Immersion raises PB, thereby compressing gases in the lungs
The average PB at sea level is 760 mm Hg. In other words, if you stand at sea level, the column of air extending from your feet upward for several tens of kilometers through the atmosphere exerts a pressure of 1 atmosphere (atm). In a deep mine shaft, over which the column of air is even taller, PB is higher still. However, it is only when diving underwater that humans can experience extreme increases in PB. A column of fresh water extending from the earth's surface upward 10.3 m exerts an additional pressure of 760 mm Hg—as much as a column of air extending from sea level to tens of kilometers skyward. The same is true for a column of water extending from the surface of a lake to a depth of 10.3 m. For seawater, which has a density ~2.5% greater than that of fresh water, the column must be only 10 m to exert 1 atm of pressure. Because liquid water is virtually incompressible, PB increases linearly with the height (weight) of the column of water (Fig. 61-1). Ten meters below the surface of the sea, PB is 2 atm, 1 atm for the atmospheric pressure plus 1 atm for the column of water. As the depth increases to 20 m and then to 30 m, PB increases to 3 atm, then 4 atm, and so on.
FIGURE 61-1 Pressures at increasing depth of immersion. The pressure at the surface of the ocean is 1 atm and increases by 1 atm for each 10 m of immersion in seawater.
Increased external water pressure does not noticeably compress the body's fluid and solid components until a depth of ~1.5 km. However, external pressure compresses each of the body's air compartments to an extent that depends on the compliance of the compartment. In compliant cavities such as the intestines, external pressure readily compresses internal gases. In relatively stiff cavities, or those that cannot equilibrate readily with external pressure, increases of external pressure can distort the cavity wall and result in pain or damage. For example, if the eustachian tube is blocked, the middle-ear pressure cannot equilibrate with external pressure, and blood fills the space in the middle ear or the tympanic membrane ruptures.
According to Boyle's law, N26-8 pressure and volume vary inversely with each other. Thus, if the chest wall were perfectly compliant, a breath-holding dive to 10 m below the surface would double the pressure and compress the air in the lungs to half its original volume. Aquatic mammals can dive to extreme depths because rib flexibility allows the lungs to empty. Whales, for example, can extend a breath-hold dive for up to 2 hours, descending to depths as great as 900 m (91 atm) without suffering any ill effects. The human chest wall does not allow complete emptying of the lungs—except in a few trained individuals, and indeed the human record for a breath-hold dive is in excess of 200 m below the surface. N61-12
Decrease in Lung Volume with Depth of Immersion
Contributed by Arthur DuBois
Imagine that a person at sea level makes a maximal inspiration, achieving a total lung capacity (TLC; see p. 602) of 6 L. What happens if this individual then dives into seawater to a depth of 10 m? The PB as well as the pressure of the air in the lungs doubles to 2 atm at this depth. If the chest wall is perfectly compliant, this increase in PB would reduce the original lung volume to (6 L)/2, or 3 L. This new lung volume is only about twice the lung's normal residual volume (RV), which is normally 1.5 to 1.9 L (see p. 602).
If the person descends an additional 10 m to a total depth of 20 m, PB will now increase to 3 atm. Under these conditions, lung volume will fall to one third of its original value, or to 2 L.
A total descent to 30 m (PB = 4 atm) will reduce lung volume to one quarter of its initial value, or to about the normal RV.
Competitive freediving is organized by two international bodies: the International Association for the Development of Apnea (AIDA) and the World Underwater Federation (CMAS). These organizations recognize different disciplines, based on the permissible methods of descent and ascent. In the No-Limits Apnea category, Herbert Nitsch reached a depth of 214 m in 2007.
If the person is using a SCUBA system (see p. 1226) to breathe compressed air, then the lungs will re-expand to normal volume. If the individual at depth were to make a maximal inspiration to TLC, remove the SCUBA mouthpiece, and then rapidly ascend toward the surface, the air in the lungs would expand to a greater-than-physiological volume. Therefore, the individual would have to exhale during the ascent to prevent the lungs from overexpanding.
