State of the Art Diving Medicine2 RICHARD H. STRAUSS
Contents
Introduction Physical Principles Decompression Sickness Pathogenesis Clinical Manifestations Spinal Cord and Brain Extremities Pulmonary Other Treatment Prevention Some Hazards of Diving Gases Oxygen Toxicity Nitrogen Narcosis Barotrauma of Descent Barotrauma of Ascent Pulmonary Barotrauma Air Embolism Breath-hold Diving Breath-hold Blackout Diving Reflex Negative Intrapulmonic Pressure Deep Diving (Commercial and Military) Selection of Divers: Examination and Physical Standards Physical Standards Pulmonary 1 From the Pulmonary Disease Division, Department of Medicine, Ohio State University College of Medicine, Columbus, Ohio 43210. 2 Portions of this article were adapted from the writer's chapters, "The Physics of Gases" and "Decompression Sickness," in Strauss, R. H., ed.: Diving Medicine, Grune and Stratton, New York, 1976, and from Strauss, R. H., and Yount, D. E.: Decompression sickness, Am Sci, 1977,65, 598.
Neurologic Cardiovascular Vision Musculoskeletal Otolaryngology Temporary Disqualifications Examination Required Further Reading Introduction
In recent years there has been a marked increase in the number of persons involved in sport and commercial diving. In the United States, more than 200,000 persons are trained each year in the use of scuba (self-contained underwater breathing apparatus) (1). Furthermore, breath-hold diving is used by many persons as a simple means to explore the underwater world. Although the dangers of diving have been popularly associated with great depths, it is important to recognize that both shallow breathhold and scuba diving—even in a swimming pool—present very real risks to the diver. This paper deals primarily with problems associated with diving for pleasure (sport diving). Commercial and military diving are mentioned to illustrate certain principles. The discussion of hyperbaric therapy is limited to problems related to diving. The risks of diving are due largely to the breathing of gases as ambient pressure increases during descent or decreases during ascent in water. Thus, the physician with training in pulmonary medicine is well prepared in a general sense to deal with diving-related problems. This paper will review the various clinical syndromes directly related to diving, with special emphasis on the pathophysiology of these events. Because
AMERICAN REVIEW OF RESPIRATORY DISEASE, VOLUME 119, 1979
1001
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RICHARD H. STRAUSS
these syndromes are associated with the effects of gases at altered ambient pressures, the physical principles that govern such effects must be reviewed. Physical Principles People normally live at the bottom of a sea of air. The weight of this air exerts a pressure on the body surface that is denned at sea level as 1 atmosphere. Atmospheric pressure decreases relatively slowly with increasing altitude. In Denver, at an altitude of 5,221 feet, ambient pressure is 0.83 atmosphere. Under water, however, small changes in depth result in significant changes in pressure. A resident of Denver can return to 1 atmosphere of pressure by diving 6 feet below the surface of a swimming pool. A column of liquid exerts a pressure that is proportional to its height, density, and the acceleration of gravity. At a depth of 33 feet, seawater exerts an additional pressure of 1 atmosphere on the submerged diver—a total pressure twice that to which he is exposed at sea level. (A list of pressure equivalents is given in table 1.) The tissues of the body are composed primarily of water, which is nearly incompressible and is thus unaffected by pressures within the usual diving range. Gases, however, are compressible. The behavior of gases is well described by the ideal gas law: PV = n R T , where P is absolute pressure, V is volume, n is the number of moles of gas, R is the universal gas constant, and T is the absolute temperature. Several simpler gas laws originate from the ideal gas law and are commonly used under conditions associated with diving, Boyle's law states that at a constant temperature the volume of a given mass of gas is inversely proportional to its pressure. Stated mathematically: PV = K, where K is a constant. Thus, if absolute pressure is doubled, the volume of a mass of gas is halved, TABLE 1 PRESSURE EQUIVALENTS 1 atmosphere
= = = = = =
33 feet 34 feet 2 9 . 9 in 760 m m
of seawater (fsw) of fresh w a t e r Hg Hg
1 4 . 7 p o u n d s p e r s q u a r e i n c h (psi) 1 kg/cm2
DEPTH
GAUGE ABSOLUTE PRESSURE PRESSURE
GAS VOLUME
66 feet
2 atm
3 atm
j . ' y . ' i f Vz vol
99 feet
3 atm
4 atm
| y . ' . ' . l % vol
DENSITY
3 units 4 units
Fig. 1. Gas volume decreases as absolute pressure increases. Gauge pressure is zero at the surface. Thus, gauge pressure equals absolute pressure less one atmosphere (from Strauss, R. H., ed.: Diving Medicine, Grune and Stratton, New York, 1976; used by permission).
Gas volume changes are particularly noticeable near the surface (figure 1). In addition to the pressure and volume changes that effect gas spaces during submersion, there are also changes in the partial pressures of individual gases within these spaces. Dalton's law of partial pressure states: "In a mixture of gases, the pressure exerted by each gas is the same as it would exert if it alone occupied the same volume; and the total pressure is the sum of the partial pressures of the component gases." As ambient pressure increases, the total pressure of a gas mixture increases. As total pressure increases, the partial pressure of each gas within the mixture increases proportionally, although its percentage remains constant. In general, the biologic effects of a gas depend on its partial pressure. This is because both diffusion and the amount of gas dissolved in a solvent are proportional to partial pressure. Thus, supplying the proper amount of 0 2 to tissue depends on the partial pressure of 0 2 and not merely on the total gas pressure or the percentage of 0 2 . C 0 2 and N 2 balance are similarly dependent on the partial pressure of the respective gas. Henry's law states that at a given temperature, the mass of a gas dissolved in a given volume of solvent is proportional to the pressure of the gas with which it is in equilibrium. Thus, as pressure increases during scuba diving, more and more N 2 is dissolved in the body. During ascent, this N 2 comes out of solution and, under certain circumstances, may cause decompression sickness. A person who goes underwater has several choices (figure 2). (1) He can ride in a vessel, the hull of which is designed to withstand hydro-
1003
DIVING MEDICINE
Submarine
Breath-hold Diving
Scuba Diving
1 atm
1 atm
* 1 atm
air seawater
~T ~T ~T 1 atm
5\
99 feet
>
*4 atm*. J
• • • . •t• • 4 atm •
ation becomes more difficult as depth increases. This occurs because more molecules of air must flow through the orifice of the regulator for each breath. Much of the resistance to air flow within the respiratory tract is due to turbulence and is therefore dependent on density. Flow resistance within airways increases as depth and gas density increase, but this effect is insignificant under conditions associated with sport diving. With current regulators, resistance is minimized and large volumes of air can be inspired at considerable depths without the necessity of generating uncomfortably negative inspiratory pressures. Occasionally, during severe exercise, a person's volume demand may exceed his regulator's capacity. A subsequent feeling of dyspnea may contribute to panic. Furthermore, an air tank is exhausted more quickly as depth increases. A gauge indicating tank pressure is generally used by divers so that they do not run out of air under water, a dangerous situation for several reasons. With the behavior of gases in mind, it is easy to understand the pathophysiology of most clinical syndromes associated with diving. These syndromes are discussed in the following sections.
to
Fig. 2. Within a submarine, pressure remains at 1 atmosphere absolute (the pressure at sea level). In breathhold diving, the lungs are compressed, and the gas pressure within them is approximately the same as the surrounding (ambient) pressure. In scuba diving, gas is supplied at ambient pressure so that normal respiration can continue (from Strauss, R. H., ed.: Diving Medicine, Grune and Stratton, New York, 1976; used by permission).
static pressure so that ambient pressure remains at 1 atmosphere. Under these circumstances, there are no volume or pressure changes within the body. (2) He can hold his breath and dive. Gas pressure within the lungs approximates ambient pressure, and the volume within the thorax must decrease proportionately. (3) The diver can submerge while breathing compressed gas from scuba equipment. Under this circumstance, gas pressure within the lung remains close to ambient pressure, but lung volumes remain normal because the person continues to breathe while underwater. A demand regulator releases gas from a tank to the respiratory tract when the mouth pressure decreases to slightly less than ambient pressure during inspiration or as depth increases. Expired gas is released into the water as bubbles. Equipment worn by a scuba diver is shown in figure 3. With certain types of scuba regulators, inspir-
Decompression Sickness Decompression sickness first became a problem in the 1800s when men began working in the compressed-air environment of tunnels and caissons, the closed underwater compartments used in the building of bridge foundations. While caissons and tunnels are being constructed below water level, air is maintained at a pressure slightly greater than that of the water to keep water out. After returning to the surface, early compressed-air workers sometimes noticed steady, boring pains, similar to a toothache, most often in the hip or knee joints. "One pays only on leaving," it was said of such work. The pains Air tank
Snorkel
Wet suit Face mask Swim fins
Regulator
Inflatable vest Weight belt
Fig. 3. Equipment used in scuba diving (after U.S. Navy Diving Manual [28], from Strauss, R. H. ed.: Sports Medicine and Physiology, W. B. Saunders, Philadelphia, 1979; used by permission).
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RICHARD H. STRAUSS
started within a few minutes or hours after surfacing and lasted several hours or longer. The afflicted men limped and were said by co-workers to be doing the "Grecian bend," a contortionist posture in walking assumed by fashionable ladies at the time (2). "The bends" and "caisson disease" are loosely synonymous with what we today call decompression sickness. The disease may affect not only the limbs directly, but can also damage the central nervous system. Paraplegia is a particularly serious problem that occurs among sport divers today. Decompression sickness is caused by the formation of gas bubbles in the blood and body tissues when ambient pressure is decreased. T o understand the pathogenesis of this disease, the factors that lead to the accumulation of N 2 in body tissues and the subsequent formation of bubbles must be understood. Gas absorption by the body is a critical factor in decompression sickness. As mentioned previously, the quantity of a given gas dissolved in a tissue is proportional to the partial pressure of that gas within the tissue. As a scuba diver descends from the surface to a depth of 66 feet, the pressure surrounding him increases from one atmosphere absolute (ATA) to 3 ATA, and the partial pressure of N 2 triples. As a result, a gradient exists for the net flow of N 2 from the alveoli to the blood and finally into tissue. After some time at depth, equilibrium will be reached, and all tissues will contain about 3 times as much N 2 as before the dive. The uptake of gas by a tissue is rapid immediately after a pressure increase (figure 4). However, the gradient for transport of gas into tissue decreases as the tissue approaches saturation, so that the uptake of gas decreases exponentially with time. The time required for a tissue to reach equilibrium depends on both the solubility of the gas in the tissue and, generally, the rate at which gas is brought to the tissue by blood. The rate of perfusion of tissues by blood can vary widely. A well-perfused tissue, such as the brain, which reaches equilibrium within minutes (3), is called a "fast" tissue. In contrast, fatty tissue, with poor perfusion and a high solubility for gases such as N 2 , requires longer to reach equilibrium and is known as a "slow" tissue. Diffusion of gas within a tissue is rarely a rate-limiting step (4) because capillaries generally lie so closely together that diffusion distances are small. When ambient pressure is decreased, the loss
>,
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\
\
FAST n SSUE
1 1 ,-'' 1 /
LOW
>o-
\
INITIAL
TISSUE
DECOMPRESSION
COMPRESSION
TIME
Fig. 4. When ambient pressure is increased during breathing of compressed air, the pressure of the inert gas (N2) in the alveoli changes immediately. The pressure of N2 in various tissues increases gradually, however, at a rate that becmes slower as saturation is approached. The initial compression (Pj-P2) results in supersaturation of the "fast" tissue, which is intended to cause rapid loss of gas but, it is hoped, no significant bubble formation. The "slow" tissue continues to absorb gas, but at a slower rate (from Strauss, R. H., ed.: Diving Medicine, Grune and Stratton, New York, 1976; used by permission).
