When human beings descend beneath the sea, the pressure around them increases tremendously. To keep the lungs from collapsing, air must be supplied at very high pressure to keep them inflated. This exposes the blood in the lungs to extremely high alveolar gas pressure, a condition called hyperbarism. Beyond certain limits, these high pressures cause tremendous alterations in body physiology and can be lethal.
Relationship of Pressure to Sea Depth
A column of seawater 33 feet (10.1 meters) deep exerts the same pressure at its bottom as the pressure of the atmosphere above the sea. Therefore, a person 33 feet beneath the ocean surface is exposed to 2 atmospheres pressure, 1 atmosphere of pressure caused by the weight of the air above the water and the second atmosphere by the weight of the water itself. At 66 feet the pressure is 3 atmospheres, and so forth, in accord with the table in Figure 44-1.
Figure 44-1 Effect of sea depth on pressure (top table) and on gas volume (bottom).
Effect of Sea Depth on the Volume of Gases—Boyle’s Law
Another important effect of depth is compression of gases to smaller and smaller volumes. The lower part of Figure 44-1 shows a bell jar at sea level containing 1 liter of air. At 33 feet beneath the sea, where the pressure is 2 atmospheres, the volume has been compressed to only one-half liter, and at 8 atmospheres (233 feet) to one-eighth liter. Thus, the volume to which a given quantity of gas is compressed is inversely proportional to the pressure. This is a principle of physics called Boyle’s law, which is extremely important in diving physiology because increased pressure can collapse the air chambers of the diver’s body, especially the lungs, and often causes serious damage.
Many times in this chapter it is necessary to refer to actual volume versus sea-level volume. For instance, we might speak of an actual volume of 1 liter at a depth of 300 feet; this is the same quantity of air as a sea-level volume of 10 liters.
Effect of High Partial Pressures of Individual Gases on the Body
The individual gases to which a diver is exposed when breathing air are nitrogen, oxygen, and carbon dioxide; each of these at times can cause significant physiologic effects at high pressures.
Nitrogen Narcosis at High Nitrogen Pressures
About four fifths of the air is nitrogen. At sea-level pressure, the nitrogen has no significant effect on bodily function, but at high pressures it can cause varying degrees of narcosis. When the diver remains beneath the sea for an hour or more and is breathing compressed air, the depth at which the first symptoms of mild narcosis appear is about 120 feet. At this level the diver begins to exhibit joviality and to lose many of his or her cares. At 150 to 200 feet, the diver becomes drowsy. At 200 to 250 feet, his or her strength wanes considerably, and the diver often becomes too clumsy to perform the work required. Beyond 250 feet (8.5 atmospheres pressure), the diver usually becomes almost useless as a result of nitrogen narcosis if he or she remains at these depths too long.
Nitrogen narcosis has characteristics similar to those of alcohol intoxication, and for this reason it has frequently been called “raptures of the depths.” The mechanism of the narcotic effect is believed to be the same as that of most other gas anesthetics. That is, it dissolves in the fatty substances in neuronal membranes and, because of its physical effect on altering ionic conductance through the membranes, reduces neuronal excitability.
Oxygen Toxicity at High Pressures
Effect of Very High PO2 on Blood Oxygen Transport
When the PO2 in the blood rises above 100 mm Hg, the amount of oxygen dissolved in the water of the blood increases markedly. This is shown in Figure 44-2, which depicts the same oxygen-hemoglobin dissociation curve as that shown in Chapter 40 but with the alveolar PO2 extended to more than 3000 mm Hg. Also depicted by the lowest curve in the figure is the volume of oxygen dissolved in the fluid of the blood at each PO2 level. Note that in the normal range of alveolar PO2 (below 120 mm Hg), almost none of the total oxygen in the blood is accounted for by dissolved oxygen, but as the oxygen pressure rises into the thousands of millimeters of mercury, a large portion of the total oxygen is then dissolved in the water of the blood, in addition to that bound with hemoglobin.
Figure 44-2 Quantity of oxygen dissolved in the fluid of the blood and in combination with hemoglobin at very high PO2s.