In a breath-hold dive that is deep enough to double PB, alveolar will also double to 80 mm Hg (see p. 1225). Because this value is substantially higher than the of mixed-venous blood at sea level (46 mm Hg), the direction of CO2 diffusion across the blood-gas barrier reverses, alveolar CO2 enters pulmonary-capillary blood, and thus arterial increases. In time, metabolically generated CO2 accumulates in the blood and eventually raises mixed-venous to values higher than alveolar , so CO2 diffusion again reverses direction and CO2 diffuses into the alveoli. The increase in arterial can reduce the duration of the dive by increasing ventilatory drive (see p. 716). During a rapid ascent phase of a breath-hold dive, the fall in PB leads to a fall in alveolar and , which promotes the exit of both gases from the blood and thus a rapid fall in both arterial (a) and . The fall in reduces the drive to breathe. The fall in —and thus cerebral —can lead to deep-water blackout. N61-13
Contributed by Arthur DuBois
Imagine that a person excessively hyperventilates before taking a deep breath and attempting to swim a long distance underwater. During the underwater exercise, arterial will fall, and the person may become hypoxic before the arterial rises sufficiently to increase the drive to ventilate and cause the swimmer to surface. The result can be shallow-water blackout and—if help is not close at hand—drowning.
Although it may be intuitive to overbreathe in preparation for a long underwater swim, beware of too much of a good thing: two deep breaths are acceptable, but prolonged hyperventilation can be fatal.
SCUBA divers breathe compressed air to maintain normal lung expansion
Technical advances have made it possible for divers to remain beneath the water surface for periods longer than permitted by a single breath-hold. One of the earliest devices was a diving bell that surrounded the diver on all sides except the bottom. Such a bell was reportedly used by Alexander the Great in 330 BC and then improved by Sir Edmund Halley in 1716 (Fig. 61-2). N61-14 By the early 19th century, pumping compressed air from above the water surface through a hose to the space underneath the bell kept water out of the bell. In all of these cases, the diver breathed air at the same pressure as the surrounding water. Although the pressures both surrounding the diver's chest and inside the airways were far higher than at sea level, the pressure gradient across the chest wall was normal. Thus, the lungs were normally expanded.
FIGURE 61-2 Diving bell. Between 1716 and 1721, Halley, the astronomer who gave his name to the comet, designed and built a wooden diving bell with an open bottom. Because the bell was at a relatively shallow depth (~12 m), the water rose only partly into the bell. In Halley's system, the air was replenished from a barrel that was open at the bottom and weighted with lead to sink beneath the diving bell. Thus, the air pressure in the barrel was higher than that in the bell. The diver used a valve to regulate airflow into the bell. This design was in use for a century, until a practical pump was available for pumping air directly from the surface. The lower part of the figure illustrates what would have happened if Halley's bell had been lowered to much larger depths. The greater the depth, the greater the water pressure. Because the air pressure inside the bell must be the same as the water pressure, the air volume progressively decreases at greater depths, and the water level rises inside the bell. N61-14
The Diving Bell
Contributed by Arthur DuBois, translated by Ulrich Hopfer
The following is a translation of a passage from a book (written in German) titled Diseases of Air Pressure with Special Considerations of So-called Caisson Disease by Dr. Richard Heller, Dr. Wilhelm Mager, and Hermann von Schroetter, PhD, MD.
“There are several reports that Aristotle had the idea to provide air to divers underwater by using an air tube. One also hears from Figuier that a diver apparatus was used in Venice in the beginning of the 17th century. This apparatus was called ‘Cornemuse’ or ‘Capuchon’ and used a bellow to provide air.* Nevertheless, the first certain information we have is that Denys Papin had the idea to renew air in diver bells by way of bellows and valves to prolong the time to remain underwater.
“Therefore, a new period of diving begins with Papin and Halley, who actually put the idea into practice in 1716. The new period brings about the most important progress in this area.
“The invention of the Cornemuse, as well as the inventions of Papin and Halley, constitute the beginning of the diving apparatus in use today.
“Papin dealt already in 1672, in a theoretical publication with Huygens, with the influence of changes in air pressure and gave an explanation why animals die under a vacuum chamber venting valve.