of gas from tissue is believed to be analogous to gas uptake as long as bubbles do not form. If bubbles are present within the tissue, however, some gas will diffuse into the bubbles, instead of leaving the body. Decompression is thus more efficient if bubble formation is avoided in the first place. When the cork is removed from a bottle of champagne, bubbles appear. During storage, the liquid is in equilibrium with the gas at its surface (mainly C0 2 ) and is saturated with this gas at a pressure greater than 1 atmosphere. When the bottle is uncorked, the ambient pressure is suddenly decreased. Gas pressure within the liquid does not decrease immediately, because equilibration of gas by diffusion through the surface of the unstirred liquid would require days. The champagne suddenly becomes supersaturated—that is, the surrounding pressure is less than the total gas pressure within the liquid. Supersaturation is a necessary condition for the type of bubble formation and growth discussed here. The formation of bubbles in divers on ascent is somewhat analogous to the formation of bubbles in champagne when the bottle is uncorked. For a bubble to grow from "nothing" to a finite size, it must go through 2 distinct phases: (1) the formation of a small bubble where noth-
DIVING MEDICINE
ing was previously observable, and (2) the growth of a small bubble into a large one. The mechanism of bubble formation in animals is poorly understood. It appears that some sort of nuclei for bubble formation exist in animals, because bubbles begin to form when the supersaturation pressure is in the range of a few atmospheres or less, as in decompression. In principle, bubbles can form without nuclei, but in pure water this is believed to require a supersaturation pressure on the order of 1,000 atmospheres (5, 6)—almost the maximal depth of the sea. Work with transparent shrimp and with rats suggests that animals normally have gas nuclei that can be crushed partially by increased hydrostatic pressure, thereby decreasing bubble formation on subsequent decompression (7, 8). A nucleus is different from a small bubble because the nucleus is stable. Surface tension (7) tends to make a bubble smaller. Laplace's law states that pressure within a bubble due to surface tension (P7) is given by the equation:
where r is the radius of the bubble. For large bubbles, P7 is negligible; however, as a bubble becomes smaller, P7 increases, which tends to force gas into solution and make the bubble collapse. Indeed, it is difficult to imagine how a very small bubble can exist at all. The mechanism by which a nucleus is stabilized is not entirely clear. One hypothesis is that certain molecules that resist the surface tension become increasingly concentrated at the surface of a bubble as it becomes smaller (9, 10). Eventually this produces a small, stable pocket of gas, then called a nucleus. As an alternative to the existence of nuclei, it has been suggested that bubbles may form readily at aqueous-lipid interfaces within animals due to decreased surface tension at such locations (11). For an existing bubble to grow, the total gas pressure within the bubble (P bubble ) must be greater than the pressures tending to constrict or crush it. Crushing pressures include those due to surface tension (P7) and to ambient pressure (P a m b i e n t ). In addition, because of its structure and osmotic balance, tissue tends to resist being deformed and thus causes tissue pressure (PtiSSue)The necessary condition for bubble growth is then: ^bubble > "ambient ~*~ ^tissue "^ *Vm
This condition can be satisfied if the tissue is
1005
sufficiently supersaturated and if gas is free to diffuse from the tissue into the bubble. Conversely, bubbles will shrink if the preceding inequality is reversed. Gas within a bubble tends to equilibrate with gas in the surrounding tissue. Therefore, the necessary condition for bubble growth after decompression from a dive using compressed air can be rewritten in terms of the gas partial pressures within the tissue: PN 2 + Po 2 + Pco 2 + PH 2 O > P a m b i e n t + P tigsue + P 7 . During ascent, supersaturation must be controlled so that bubbles do not form and grow sufficiently to cause decompression sickness. After several decades of experience and research, there are now guidelines as to how abrupt a decrease in pressure causes the disease. Thus, divers and others exposed to increased pressure can usually avoid this danger by decreasing the pressure gradually. Prevention of decompression sickness is discussed later in this paper. Pathogenesis In severe cases of decompression sickness, in which the diver or laboratory animal has died, bubbles have been reported everywhere: within blood vessels, presumably having impeded circulation; extravascularly, distorting tissues; and possibly within cells (12). In the more common, nonlethal form of decompression sickness, the location of bubbles is less clear. After some dives, bubbles can be detected in the venous circulation because they reflect ultrasonic signals of a Doppler flow meter (13), even though decompression sickness has not occurred. There appears to be a correlation between increasing numbers of bubbles and the severity of some types of decompression sickness (14). Numerous changes in the blood have been noted after decompression (15): clumping of red cells, formation of rouleaux, sludging of blood in small vessels, and a decrease in the number of platelets. Hematologic changes are believed to be largely a result of the gas-blood interface of bubbles. Hemoconcentration occurs, possibly from increased capillary permeability. In addition, the osmotic activity of dissolved gases has been suggested as a mechanism for fluid shifts (16). Decompression sickness is associated with release into blood of a "Smooth Muscle Acting Factor," which causes constriction of blood vessels and bronchi and potentiates bradykinin (17). Numerous other biologically active sub-
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RICHARD H. STRAUSS
stances associated with stress have been observed in decompression sickness. Clinical Manifestations Symptoms may appear during or immediately after decompression or, more usually, after a delay of minutes to hours. The delay may be due in part to the growth of bubbles and, perhaps more important, to the gradual progression of pathologic processes, such as swelling, after the original damage to tissue by bubbles. Spinal Cord and Brain Central nervous system "bends" is an especially serious types of decompression sickness because it can cause permanent nerve damage, such as paraplegia. Approximately one-half of 100 cases of decompression sickness treated recently in Hawaii involved the central nervous system (18); almost all of the victims were recreational divers. Neurologic lesions often involve the spinal cord, particularly the thoracic segments, but also the upper lumbar and lower cervical segments. The white matter of the cord, rather than the gray matter, is generally affected (19, 20). The primary cause of damage appears to be evolution of bubbles within the venous vertebral plexus, leading to stasis and obstruction of blood (21). Early lesions consist of small hemorrhages followed by degeneration of nerve fibers (19). It is important that the diver and his physician recognize the early manifestations of spinal cord decompression sickness, because immediate treatment in a recompression chamber may result in recovery, whereas delay significantly decreases the chances of a good outcome. Soon after surfacing, the diver's first symptom may be transient back pain with radiation to the abdomen, which he often attributes to the lifting of air tanks. Therefore, the first manifestation to catch the diver's attention is usually a feeling of "pins and needles" in the legs—that is, paresthesia and hypesthesia. Next, the legs become weak and the walk unsteady; the diver often cannot initiate urination, although his bladder may be distended. Finally, paralysis below the waist or neck may ensue (22). The condition appears to be similar to that of a spinal fracture with cord injury; however, the diver is more fortunate because with prompt treatment his chances for recovery are much better. Brain damage is less frequent than spinal cord damage. Manifestations include visual disturbances, hemiplegia, and unconsciousness. Vertigo
("the staggers") may result from damage to the brain or inner ear. The maximal rate at which a diver can ascend safely to the surface or to a decompression stop is believed to be 60 feet per min. Injury to the central nervous system is often associated with marginally adequate decompression and an unusually rapid rate of ascent in an emergency situation, such as running out of air during a dive. When decompression procedures have been violated badly, symptoms may appear immediately and progress to paralysis within minutes. Even when standard practices are followed, decompression sickness occurs occasionally and may progress during several hours. Extremities Limb pain is another common symptom of decompression sickness. Although pain may occur at many locations in the extremities, shoulder and elbow joints are the most frequent sites in divers, as contrasted to hip and knee joints in tunnel workers. The pain is usually steady, but occasionally may be throbbing. It reaches a peak in minutes or hours and often subsides spontaneously several hours later, even if left untreated. The mechanism of pain production is unclear. T h e arm or leg usually looks completely normal, there is little tenderness, and moderate joint motion is well tolerated. Treatment by recompression helps to relieve the pain and may decrease subsequent tissue damage. Pain in the extremities may also result from local injury unnoticed in the excitement of the dive. Such injuries bear characteristics of trauma, e.g. swelling, discoloration, tenderness, and exacerbation of pain on motion. Osteonecrosis is probably a late consequence of inadequate decompression and was much more frequent in the past than at present. Patches of bone die but may not become visible on roentgenograms for months or years after diving. Often the person has no symptoms. However, if the necrotic patches of bone are near a joint surface such as the shoulder or hip, the joint may collapse and cause crippling (23-25). Pulmonary Some of the bubbles formed in the vasculature of systemic tissues are carried by venous blood to the lungs. Most of these bubbles lodge in small pulmonary vessels, although a fraction may reach the systemic arterial circulation (26). In most cases of decompression sickness, no pulmonary
1007
DIVING MEDICINE
manifestations appear, even though bubbles may be detected in the venous circulation. The degree of pulmonary embolization by gas necessary to cause symptoms is unknown; release of vasoactive substances and reflex mechanisms probably contribute to pathogenesis. The pulmonary syndrome is called "the chokes" by divers and is characterized by substernal chest pain, dyspnea, and cough. Symptoms are aggravated by deep inspiration and by smoking (27). In animals, clinical signs of the syndrome are accompanied by increased pulmonary arterial pressure and hypoxemia (21). Pulmonary edema may also occur. The chokes is an extremely serious form of decompression sickness. Without recompression, circulatory collapse and death may follow, whereas recompression results in complete relief within minutes in most cases. Other "Skin bends" is sometimes seen in scuba divers, but more often follows simulated dives in chambers when the skin is in direct contract with the compressed gas. The affected skin, usually on the back or elsewhere on the trunk, itches and burns. If these are the only manifestations, skin bends is frequently left untreated or is treated by breathing 0 2 at 1 atmosphere. If discoloration (marbling) appears, chamber treatment is advisable. Fatigue much greater than that expected from the work performed sometimes follows marginal or inadequate decompression. It may or may not be associated with other signs of decompression sickness. Treatment The standard treatment for decompression sickness is to place the victim in a hyperbaric (high-pressure) chamber and increase the air pressure to 2.8 ATA (equivalent to 60 feet of seawater) over one or 2 min (28). The patient then breathes pure 0 2 intermittently by mask (figure 5). The increased ambient pressure causes bubbles to diminish in size. Breathing 0 2 , rather than air, increases the gradient for diffusion of inert gas from bubbles and tissue out of the body. Oxygenation of tissues is also increased. However, because increased partial pressures of 0 2 can cause 0 2 toxicity, in particular, convulsions, air is breathed intermittently for periods of 5 min or more. Ancillary treatment may in-
0
1
2 TIME
3
4
5
(hours)
Fig. 5. Victims of decompression sickness are placed in a pressurized chamber where the breathe pure 0 2 . To avoid oxygen toxicity, air is breathed for intermittent periods of 5 min or longer, according to the U.S. Navy treatment schedule shown (28) (from Strauss, R. H., and Prockop, L. D.: Decompression sickness among scuba divers, JAMA, 1973, 223, 637; used by permission).
clude corticosteroids to decrease nervous tissue edema, and plasma expanders and intravenous fluids to increase circulating blood volume. Treatment can be dramatically effective if it is begun early enough, when symptoms are beginning to develop and tissue damage is mild. However, as time progresses, tissue damage increases, and even if all bubbles disappear with hyperbaric treatment, healing requires days or weeks and may not be complete. Decompression sickness that involves the central nervous system is a medical emergency. The victim should be given 0 2 continuously by mask and transported to a recompression chamber by the fastest means possible. (If an aircraft is used, cabin pressure should remain as close to 1 atmosphere as possible; the time saved by air transportation is believed to more than compensate for a moderate decrease in ambient pressure). The treatment schedule shown in figure 5 is often used to treat scuba divers. Other schedules are used for deeper dives, but the principles remain the same. Attempts by divers to treat themselves by recompression under water are usually unsuccessful and dangerous. Consultation concerning diving medical problems, including the location of the nearest hyperbaric chamber, can be obtained by calling (512) 536-3278 (U.S. Air Force School of Aerospace Medicine, San Antonio, Tex.), or (904) 234-4355 (U.S. Navy Experimental Diving Unit, Panama City, Fla.). The U. S. Coast Guard and state police sometimes assist with emergency transportation.
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RICHARD H. STRAUSS
Prevention A practical problem in diving is how to return to the surface in the shortest possible time without sustaining injury. This is a bit like approaching the edge of a cliff as closely as possible, for the view, without falling off. The main variable is the rate of ascent, which can be seen graphically when pressure is plotted against time, as in figure 6. Early compressed-air workers and divers were brought to the surface as fast as machinery would permit. When it became evident that this caused damage, a slower, constant rate of ascent was used, but this still resulted in injury. In 1908 and later, the English physiologist J. S. Haldane and colleagues (Boycott, Damant, and Haldane [29]) published work that has been the basis for many decompression schedules ever since. They found that men who spent several hours at pressures up to approximately 2 ATA could be brought immediately to 1 atmosphere absolute without causing decompression sickness. From these data, they suggested that any tissue could tolerate a decrease in pressure if the ratio of tissue gas pressure to ambient pressure did not exceed 2/1. After a decrease in pressure, the diver was supposed to wait until sufficient gas was eliminated from his body to permit a further decrease in pressure. Haldane and colleagues postulated that various
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50
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Fig. 6. Decompression of several tissues postulated in 1908 by Haldane and co-workers is such that the pressure of nitrogen in any one tissue (broken lines) is never greater than approximately twice ambient pressure (solid line) (after Boycott [29]; from Strauss, R. H., ed.: Diving Medicine, Grune and Stratton, New York, 1976; used by permission).
tissues have different rates of gas uptake or loss (figure 6). The initial, large decrease in pressure had the advantage of increasing the outward diffusion gradient for gas from fast tissues and limiting further gas absorption by slow tissues. However, as diving depths became greater, the theoretical ratio of tissue gas pressure to ambient pressure had to be decreased progressively to avoid decompression sickness. The profiles of empirical decompression curves (28) now lie somewhere between the original Haldane curve and the straight line of a constant rate of decompression (linear decompression). One way to prevent bubble formation is to avoid supersaturation entirely. This is possible during very slow decompression because tissues are normally unsaturated—that is, their total gas pressure is less than ambient pressure. Such unsaturation occurs primarily because the C 0 2 that is produced by metabolism is more soluble in blood than is the 0 2 consumed and exerts a lower partial pressure (figure 7). This same unsaturation is responsible for the spontaneous resorption of air in a pneumothorax. Decompression tables based on this principle have been calculated by Hills (30). T h e degree of unsaturation, sometimes called the "oxygen window," can be increased by breathing 0 2 at partial pressures greater than normal. This technique is used to speed decompression and to increase the rate of inert gas elimination from the body during treatment of decompression sickness. Susceptibility to decompression sickness varies among persons and even in the same diver from day to day. Predisposing factors include obesity, exertion, poor physical condition, fatigue, age, cold, dehydration, and injury. Some acclimatization may occur: tunnel workers and divers appear to be less susceptible to decompression sickness when working daily than after an inactive period (31). Most careful pleasure divers in the United States use as guidelines the U.S. Navy diving tables (28), which have a historical basis in the work of Haldane, but have been modified empirically through years of experience to be generally safe. Many other decompression tables have been developed for commercial or military use. Some divers wear a decompression "meter." Although the meters are generally designed to approximate an accepted set of decompression tables and are used as an alternative to consulting the tables, the practice is not necessarily safe.
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DIVING MEDICINE
AMBIENT
= 760~ P 0z = 90mmHg
UNSATURATION = 54 mm Hg
Pco2= 40
Pp2 = 40 mm Hg nx>2 = 46
PH 2 0 = 47
PH 2 0 = 47
I
1
PN 2 =573
o -
ARTERIAL BLOOD
P
N2
= 573
TOTAL GAS PRESSURE - 706 mm Hg
VENOUS BLOOD
Fig. 7. Arterial blood is nearly saturated with gas. Venous blood and tissue are normally unsaturated; that is, the total gas pressure within them is significantly less than ambient pressure (from Strauss, R. H . , ed.: Diving Medicine, Grune and Stratton, New York, 1976; used by permission).
At present, commercially available devices involve the transfer of gas by diffusion or limited bulk flow from a compartment exposed to ambient pressure into a second compartment to which an indicator of gas pressure is attached. Gas passes into or out of the indicator compartment in proportion to ambient pressure—it is hoped in a manner somewhat analogous to that of the body. Because the tissues of the body differ in terms of gas uptake and loss, a meter with several diffusion units would mimic the body more effectively. A small electronic computer that integrates time and depth may prove to be the best decompression meter. Although diving is done in mountain lakes and other bodies of water at altitudes well above sea level, the use of sea-level decompression tables becomes less safe as altitude increases. Various decompression methods for altitude diving have been proposed, but few have been tested extensively, and some are dangerous. In Switzerland, Buhlmann and associates (32, 33) have calculated new altitude decompression tables, and after 214 test dives no cases of decompression sickness have been reported. In 1961, several members of the crew of a commercial airliner incurred decompression sickness on an intercontinental flight after scuba diving during the morning and afternoon before their evening flight (34). Other incidents of decompression sickness aboard commercial and
private aircraft after diving have been reported. Studies by Edel and co-workers (34) led to the conclusion that scuba divers who stay strictly within the depth-time limits recommended by the U.S. Navy tables for dives that do not require decompression will not develop decompression sickness if, after diving, they allow a minimum of 2 hours at the surface before flying in a pressurized aircraft (maximum cabin altitude, 8,000 feet); those who make dives beyond the no-decompression limits should allow a surface interval of 24 hours to avoid the risk of decompression sickness. More recently, researchers have recommended a wait of 4 hours between no-decompression diving and flying. Commercial pilots are not permitted to fly for 24 hours after scuba diving, and persons who may exceed 8,000 feet in altitude should follow the same rule. Although several women have done scuba diving during pregnancy without apparent detrimental effects to the fetus, the safety of this practice has not been established. Gas bubbles have been observed in the circulation of fetal sheep using a standard decompression table, although the mother was unaffected (35). Fetal risks include not only decompression sickness but also hyperoxia, hypoxia, and hypercapnea. The Undersea Medical Society recommends that the woman who is, or may be, pregnant be discouraged from diving (36).