Effect of High Alveolar PO2 on Tissue PO2
Let us assume that the PO2 in the lungs is about 3000 mm Hg (4 atmospheres pressure). Referring to Figure 44-2, one finds that this represents a total oxygen content in each 100 milliliters of blood of about 29 volumes percent, as demonstrated by point A in the figure—this means 20 volumes percent bound with hemoglobin and 9 volumes percent dissolved in the blood water. As this blood passes through the tissue capillaries and the tissues use their normal amount of oxygen, about 5 milliliters from each 100 milliliters of blood, the oxygen content on leaving the tissue capillaries is still 24 volumes percent (point B in the figure). At this point, the PO2 is approximately 1200 mm Hg, which means that oxygen is delivered to the tissues at this extremely high pressure instead of at the normal value of 40 mm Hg. Thus, once the alveolar PO2 rises above a critical level, the hemoglobin-oxygen buffer mechanism (discussed in Chapter 40) is no longer capable of keeping the tissue PO2 in the normal, safe range between 20 and 60 mm Hg.
Acute Oxygen Poisoning
The extremely high tissue PO2 that occurs when oxygen is breathed at very high alveolar oxygen pressure can be detrimental to many of the body’s tissues. For instance, breathing oxygen at 4 atmospheres pressure of oxygen (PO2 = 3040 mm Hg) will cause brain seizures followed by coma in most people within 30 to 60 minutes. The seizures often occur without warning and, for obvious reasons, are likely to be lethal to divers submerged beneath the sea.
Other symptoms encountered in acute oxygen poisoning include nausea, muscle twitchings, dizziness, disturbances of vision, irritability, and disorientation. Exercise greatly increases the diver’s susceptibility to oxygen toxicity, causing symptoms to appear much earlier and with far greater severity than in the resting person.
Excessive Intracellular Oxidation as a Cause of Nervous System Oxygen Toxicity—“Oxidizing Free Radicals.”
Molecular oxygen (O2) has little capability of oxidizing other chemical compounds. Instead, it must first be converted into an “active” form of oxygen. There are several forms of active oxygen called oxygen free radicals. One of the most important of these is the superoxide free radical 
, and another is the peroxide radical in the form of hydrogen peroxide. Even when the tissue PO2 is normal at the level of 40 mm Hg, small amounts of free radicals are continually being formed from the dissolved molecular oxygen. Fortunately, the tissues also contain multiple enzymes that rapidly remove these free radicals, including peroxidases, catalases, and superoxide dismutases. Therefore, so long as the hemoglobin-oxygen buffering mechanism maintains a normal tissue PO2, the oxidizing free radicals are removed rapidly enough that they have little or no effect in the tissues.
Above a critical alveolar PO2 (above about 2 atmospheres PO2), the hemoglobin-oxygen buffering mechanism fails, and the tissue PO2 can then rise to hundreds or thousands of millimeters of mercury. At these high levels, the amounts of oxidizing free radicals literally swamp the enzyme systems designed to remove them, and now they can have serious destructive and even lethal effects on the cells. One of the principal effects is to oxidize the polyunsaturated fatty acids that are essential components of many of the cell membranes. Another effect is to oxidize some of the cellular enzymes, thus damaging severely the cellular metabolic systems. The nervous tissues are especially susceptible because of their high lipid content. Therefore, most of the acute lethal effects of acute oxygen toxicity are caused by brain dysfunction.
Chronic Oxygen Poisoning Causes Pulmonary Disability
A person can be exposed to only 1 atmosphere pressure of oxygen almost indefinitely without developing the acute oxygen toxicity of the nervous system just described. However, after only about 12 hours of 1 atmosphere oxygen exposure, lung passageway congestion, pulmonary edema, and atelectasis caused by damage to the linings of the bronchi and alveoli begin to develop. The reason for this effect in the lungs but not in other tissues is that the air spaces of the lungs are directly exposed to the high oxygen pressure, but oxygen is delivered to the other body tissues at almost normal Po2 because of the hemoglobin-oxygen buffer system.
Carbon Dioxide Toxicity at Great Depths in the Sea
If the diving gear is properly designed and functions properly, the diver has no problem due to carbon dioxide toxicity because depth alone does not increase the carbon dioxide partial pressure in the alveoli. This is true because depth does not increase the rate of carbon dioxide production in the body, and as long as the diver continues to breathe a normal tidal volume and expires the carbon dioxide as it is formed, alveolar carbon dioxide pressure will be maintained at a normal value.
In certain types of diving gear, however, such as the diving helmet and some types of rebreathing apparatuses, carbon dioxide can build up in the dead space air of the apparatus and be rebreathed by the diver. Up to an alveolar carbon dioxide pressure (PCO2) of about 80 mm Hg, twice that in normal alveoli, the diver usually tolerates this buildup by increasing the minute respiratory volume a maximum of 8- to 11-fold to compensate for the increased carbon dioxide. Beyond 80 mm Hg alveolar PCO2, the situation becomes intolerable, and eventually the respiratory center begins to be depressed, rather than excited, because of the negative tissue metabolic effects of high PCO2. The diver’s respiration then begins to fail rather than to compensate. In addition, the diver develops severe respiratory acidosis and varying degrees of lethargy, narcosis, and finally even anesthesia, as discussed in Chapter 42.