“Edm. Halley, the famous Astronomer and Secretary of the English Society of Sciences, wrote up his experiences in 1716 in the ‘Transactions anglic’ under the title of ‘The art of living under water.’
“For low depths, the air delivery into the diving bell was achieved by two leather tubes, whereby one was used to pump in air with a bellows and the other allowed the air to escape. This arrangement with bellows did not work for greater depths of over 3 fathoms [i.e., 18 feet or ~5.5 m]. For these depths, barrels with air would be lowered into the water, while the used air was released into the water through a valve. Halley lowered himself together with 4 other persons to a depth of 9–10 fathoms, about 17 m, in 1721, whereby 7-8 barrels of air had to be used.
“His diving bell was made of wood, 8 feet high, in the form of a cut-off cone, with 3 feet diameter at the apex and 5 feet at the base [see Fig. 61-2]. The diving bell had a cap of lead. Additional lead weights were fastened at the lower edge so that the bell could sink to the bottom of the sea…. Glass in the ceiling served as window. There was a valve in the dome, through which the used-up, warm air could escape. A type of platform was attached to the free edge of the bell with ropes and fixed in place through weights. Divers would use this platform.
“The entire apparatus was fastened to the main spreader of a ship used to move the bell to its destination. To renew air when the bell was underwater, Halley used two small barrels of 160 L each and lowered the barrels with the aid of weights. The barrels were connected to the bell via a leather tube that was puttied with wax and oil into the cover of the barrel. A hole in the bottom of the barrel allowed water to enter it thus generating pressure to move the air into the bell.
“The barrels were moved to the surface, refilled with air and re-lowered on a signal. The diver serviced the tubes, brought them into the bell, and regulated the airflow through valves at the end of the tubes.
“Nevertheless, the divers suffered, as described by Halley, from the significant increase in temperature within the bell due to compression of the air so that any stay in the bell was difficult. Moreover, he describes that the workers had pain in their ears, and nosebleeds once they were back at the surface.
“During this time, there was also remarkable progress in efforts to get air travel going. On August 8, 1709, the Portuguese Pater Bartholomeo Laurenco de Gussmann lifted himself up in the air with an airship constructed by him in the Indian House in Lisbon and in front of King John V and the entire court. Unfortunately, he got stuck at the roof of the palace and crashed. His device consisted of stiffened paper and the uplifting was caused by heated air. … As often seen in the history, this great invention was snagged by an unfortunate, small obstruction so that the inventor got forgotten.”
*This apparatus was supposed to contain a pipe with an enlargement at the lower end that could go over the head of the diver. This pipe provided air driven by bellows, while another pipe returned exhaled air to the surface.
The conditions are essentially the same in a modern-day caisson, a massive, hollow, pressurized structure that functions like a large diving bell. Once again, the pressure inside the caisson (3 to 4 atm) has to be high enough to prevent water at the bottom of the caisson from entering. Several workers (“sand hogs”) at the bottom of the caisson may excavate material from the bottom of a river for constructing tunnels or foundations of bridges.
Technical advances also extended to individual divers, who first wore diving suits with spherical helmets over their heads (Fig. 61-3A). The air inside these helmets was pressurized to match exactly the pressure of the water in which they were diving. In 1943, Jacques Cousteau perfected the self-contained underwater breathing apparatus, or SCUBA, that replaced cumbersome gear and increased the mobility and convenience of an underwater dive (see Fig. 61-3B). N61-15
FIGURE 61-3 Devices for breathing underwater. A, Compressed air, pumped from the surface to the diver, keeps the pressure inside the helmet slightly higher than that of the surrounding water. B, SCUBA is an acronym for self-contained underwater breathing apparatus.
Diving Helmets and the SCUBA System
Contributed by Arthur DuBois
In the diving helmet shown in Figure 61-3A, a nonreturn valve was placed at the point where the air hose met the helmet. This device prevented air from escaping from the helmet in case the hose were to rupture.
The SCUBA system devised by Jacques Cousteau (see Fig. 61-3B) consists of five major elements:
1. A tank of gas compressed to a pressure that exceeds the highest pressures that the diver will encounter during the dive.