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RICHARD H. STRAUSS
Some Hazards of Diving Gases
T h e gas mixture that is breathed by a diver must be free of contaminants such as CO and oil vapor. In addition, 2 gases that are normally breathed—0 2 and N 2 —become hazardous at increased partial pressures. Oxygen Toxicity Breathing 0 2 at increased ambient pressures can cause grand mal seizures, which in a scuba diver, generally lead to drowning. Therefore, the sport diver should never breathe pure 0 2 under water. Occasionally, the U.S. Navy uses a closedcircuit rebreather system to avoid release of tell-tale bubbles into the water. In this system, 0 2 is rebreathed after the removal of C 0 2 . The probability of convulsions increases as ambient pressure and time at pressure increase (37). T h e maximal allowable depth using this system is 25 feet of sea water (fsw). Within a hyperbaric chamber, 100 per cent 0 2 is breathed at pressures of as much as 2.8 ATA (60 fsw) in the treatment of decompression sickness and air embolism (figure 5). T o decrease the incidence of convulsions, 5-min periods of breathing air are interspersed during 0 2 breathing. Localized muscular twitching, particularly noticeable in the face, as well as nausea and vertigo, may precede convulsions. If seizures or premonitory signs appear, the oxygen mask is removed and the patient is protected from injury. Seizures are generally of brief duration. After 15 min of air breathing, the patient can often return to 0 2 treatment without subsequent convulsions. T h e mechanism of central nervous system 0 2 toxicity is unclear. Exposure to 0 2 at high pressures is associated with several neural changes: the concentration of 7-aminobutyric acid decreases in the brain; certain enzymes that support oxidative metabolism are altered; and cellular membranes are damaged through oxidation of lipids and sulfhydryl groups (38). Pulmonary 0 2 toxicity is not a problem among scuba divers. It can occur among saturation divers who live in chambers for days and breathe gas mixtures in which the partial pressure of 0 2 exceeds approximately 0.5 ATA. Such conditions occur because the time required for decompression from a dive can be shortened by increasing the Po 2 of inspired air, but at increased risk of 0 2 toxicity. Pulmonary 0 2 toxicity has been reviewed extensively elsewhere (3941).
Nitrogen Narcosis Nitrogen narcosis is called by the French Vivresse des grandes profondeurs—rapture of the deep (42). It occurs because the N 2 in air acts progressively as a general anesthetic as its partial pressure increases. Martini's Law, a fanciful rule of thumb, states that each 50-foot increment in depth is equal in effect to one martini on an empty stomach. Manifestations of narcosis occur almost immediately and include impairment of judgment, memory, ability to do arithmetic, and fine movements. The mechanism of nitrogen narcosis is unclear. One hypothesis is that N 2 , which dissolves predominantly in the lipid portion of nerves, causes a small but significant expansion in lipid volume. This, in turn, is believed to alter membrane characteristics such that synaptic transmission is decreased and permeability to ions is increased (43,44). Most other physiologically inert gases, such as neon and xenon, also have narcotic properties at increased pressures. Helium appears to be the single exception. It is substituted for N 2 as the inert breathing gas in military and commercial dives deeper than approximately 150 feet. Helium is too expensive for recreational use. Nitrogen narcosis is one reason to limit sport diving to approximately 130 feet in depth. An intoxicated diver is an unsafe diver. Unfortunately, many divers do not recognize that their judgment is impaired at depths greater than 100 feet. Barotrauma of Descent
Barotrauma of descent, or "squeeze," is a process in which ambient pressure increases, but pressure within an unventilated gas space does not. The term is also used to describe the result of such a process—usually hemorrhage. For squeeze to occur, (i) a gas space must exist that is not entirely collapsible, and (2) the gas within the space must not equilibrate fully with gas at ambient pressure, Middle ear squeeze is a common problem among divers. As a scuba diver descends and water pressure increases, he normally opens his eustachian tubes every few feet so that air can flow into the middle ear cavity (figure 8). By this method of "equalizing" pressure, the pressure across the tympanic membrane is kept small and no damage occurs. However, if pressure is not equalized during descent, as when the eustachian tube is edematous during an upper respiratory infection or allergy, damage may occur.
DIVING MEDICINE
Semicircular canals
Fig. 8. Simplified diagrammatic drawing of the ear. The external auditory canal, middle ear, and eustachian tube contain air. The fluid-filled inner ear is subdivided into the perilymphatic and endolymphatic spaces, which connect to the subarachnoid space by the cochlear duct and endolymphatic duct, respectively (from Farmer, J. C , and Thomas, W. G.: Ear and sinus problems in diving, in Diving Medicine, R. H. Strauss, ed.: Grune and Stratton, New York, 1976; used by permission).
Vessels within the lining of the middle ear contain blood at approximately ambient pressure. When the pressure within the middle ear is sufficiently less than ambient pressure, the walls of small vessels rupture and hemorrhage occurs. The examining physician can see hemorrhage that occurs within the tympanic membrane. The degree of hemorrhage usually reflects the severity of the barotrauma, and sometimes blood accumulates within the middle ear. The tympanic membrane may itself be ruptured, and cold water that enters the middle ear can cause vertigo and disorientation under water—a hazardous state. The treatment for ear squeeze is to avoid diving until the ear has healed and all symptoms have cleared (45). A decongestant may be used. Ear squeeze generally can be avoided if the diver simply heeds the warning of ear pain. On feeling any ear pain, the diver should stop his descent, ascend a few feet, and try to equalize ear pressure. If the ears cannot be equalized, the dive should be terminated. Diving should be avoided when respiratory infection or allergy is present. Squeeze can affect any gas space that does not equilibrate with ambient pressure. Eye goggles are not worn because they can result in conjunctival hemorrhage. The diver's face mask encloses
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his nose as well as eyes so that compressed air can reach the mask. Sinus squeeze causes pain over the affected sinus and sometimes results in extravasation of blood, which may be observed in the face mask on surfacing. Many divers can equalize ear pressure without conscious effort, but others use maneuvers such as trying to exhale forcefully against the pinched nose to force air through the eustachian tubes. This maneuver is occasionally associated with sudden deafness and tinnitus, usually in one ear. A probable mechanism is that increased pressure in the thorax and abdomen is transmitted to the cerebrospinal fluid as blood engorges veins within the spinal column. The increased pressure is in turn transmitted from the cerebrospinal fluid, via the endolymphatic and cochlear ducts, to the fluid of the inner ear (figure 8). The increased perilymphatic pressure tends to rupture the round or oval window of the inner ear with loss of fluid into the middle ear, which is at a lower pressure. T h e neural portion of the inner ear is damaged in the process (46,47). Many experienced divers assimilate a method of equalizing ear pressure that may well be safer (Frenzel maneuver). They increase pressure within the pharynx by occluding the nose, closing the glottis, and then contracting the pharyngeal muscles. Air is thus forced through the eustachian tubes without altering thoracic pressure. This can be performed with the mouth open or with a regulator in place because the tongue and soft palate occlude the posterior oral cavity. Barotrauma rarely affects the ears during ascent because the eustachian tube acts somewhat like a one-way valve. Air escapes from the middle ear with relative ease, although it may enter with difficulty. Still, occasional divers become vertiginous during ascent (alternobaric vertigo). It is believed that this occurs when the pressure within one or both middle ears exceeds ambient pressure by a critical amount (48, 49). Symptoms usually stop when the surface is reached. Transient vertigo has also been observed in divers during descent. Barotrauma of Ascent
As ambient pressure is decreased during ascent, gas within the lungs tends to expand in accordance with Boyle's law. This effect becomes especially important at shallow depths where a relatively small change in depth can lead to a
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large change in gas volume. Thus, a 33-foot ascent from 99 feet (4 ATA) to 66 feet (3 ATA) changes gas volume by the ratio 4/3, an increase of 33 per cent. However, ascent from a depth of 33 feet (2 ATA) to the surface (1 ATA) leads to a doubling of gas volume. Pulmonary Barotrauma The ascending scuba diver must permit expanding gas to escape from his lungs, either by breathing normally or, in case of an equipment problem, by exhaling continuously. Failure to do this can lead to overdistension of the lungs, tearing of lung tissue, and escape of air from alveoli. The extra-alveolar air may travel to any of several locations: (1) small amounts may dissect no farther than the interstitial tissue of the lung, (2) dissection may occur along vessels to the mediastinum and then to subcutaneous tissue or elsewhere (50, 51), (3) air may enter pulmonary vessels and be carried to distant parts of the body as arterial emboli; and (4) pneumothorax may occur. Extra-alveolar air is sometimes asymptomatic (52). Overdistension of the lungs, not merely the difference between alveolar pressure and that outside the chest, is responsible for damage to lung tissue. In experiments with anesthetized dogs, lung rupture occurred when intrapulmonic pressure exceeded ambient pressure by 80 mm Hg. Yet much higher pressures could be tolerated without damage when the thorax and abdomen were bound in order to limit expansion (53). Comparable findings have been noted in fresh cadavers. Coughing results in high intraalveolar pressures, but generally does not cause lung rupture. Air embolism has occurred under conditions in which observers were sure that breath holding had not occurred. It is hypothesized that local obstruction to egress of air may be responsible for barotrauma to lung tissue. Potential causes of obstruction include broncholiths, gas-filled cysts, active asthma, and viscous secretions. Persons with obstruction to egress of air should not dive. Occasional persons suffer from air embolism without any apparent cause. Air Embolism The mechanism by which air enters pulmonary vessels is not entirely clear. It is believed that small vessels rupture as lung tissue is overstretched. Air may not enter the circulatory system until the high intra-pulmonic pressure is relieved by the resumption of breathing and
pulmonary circulation is restored. Bubbles are carried quickly to the heart and then by the arterial system to various parts of the body. The bubbles lodge in small arterial vessels, occluding circulation beyond that point. They are stabilized by surface tension; loss of gas by diffusion is slow. Air embolism to the brain generally becomes apparent within seconds as a stroke-like syndrome. A typical history is that of a scuba diver who ascends rapidly, often under emergency conditions, reaches the surface, gasps, and sinks unconscious into the water. If not rescued, the diver drowns. Almost any sign of cerebral damage may appear, including focal paralysis, paresthesias, or visual disturbances. Hemoptysis sometimes occurs. Trainees should remember that cerebral air embolism has occurred on several occasions during scuba practice in a standard swimming pool. (Decompression sickness does not occur under such shallow conditions.) Cerebral air embolism is a medical emergency and treatment in a hyperbaric chamber should be initiated as soon as possible. The patient should be transported in the Trendelenberg position, lying on his left side. This position is believed to decrease the chances of additional gas emboli reaching the brain and may possibly improve cerebral circulation impaired by gas emboli. T h e patient should breathe 0 2 continuously through a mask with a seal that assures a high inspired Po 2 . In the presure chamber, an often used treatment schedule is similar to that used for decompression sickness (figure 5), except that initial pressurization is to 165 fsw (6 ATA) with air breathing for 15 to 30 min (28). This initial high pressure is believed to decrease the size of bubbles sufficiently to permit them to be carried to smaller vessels, thus decreasing the size of the affected area (54). Bubble absorption also begins. Chamber pressure is subsequently decreased to 60 fsw so that 0 2 may be breathed with only a small risk of convulsions. Corticosteroids are administered to minimize cerebral edema. Although massive cerebral air embolism leads to death within minutes, those victims who reach a hyperbaric chamber while still alive have an excellent chance for full recovery. Cerebral air embolism is often accompanied by mediastinal emphysema sufficient to be visible on roentgenograms. Subcutaneous emphysema, palpable particularly in the supraclavicular fossae, may also be present. Mediastinal and subcutaneous emphysema do not require treatment in
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a pressure chamber if they occur without manifestations of air embolism and if they are asymptomatic or cause only mild symptoms such as substernal discomfort or voice change. The breathing of 0 2 by mask is usually sufficient treatment. Pneumothorax occurs infrequently as a result of pulmonary overdistension in diving. In contrast, during the use of positive pressure breathing in patients, pneumothorax is well known and cerebral gas embolism is rare. Uncomplicated pneumothorax in a diver is treated in the usual manner. If it accompanies cerebral air embolism, the latter must be treated in a chamber. As ambient pressure increases, additional air may enter the pneumothorax. When ambient pressure is subsequently decreased, a tension pneumothorax may result and require treatment. A chest tube may be inserted prophylactically before decompression. Breath-hold Diving
Many of the interesting forms of sea life that can be viewed by a scuba diver can also be seen by a breath-hold diver. The abundance of life decreases as water becomes deeper because sun light is the foundation of the food chain, and water acts as a filter for light. Breath-hold diving is simpler, cheaper, and safer than scuba diving, but often requires more exertion in the water. Basic equipment consists of a face mask for clear vision under water, fins to aid propulsion, and a snorkel (breathing tube) so that the diver can breathe at the surface without lifting his or her face from the water (figure 3). Persons who merely wish to swim at the surface and look at the bottom can do so with little expenditure of energy, given calm water conditions. Anyone who performs breath-hold dives should be aware of the danger associated with hyperventilation. Breath-hold Blackout Each year, a number of persons die from loss of consciousness (blackout) under water and subsequent drowning. Breath-hold blackout occurs almost exclusively in young males who are demonstrating how far they can swim under water or how long they can remain submerged. Many such incidents occur in guarded swimming pools (55). Swimmers often learn through experience that, by hyperventilating immediately before submerging, they can extend their time under water. However, unless alerted to the danger, they fail to realize that this maneuver can lead to loss of consciousness without warning. The mechanism of breath-hold blackout be-
comes clear when alveolar gases are examined during breath holding (56-58). Such measurements have been made using a rebreathing technique. That alveolar Po 2 decreases steadily during breath holding and that Pco 2 increases more slowly is shown in figure 9. These changes are more pronounced during exercise (56-58). When a person tries to hold his or her breath as long as possible, he or she is forced to terminate breath holding at a time (the breaking point) when the urge to breathe can no longer be suppressed. The breaking point is determined primarily by alveolar (arterial) Pco 2 , but other factors such as arterial Po 2 , attention, motivation, and lung volume play a role (59). Greater lung volumes permit longer breath holding, and sport divers usually inspire to nearly maximal lung volume before diving. Voluntary breath holding without hyperventilation (figure 9) is terminated even in highly motivated adults before alveolar Po 2 is sufficiently low to cause unconsciousness. (Small children may prolong breath holding to the point of cyanosis, unconsciousness, and convulsions [60]). However, hyperventilation can significantly decrease alveolar Pco 2 and body stores of C 0 2 so that the urge to breathe is delayed during subsequent breath holding. Unfortunately, hyperventilation increases body stores of 0 2 only slightly; alveolar Po 2 may approach 140 mm Hg, but the quantity of 0 2 in the blood is little increased because arterial hemoglobin is normally almost fully saturated with 0 2 . As a result, after hyperventilation arterial Po 2 may
l i m e , Seconds
Fig. 9. Alveolar Po2 and Pco2 during breath holding with air. Resting consumption of 0 2 (Vo2) = 320 ml/min. Work was mild: Vo2 = 580 ml/min (from Lanphier, E. H., and Rahn, H.: Alveolar gas exchange during breath holding with air, J Appl Physiol, 1963, 18, 478; used by permission).