Decompression of the Diver After Excess Exposure to High Pressure
When a person breathes air under high pressure for a long time, the amount of nitrogen dissolved in the body fluids increases. The reason for this is the following: Blood flowing through the pulmonary capillaries becomes saturated with nitrogen to the same high pressure as that in the alveolar breathing mixture. And over several more hours, enough nitrogen is carried to all the tissues of the body to raise their tissue Pn2 also to equal the Pn2 in the breathing air.
Because nitrogen is not metabolized by the body, it remains dissolved in all the body tissues until the nitrogen pressure in the lungs is decreased back to some lower level, at which time the nitrogen can be removed by the reverse respiratory process; however, this removal often takes hours to occur and is the source of multiple problems collectively called decompression sickness.
Volume of Nitrogen Dissolved in the Body Fluids at Different Depths
At sea level, almost exactly 1 liter of nitrogen is dissolved in the entire body. Slightly less than one half of this is dissolved in the water of the body and a little more than one half in the fat of the body. This is true because nitrogen is five times as soluble in fat as in water.
After the diver has become saturated with nitrogen, the sea-level volume of nitrogen dissolved in the body at different depths is as follows:
|
Feet |
Liters |
|
0 |
1 |
|
33 |
2 |
|
100 |
4 |
|
200 |
7 |
|
300 |
10 |
Several hours are required for the gas pressures of nitrogen in all the body tissues to come nearly to equilibrium with the gas pressure of nitrogen in the alveoli. The reason for this is that the blood does not flow rapidly enough and the nitrogen does not diffuse rapidly enough to cause instantaneous equilibrium. The nitrogen dissolved in the water of the body comes to almost complete equilibrium in less than 1 hour, but the fat tissue, requiring five times as much transport of nitrogen and having a relatively poor blood supply, reaches equilibrium only after several hours. For this reason, if a person remains at deep levels for only a few minutes, not much nitrogen dissolves in the body fluids and tissues, whereas if the person remains at a deep level for several hours, both the body water and body fat become saturated with nitrogen.
Decompression Sickness (Synonyms: Bends, Compressed Air Sickness, Caisson Disease, Diver’s Paralysis, Dysbarism)
If a diver has been beneath the sea long enough that large amounts of nitrogen have dissolved in his or her body and the diver then suddenly comes back to the surface of the sea, significant quantities of nitrogen bubbles can develop in the body fluids either intracellularly or extracellularly and can cause minor or serious damage in almost any area of the body, depending on the number and sizes of bubbles formed; this is called decompression sickness.
The principles underlying bubble formation are shown in Figure 44-3. In Figure 44-3A, the diver’s tissues have become equilibrated to a high dissolved nitrogen pressure (Pn2 = 3918 mm Hg), about 6.5 times the normal amount of nitrogen in the tissues. As long as the diver remains deep beneath the sea, the pressure against the outside of his or her body (5000 mm Hg) compresses all the body tissues sufficiently to keep the excess nitrogen gas dissolved. But when the diver suddenly rises to sea level (Figure 44-3B), the pressure on the outside of the body becomes only 1 atmosphere (760 mm Hg), while the gas pressure inside the body fluids is the sum of the pressures of water vapor, carbon dioxide, oxygen, and nitrogen, or a total of 4065 mm Hg, 97 percent of which is caused by the nitrogen. Obviously, this total value of 4065 mm Hg is far greater than the 760 mm Hg pressure on the outside of the body. Therefore, the gases can escape from the dissolved state and form actual bubbles, composed almost entirely of nitrogen, both in the tissues and in the blood where they plug many small blood vessels. The bubbles may not appear for many minutes to hours because sometimes the gases can remain dissolved in the “supersaturated” state for hours before bubbling.
Figure 44-3 Gaseous pressures both inside and outside the body, showing (A) saturation of the body to high gas pressures when breathing air at a total pressure of 5000 mm Hg, and (B) the great excesses of intrabody pressures that are responsible for bubble formation in the tissues when the lung intra-alveolar pressure body is suddenly returned from 5000 mm Hg to normal pressure of 760 mm Hg.
Symptoms of Decompression Sickness (“Bends”)
The symptoms of decompression sickness are caused by gas bubbles blocking many blood vessels in different tissues. At first, only the smallest vessels are blocked by minute bubbles, but as the bubbles coalesce, progressively larger vessels are affected. Tissue ischemia and sometimes tissue death result.