2. A reducing valve that delivers gas from the tank to the diver's hose at a pressure of 6 to 7 atm.
3. A “demand” breathing valve for inspiration, triggered to open by the slight decrease in pressure caused by the diver's inspiration. This valve delivers the air mixture to the diver at the ambient pressure.
4. An exhaust valve that allows expired air to be released at a pressure that is slightly higher than the ambient pressure.
5. A face mask or mouthpiece with a gas-delivery system that has a small ventilatory dead space (see p. 675).
Deep dives for extended periods of time require training and carry the risk of drowning secondary to muscle fatigue and hypothermia. Air flotation and thermal insulation of the diving suit lessen these hazards. For reasons that will become apparent, use of any of these techniques while breathing room air carries additional hazards, including nitrogen narcosis, O2 toxicity, and problems with decompression.
Increased alveolar can cause narcosis
Descending beneath the water causes the inspired —nearly 600 mm Hg at sea level (see Table 26-1)—to increase as PB increases. According to Henry's law (see Box 26-2), the increased will cause more N2to dissolve in pulmonary-capillary blood and, eventually, the body's tissues. The dissolved [N2] in various compartments begins to increase immediately but may take many hours to reach the values predicted by Henry's law. Because of its high lipid solubility, N2 dissolves readily in adipocytes and in membrane lipids. A high reduces the ion conductance of membranes, and therefore neuronal excitability, by mechanisms that are similar to those of gas anesthetics. Diving to increased depths (e.g., 4 to 5 atm) while breathing compressed air causes nitrogen narcosis. Mild nitrogen narcosis resembles alcohol intoxication (e.g., loss of psychosocial inhibitions). According to “Martini's law,” each 15 m of depth has the effects of drinking an additional martini. Progressive narcosis occurs with increasing depth or time of the dive and is accompanied by lethargy and drowsiness, rapid onset of fatigue, and, eventually, a loss of consciousness. Because it develops insidiously, nitrogen narcosis poses a potentially fatal threat to divers who are not aware of the risks.
Increased alveolar can lead to O2 toxicity
At sea level, dry inspired air has a of 159 mm Hg. However, the alveolar (A) of a healthy person at sea-level air is ~101 mm Hg, reduced from 159 mm Hg by humidification in the airways and removal of O2by gas exchange with the blood (see p. 681). at sea level is very close to (within ~10 mm Hg) and nearly saturates Hb, to yield an arterial O2 content of ~20 mL/dL blood (Fig. 61-4, red curve). As PB—and therefore arterial —increases at greater depths, the O2 bound to Hb increases very little. However, according to Henry's law (see p. 593), the O2 that is physically dissolved in the water of blood increases linearly (see Fig. 61-4, black line). Thus, the increment of total O2 content at depth reflects dissolved O2 (see Fig. 61-4, blue curve).
FIGURE 61-4 O2 content of blood at high pressures. The red curve is the same Hb-O2 dissociation curve as that in Figure 29-3, except that the range is extended to very high values of .
During a breath-hold dive to 5 atm, or in a hyperbaric chamber pressurized to 5 atm, arterial increases to ~700 mm Hg, slightly higher than when breathing 100% O2 at sea level. Exposure to such a high has no ill effects for up to several hours. However, prolonged exposure damages the airway epithelium and smooth muscle, causing bronchiolar and alveolar membrane inflammation and, ultimately, pulmonary edema, atelectasis, fibrin formation, and lung consolidation. These effects are the result of inactivation of several structural repair enzymes and oxidation of certain cellular constituents.
