless of the nitrogen pressure involved. For example, if the diver had been taken to 33 fsw instead of 100, it would have taken just as long to saturate him completely and to bring his nitrogen pressures to equilibrium. In this case, the original gradient between alveolar air and the tissues would have been only 0.8 ata instead of 2.4 ata. Because of this, the amount of nitrogen delivered to tissues by each round of blood circulation would have been smaller from the beginning. Less nitrogen would have to be delivered to saturate him at 33 fsw, but the slower rate of delivery would cause the total time required to be the same.

3-10.4.2 Other Inert Gases. When any other inert gas, such as helium, is used in the breathing mixture, the body tissues become saturated with that gas in the same process as for nitrogen. However, the time required to reach saturation is different for each gas.

The actual total pressure of gases in a tissue may achieve significant supersaturation or subsaturation during the gas exchange when one gas replaces another in body tissues without a change in ambient pressure (isobaric gas exchange).

3-10.5 Desaturation of Tissues. The process of desaturation is the reverse of saturation (Figure 3-18). If the arterial pressure of the gas in the lungs is reduced, either through a change in pressure or a change in the breathing medium, the new pressure gradient induces the nitrogen to diffuse from the tissues to the blood, from the blood to the gas in the lungs, and then out of the body with the expired breath. Some parts of the body desaturate more slowly than others for the same reasons that they saturate more slowly: poor blood supply or a greater capacity to store gas.

Figure 3-18. Desaturation of Tissues. The desaturation process is essentially the reverse of saturation. When pressure of inert gas is lowered, blood is cleared of excess gas as it goes through the lungs. Blood then removes gas from the tissues at rates depending on amount of blood that flows through them each minute. Tissues with poor blood supply (as in C in upper sketch) or large gas capacity will lag behind and may remain partially saturated after others have cleared (see lower diagram). If dive is long enough to saturate each tissue, long decompression stops are required to desaturate the tissue enough so that bubbles will not form in it on ascent.

3-10.5.1 Saturation/Desaturation Differences. There is a major difference between saturation and desaturation. The body accommodates large and relatively sudden increases in the partial pressure of the inspired gas without ill effect. The same is not true for desaturation, however, where a high pressure gradient (toward the outside) can lead to serious problems.

A diver working at a depth of 100 fsw is under a total pressure of 4 ata. The partial pressure of the nitrogen in the air he is breathing is approximately 3.2 ata (80 percent of 4 ata). If his body is saturated with nitrogen, the partial pressure of the nitrogen in his tissues is also 3.2 ata. If the diver were to quickly ascend to the surface, the total hydrostatic pressure on his tissues would be reduced to 1 ata, whereas the tissue nitrogen tension would remain momentarily at 3.2 ata.

3-10.5.2 Bubble Formation. A dissolved gas can have a tension higher than the total pressure in the body. If a tissue is supersaturated with gas to this degree, the gas eventually separates from solution in the form of bubbles. Bubbles of nitrogen forming in the tissues and blood result in the condition known as decompression sickness. These bubbles can put pressure on nerves, damage delicate tissues, block the flow of blood to vital organs and induce biochemical changes and blood clotting. Symptoms may range from skin rash to mild discomfort and pain in the joints and muscles, paralysis, numbness, hearing loss, vertigo, unconsciousness, and in extreme cases, death.

Fortunately, the blood and tissues can hold gas in supersaturated solution to some degree without serious formation of bubbles. This permits a diver to ascend a few feet without experiencing decompression sickness, while allowing some of the excess gas to diffuse out of the tissues and be passed out of his body. By progressively ascending in increments and then waiting for a period of time at each level, the diver eventually reaches the surface without experiencing decompression sickness.

3-10.6 Decompression Sickness. As has been discussed, when a diver's blood and tissues have taken up nitrogen or helium in solution at depth, reducing the external pressure on ascent can produce a state of supersaturation, as has been discussed. If the elimination of dissolved gas, via the circulation and the lungs, fails to keep up with the reduction of external pressure, the degree of supersaturation may reach the point at which the gas can no longer stay in solution. The situation then resembles what happens when a bottle of carbonated beverage is uncapped.