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RICHARD H. STRAUSS
decrease to the point that consciousness is lost before arterial Pco 2 is sufficiently increased to result in a strong urge to breathe. The stimulus to breathing furnished by low arterial Po 2 is weak enough to be ignored by a highly motivated person. A practical guideline for divers is to take only one or 2 deep breaths before submerging. Pressure changes during diving can increase further the chances for unconsciousness. As water pressure increases, lung volume decreases and both alveolar Po 2 and Pco 2 increase (figure 10) (61). During submergence, alveolar Po 2 may become quite low. Upon ascent, the ambient pressure decreases and gas within the lung expands. Alveolar Po 2 then decreases even further and may result in loss of consciousness. During ascent, alveolar Pco 2 also decreases and the urge to breathe diminishes—a paradoxic event in terms of survival. Diving Reflex When whales, seals, or other aquatic mammals dive, cardiovascular changes occur that result in the conservation of 0 2 . Seals can swim underwater for 20 min (62), and some whales can remain submerged for one hour. During a dive by such an animal, the circulation of blood is essentially restricted to the heart, lungs, and brain. Vasoconstriction severely limits blood flow to the remainder of the body, including the working muscles (63, 64). Cardiac output decreases and heart rate decreases—to 16 beats per min in freeswimming seals (62). This response is known as the diving reflex. When the animal returns to the surface and breathes, peripheral circulation is restored and lactic acid, which has accumulated in the anaerobic muscle, enters the blood stream and is subsequently metabolized. After a long dive, the whale must remain at the surface for several minutes, a fact that whalers have long used to their advantage. Some humans exhibit bradycardia and vasoconstriction during breath-hold diving. These changes result in part from breath holding itself, but are augmented by exposure of skin, especially the face, to cool water (65-67). There is no clear evidence that the bradycardia response significantly conserves 0 2 in human divers. Negative Intrapulmonic Pressure In a person who breathes surface air while immersed to the neck in water, external chest pressure exceeds intrapulmonic (intra-alveolar) pressure by the weight of the column of water at a given point on the chest. This hydrostatic
(H 0
.
1
.
1
20 40 T i m e , Seconds
.
!(>0
Fig. 10. Po2 and Pco2 during 80-sec simulated dives (in a pressure chamber) preceded by hyperventilation (from Lanphier, E. H., and Rahn, H.: Alveolar gas exchange during breath-hold diving, J Appl Physiol, 1963, 18, 471; used by permission).
pressure causes a moderate decrease in expiratory reserve volume and a small decrease in vital capacity. Such changes are comparable to those found during negative pressure breathing in air. During immersion to the neck in the sitting position, approximately one fourth of the decrease in expiratory reserve volume is accounted for by the hydrostatic pressure of the water on the abdomen and most of the remainder by the pressure on the thorax (68). (The scuba diver swimming in the horizontal position with a good regulator at his mouth must generate a slightly negative intrapulmonic pressure for inhalation and a slightly positive pressure for exhalation. If he assumes an upright position, the pressure differences become similar to those during immersion to the neck.) Swimmers and divers have long noted a tendency for increased production of urine after they enter the water. Such diuresis has been documented and is believed to be caused by an increase in thoracic blood volume that results from negative intrapulmonic pressure, as well as from loss of the effect of gravity on the circulation. Stimulation of stretch receptors in the left atrium of the heart results in decreased secretion of antidiuretic hormone and associated diuresis (69, 70). Water temperature may also play a role. For many years, a breath-hold diver's maximal depth was believed to be determined by the point
DIVING MEDICINE
at which his total lung capacity was compressed to his residual volume (RV). If a subject's RV were 20 per cent of his total lung capacity, the depth limit would be 5 ATA (132 feet). It was predicted that further descent would rapidly result in negative intrapulmonic pressures leading to lung squeeze: rupture of vessels with extravasation of blood as seen in ear squeeze. However, one extensively studied subject dived to 240 feet (71), and even deeper breath-hold dives have been recorded. Although external pressure can compress the rib cage and raise the diaphragm to decrease residual volume, an important factor may be the shift of blood from the peripheral to thoracic blood vessels as intrapulmonic pressure becomes negative. A shift of 600 ml of blood has been estimated experimentally (72). Such blood shifts would lead to additional compression of the gas in the lungs and would permit diving to depths greater than those previously predicted. Among sport divers, lung squeeze has rarely proved to be a problem. A possible case has been reported in a diver who apparently lost consciousness and then sank while apneic (73). Those divers who attempt breath-holding depth records may yet be able to demonstrate the syndrome. Deep Diving (Commercial and Military) Military uses of deep diving include salvage and rescue operations. However, the major impetus for extending the depth at which divers can work is the recovery of undersea oil. Whenever possible, the oil industry avoids using divers in deep water because such operations are time-consuming and expensive. Decompression after even a brief deep dive may require several days at a cost of thousands of dollars per day. It is not surprising that undersea robots and armored diving suits, within which the operator remains at one atmosphere, are used increasingly. Still, some jobs are done most effectively by divers, who currently work as deep as 1,000 feet. Much of the present research in diving medicine focuses on the practical problems of extending divers' working depth in the sea and increasing safety at all depths. In dives greater than approximately 150 feet, helium is used as the main inert breathing gas to avoid narcosis. Sufficient 0 2 is added to result in an inspired Po 2 slightly greater than normal. At a depth of 500 feet, a gas mixture with a Po 2 of 200 mm Hg is 1.63 per cent 0 2 . This is insufficient to support a flame, but respiration proceeds well. The breathing of helium causes the voice to
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sound like "Donald Duck." This occurs because helium conducts sound more rapidly than does air, resulting in an upward shift in resonance frequency components in the vocal tract (74, 75). The effect becomes more pronounced as depth increases so that direct conversations are unintelligible. Electronic unscramblers are used to alter voice characteristics so that speech can be understood. Exposure of persons to great pressures is associated with tremors and decreased manual dexterity. This problem is termed the high pressure nervous syndrome and may result from a decrease in the lipid volume of nerves. (Lipids are more compressible than water.) Adding a small amount of N 2 to the breathing mixture helps to counteract the high pressure nervous syndrome (76), possibly by increasing lipid volume. Rapid compression makes the symptoms worse. Avoidance of decompression sickness is the most time-consuming problem. Because decompression from high pressures requires several days, "saturation diving" is frequently used. After 12 to 24 hours at a given pressure, the diver's body has absorbed as much inert gas as it can and is said to be saturated with that gas. Additional time under pressure does not add to decompression time. Thus, the diver can remain for many days at the pressure at which he must work, generally living in a pressure chamber within a ship or surface rig. He is lowered to the work site in a diving bell, which can be detached from the larger chamber. When water pressure equals the gas pressure within the bell, the hatch in the floor is opened and the diver enters the water. When the job is finished the diver is decompressed in the larger chamber at a rate of approximately 100 feet of seawater pressure per day. Faster methods of decompression are sought continually. Increasing the Po 2 of the inspired gas speeds the loss of inert gas from the body, but is limited by pulmonary 0 2 toxicity. Inspired Po 2 that is to be maintained for several days generally does not exceed 0.5 atmosphere. Helium, N 2 , or any mixture of inert gases can cause decompression sickness. However, differences in solubility and diffusivity between gases can sometimes be used to advantage. During decompression from a dive in which helium was breathed, the inert gas can be changed to N 2 as the surface is approached. After the change, helium leaves the body more rapidly than N 2 enters it, and the total inert gas load is decreased. Decompression time can thus be shortened (77). What is the ultimate depth limit for divers?
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The answer is unknown and research continues. Humans have worked within a chamber at a pressure equivalent to 2,001 feet (61 ATA) (78). It has been suggested that alveolar ventilation may be the limiting factor. Gases become more dense when compressed, and concomitantly, resistance to flow within airways increases. The ability to perform moderate exercise is required under water, and increased ventilation is therefore necessary. One group of persons in a dry chamber was able to exercise at heavy work loads while breathing a neon-helium-0 2 mixture with a density of 25 g per liter (79). This density is approximately 22 times that of air at sea level and is equivalent to that of a helium-0 2 mixture at 5,000 feet of seawater. In contrast, persons exercising under water within a wet chamber while breathing a less dense gas mixture (helium-0 2 , 7.3 g per liter) were forced to stop exercise at lighter work loads because of severe dyspnea (80). The differences may be due to factors related to the underwater versus dry pressure environment. As gas density increases, diffusion of one gas through another (binary diffusion) becomes slower. It has been suggested that diffusion of 0 2 or C 0 2 through the layer of unmixed gas within the alveoli might be impaired sufficiently, increasing stratified inhomogeneity, to create problems in gas exchange at great depths (81, 82). This effect may be opposed, at least initially, by increased intrapulmonary gas mixing or by improved ventilation/perfusion matching (83) as gas density increases. If humans could breathe liquid rather than gas, many of the problems associated with diving, including decompression requirements, would be eliminated. Anesthetized dogs have been ventilated successfully with a fluorocarbon liquid for one hour (84). The solubility of 0 2 and CO a in this liquid is sufficiently high to support the dogs' resting respiratory needs. In humans, however, maximal ventilation with a liquid has been estimated at 4 liter per min (85). This would apply even if ventilation were assisted externally because airways would collapse during expiration. Given so small a ventilatory limit, the quantity of gas transported by a volume of liquid must be large. Sufficient 0 2 could be dissolved in fluorocarbon liquid by exposing it to 0 2 under hyperbaric conditions. However, at present, insufficient C 0 2 can be dissolved in the liquid at Pco 2 values compatible with life to support human respiration during exercise or even at rest. If such problems were solved, the ultimate depth limit would probably be determined by
hydrostatic pressure. Many biologic processes are affected adversely by altered pressures (86). Whales are believed to dive to 3,000 feet. However, when liquid-breathing mice are subjected to a pressure equal to 5,400 feet of seawater (166 atmospheres), they stop breathing (87). Humans' hydrostatic pressure limit could well be within such a range. Selection of Divers: Examination and Physical Standards*
The type of diving planned and the diving background of the candidate must be considered (28, 88-93). In general, standards are more strict for a beginning student than for experienced divers. Some conditions (e.g., subpleural blebs or aircontaining pulmonary cysts) are clearly disqualifying for all diving. It may be seen, however, that commercial and naval diving standards are more rigid than those for a sport diver who can select the conditions and timing of his pleasure dives. For commercial divers, the legal liability of a diving school or diving company and the relative remoteness of most commercial diving operations—in time as well as distance—from definitive medical care facilities are additional considerations. A diver in saturation at 1,000 fsw in a chamber may require 6 to 10 days of decompression before evacuation to a hospital intensive care unit. Even after an ill or injured diver has been decompressed, adverse weather conditions can halt helicopter operations or preclude safe transfer at sea to rescue vessels for days at a time. Freedom from musculoskeletal or other disabilities that impair efficiency or job longevity is an important consideration in commercial diving. Skin conditions that might be insignificant in sport divers (e.g., chronic furunculosis) would be disqualifying for scientific or commercial saturation diving. Conditions that could cause alteration of consciousness underwater (e.g., seizure disorders, insulin-dependept diabetes mellitus, and cardiac arrhythmias) are always disqualifying for any type of diving. Responsibility to other divers is a consideration. A diver may be willing to take a calculated risk with regard to his own safety, but if an acci* This section is reprinted from Davis, J. C, Kindwall, E. P., and Youngblood, D. A.: Selection of divers: Examination and physical standards, in Weekly Update: Hyperbaric and Undersea Medicine, Jefferson ,C. Davis, ed., Biomedia Inc., Princeton, 1978, pp. 1-7. Reprinted by permission.
DIVING MEDICINE
dent occurred, other divers could be injured or killed in rescue attempts. T h e decisions of the examining physician must include this possibility and not be clouded by the candidate's willingness to take a chance. With the infinite array of borderline decisions that must be considered, the examining physician must know the diving environment. T h e best way to acquire this knowledge is for the physician to be a diver. Physical Standards Specific physical standards have been established and published by various agencies—the U.S. Navy, the Occupational Safety and Health Administration (OSHA), the National Oceanic and Atmospheric Administration (NOAA), scuba certifying organizations, and commercial diving companies.* It is not our intent to review the provisions of these references but rather to draw on our personal experiences to comment on rationale in key areas. Some conditions are obviously always disqualifying for any type of diving, so we will dispense with those first, then move on to the controversial areas. T h e standard disqualifying conditions are the following: (1) Any history of seizure disorder (except febrile convulsions in infancy) or during the period after a head injury when a neurologist believes the patient is at risk for post-traumatic epilepsy. (2) Recurrent or unexplained episodes of syncope, whether cardiovascular or neurogenic. (3) Insulin-dependent diabetes mellitus. T h e risk of an insulin reaction under water is increased by the ever present possibility of the need for sudden bursts of energy expenditure in emergencies or the need for unexpected hard swimming against current. Diabetes mellitus that is well controlled by diet alone might be waived for sport divers. In some regulations, however, diabetes of any degree is a disqualification for diving. (4) Coronary artery disease. Heavy exertion in the water as well as topside work—carrying and donning diving equipment and climbing into boats—must be added to the risk of sudden incapacitation under water. A history of myocardial infarction is always disqualifying in the opinion * Many American commercial divers work in places subject to the regulations of other nations (e.g., United Kingdom, Norway, and Australia), and U.S. physicians certifying such divers "fit to dive" may have to be "approved" to do so by the government of the particular country.