A prolonged elevation of also has detrimental effects on nonpulmonary tissues, including the central nervous system (CNS). Exposure to an ambient of ~1500 mm Hg (e.g., breathing room air at ~10 atm) for as little as 30 to 45 minutes can cause seizures and coma. Preliminary symptoms of O2 toxicity include muscle twitching, nausea, disorientation, and irritability. The toxic effects of O2 occur because free radicals (e.g., superoxide anion and peroxide free radicals; see pp. 1238–1239) oxidize the polyunsaturated fatty-acid component of cell membranes as well as enzymes that are involved in energy metabolism. At the more modest levels that normally prevail at sea level, scavenger enzymes such as superoxide dismutase (see p. 1238) eliminate the relatively few radicals formed. N61-16
Effect of SCUBA Diving on Alveolar
Contributed by Emile Boulpaep, Walter Boron
If a diver were instantaneously submerged to a depth of 10 m in seawater (i.e., with a doubling of PB), in the absence of ventilation, alveolar would double (see p. 1225). If the diver is not ventilating, alveolar would exceed pulmonary-capillary . As a result, CO2 would diffuse slowly into the blood and raise arterial [CO2]. The result would be a gradually developing respiratory acidosis (see p. 633). However, in real life, SCUBA divers breathe as they descend to depth gradually. This ventilation prevents alveolar from rising beyond the value at sea level. In the new steady state—assuming that both the body's CO2 production rate () and the alveolar ventilation () remain constant—the alveolar CO2 at depth will be the same as that at sea level (see Equation 31-9).
Using helium to replace inspired N2 and O2 avoids nitrogen narcosis and O2 toxicity
Several occupations—including deep mining, caisson work, and deep diving N61-17—require people to spend extended periods at a PB greater than that at sea level.
Contributed by Arthur DuBois
In deep mining, workers descend down a shaft to depths as great as 2.4 km below the surface. Just as PB falls with ascent to a high altitude, it rises with descent to a great depth in a mine, doubling approximately every 5.5 km of depth. Nevertheless, 2.4 km below the earth's surface, PB is only ~1.4 atm, which presents little problem to the miner. The greatest health hazards for the deep miner are from exposure to high temperature (ambient temperature increases by 1°C every ~300 m), from humidity (miners use a fine water spray to minimize dust), and from inspiration of particulates.
Caisson workers rarely experience >3 or 4 atm, and only for relatively brief periods. Because nitrogen narcosis begins to appear only at ~5 atm of room air after more than an hour, and because oxygen toxicity only begins to appear at ~10 atm of room air after >30 min, caisson workers can avoid the adverse effects of increased PB while they are in the caisson. However, caisson workers may have major difficulties caused by decompression when exiting the caisson.
Divers may spend hours, days, or even weeks at depths between 60 m and 300 m below the water surface. They wear diving suits when working and live in compression chambers when at “leisure.” Deep divers who spend days or weeks at high PB must breathe special gas mixtures to avoid nitrogen narcosis and oxygen toxicity.
During an extended dive or other exposure to high pressure (one exceeding several hours), the body's tissues gradually equilibrate with the high-pressure gases that one has been breathing. This equilibrated state is referred to by the misnomer saturation. At sea level, the human body normally contains ~1 L of dissolved N2, equally distributed between the body's water and fat compartments. As rises, the N2equilibrates only slowly with the body's lipid stores because adipose tissue is relatively underperfused. Although a deep dive of several minutes does not provide sufficient time to equilibrate the fat with N2, one of several hours' duration does. At equilibrium—as required by Henry's law—the volume of N2 dissolved in the tissues is proportional to alveolar . Thus, if the body normally dissolves 1 L of N2 at a PB of 1 atm, it will ultimately dissolve 4 L of N2 at a PB of 4 atm. These same principles apply to O2, although with different solubilities and speeds of equilibration in various tissues.
The adverse effects of N2 and O2 depend on the amount of gas that is dissolved in tissues. The amount, in turn, increases with the dive's depth (i.e., partial pressure of the gas) and duration (i.e., how close the gas is to achieving equilibrium with various tissues). Thus, the length of time that a diver can spend safely underwater is inversely proportional to the depth of the dive.
To prevent nitrogen narcosis in saturation diving conditions, divers must partly or completely replace N2 with another inert gas. Helium is the replacement gas of choice for four reasons: N61-18
Properties of Helium
Contributed by Ethan Nadel
Helium is an odorless, tasteless, and colorless gas. Compared to N2, it has a lower solubility in water, which means that it dissolves in tissues to a lesser extent. In fact, helium has the lowest water solubility of all gases.