3-10.6.1 Direct Bubble Effects. Supersaturated tissues may result in bubble formation in tissue or in the bloodstream. Also, bubbles may arise from the lung and enter the bloodstream from pulmonary overinflation (arterial gas embolism). Once in the bloodstream these bubbles will cause symptoms depending only on where they end up, not on their source. These bubbles may exert their effects directly in several ways:

■ Direct blockage of arterial blood supply leading to tissue hypoxia, tissue injury, and death. This is called embolism and may occur from pulmonary damage (arterial gas embolism) or from the bubbles reaching the arterial circulation during decompression. The mechanism usually causes cerebral (brain) symptoms.

■ Venous congestion from bubbles or slow blood flow and sludging, which leads to increased back pressure. This increased back pressure leads to hypoxia, tissue injury, and death. This is one of the mechanisms of injury in Spinal Cord DCS.

■ Direct pressure on surrounding tissue (autochthonous bubbles) causing stretching, pressure on nerve endings, or direct mechanical damage. This is another mechanism for Spinal Cord DCS and may be a mechanism for Musculoskeletal DCS.

■ Bubbles blocking blood flow in the lungs that leads to decreased gas exchange, hypoxia, and hypercarbia. This is the mechanism of damage in Pulmonary DCS.

The time course for these Direct Bubble Effects is short (a few minutes to hours). The only necessary treatment for Direct Bubble Effects is recompression. This will compress the bubble to a smaller diameter. This restores blood flow, decreases venous congestion and improves gas exchange in the lungs and tissues. It also increases the speed at which the bubbles outgas and collapse.

3-10.6.2 Indirect Bubble Effects. Bubbles may also exert their effects indirectly because a bubble present in a blood vessel acts like a foreign body. The body reacts as it would if there were a cinder in the eye or a splinter in the hand. The body's defense mechanisms become alerted and try to reject the foreign body. This try at rejection includes the following:

■ Blood vessels become "leaky" (due to chemical release). Blood plasma leaks out while blood cells remain inside. The blood becomes thick and causes sludging and decreased pressure downstream, with possible shock.

The platelet system becomes active and the platelets gather at the site of the bubble causing a clot to form.

The injured tissue releases fats that clump together in the bloodstream. These act as emboli, causing tissue hypoxia.

Injured tissues release histamine and histamine-like substances, causing edema, which leads to allergic-type problems of shock and respiratory distress.

Bubble reaction takes place in a longer period (up to 30 minutes or more) than the direct effects. Because the non-compressible clot replaces a compressible bubble, recompression alone is not enough. To restore blood flow and relieve hypoxia, hyperbaric treatment and other therapies are often required.

3-10.6.3 Symptoms of Decompression Sickness. The resulting symptoms depend on the location and size of the bubble or bubbles. Symptoms include pain in joints, muscles or bones when a bubble is in one of these structures. Bubble formation in the brain can produce blindness, dizziness, paralysis and even unconsciousness and convulsion. When the spinal cord is involved, paralysis and/or loss of feeling can occur. Bubbles in the inner ear produce hearing loss and vertigo. Bubbles in the lungs can cause coughing, shortness of breath, and hypoxia, a condition referred to as "the chokes." This condition often proves fatal. Skin bubbles produce itching or rash or both. Unusual fatigue or exhaustion after a dive is prob ably also due to bubbles in unusual locations and the biochemical changes they have induced. Decompression sickness that affects the central nervous system (brain or spinal cord) or lungs can produce serious disabilities and may even threaten life if not treated promptly and properly. When other areas such as joints are affected, the condition may produce excruciating pain and lead to local damage if not treated, but life is seldom threatened.

3-10.6.4 Treating Decompression Sickness. Treatment of decompression sickness is accomplished by recompression. This involves putting the victim back under pressure to reduce the size of the bubbles to cause them to go back into solution and to supply extra oxygen to the hypoxic tissues. Treatment is done in a recompression chamber, but can sometimes be accomplished in the water if a chamber cannot be reached in a reasonable period of time. Recompression in the water is not recommended, but if undertaken, must be done following specified procedures. Further discussion of the symptoms of decompression sickness and a complete discussion of treatment are presented in volume 5.