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of most physicians but possible exceptions in sport diving will be discussed subsequently. (5) Sickle-cell disease or trait. Heavy exertion in cold water increases the risk of sickling, and if blood flow were compromised in decompression sickness, the local areas of hypoxia could cause sickling and compound the problem. Moreover, aseptic bone necrosis has been associated with sickle-cell disorders. (6) Middle ear surgery with placement of a prosthesis in the conduction chain. Displacement during pressure changes could cause permanent derangement of the surgical repair. (7) Persistent inability to equalize pressure in the middle ear by the Valsalva or Frenzel maneuvers. Re-examination after correction of a deviated nasal septum, removal of nasal polyps, desensitization in allergk rhinitis, or clearing of acute coryza may remove this disqualification. (8) Meniere's disease. (?) History of pulmonary overpressure accident. Aside from those cases which occur because of panic and a breath-holding ascent or the presence of air-containing pulmonary cysts or blebs, cases have occurred o n normal ascent in which no pulmonary pathology is detectable. T h e potentially fatal consequences of arterial gas embolism make any risk of a recurrence unacceptable. Despite normal results of pulmonary function testing, a candidate cannot be cleared for diving because small areas of local pulmonary gas trapping cannot be detected. These areas may have caused the original event, or, in the case of breath-holding ascent, residual damage may make recurrence more likely. (10) Air-containing pulmonary cysts or blebs are always disqualifying for any type of diving. In this, as well as all forms of barotrauma, the physician should remember that Boyle's law dictates the greatest volume changes in trapped gas at shallow depths. Thus, clearing a patient to do only shallow, compressed-gas diving would be especially dangerous. (11) Significant obstructive pulmonary disease. Minimal pulmonary function values that have been suggested are vital capacity, forced expiratory volume in one second, and maximal voluntary ventilation 75% of predicted. It must be reemphasized, however, that the usual pulmonary function tests cannot detect potentially dangerous local air-trapping areas. (12) Chronic alcoholism. Besides errors in judgment during periods of intoxication or hangover, aseptic bone necrosis is a known concomitant of alcoholism per se. Roentgenographically, it is
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not possible to distinguish this etiology from that of dysbaric osteonecrosis. Conditions in which there is significant disagreement among authorities or in which answers are not based on studies or extensive experience are more difficult. In the following discussion, we will try to summarize both sides of each issue and give our own opinions. Pulmonary Asthma. Because of the increased risk of local air trapping and pulmonary overpressure accidents on ascent with exertion or cold-induced bronchospasm, one recommendation is disqualification for any history of asthma beyond early childhood. At the other extreme are those who believe that the filtered, clean air used in diving should not cause bronchospasm; hence, except during periods of asthmatic attacks, diving can be approved. In our experience, a history of bronchial asthma is disqualifying if there have been any attacks within 2 years, if medication is needed for control, or if bronchospasm has ever been associated with exertion or inhalation of cold air. Pneumothorax. Some authorities advise against diving after any pneumothorax—spontaneous, traumatic, or surgical. They believe the risk of undetectable local air trapping by scarring and adhesive bands is too great. Others argue that with traumatic pneumothorax, chest surgery, or hemopneumothorax, the pleural scarring induced is protective; after a chamber pressure test, experienced divers with normal pulmonary functions and chest roentgenograms may be requalified. Our own view of this most difficult decision revolves around these 2 divergent opinions. Any history of chest surgery or pneumothorax should disqualify a candidate for any type of diving training. There is no need to assume any risk. In the case of an experienced scientific or commercial diver whose livelihood depends on diving, some people recommend the more liberal approach, except in the case of spontaneous pneumothorax with its established high recurrence rate even at sea level. Some regulations, however, strictly forbid diving after any perforating chest injury or open chest surgery. Neurologic Migraine. Many affected people take part in sport diving with no evidence of any effect. We could make a case for disqualification by citing the changes in vascular tone caused by C 0 2 im-
balance and so forth, but in sport diving, we recognize only one significant problem. Severe migraine-intensity headache with scintillating scotomata is seen as decompression sickness or arterial gas embolism symptoms. A migraine attack after diving may require compression therapy to ensure that a case of decompression sickness or gas embolism is not masquerading as a migraine attack. Frankly, we do not see this as a valid contraindication to sport diving. Commercial diving poses a quite different problem, so migraine is totally disqualifying. Whereas the sport diver can easily avoid diving during attacks, unpredictable periods of incapacitation make commercial diving with migraine unacceptable. History of neurologic decompression sickness with residual deficit. This condition is disqualifying. The precise microcirculatory status at the involved site of the spinal cord or brain has not been defined. The possibility that such areas may be less well perfused and susceptible to further decompression insult must be considered. Paraplegia. Paraplegia after traumatic transection of the cord is not a contraindication to sport diving, provided the subject has sufficient pulmonary function to breath-hold to the bottom of a pool. The Participating Pioneer of Sport for the Disabled advises the use of a buddy, however, to guard the trailing legs against injury, particularly over coral. Psychiatric. Psychiatric considerations are complex. However, one criterion is whether or not you would trust the candidate with your life. Cardiovascular Myocardial infarction. A history of myocardial infarction is an absolute disqualification for further diving under most circumstances. A possible exception has been suggested in the case of an experienced sport scuba diver who will not accept a blanket disqualification. If the patient is more than one year postinfarction, has no angina or arrhythmias, has normal exercise tolerance, and is re-evaluated by a cardiologist at 6month intervals, some authorities have reluctantly agreed to permit such a patient to return to sport diving after the patient fully understands the risk. Both the patient and fellow divers must understand the risk of drowning due to a recurrence under water. Hypertension. Diving itself has no effect on hypertension, but good medical practice requires drug control at some point. If more than a mild diuretic and dietary and weight controls is re-
DIVING MEDICINE
quired in the form of antihypertensive drugs, diving must be discontinued. Vision In commercial diving, the established standards for acuity correctable to 20/20 and normal color vision are for topside and chamber work. Most underwater work is in such low visibility that most tasks are performed mainly by touch. In fact, one current study has demonstrated an advantage to blind divers doing mechanical underwater tasks in zero-visibility water. In sport diving, corrective lenses can be mounted in scuba face masks, or contact lenses can be worn. Soft contact lenses are permissible. Musculoskeletal For commercial diving, there is great sensitivity to the need to reject all candidates with conditions that might predispose to aseptic bone necrosis. Besides alcoholism and sickle-cell disorders, a major disqualifying factor is a history of systemic corticosteroid administration for a prolonged period. It is not known whether the steroids themselves or the underlying disorder (e.g., lupus) represent the cause of the increased risk of aseptic necrosis. Jones (90) has pointed out, however, that only patients who have received the steroid equivalent of 500 mg of prednisone appear to be at increased risk because of steroids. Otolaryngology Hearing acuity. Hearing acuity is of no concern in sport diving. In commercial diving, however, it is vital to understand communications from topside. An on-the-job test may be required to make this determination despite audiometric findings. Labyrinthine window rupture after successful repair. Opinions are divided on this condition because our experience base is so small. Perforation of the tympanic membrane. Until fully healed, this condition is disqualifying for scuba diving. An exception might be an experienced helmet diver, caisson worker, or hyperbaric chamber worker whose tympanic membrane is not exposed to water. Temporary Disqualifications Upper or lower respiratory infection. Upper or lower respiratory infection that causes inability to equalize pressure in the ears, sinuses, or lungs due to mucous plugs or bronchospasm is a temporary disqualification.
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Pregnancy. Studies in animals have shown significant species variation in the susceptibility for bubble formation in fetal circulation. Much more experimental work will be required before we can exclude the risk of intra- or extravascular gas separation in the fetus during decompression from a dive that is safe for the mother. Recent fractures or sprains. Recent fractures or sprains that interfere with local tissue perfusion for normal inert gas uptake and elimination are disqualifies. Some studies have shown an increased risk of bends at such sites. Drugs. Besides the obvious dangers of diving under the influence of alcohol or psychotropic drugs, prescribed medications must be considered. In general, it is not only the side effects of the drug with the unknown potentiating effect of nitrogen narcosis that represent hazards, but also the underlying disorder requiring medication. Even acute coryza requiring antihistamines or decongestants may not only cause difficulty equalizing ears and sinuses, but may represent a risk because of distraction. Tranquilizers not only dull alertness, but if anxiety is of such a degree to require their use, the patient should not dive. Inguinal hernia. Until successfully repaired, inguinal hernia provides the possibility of trapped gastrointestinal gas expansion and strangulation on ascent. Furthermore, various phases of all types of diving require lifting and other forms of exertion. Physical fitness. Most commercial diving requires adequate strength and endurance to perform heavy manual labor. Sport scuba diving is deceptively easy—until an emergency occurs or unexpected currents require long, hard swims in heavy surface action or against a current. The sport diver should be capable of such activity before embarking on any dive. The high N 2 content and poor perfusion of adipose tissue predispose the truly obese person to decompression sickness, besides having an effect on endurance. Skin-fold measurements below the scapula and over the triceps, or body composition studies, are a better guide to disqualifying obesity than height-weight tables. Increased skin-fold thickness in other areas (e.g., abdomen) does not seem to be correlated with an increased risk of decompression sickness. Examination Required The agency or company to which the diver is applying will provide a form calling for specific tests. In general, an examination should be adequate to discover any of the factors discussed.
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For any form of diving, the m i n i m u m components of an e x a m i n a t i o n are the following: (i) a history a n d review of systems, (2) a complete physical e x a m i n a t i o n with emphasis o n the otorhinolaryngeal, p u l m o n a r y , a n d cardiovascular systems, (3) inspiratory chest roentgenograms (posteroanterior a n d lateral), (4) baseline electrocardiogram (desirable for all applicants a n d m a n d a t o r y for those m o r e t h a n 40 years of age), stress electrocardiography a n d special studies as indicated, (5) complete neurologic e x a m i n a t i o n to establish a baseline in case of decompression sickness or gas embolism, (6) complete blood count, urinalysis, serology, a n d sickle-cell studies in susceptible p o p u l a t i o n s .
Further Reading I n t r o d u c t o r y books i n t e n d e d for the practicing physician include Diving Medicine, R. H . Strauss, ed. (94); Diving and Subaquatic Medicine, by C. E d m o n d s , C. Lowry, a n d J. P e n n e father (95); and Underwater Medicine, by S. Miles a n d D . E. Mackay (96). A m o r e complete, research-oriented text is The Physiology and Medicine of Diving, P. B. B e n n e t t a n d D. H . Elliott, eds. (97). Diving techniques are described in detail in the U.S. Navy Diving Manual (28) a n d t h e NO A A Diving Manual (93). A book popularly used in t h e t r a i n i n g of recreational divers is The New Science of Skin and Scuba Diving (98). Acknowledgment T h e writer wishes to thank the following persons for reviewing and commenting on this paper: Albert B. Craig, Jr., M.D., Jefferson C. Davis, M.D., Eric P. Kindwall, M.D., Herbert A. Saltzman, M.D., and Michael E. Whitcomb, M.D.
References 1. Egstrom, G. H.: U.C.L.A. Diving Safety Research Program, Underwater Kinesiology Laboratory, University of California, Los Angeles. Personal communication, 1979. 2. Kindwall, E. P.: A short history of diving and diving medicine, in Diving Medicine, R. H. Strauss, ed., Grune and Stratton, New York, 1976, p.l. 3. Kety, S. S.: T h e cerebral circulation, in Handbook of Physiology, vol. 3, J. Field, ed., American Physiology Society, Washington, D. C , 1960, p. 1751. 4. Ohta, Y., Song, S. H., Groom, A. C , and Farhi, L. E.: Is inert gas washout from the tissues limited by diffusion?, J Appl Physiol, 1978, 45, 903.
5. Apfel, R. E.: T h e tensile strength of liquids, Sci Am, 1972,227,58. 6. Yount, D. E., and Kunkle, T . D.: Gas nucleation in the vicinity of solid hydrophobic spheres, J Appl Physics, 1975, 46, 4484. 7. Evans, A., and Walder, D. N.: Significance of gas micronuclei in the aetiology of decompression sickness, Nature, 1969, 222,251. 8. Vann, R. D., Grimstad, J. J., Nielsen, C. H., and Carey, B. A.: T h e rat as a decompression model: Evidence for pre-existing gaseous micronuclei (abstract), Undersea Biomed Res, 1978, 5,25. 9. Sirotyuk, M. G.: Stabilization of gas bubbles in water, Soviet Physics-Acoustics, 1970,16,237. 10. Yount, D. E., Kunkle, T. D., D'Arrigo, J. S., Ingle, F. W., Yeung, C. M., and Beckman, E. L.: Stabilization of gas cavitation nuclei by surface active compounds, Aviat Space Environ Med, 1977,^,185. 11. Hills, B. A.: Decompression sickness: A study of cavitation at the liquid-liquid interface. Aerosp Med, 1967,35,814. 12. Harvey, E. N., Barnes, D. K., McElroy, W. D., Whiteley, A. H., Pease, D. C , and Cooper, K. W.: Bubble formation in animals, J Cell Physiol, 1944, 24, 1, 23, 117. T h e effect of mechanical disturbance on bubble formation in single cells and tissues after saturation with extra high gas pressures, J Cell Physiol, 1946, 28, 325. 13. Smith, K. H., and Spencer, M. P.: Doppler indices of decompression sickness: Their evaluation and use, Aerosp Med, 1970, 41, 1396. 14. Neuman, T . S., Hall, D. A., and Linaweaver, P. G., Jr.: Gas phase separation during decompression in man: Ultrasound monitoring, Undersea Biomed Res, 1976,3,121. 15. Philip, R. B.: A review of blood changes associated with compression-decompression: Relationship to decompression sickness, Undersea Biomed Res, 1974, i , 117. 16. Kylstra, J. A., Longmuir, I. S., and Grace, M.: Dysbarism: Osmosis caused by dissolved gas?, Science, 1968,161,289. 17. Chryssanthou, C. P.: Humoral factors in the pathogenesis of decompression sickness (DS), in DCIEM Conference Proceedings, No. 73-CP-960, K. N. Ackles, ed., Department of National Defense, Downsview, Ontario, Canada, 1973, p. 165. 18. Erde, A. E., and Edmonds, C : Decompression sickness: A clinical series, J Occup Med, 1975, 17, 324. 19. Haymaker, W., and Johnston, A. D.: Pathology of decompression sickness, Milit Med, 1955, 117, 285. 20. Palmer, A. C , Blakemore, W. F., Payne, J. E., and Sillence, A.: Decompression sickness in the goat: Nature of brain and spinal cord lesions at 48 hours, Undersea Biomed Res, 1978, 5, 275. 21. Bove, A. A., Hallenbeck, J. M., and Elliott,