The density of helium is nearly an order of magnitude lower than that of nitrogen (0.178 × 10–3 g/cm3 versus 1.25 × 10–3 g/cm3), so that the Reynolds number (Re; see Equation 27-11) is reduced by a similar factor. Thus, at the same air velocity, helium is far less likely to exceed Re and thereby engage in turbulent flow. Because turbulent flow increases the effective airway resistance (see p. 617), helium will have a lower effective airway resistance than nitrogen.
The viscosity of helium (194 µP at 20°C) is not markedly different from that of nitrogen (178 µP at 27.4°C). Thus, according to Poiseuille's law (see Equation 27-8), the resistance under laminar flow conditions would be very similar for helium and nitrogen—assuming that the length and radius of the airway is unchanged.
Lenntech. Helium—He: Chemical properties of helium—health effects of helium. http://www.lenntech.com/Periodic-chart-elements/He-en.htm [Accessed July 13, 2015].
Lenntech. Nitrogen—N: Chemical properties of nitrogen—health effects of nitrogen—environmental effects of nitrogen. http://www.lenntech.com/Periodic-chart-elements/N-en.htm [Accessed July 13, 2015].
Weast RC. Handbook of Chemistry and Physics. 59th ed. CRC Press: Boca Raton, FL; 1978–1979.
1. Helium has only a fraction of the narcotizing effect of N2.
2. Helium dissolves in the tissues to a lesser extent than N2.
3. Helium has a lower density than N2 and this lowers effective airway resistance. However, the low density of helium facilitates convective “air” cooling around the body, so that heat loss is increased. Thus, ambient temperature must be higher in a high-helium compression chamber.
4. During the decompression phase of a dive, helium diffuses out of the tissues more rapidly than does N2, which alleviates most of the problems associated with decompression.
To prevent O2 toxicity in saturation diving conditions, divers must reduce the fraction of inspired air that is O2 () in the compressed-gas mixture. Thus, at a PB of 10 atm, an of 2% O2 in helium will provide the same inspired as room air does at sea level (i.e., of ~20% O2 at a PB of 1 atm). Of course, the diver must monitor the inspired , which is the physiologically relevant parameter.
After an extended dive, one must decompress slowly to avoid decompression illness
Although the preceding three sections have focused on problems divers face while at great depths, serious difficulties also arise if—after a deep saturation dive—the diver returns to the surface too quickly. At the end of a saturation dive, is at the same high value in the alveoli and most tissues. As PB falls during ascent, alveolar will fall as well, which creates a gradient from the mixed-venous blood to the alveolar air. Washout of N2 from the blood creates a gradient from tissues to blood. To allow enough time for the dissolved N2 to move from tissues to blood to alveoli, N61-19 a diver must rise to the surface slowly (no faster than ~3 m/hr). Because N2 exits from water much faster than it does from fat, the total elimination of N2 has two components: some compartments empty quickly (e.g., blood), and some empty slowly (e.g., joints, fat, eyeballs).
The Oxygen Window
Contributed by Arthur DuBois
The extra nitrogen can be eliminated without forming bubbles in the venous blood because of something called the oxygen window. This window occurs because the sum of gas pressures in the venous blood leaving the tissues is less than the sum of gas pressures in the arterial blood entering the tissues. The reason for this is that—for a resting person at sea level—the partial pressure of oxygen falls from an arterial level of 100 mm Hg to a venous tension of 40 mm Hg, whereas the carbon dioxide tension rises only from 40 to 46 mm Hg; this difference leaves a “window” of 100 − 40 − 6 = 54 mm Hg, the so-called oxygen window, into which nitrogen can move from the tissues into the blood—in an amount that corresponds to a partial pressure of 54 mm Hg in the blood—without raising the sum of pressures of the gases above the water pressure surrounding the body. The nitrogen dissolved at 54 mm Hg is carried from the tissues to the alveolar air without forming bubbles in the bloodstream as the person ascends at a rate of 3 m/hr following a saturation dive because in 1 hour, the dissolved nitrogen carried to the lungs in the oxygen window is expired and leaves the body.