In most people with decompression sickness, the symptoms are pain in the joints and muscles of the legs and arms, affecting 85 to 90 percent of those persons who develop decompression sickness. The joint pain accounts for the term “bends” that is often applied to this condition.
In 5 to 10 percent of people with decompression sickness, nervous system symptoms occur, ranging from dizziness in about 5 percent to paralysis or collapse and unconsciousness in as many as 3 percent. The paralysis may be temporary, but in some instances, damage is permanent.
Finally, about 2 percent of people with decompression sickness develop “the chokes,” caused by massive numbers of microbubbles plugging the capillaries of the lungs; this is characterized by serious shortness of breath, often followed by severe pulmonary edema and, occasionally, death.
Nitrogen Elimination from the Body; Decompression Tables
If a diver is brought to the surface slowly, enough of the dissolved nitrogen can usually be eliminated by expiration through the lungs to prevent decompression sickness. About two thirds of the total nitrogen is liberated in 1 hour and about 90 percent in 6 hours.
Decompression tables that detail procedures for safe decompression have been prepared by the U.S. Navy. To give the student an idea of the decompression process, a diver who has been breathing air and has been on the sea bottom for 60 minutes at a depth of 190 feet is decompressed according to the following schedule:
10 minutes at 50 feet depth
17 minutes at 40 feet depth
19 minutes at 30 feet depth
50 minutes at 20 feet depth
84 minutes at 10 feet depth
Thus, for a work period on the bottom of only 1 hour, the total time for decompression is about 3 hours.
Tank Decompression and Treatment of Decompression Sickness
Another procedure widely used for decompression of professional divers is to put the diver into a pressurized tank and then to lower the pressure gradually back to normal atmospheric pressure, using essentially the same time schedule as noted earlier.
Tank decompression is even more important for treating people in whom symptoms of decompression sickness develop minutes or even hours after they have returned to the surface. In this case, the diver is recompressed immediately to a deep level. Then decompression is carried out over a period several times as long as the usual decompression period.
“Saturation Diving” and Use of Helium-Oxygen Mixtures in Deep Dives
When divers must work at very deep levels—between 250 feet and nearly 1000 feet—they frequently live in a large compression tank for days or weeks at a time, remaining compressed at a pressure level near that at which they will be working. This keeps the tissues and fluids of the body saturated with the gases to which they will be exposed while diving. Then, when they return to the same tank after working, there are no significant changes in pressure, so decompression bubbles do not occur.
In very deep dives, especially during saturation diving, helium is usually used in the gas mixture instead of nitrogen for three reasons: (1) it has only about one-fifth the narcotic effect of nitrogen; (2) only about one half as much volume of helium dissolves in the body tissues as nitrogen, and the volume that does dissolve diffuses out of the tissues during decompression several times as rapidly as does nitrogen, thus reducing the problem of decompression sickness; and (3) the low density of helium (one seventh the density of nitrogen) keeps the airway resistance for breathing at a minimum, which is very important because highly compressed nitrogen is so dense that airway resistance can become extreme, sometimes making the work of breathing beyond endurance.
Finally, in very deep dives it is important to reduce the oxygen concentration in the gaseous mixture because otherwise oxygen toxicity would result. For instance, at a depth of 700 feet (22 atmospheres of pressure), a 1 percent oxygen mixture will provide all the oxygen required by the diver, whereas a 21 percent mixture of oxygen (the percentage in air) delivers a PO2 to the lungs of more than 4 atmospheres, a level very likely to cause seizures in as little as 30 minutes.
Scuba (Self-Contained Underwater Breathing Apparatus) Diving
Before the 1940s, almost all diving was done using a diving helmet connected to a hose through which air was pumped to the diver from the surface. Then, in 1943, French explorer Jacques Cousteau popularized a self-contained underwater breathing apparatus, known as the SCUBA apparatus. The type of SCUBA apparatus used in more than 99 percent of all sports and commercial diving is the open-circuit demand system shown in Figure 44-4. This system consists of the following components: (1) one or more tanks of compressed air or some other breathing mixture, (2) a first-stage “reducing” valve for reducing the very high pressure from the tanks to a low pressure level, (3) a combination inhalation “demand” valve and exhalation valve that allows air to be pulled into the lungs with slight negative pressure of breathing and then to be exhaled into the sea at a pressure level slightly positive to the surrounding water pressure, and (4) a mask and tube system with small “dead space.”
Figure 44-4 Open-circuit demand type of SCUBA apparatus.