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D. H.: Circulatory responses to venous air embolism and decompression sickness in dogs, Undersea Biomed Res, 1974,1, 207. Strauss, R. H., and Prockop, L. D.: Decompression sickness among scuba divers, JAMA, 1973, 223, 637. Kawashima, M., Hayashi, K., Torisu, T., and Kitano, M.: Histopathology of the early stage of osteonecrosis in divers, Undersea Biomed Res, 1977, 4,409. Hunter, W. L., Biersner, R. J., Sphar, R. L., and Harvey, C. A.: Aseptic bone necrosis among U.S. Navy divers: Survey of 934 nonrandomly selected personnel, Undersea Biomed Res, 1978, 5,25. Wade, C. E., Hayashi, E. M., Cashman, T. M., and Beckman, E. L.: Incidence of dysbaric osteonecrosis in Hawaii's diving fishermen, Undersea Biomed Res, 1978,5,137. Spencer, M. P., and Oyama, Y.: Pulmonary capacity for dissipation of venous gas emboli, Aerosp Med, 1971,42, 822. Behnke, A. R.: Decompression sickness, Milit Med, 1955,117,257. U.S. Navy Diving Manual, Department of the Navy, Washington, D. C , 1973. Boycott, A. E., Damant, G. C. C , and Haldane, J. S.: The prevention of compressed-air illness, J Hyg (Camb), 1908,8,342. Hills, B. A.: Biophysical aspects of decompression, in The Physiology and Medicine of Diving and Compressed Air Work, P. B. Bennett and D. H. Elliott, ed., Bailliere Tindall, London, 1975, pp. 366-391. Behnke, A. R.: Decompression sickness: Advances and interpretations, Aerosp Med, 1971, 42,255. Buhlmann, A. A., Schibli, R., and Gehring, H.: Experimentelle Untersuchungen iiber die Dekompression nach Tauchgangen in Bergseen bei vermindertem Luftdruck, Schweiz Med Wochenschr, 1973,103, 378. Boni, M., Schibli, R., Nussberger, P., and Buhlmann, A. A.: Diving at diminished atmospheric pressure: Air-decompression tables for different altitudes, Undersea Biomed Res, 1976,3,189. Edel, P. O., Carroll, J. J., Honaker, R. W., and Beckman, E. L.: Interval at sea-level pressure required to prevent decompression sickness in humans who fly in commercial aircraft after diving, Aerosp Med, 1969,40,1105. Fife, W. P., Simmang, C , and Kitzman, J. V.: Susceptibility of fetal sheep to acute decompression sickness, Undersea Biomed Res, 1978, 5,287. Pressure. Newsletter of the Undersea Medical Society, Inc., Bethesda, December 1978, p. 1. Lanphier, E. H.: Use of nitrogen-oxygen mixtures in diving, in Proceedings of the First Symposium of Underwater Physiology, L. G. Goff,
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ed., National Academy of Sciences-National Research Council, Washington, D. C , 1955, p. 74. Wood, J. D.: Oxygen toxicity, in The Physiology and Medicine of Diving and Compressed Air Work, P. B. Bennett and D. H. Elliott, ed., Bailliere Tindall, London, 1975, p. 166. Clark, J. M., and Lambertsen, C. J.: Pulmonary oxygen toxicity: A review, Pharmacol Rev, 1971, 23, 37. Wolfe, W. G., and DeVries, W. C : Oxygen toxicity, Annu Rev Med, 1975,26,203. Hendricks, P. L., Hall, D. A., Hunter, W. L., Jr., and Haley, P. J.: Extension of pulmonary 0 2 tolerance in man at 2 ATA by intermittent 0 2 exposure, J Appl Physiol, 1977, 42, 593. Cousteau, J. Y.: The Silent World, Harper and Row, New York, 1953, p. 34. Miller, K. W., Paton, W. D. M., Smith, R. A., and Smith, E. B.: The pressure reversal of general anesthesia and the critical volume hypothesis, Mol Pharmacol, 1973,9,131. Bennett, P. B.: Inert gas narcosis, in The Physiology and Medicine of Diving and Compressed Air Work, P. B. Bennett and D. H. Elliott, ed., Bailliere Tindall, London, 1975, p. 207. Farmer, J. C , and Thomas, W. G.: Ear and sinus problems in diving, in Diving Medicine, R. H. Strauss, ed., Grune aaad Stratton, New York, 1976, p.109. Edmonds, C , Freeman, P., and Tonkin, J.: Fistula of the round window in diving, Trans Am Acad Ophthalmol Otolaryngol, 1974, 78, 444. Freeman, P., Tonkin, J., and Edmonds, C: Rupture of the round window membrane in inner ear barotrauma, Arch Otolaryngol, 1974, 99, 437. Tjernstrom, O.: Further studies on alternobaric vertigo, Acta Otolaryngol (Stockh), 1974, 78, 221. Tjernstrom, O.: Middle ear mechanics and alternobaric vertigo, Acta Otolaryngol (Stockh), 1974,78,376. Macklin, C. C : Pneumothorax with massive collapse from experimental local over-inflation of the lung substance, Can Med Assoc J, 1937, 36, 414. Macklin, C. C : Transport of air along sheaths of pulmonic blood vessels from alveoli to mediastinum, Arch Intern Med, 1939, 64,913. James, R. E.: Extra-alveolar air resulting from submarine escape training: A post-training roentgenographic survey of 170 submariners, Naval Submarine Med Res Lab Report No. 550, 1968. Schaefer, K. E., McNulty, W. P., Jr., Carey, C , and Liebow, A. A.: Mechanisms in development of interstitial emphysema and air embolism on decompression from depth, J Appl Physiol, 1958, 13, 15. Waite, C. L., Mazzone, W. F., Greenwood, M. E., and Larsen, R. T.: Dysbaric cerebral air embolism, in Underwater Physiology, C. J. Lambertsen, ed., Williams and Wilkins, Baltimore, 1967,
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termining the limits of depths in breathhold p.205. diving, Science, 1968,162, 1020. 55. Craig, A. B., Jr.: Summary of 58 cases of loss of consciousness during underwater swimming and 72. Craig, A. B., Jr.: Depth limits of breath hold diving (an example of Fennology), Respir Phydiving, Med Sci Sports, 1976,8,171. siol, 1968,5, 14. 56. Craig, A. B., Jr.: Causes of loss of consciousness during underwater swimming, J Appl Physiol, 73. Strauss, M. B., and Wright, P. W.: Thoracic squeeze diving casualty, Aerosp Med, 1971, 42, 1961,1^,583. 673. 57. Lanphier, E. H., and Rahn, H.: Alveolar gas 74. Morrow, C. T.: Speech in deep-submergence atexchange during breath holding with air, J mospheres, J Acoust Soc Am, 1971, 50, 715. Appl Physiol, 1963,18, 478. 58. Craig, A. B., Jr., and Harley, A. D.: Alveolar gas 75. Underwater communications in The Underwater Handbook, C. W. Shilling, M. Werts, and exchange during breath-hold dives, J Appl PhyN. Schandelmeier, ed., Plenum Press, New York, siol, 1968, 24,182. 1976, p. 811. 59. Mithoefer, J. C : T h e breaking point of breath holding, in Physiology of Breath-Hold Diving 76. Hunter, W. L., and Bennett, P.B.: T h e causes, mechanisms and prevention of the high pressure and the Ama of Japan, H. Rahn and R. Yokonervous syndrome, Undersea Biomed Res, 1974, yama, ed., National Academy of Sciences-National Research Council, Washington, D. C , 1,1. 1965, pp. 195-205. 77. Keller, H., and Buhlmann, A. A.: Deep diving 60. Bridge, E. M., Livingston, S., and Tietze, C : and short decompression by breathing mixed Breath-holding spells, J Pediatr, 1943, 23, 539. gases, J Appl Physiol, 1965, 20,1267. 61. Lanphier, E. H., and Rahn, H.: Alveolar gas 78. Fructus, X., Agarate, C , Naquet, R., and Rosexchange during breath-hold diving, J Appl tain, J. C : Postponing the "high pressure nerPhysiol, 1963,18,471. vous syndrome" to 1640 feet and beyond, in Underwater Physiology V, C. J. Lambertsen, ed., 62. Kooyman, G. L., and Campbell, W. B.: Heart Federation of American Societies for Experimenrates in freely diving Weddell seals, Comp Biotal Biology, Bethesda, 1976, pp. 21-33. chem Physiol, 1972,43, 31. 63. Scholander, P. F.: T h e master switch of life, Sci 79. Lambertsen, C. J., Gelfand, R., Peterson, R., Strauss, R., Wright, W. B., Dickson, J. G., Puglia, Am, December 1963, p. 92. C , and Hamilton, R. W.: Human tolerance to 64. Eisner, R., and Scholander, P. F.: Circulatory He, Ne and N 2 at respiratory gas densities adaptations to diving in animals and man, in equivalent to H e - 0 2 breathing at depths of Physiology of Breath-Hold Diving and the Ama 1200, 3000, 4000 and 5000 feet of sea water (preof Japan, H. Rahn, ed., National Academy of dictive studies III), Aviat Space Environ Med, Sciences-National Research Council, Washing1977,^,843. ton, D. C , 1965, pp. 281-294. 65. Song, S. H., Lee, W. K., Chung, Y. A., and Hong, 80. Dwyer, J., Saltzman, H. A., and O'Bryan, R.: Maximal physical-work capacity of man at 43.4 S. K.: Mechanism of apneic bradycardia in man, ATA, Undersea Biomed Res, 1977,4, 359. J Appl Physiol, 1969, 27, 323. 66. Heistad, D. D., Abboud, F. M., and Eckstein, 81. Lanphier, E. H.: Interactions of factors limiting performance at high pressures, in Underwater J. W.: Vasoconstrictor response to simulated divPhysiology, C. J. Lambertsen, ed., Williams and ing in man, J Appl Physiol, 1968, 25,542. Wilkins, Baltimore, 1967, p. 375. 67. Olsen, C. R., Fanestil, D. D., and Scholander, P. F.: Some effects of breath holding and apneic 82. Chouteau, J.: Respiratory gas exchange in animals during exposure to extreme ambient presunderwater diving on cardiac rhythm in man, sures, in Underwater Physiology, C. J. LambertJ Appl Physiol, 1962,17,461. sen, ed., Academic Press, New York, 1971, p. 385. 68. Craig, A. B., Jr., and Dvorak, M.: Expiratory reserve volume and vital capacity of the lungs 83. Martin, R. R., Zutter, M., and Anthonisen, N. R.: Pulmonary gas exchange in dogs breathduring immersion in water, J Appl Physiol, ing SF 6 at 4 ATA, J Appl Physiol, 1972, 83, 86. 1915,38,5. 69. Gauer, O. H., and Henry, J. P.: Circulatory 84. Matthews, W. H., Balzer, R. H., Shelburne, J. D., Pratt, P. C , and Kylstra, J. A.: Steady-state basis of fluid volume control, Physiol Rev, 1963, gas exchange in normothermic, anesthetized, 43, 423. liquid-ventilated dogs, Undersea Biomed Res, 70. McCally, M.: Body fluid volumes and the renal 1978,5,341. response to immersion, in Physiology of BreathHold Diving and the Ama of Japan, H. Rahn, 85. Kylstra, J. A.: Liquid breathing, Undersea Bioed., National Academy of Sciences-National Remed Res, 1974,1, 259. search Council, Washington, D. C , 1965. 86. MacDonald, A. G.: Hydrostatic pressure phy71. Schaefer, K. E., Allison, R. D., Dougherty, J. H., siology, in The Physiology and Medicine of DivCarey, C. R., Walker, R., Yost, F., and Parker, ing and Compressed Air Work, P. B. Bennett D: Pulmonary and circulatory adjustments deand D. H. Elliott, ed., Bailliere Tindall, Lon-
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don, 1975, p. 78. 87. Kylstra, J. A., Nantz, R., Crowe, J., Wagner, W., and Saltzman, H. A.: Hydraulic compression of mice to 166 atmopsheres, Science, 1967, 158, 793. 88. Aquadro, C. F.: Examination and selection of personnel for work in underwater environment, J Occup Med, 1965, 7,619. 89. Boettcher, W. M.: Epidemiological and etiological considerations in osteonecrosis, in Dysbarism-related Osteonecrosis, E. L. Beckman and D. H. Elliott, ed., U.S. Government Printing Office, Washington, D. C., 1974, p. 87. 90. Jones, J. P., Jr.: Osteonecrosis associated with metabolic disease and corticosteroid therapy, in Dysbarism-related Osteonecrosis, E. L. Beckman and D. H. Elliott, ed., U.S. Government Printing Office, Washington, D. C., 1974, p. 91. 91. Kindwall, E. P.: Medical aspects of commercial diving and compressed air work, in Occupation-
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al Medicine, C. Zenz, ed., Yearbook Medical Publishers, Chicago, 1975, p. 361. Medical fitness and medical examinations, in British Sub-Aqua Club Diving Manual, British Sub-Aqua Club, London, 1977, p. 46. NOAA Diving Manual, U.S. Government Printing Office, Washington, D. C , 1975. Stauss, R. H., ed.: Diving Medicine, Grune and Stratton, New York, 1976. Edmonds, C , Lowry, C , and Pennefather, J.: Diving and Subaquatic Medicine, 1976, Diving Medical Centre, Mosman, Australia, 1976. Miles, S., and Mackay, D. E.: Underwater Medicine, J. B. Lippincott, Philadelphia, 1976. Bennett, P. B., and Elliott, D. H.: The Physiology and Medicine of Diving and Compressed Air Work, Bailliere Tindall, London, 1975. Empleton, E. B., ed.: The New Science of Skin and Scuba Diving, Association Press, New York, 1975.
Contents
Introduction Physical Principles Decompression Sickness Pathogenesis Clinical Manifestations Spinal Cord and Brain Extremities Pulmonary Other Treatment Prevention Some Hazards of Diving Gases Oxygen Toxicity Nitrogen Narcosis Barotrauma of Descent Barotrauma of Ascent Pulmonary Barotrauma Air Embolism Breath-hold Diving Breath-hold Blackout Diving Reflex Negative Intrapulmonic Pressure Deep Diving (Commercial and Military) Selection of Divers: Examination and Physical Standards Physical Standards Pulmonary 1 From the Pulmonary Disease Division, Department of Medicine, Ohio State University College of Medicine, Columbus, Ohio 43210. 2 Portions of this article were adapted from the writer's chapters, "The Physics of Gases" and "Decompression Sickness," in Strauss, R. H., ed.: Diving Medicine, Grune and Stratton, New York, 1976, and from Strauss, R. H., and Yount, D. E.: Decompression sickness, Am Sci, 1977,65, 598.
Neurologic Cardiovascular Vision Musculoskeletal Otolaryngology Temporary Disqualifications Examination Required Further Reading Introduction
In recent years there has been a marked increase in the number of persons involved in sport and commercial diving. In the United States, more than 200,000 persons are trained each year in the use of scuba (self-contained underwater breathing apparatus) (1). Furthermore, breath-hold diving is used by many persons as a simple means to explore the underwater world. Although the dangers of diving have been popularly associated with great depths, it is important to recognize that both shallow breathhold and scuba diving—even in a swimming pool—present very real risks to the diver. This paper deals primarily with problems associated with diving for pleasure (sport diving). Commercial and military diving are mentioned to illustrate certain principles. The discussion of hyperbaric therapy is limited to problems related to diving. The risks of diving are due largely to the breathing of gases as ambient pressure increases during descent or decreases during ascent in water. Thus, the physician with training in pulmonary medicine is well prepared in a general sense to deal with diving-related problems. This paper will review the various clinical syndromes directly related to diving, with special emphasis on the pathophysiology of these events. Because
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these syndromes are associated with the effects of gases at altered ambient pressures, the physical principles that govern such effects must be reviewed. Physical Principles People normally live at the bottom of a sea of air. The weight of this air exerts a pressure on the body surface that is denned at sea level as 1 atmosphere. Atmospheric pressure decreases relatively slowly with increasing altitude. In Denver, at an altitude of 5,221 feet, ambient pressure is 0.83 atmosphere. Under water, however, small changes in depth result in significant changes in pressure. A resident of Denver can return to 1 atmosphere of pressure by diving 6 feet below the surface of a swimming pool. A column of liquid exerts a pressure that is proportional to its height, density, and the acceleration of gravity. At a depth of 33 feet, seawater exerts an additional pressure of 1 atmosphere on the submerged diver—a total pressure twice that to which he is exposed at sea level. (A list of pressure equivalents is given in table 1.) The tissues of the body are composed primarily of water, which is nearly incompressible and is thus unaffected by pressures within the usual diving range. Gases, however, are compressible. The behavior of gases is well described by the ideal gas law: PV = n R T , where P is absolute pressure, V is volume, n is the number of moles of gas, R is the universal gas constant, and T is the absolute temperature. Several simpler gas laws originate from the ideal gas law and are commonly used under conditions associated with diving, Boyle's law states that at a constant temperature the volume of a given mass of gas is inversely proportional to its pressure. Stated mathematically: PV = K, where K is a constant. Thus, if absolute pressure is doubled, the volume of a mass of gas is halved, TABLE 1 PRESSURE EQUIVALENTS 1 atmosphere
= = = = = =
33 feet 34 feet 2 9 . 9 in 760 m m
of seawater (fsw) of fresh w a t e r Hg Hg
1 4 . 7 p o u n d s p e r s q u a r e i n c h (psi) 1 kg/cm2
DEPTH
GAUGE ABSOLUTE PRESSURE PRESSURE
GAS VOLUME
66 feet
2 atm
3 atm
j . ' y . ' i f Vz vol
99 feet
3 atm
4 atm
| y . ' . ' . l % vol
DENSITY
3 units 4 units
Fig. 1. Gas volume decreases as absolute pressure increases. Gauge pressure is zero at the surface. Thus, gauge pressure equals absolute pressure less one atmosphere (from Strauss, R. H., ed.: Diving Medicine, Grune and Stratton, New York, 1976; used by permission).