Too rapid an ascent causes the N2 in the tissues—previously dissolved under high pressure—to leave solution and form bubbles as PB falls. This process is identical to the formation of gas bubbles when one opens a bottle of a carbonated beverage that had been capped under high pressure. Similar problems can occur in pilots who bail out from a pressurized aircraft at high altitude and in divers who ascend to altitude or become aircraft passengers (i.e., are exposed to a lower-than-normal PB) too soon after completing a dive that, by itself, would not cause difficulties.
During a too-rapid decompression, bubble formation can occur in any tissue in which N2 has previously been dissolved. Decompression illness (DCI) N61-20 is the general term for two major types of clinical disorder:
For a discussion of dysbarism—medical conditions resulting from changes in barometric (i.e., ambient) pressure—visit http://emedicine.medscape.com/article/769902-overview (accessed July 2015).
For a discussion of decompression illness, visit http://www.medscape.com/viewarticle/710379_6 (accessed July 2015).
For a discussion of decompression sickness, visit http://emedicine.medscape.com/article/769717-overview (accessed July 2015).
1. Decompression sickness (DCS) is caused by local bubble formation, either in tissues or in venous blood. In tissues, the distortion produced by these bubbles can affect function and cause itching or pain. In veins, the bubbles can cause obstruction, leading to capillary leaks. Mild or type I DCS can include short-lived mild pains (“niggles”), pruritus, a skin rash, and deep throbbing pain (bends), resulting from bubbles that form in muscles and joints. Serious or type II DCS can include symptoms in the CNS, lungs, and circulatory system. The CNS disorder—most commonly involving the spinal cord—reflects bubble formation in the myelin sheath of axons, which compromises nerve conduction. Symptoms may range from dizziness—the staggers—to paralysis. Pulmonary symptoms—the chokes—result from bubbles that originate in the systemic veins and travel as gas emboli to lodge in the pulmonary circulation, and include burning pain on inspiration, cough, and respiratory distress. In the circulatory system, bubbles not only can obstruct blood flow but also can trigger the coagulation cascade (see pp. 440–444), leading to the release of vasoactive substances. Hypovolemic shock is also a part of this syndrome.
2. Arterial gas embolization (AGE) is caused by bubbles that enter the systemic arterial blood via either tears in the alveoli or right-to-left shunts (e.g., a patent foramen ovale) and then become wedged in the brain or other organs. Large arterial gas emboli can have catastrophic consequences unless the victim receives immediate recompression treatment.
Figure 61-5 shows how long a diver can spend at various depths—breathing room air—without having to undergo a decompression protocol during the ascent. For example, a dive to 8 m can last indefinitely without any ill effects during the ascent. A dive of 25 minutes' duration will not provide sufficient time to saturate the tissues unless the dive exceeds 40 m. However, a longer dive at 40 m will require a decompression program. For instance, a 20-minute dive to a depth of 90 m requires nearly 3 hours of decompression time. Thus, the rate at which a diver should ascend to avoid DCI depends on both the depth and the duration of the dive. Divers use detailed tables to plan their rate of ascent from a deep dive.
FIGURE 61-5 Need for decompression as a function of depth and duration of dive. If the dive is sufficiently brief or sufficiently shallow, no decompression is required (teal area). For greater depths or longer durations, a decompression protocol is required (salmon area). (Data from Duffner GJ: Medical problems involved in underwater compression and decompression. Ciba Clin Symp 10:99–117, 1958.)
The best treatment for DCI is to recompress the diver in a hyperbaric chamber. Recompression places the gases back under high pressure, forcing them to redissolve in the tissues, a process that instantly relieves many symptoms. Once the diver is placed under high pressure, decompression can be carried out at a deliberate and supervised pace. N61-21
Contributed by Emile Boulpaep, Walter Boron
U.S. Navy Treatment Table 6—discussed in the review by Vann and colleagues listed below (see their Fig. 5)—is commonly used to treat type II DCS. Other Navy tables describe treatment protocols for other situations.
United States Navy. 6th rev. Naval Sea Systems Command: Washington, DC; 2008. US Navy Diving Manual. vol 5 [Diving Medicine and Recompression Chamber Operations. NAVSEA 0910-LP-106-0957].
Vann RD, Butler FK, Mitchell SJ, Moon RE. Decompression illness. Lancet. 2011;377:153–164.