The demand system operates as follows: The first-stage reducing valve reduces the pressure from the tanks so that the air delivered to the mask has a pressure only a few mm Hg greater than the surrounding water pressure. The breathing mixture does not flow continually into the mask. Instead, with each inspiration, slight extra negative pressure in the demand valve of the mask pulls the diaphragm of the valve open, and this automatically releases air from the tank into the mask and lungs. In this way, only the amount of air needed for inhalation enters the mask. Then, on expiration, the air cannot go back into the tank but instead is expired into the sea.
The most important problem in use of the self-contained underwater breathing apparatus is the limited amount of time one can remain beneath the sea surface; for instance, only a few minutes are possible at a 200-foot depth. The reason for this is that tremendous airflow from the tanks is required to wash carbon dioxide out of the lungs—the greater the depth, the greater the airflow in terms of quantity of air per minute that is required, because the volumeshave been compressed to small sizes.
Special Physiologic Problems in Submarines
Escape from Submarines
Essentially the same problems encountered in deep-sea diving are often met in relation to submarines, especially when it is necessary to escape from a submerged submarine. Escape is possible from as deep as 300 feet without using any apparatus. However, proper use of rebreathing devices, especially when using helium, theoretically can allow escape from as deep as 600 feet or perhaps more.
One of the major problems of escape is prevention of air embolism. As the person ascends, the gases in the lungs expand and sometimes rupture a pulmonary blood vessel, forcing the gases to enter the vessel and cause air embolism of the circulation. Therefore, as the person ascends, he or she must make a special effort to exhale continually.
Health Problems in the Submarine Internal Environment
Except for escape, submarine medicine generally centers on several engineering problems to keep hazards out of the internal environment. First, in atomic submarines, there exists the problem of radiation hazards, but with appropriate shielding, the amount of radiation received by the crew submerged beneath the sea has been less than normal radiation received above the surface of the sea from cosmic rays.
Second, poisonous gases on occasion escape into the atmosphere of the submarine and must be controlled rapidly. For instance, during several weeks’ submergence, cigarette smoking by the crew can liberate enough carbon monoxide, if not removed rapidly, to cause carbon monoxide poisoning. And, on occasion, even Freon gas has been found to diffuse out of refrigeration systems in sufficient quantity to cause toxicity.
Hyperbaric Oxygen Therapy
The intense oxidizing properties of high-pressure oxygen (hyperbaric oxygen) can have valuable therapeutic effects in several important clinical conditions. Therefore, large pressure tanks are now available in many medical centers into which patients can be placed and treated with hyperbaric oxygen. The oxygen is usually administered at PO2s of 2 to 3 atmospheres of pressure through a mask or intratracheal tube, whereas the gas around the body is normal air compressed to the same high-pressure level.
It is believed that the same oxidizing free radicals responsible for oxygen toxicity are also responsible for at least some of the therapeutic benefits. Some of the conditions in which hyperbaric oxygen therapy has been especially beneficial follow.
Probably the most successful use of hyperbaric oxygen has been for treatment of gas gangrene. The bacteria that cause this condition, clostridial organisms, grow best under anaerobic conditions and stop growing at oxygen pressures greater than about 70 mm Hg. Therefore, hyperbaric oxygenation of the tissues can frequently stop the infectious process entirely and thus convert a condition that formerly was almost 100 percent fatal into one that is cured in most instances by early treatment with hyperbaric therapy.
Other conditions in which hyperbaric oxygen therapy has been either valuable or possibly valuable include decompression sickness, arterial gas embolism, carbon monoxide poisoning, osteomyelitis, and myocardial infarction.
Bibliography
Butler P.J. Diving beyond the limits. News Physiol Sci. 2001;16:222.
Leach R.M., Rees P.J., Wilmshurst P. Hyperbaric oxygen therapy. BMJ. 1998;317:1140.
Lindholm P., Lundgren C.E. The physiology and pathophysiology of human breath-hold diving. J Appl Physiol. 2009;106:284.
Moon R.E., Cherry A.D., Stolp B.W., et al. Pulmonary Gas Exchange in Diving. J Appl Physiol. 2008. [Epub ahead of print]
Neuman T.S. Arterial gas embolism and decompression sickness. News Physiol Sci. 2002;17:77.
Pendergast D.R., Lundgren C.EG. The physiology and pathophysiology of the hyperbaric and diving environments. J Appl Physiol. 2009;106:274.
Thom S.R. Oxidative stress is fundamental to hyperbaric oxygen therapy. J Appl Physiol. 2008. doi:10.1152/japplphysiol.91004