Gas volume changes are particularly noticeable near the surface (figure 1). In addition to the pressure and volume changes that effect gas spaces during submersion, there are also changes in the partial pressures of individual gases within these spaces. Dalton's law of partial pressure states: "In a mixture of gases, the pressure exerted by each gas is the same as it would exert if it alone occupied the same volume; and the total pressure is the sum of the partial pressures of the component gases." As ambient pressure increases, the total pressure of a gas mixture increases. As total pressure increases, the partial pressure of each gas within the mixture increases proportionally, although its percentage remains constant. In general, the biologic effects of a gas depend on its partial pressure. This is because both diffusion and the amount of gas dissolved in a solvent are proportional to partial pressure. Thus, supplying the proper amount of 0 2 to tissue depends on the partial pressure of 0 2 and not merely on the total gas pressure or the percentage of 0 2 . C 0 2 and N 2 balance are similarly dependent on the partial pressure of the respective gas. Henry's law states that at a given temperature, the mass of a gas dissolved in a given volume of solvent is proportional to the pressure of the gas with which it is in equilibrium. Thus, as pressure increases during scuba diving, more and more N 2 is dissolved in the body. During ascent, this N 2 comes out of solution and, under certain circumstances, may cause decompression sickness. A person who goes underwater has several choices (figure 2). (1) He can ride in a vessel, the hull of which is designed to withstand hydro-
1003
DIVING MEDICINE
Submarine
Breath-hold Diving
Scuba Diving
1 atm
1 atm
* 1 atm
air seawater
~T ~T ~T 1 atm
5\
99 feet
>
*4 atm*. J
• • • . •t• • 4 atm •
ation becomes more difficult as depth increases. This occurs because more molecules of air must flow through the orifice of the regulator for each breath. Much of the resistance to air flow within the respiratory tract is due to turbulence and is therefore dependent on density. Flow resistance within airways increases as depth and gas density increase, but this effect is insignificant under conditions associated with sport diving. With current regulators, resistance is minimized and large volumes of air can be inspired at considerable depths without the necessity of generating uncomfortably negative inspiratory pressures. Occasionally, during severe exercise, a person's volume demand may exceed his regulator's capacity. A subsequent feeling of dyspnea may contribute to panic. Furthermore, an air tank is exhausted more quickly as depth increases. A gauge indicating tank pressure is generally used by divers so that they do not run out of air under water, a dangerous situation for several reasons. With the behavior of gases in mind, it is easy to understand the pathophysiology of most clinical syndromes associated with diving. These syndromes are discussed in the following sections.
to
Fig. 2. Within a submarine, pressure remains at 1 atmosphere absolute (the pressure at sea level). In breathhold diving, the lungs are compressed, and the gas pressure within them is approximately the same as the surrounding (ambient) pressure. In scuba diving, gas is supplied at ambient pressure so that normal respiration can continue (from Strauss, R. H., ed.: Diving Medicine, Grune and Stratton, New York, 1976; used by permission).
static pressure so that ambient pressure remains at 1 atmosphere. Under these circumstances, there are no volume or pressure changes within the body. (2) He can hold his breath and dive. Gas pressure within the lungs approximates ambient pressure, and the volume within the thorax must decrease proportionately. (3) The diver can submerge while breathing compressed gas from scuba equipment. Under this circumstance, gas pressure within the lung remains close to ambient pressure, but lung volumes remain normal because the person continues to breathe while underwater. A demand regulator releases gas from a tank to the respiratory tract when the mouth pressure decreases to slightly less than ambient pressure during inspiration or as depth increases. Expired gas is released into the water as bubbles. Equipment worn by a scuba diver is shown in figure 3. With certain types of scuba regulators, inspir-
Decompression Sickness Decompression sickness first became a problem in the 1800s when men began working in the compressed-air environment of tunnels and caissons, the closed underwater compartments used in the building of bridge foundations. While caissons and tunnels are being constructed below water level, air is maintained at a pressure slightly greater than that of the water to keep water out. After returning to the surface, early compressed-air workers sometimes noticed steady, boring pains, similar to a toothache, most often in the hip or knee joints. "One pays only on leaving," it was said of such work. The pains Air tank
Snorkel
Wet suit Face mask Swim fins
Regulator
Inflatable vest Weight belt
Fig. 3. Equipment used in scuba diving (after U.S. Navy Diving Manual [28], from Strauss, R. H. ed.: Sports Medicine and Physiology, W. B. Saunders, Philadelphia, 1979; used by permission).
1004
RICHARD H. STRAUSS
started within a few minutes or hours after surfacing and lasted several hours or longer. The afflicted men limped and were said by co-workers to be doing the "Grecian bend," a contortionist posture in walking assumed by fashionable ladies at the time (2). "The bends" and "caisson disease" are loosely synonymous with what we today call decompression sickness. The disease may affect not only the limbs directly, but can also damage the central nervous system. Paraplegia is a particularly serious problem that occurs among sport divers today. Decompression sickness is caused by the formation of gas bubbles in the blood and body tissues when ambient pressure is decreased. T o understand the pathogenesis of this disease, the factors that lead to the accumulation of N 2 in body tissues and the subsequent formation of bubbles must be understood. Gas absorption by the body is a critical factor in decompression sickness. As mentioned previously, the quantity of a given gas dissolved in a tissue is proportional to the partial pressure of that gas within the tissue. As a scuba diver descends from the surface to a depth of 66 feet, the pressure surrounding him increases from one atmosphere absolute (ATA) to 3 ATA, and the partial pressure of N 2 triples. As a result, a gradient exists for the net flow of N 2 from the alveoli to the blood and finally into tissue. After some time at depth, equilibrium will be reached, and all tissues will contain about 3 times as much N 2 as before the dive. The uptake of gas by a tissue is rapid immediately after a pressure increase (figure 4). However, the gradient for transport of gas into tissue decreases as the tissue approaches saturation, so that the uptake of gas decreases exponentially with time. The time required for a tissue to reach equilibrium depends on both the solubility of the gas in the tissue and, generally, the rate at which gas is brought to the tissue by blood. The rate of perfusion of tissues by blood can vary widely. A well-perfused tissue, such as the brain, which reaches equilibrium within minutes (3), is called a "fast" tissue. In contrast, fatty tissue, with poor perfusion and a high solubility for gases such as N 2 , requires longer to reach equilibrium and is known as a "slow" tissue. Diffusion of gas within a tissue is rarely a rate-limiting step (4) because capillaries generally lie so closely together that diffusion distances are small. When ambient pressure is decreased, the loss
>,
>„
1
-
/ 1
/
/
L
/
\
\
\
FAST n SSUE
1 1 ,-'' 1 /
LOW
>o-
\
INITIAL
TISSUE
DECOMPRESSION
COMPRESSION
TIME
Fig. 4. When ambient pressure is increased during breathing of compressed air, the pressure of the inert gas (N2) in the alveoli changes immediately. The pressure of N2 in various tissues increases gradually, however, at a rate that becmes slower as saturation is approached. The initial compression (Pj-P2) results in supersaturation of the "fast" tissue, which is intended to cause rapid loss of gas but, it is hoped, no significant bubble formation. The "slow" tissue continues to absorb gas, but at a slower rate (from Strauss, R. H., ed.: Diving Medicine, Grune and Stratton, New York, 1976; used by permission).
of gas from tissue is believed to be analogous to gas uptake as long as bubbles do not form. If bubbles are present within the tissue, however, some gas will diffuse into the bubbles, instead of leaving the body. Decompression is thus more efficient if bubble formation is avoided in the first place. When the cork is removed from a bottle of champagne, bubbles appear. During storage, the liquid is in equilibrium with the gas at its surface (mainly C0 2 ) and is saturated with this gas at a pressure greater than 1 atmosphere. When the bottle is uncorked, the ambient pressure is suddenly decreased. Gas pressure within the liquid does not decrease immediately, because equilibration of gas by diffusion through the surface of the unstirred liquid would require days. The champagne suddenly becomes supersaturated—that is, the surrounding pressure is less than the total gas pressure within the liquid. Supersaturation is a necessary condition for the type of bubble formation and growth discussed here. The formation of bubbles in divers on ascent is somewhat analogous to the formation of bubbles in champagne when the bottle is uncorked. For a bubble to grow from "nothing" to a finite size, it must go through 2 distinct phases: (1) the formation of a small bubble where noth-
DIVING MEDICINE
ing was previously observable, and (2) the growth of a small bubble into a large one. The mechanism of bubble formation in animals is poorly understood. It appears that some sort of nuclei for bubble formation exist in animals, because bubbles begin to form when the supersaturation pressure is in the range of a few atmospheres or less, as in decompression. In principle, bubbles can form without nuclei, but in pure water this is believed to require a supersaturation pressure on the order of 1,000 atmospheres (5, 6)—almost the maximal depth of the sea. Work with transparent shrimp and with rats suggests that animals normally have gas nuclei that can be crushed partially by increased hydrostatic pressure, thereby decreasing bubble formation on subsequent decompression (7, 8). A nucleus is different from a small bubble because the nucleus is stable. Surface tension (7) tends to make a bubble smaller. Laplace's law states that pressure within a bubble due to surface tension (P7) is given by the equation:
where r is the radius of the bubble. For large bubbles, P7 is negligible; however, as a bubble becomes smaller, P7 increases, which tends to force gas into solution and make the bubble collapse. Indeed, it is difficult to imagine how a very small bubble can exist at all. The mechanism by which a nucleus is stabilized is not entirely clear. One hypothesis is that certain molecules that resist the surface tension become increasingly concentrated at the surface of a bubble as it becomes smaller (9, 10). Eventually this produces a small, stable pocket of gas, then called a nucleus. As an alternative to the existence of nuclei, it has been suggested that bubbles may form readily at aqueous-lipid interfaces within animals due to decreased surface tension at such locations (11). For an existing bubble to grow, the total gas pressure within the bubble (P bubble ) must be greater than the pressures tending to constrict or crush it. Crushing pressures include those due to surface tension (P7) and to ambient pressure (P a m b i e n t ). In addition, because of its structure and osmotic balance, tissue tends to resist being deformed and thus causes tissue pressure (PtiSSue)The necessary condition for bubble growth is then: ^bubble > "ambient ~*~ ^tissue "^ *Vm
This condition can be satisfied if the tissue is
1005
sufficiently supersaturated and if gas is free to diffuse from the tissue into the bubble. Conversely, bubbles will shrink if the preceding inequality is reversed. Gas within a bubble tends to equilibrate with gas in the surrounding tissue. Therefore, the necessary condition for bubble growth after decompression from a dive using compressed air can be rewritten in terms of the gas partial pressures within the tissue: PN 2 + Po 2 + Pco 2 + PH 2 O > P a m b i e n t + P tigsue + P 7 . During ascent, supersaturation must be controlled so that bubbles do not form and grow sufficiently to cause decompression sickness. After several decades of experience and research, there are now guidelines as to how abrupt a decrease in pressure causes the disease. Thus, divers and others exposed to increased pressure can usually avoid this danger by decreasing the pressure gradually. Prevention of decompression sickness is discussed later in this paper. Pathogenesis In severe cases of decompression sickness, in which the diver or laboratory animal has died, bubbles have been reported everywhere: within blood vessels, presumably having impeded circulation; extravascularly, distorting tissues; and possibly within cells (12). In the more common, nonlethal form of decompression sickness, the location of bubbles is less clear. After some dives, bubbles can be detected in the venous circulation because they reflect ultrasonic signals of a Doppler flow meter (13), even though decompression sickness has not occurred. There appears to be a correlation between increasing numbers of bubbles and the severity of some types of decompression sickness (14). Numerous changes in the blood have been noted after decompression (15): clumping of red cells, formation of rouleaux, sludging of blood in small vessels, and a decrease in the number of platelets. Hematologic changes are believed to be largely a result of the gas-blood interface of bubbles. Hemoconcentration occurs, possibly from increased capillary permeability. In addition, the osmotic activity of dissolved gases has been suggested as a mechanism for fluid shifts (16). Decompression sickness is associated with release into blood of a "Smooth Muscle Acting Factor," which causes constriction of blood vessels and bronchi and potentiates bradykinin (17). Numerous other biologically active sub-
1006
RICHARD H. STRAUSS
stances associated with stress have been observed in decompression sickness. Clinical Manifestations Symptoms may appear during or immediately after decompression or, more usually, after a delay of minutes to hours. The delay may be due in part to the growth of bubbles and, perhaps more important, to the gradual progression of pathologic processes, such as swelling, after the original damage to tissue by bubbles. Spinal Cord and Brain Central nervous system "bends" is an especially serious types of decompression sickness because it can cause permanent nerve damage, such as paraplegia. Approximately one-half of 100 cases of decompression sickness treated recently in Hawaii involved the central nervous system (18); almost all of the victims were recreational divers. Neurologic lesions often involve the spinal cord, particularly the thoracic segments, but also the upper lumbar and lower cervical segments. The white matter of the cord, rather than the gray matter, is generally affected (19, 20). The primary cause of damage appears to be evolution of bubbles within the venous vertebral plexus, leading to stasis and obstruction of blood (21). Early lesions consist of small hemorrhages followed by degeneration of nerve fibers (19). It is important that the diver and his physician recognize the early manifestations of spinal cord decompression sickness, because immediate treatment in a recompression chamber may result in recovery, whereas delay significantly decreases the chances of a good outcome. Soon after surfacing, the diver's first symptom may be transient back pain with radiation to the abdomen, which he often attributes to the lifting of air tanks. Therefore, the first manifestation to catch the diver's attention is usually a feeling of "pins and needles" in the legs—that is, paresthesia and hypesthesia. Next, the legs become weak and the walk unsteady; the diver often cannot initiate urination, although his bladder may be distended. Finally, paralysis below the waist or neck may ensue (22). The condition appears to be similar to that of a spinal fracture with cord injury; however, the diver is more fortunate because with prompt treatment his chances for recovery are much better. Brain damage is less frequent than spinal cord damage. Manifestations include visual disturbances, hemiplegia, and unconsciousness. Vertigo
("the staggers") may result from damage to the brain or inner ear. The maximal rate at which a diver can ascend safely to the surface or to a decompression stop is believed to be 60 feet per min. Injury to the central nervous system is often associated with marginally adequate decompression and an unusually rapid rate of ascent in an emergency situation, such as running out of air during a dive. When decompression procedures have been violated badly, symptoms may appear immediately and progress to paralysis within minutes. Even when standard practices are followed, decompression sickness occurs occasionally and may progress during several hours. Extremities Limb pain is another common symptom of decompression sickness. Although pain may occur at many locations in the extremities, shoulder and elbow joints are the most frequent sites in divers, as contrasted to hip and knee joints in tunnel workers. The pain is usually steady, but occasionally may be throbbing. It reaches a peak in minutes or hours and often subsides spontaneously several hours later, even if left untreated. The mechanism of pain production is unclear. T h e arm or leg usually looks completely normal, there is little tenderness, and moderate joint motion is well tolerated. Treatment by recompression helps to relieve the pain and may decrease subsequent tissue damage. Pain in the extremities may also result from local injury unnoticed in the excitement of the dive. Such injuries bear characteristics of trauma, e.g. swelling, discoloration, tenderness, and exacerbation of pain on motion. Osteonecrosis is probably a late consequence of inadequate decompression and was much more frequent in the past than at present. Patches of bone die but may not become visible on roentgenograms for months or years after diving. Often the person has no symptoms. However, if the necrotic patches of bone are near a joint surface such as the shoulder or hip, the joint may collapse and cause crippling (23-25). Pulmonary Some of the bubbles formed in the vasculature of systemic tissues are carried by venous blood to the lungs. Most of these bubbles lodge in small pulmonary vessels, although a fraction may reach the systemic arterial circulation (26). In most cases of decompression sickness, no pulmonary
1007
DIVING MEDICINE
manifestations appear, even though bubbles may be detected in the venous circulation. The degree of pulmonary embolization by gas necessary to cause symptoms is unknown; release of vasoactive substances and reflex mechanisms probably contribute to pathogenesis. The pulmonary syndrome is called "the chokes" by divers and is characterized by substernal chest pain, dyspnea, and cough. Symptoms are aggravated by deep inspiration and by smoking (27). In animals, clinical signs of the syndrome are accompanied by increased pulmonary arterial pressure and hypoxemia (21). Pulmonary edema may also occur. The chokes is an extremely serious form of decompression sickness. Without recompression, circulatory collapse and death may follow, whereas recompression results in complete relief within minutes in most cases. Other "Skin bends" is sometimes seen in scuba divers, but more often follows simulated dives in chambers when the skin is in direct contract with the compressed gas. The affected skin, usually on the back or elsewhere on the trunk, itches and burns. If these are the only manifestations, skin bends is frequently left untreated or is treated by breathing 0 2 at 1 atmosphere. If discoloration (marbling) appears, chamber treatment is advisable. Fatigue much greater than that expected from the work performed sometimes follows marginal or inadequate decompression. It may or may not be associated with other signs of decompression sickness. Treatment The standard treatment for decompression sickness is to place the victim in a hyperbaric (high-pressure) chamber and increase the air pressure to 2.8 ATA (equivalent to 60 feet of seawater) over one or 2 min (28). The patient then breathes pure 0 2 intermittently by mask (figure 5). The increased ambient pressure causes bubbles to diminish in size. Breathing 0 2 , rather than air, increases the gradient for diffusion of inert gas from bubbles and tissue out of the body. Oxygenation of tissues is also increased. However, because increased partial pressures of 0 2 can cause 0 2 toxicity, in particular, convulsions, air is breathed intermittently for periods of 5 min or more. Ancillary treatment may in-
0
1
2 TIME
3
4
5
(hours)
Fig. 5. Victims of decompression sickness are placed in a pressurized chamber where the breathe pure 0 2 . To avoid oxygen toxicity, air is breathed for intermittent periods of 5 min or longer, according to the U.S. Navy treatment schedule shown (28) (from Strauss, R. H., and Prockop, L. D.: Decompression sickness among scuba divers, JAMA, 1973, 223, 637; used by permission).