Modern research has shown that the symptoms caused by bubbles depend on their ultimate location and not their source. Bubbles entering the arterial circulation from the lung (pulmonary overinflation syndrome) have exactly the same effects as those arising from body tissues and cells (decompression sickness) that find their way into the arterial circulation. This means that the treatment of diseases caused by bubbles is dependent on the ultimate symptoms and symptom severity and not on the source of the bubbles.

This finding has lead to new treatment protocols in which the initial treatment for arterial gas embolism and decompression sickness is the same, recompression to 60 fsw. After that, treatment proceeds according to the patient's condition and response to therapy. Many agree with the opinion that Direct Bubble Effects are the cause of symptoms occurring early after surfacing. These cases usually respond to recompression alone. However, the longer after surfacing that symptoms appear, the more likely it is that the effect of the bubbles is responsible for symptoms, rather than the bubbles themselves. In this situation, recompression alone will be less effective.

3-10.6.5 Preventing Decompression Sickness. Prevention of decompression sickness is generally accomplished by following the decompression tables. However, individual susceptibility or unusual conditions, either in the diver or in connection with the dive, produces a small percentage of cases even when proper dive procedures are followed meticulously. To be absolutely free of decompression sickness under all possible circumstances, the decompression time specified would have to be far in excess of that normally needed. On the other hand, under ideal circumstances, some individuals can ascend safely in less time than the tables specify. This must not be taken to mean that the tables contain an unnecessarily large safety factor. The tables represent the minimum workable decompression time that permits average divers to surface safely from normal working dives without an unacceptable incidence of decompression sickness.

3-10.7 High Pressure Nervous Syndrome (HPNS). High Pressure Nervous Syndrome (HPNS) is a derangement of central nervous system function that occurs during deep helium-oxygen dives, particularly saturation dives. The cause is unknown. The clinical manifestations include nausea, fine tremor, imbalance, incoordination, loss of manual dexterity and loss of alertness. Abdominal cramps and diarrhea develop occasionally. In severe cases a diver may develop vertigo, extreme indifference to his surroundings and marked confusion such as inability to tell the right hand from the left hand. HPNS is first noted between 400 and 500 fsw and the severity appears to be both depth and compression rate dependent. With slow compression, depths of 1000 fsw may be achieved with relative freedom from HPNS. Beyond that, some HPNS may be present regardless of the compression rate. Attempts to block the appearance of the syndrome have included the addition of nitrogen or hydrogen to the breathing mixture and the use of various drugs. No method appears to be entirely satisfactory.

3-10.8 Compression Pains. Compression pains (referred to as compression arthralgia) result from increases in external pressure surrounding the body. These pains affect the joints and may occur in almost any diver. They have been experienced in the knees, shoulders, fingers, back, hips, neck, and ribs. Compression pains are often deep aching pains, similar to those of Type I decompression sickness. However, the pains may be relatively sudden in onset and initially intense. These pains may be accompanied by "popping" ofjoints or a dry, "gritty" feeling within the joint.

Symptoms are dependent on depth, rate of compression, and individual susceptibility. While primarily a problem encountered in saturation diving, symptoms may occur as shallow as 100 fsw at rapid compression rates, such as seen in air diving. In deep, helium saturation dives with slower compression rates, symptoms are more commonly seen deeper than 300 fsw. Deeper than 600 fsw, compression pains may occur even at very slow rates of compression. These pains may be severe enough to limit diver activity, travel rate and depths during downward excursions. Improvement is generally noted as time is spent at depth but, on occasion, these pains may last well into the decompression phase of the dive until shallower depths are reached. They can be distinguished from decompression sickness pain because they were present before decompression was started and do not increase in intensity with decreasing depth.

The mechanism of compression pain is unknown, but is thought to result from the sudden increase in tissue gas tension surrounding the joints causing fluid shifts and interfering with joint lubrication.

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