clude corticosteroids to decrease nervous tissue edema, and plasma expanders and intravenous fluids to increase circulating blood volume. Treatment can be dramatically effective if it is begun early enough, when symptoms are beginning to develop and tissue damage is mild. However, as time progresses, tissue damage increases, and even if all bubbles disappear with hyperbaric treatment, healing requires days or weeks and may not be complete. Decompression sickness that involves the central nervous system is a medical emergency. The victim should be given 0 2 continuously by mask and transported to a recompression chamber by the fastest means possible. (If an aircraft is used, cabin pressure should remain as close to 1 atmosphere as possible; the time saved by air transportation is believed to more than compensate for a moderate decrease in ambient pressure). The treatment schedule shown in figure 5 is often used to treat scuba divers. Other schedules are used for deeper dives, but the principles remain the same. Attempts by divers to treat themselves by recompression under water are usually unsuccessful and dangerous. Consultation concerning diving medical problems, including the location of the nearest hyperbaric chamber, can be obtained by calling (512) 536-3278 (U.S. Air Force School of Aerospace Medicine, San Antonio, Tex.), or (904) 234-4355 (U.S. Navy Experimental Diving Unit, Panama City, Fla.). The U. S. Coast Guard and state police sometimes assist with emergency transportation.
1008
RICHARD H. STRAUSS
Prevention A practical problem in diving is how to return to the surface in the shortest possible time without sustaining injury. This is a bit like approaching the edge of a cliff as closely as possible, for the view, without falling off. The main variable is the rate of ascent, which can be seen graphically when pressure is plotted against time, as in figure 6. Early compressed-air workers and divers were brought to the surface as fast as machinery would permit. When it became evident that this caused damage, a slower, constant rate of ascent was used, but this still resulted in injury. In 1908 and later, the English physiologist J. S. Haldane and colleagues (Boycott, Damant, and Haldane [29]) published work that has been the basis for many decompression schedules ever since. They found that men who spent several hours at pressures up to approximately 2 ATA could be brought immediately to 1 atmosphere absolute without causing decompression sickness. From these data, they suggested that any tissue could tolerate a decrease in pressure if the ratio of tissue gas pressure to ambient pressure did not exceed 2/1. After a decrease in pressure, the diver was supposed to wait until sufficient gas was eliminated from his body to permit a further decrease in pressure. Haldane and colleagues postulated that various
/
1
1 I
/ /
1 1
/
/
/
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'
/ 1' /
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1
f
'
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/
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y \ // y 1 1// ' s^" ^ \W
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\
y
i 1• — — — |
I^--
L 1
1
10
20
1
1
30 40 TIME IN MINUTES
1 —
50
1
60
Fig. 6. Decompression of several tissues postulated in 1908 by Haldane and co-workers is such that the pressure of nitrogen in any one tissue (broken lines) is never greater than approximately twice ambient pressure (solid line) (after Boycott [29]; from Strauss, R. H., ed.: Diving Medicine, Grune and Stratton, New York, 1976; used by permission).
tissues have different rates of gas uptake or loss (figure 6). The initial, large decrease in pressure had the advantage of increasing the outward diffusion gradient for gas from fast tissues and limiting further gas absorption by slow tissues. However, as diving depths became greater, the theoretical ratio of tissue gas pressure to ambient pressure had to be decreased progressively to avoid decompression sickness. The profiles of empirical decompression curves (28) now lie somewhere between the original Haldane curve and the straight line of a constant rate of decompression (linear decompression). One way to prevent bubble formation is to avoid supersaturation entirely. This is possible during very slow decompression because tissues are normally unsaturated—that is, their total gas pressure is less than ambient pressure. Such unsaturation occurs primarily because the C 0 2 that is produced by metabolism is more soluble in blood than is the 0 2 consumed and exerts a lower partial pressure (figure 7). This same unsaturation is responsible for the spontaneous resorption of air in a pneumothorax. Decompression tables based on this principle have been calculated by Hills (30). T h e degree of unsaturation, sometimes called the "oxygen window," can be increased by breathing 0 2 at partial pressures greater than normal. This technique is used to speed decompression and to increase the rate of inert gas elimination from the body during treatment of decompression sickness. Susceptibility to decompression sickness varies among persons and even in the same diver from day to day. Predisposing factors include obesity, exertion, poor physical condition, fatigue, age, cold, dehydration, and injury. Some acclimatization may occur: tunnel workers and divers appear to be less susceptible to decompression sickness when working daily than after an inactive period (31). Most careful pleasure divers in the United States use as guidelines the U.S. Navy diving tables (28), which have a historical basis in the work of Haldane, but have been modified empirically through years of experience to be generally safe. Many other decompression tables have been developed for commercial or military use. Some divers wear a decompression "meter." Although the meters are generally designed to approximate an accepted set of decompression tables and are used as an alternative to consulting the tables, the practice is not necessarily safe.
1009
DIVING MEDICINE
AMBIENT
= 760~ P 0z = 90mmHg
UNSATURATION = 54 mm Hg
Pco2= 40
Pp2 = 40 mm Hg nx>2 = 46
PH 2 0 = 47
PH 2 0 = 47
I
1
PN 2 =573
o -
ARTERIAL BLOOD
P
N2
= 573
TOTAL GAS PRESSURE - 706 mm Hg
VENOUS BLOOD
Fig. 7. Arterial blood is nearly saturated with gas. Venous blood and tissue are normally unsaturated; that is, the total gas pressure within them is significantly less than ambient pressure (from Strauss, R. H . , ed.: Diving Medicine, Grune and Stratton, New York, 1976; used by permission).
At present, commercially available devices involve the transfer of gas by diffusion or limited bulk flow from a compartment exposed to ambient pressure into a second compartment to which an indicator of gas pressure is attached. Gas passes into or out of the indicator compartment in proportion to ambient pressure—it is hoped in a manner somewhat analogous to that of the body. Because the tissues of the body differ in terms of gas uptake and loss, a meter with several diffusion units would mimic the body more effectively. A small electronic computer that integrates time and depth may prove to be the best decompression meter. Although diving is done in mountain lakes and other bodies of water at altitudes well above sea level, the use of sea-level decompression tables becomes less safe as altitude increases. Various decompression methods for altitude diving have been proposed, but few have been tested extensively, and some are dangerous. In Switzerland, Buhlmann and associates (32, 33) have calculated new altitude decompression tables, and after 214 test dives no cases of decompression sickness have been reported. In 1961, several members of the crew of a commercial airliner incurred decompression sickness on an intercontinental flight after scuba diving during the morning and afternoon before their evening flight (34). Other incidents of decompression sickness aboard commercial and
private aircraft after diving have been reported. Studies by Edel and co-workers (34) led to the conclusion that scuba divers who stay strictly within the depth-time limits recommended by the U.S. Navy tables for dives that do not require decompression will not develop decompression sickness if, after diving, they allow a minimum of 2 hours at the surface before flying in a pressurized aircraft (maximum cabin altitude, 8,000 feet); those who make dives beyond the no-decompression limits should allow a surface interval of 24 hours to avoid the risk of decompression sickness. More recently, researchers have recommended a wait of 4 hours between no-decompression diving and flying. Commercial pilots are not permitted to fly for 24 hours after scuba diving, and persons who may exceed 8,000 feet in altitude should follow the same rule. Although several women have done scuba diving during pregnancy without apparent detrimental effects to the fetus, the safety of this practice has not been established. Gas bubbles have been observed in the circulation of fetal sheep using a standard decompression table, although the mother was unaffected (35). Fetal risks include not only decompression sickness but also hyperoxia, hypoxia, and hypercapnea. The Undersea Medical Society recommends that the woman who is, or may be, pregnant be discouraged from diving (36).
1010
RICHARD H. STRAUSS
Some Hazards of Diving Gases
T h e gas mixture that is breathed by a diver must be free of contaminants such as CO and oil vapor. In addition, 2 gases that are normally breathed—0 2 and N 2 —become hazardous at increased partial pressures. Oxygen Toxicity Breathing 0 2 at increased ambient pressures can cause grand mal seizures, which in a scuba diver, generally lead to drowning. Therefore, the sport diver should never breathe pure 0 2 under water. Occasionally, the U.S. Navy uses a closedcircuit rebreather system to avoid release of tell-tale bubbles into the water. In this system, 0 2 is rebreathed after the removal of C 0 2 . The probability of convulsions increases as ambient pressure and time at pressure increase (37). T h e maximal allowable depth using this system is 25 feet of sea water (fsw). Within a hyperbaric chamber, 100 per cent 0 2 is breathed at pressures of as much as 2.8 ATA (60 fsw) in the treatment of decompression sickness and air embolism (figure 5). T o decrease the incidence of convulsions, 5-min periods of breathing air are interspersed during 0 2 breathing. Localized muscular twitching, particularly noticeable in the face, as well as nausea and vertigo, may precede convulsions. If seizures or premonitory signs appear, the oxygen mask is removed and the patient is protected from injury. Seizures are generally of brief duration. After 15 min of air breathing, the patient can often return to 0 2 treatment without subsequent convulsions. T h e mechanism of central nervous system 0 2 toxicity is unclear. Exposure to 0 2 at high pressures is associated with several neural changes: the concentration of 7-aminobutyric acid decreases in the brain; certain enzymes that support oxidative metabolism are altered; and cellular membranes are damaged through oxidation of lipids and sulfhydryl groups (38). Pulmonary 0 2 toxicity is not a problem among scuba divers. It can occur among saturation divers who live in chambers for days and breathe gas mixtures in which the partial pressure of 0 2 exceeds approximately 0.5 ATA. Such conditions occur because the time required for decompression from a dive can be shortened by increasing the Po 2 of inspired air, but at increased risk of 0 2 toxicity. Pulmonary 0 2 toxicity has been reviewed extensively elsewhere (3941).
Nitrogen Narcosis Nitrogen narcosis is called by the French Vivresse des grandes profondeurs—rapture of the deep (42). It occurs because the N 2 in air acts progressively as a general anesthetic as its partial pressure increases. Martini's Law, a fanciful rule of thumb, states that each 50-foot increment in depth is equal in effect to one martini on an empty stomach. Manifestations of narcosis occur almost immediately and include impairment of judgment, memory, ability to do arithmetic, and fine movements. The mechanism of nitrogen narcosis is unclear. One hypothesis is that N 2 , which dissolves predominantly in the lipid portion of nerves, causes a small but significant expansion in lipid volume. This, in turn, is believed to alter membrane characteristics such that synaptic transmission is decreased and permeability to ions is increased (43,44). Most other physiologically inert gases, such as neon and xenon, also have narcotic properties at increased pressures. Helium appears to be the single exception. It is substituted for N 2 as the inert breathing gas in military and commercial dives deeper than approximately 150 feet. Helium is too expensive for recreational use. Nitrogen narcosis is one reason to limit sport diving to approximately 130 feet in depth. An intoxicated diver is an unsafe diver. Unfortunately, many divers do not recognize that their judgment is impaired at depths greater than 100 feet. Barotrauma of Descent
Barotrauma of descent, or "squeeze," is a process in which ambient pressure increases, but pressure within an unventilated gas space does not. The term is also used to describe the result of such a process—usually hemorrhage. For squeeze to occur, (i) a gas space must exist that is not entirely collapsible, and (2) the gas within the space must not equilibrate fully with gas at ambient pressure, Middle ear squeeze is a common problem among divers. As a scuba diver descends and water pressure increases, he normally opens his eustachian tubes every few feet so that air can flow into the middle ear cavity (figure 8). By this method of "equalizing" pressure, the pressure across the tympanic membrane is kept small and no damage occurs. However, if pressure is not equalized during descent, as when the eustachian tube is edematous during an upper respiratory infection or allergy, damage may occur.
DIVING MEDICINE
Semicircular canals
Fig. 8. Simplified diagrammatic drawing of the ear. The external auditory canal, middle ear, and eustachian tube contain air. The fluid-filled inner ear is subdivided into the perilymphatic and endolymphatic spaces, which connect to the subarachnoid space by the cochlear duct and endolymphatic duct, respectively (from Farmer, J. C , and Thomas, W. G.: Ear and sinus problems in diving, in Diving Medicine, R. H. Strauss, ed.: Grune and Stratton, New York, 1976; used by permission).
Vessels within the lining of the middle ear contain blood at approximately ambient pressure. When the pressure within the middle ear is sufficiently less than ambient pressure, the walls of small vessels rupture and hemorrhage occurs. The examining physician can see hemorrhage that occurs within the tympanic membrane. The degree of hemorrhage usually reflects the severity of the barotrauma, and sometimes blood accumulates within the middle ear. The tympanic membrane may itself be ruptured, and cold water that enters the middle ear can cause vertigo and disorientation under water—a hazardous state. The treatment for ear squeeze is to avoid diving until the ear has healed and all symptoms have cleared (45). A decongestant may be used. Ear squeeze generally can be avoided if the diver simply heeds the warning of ear pain. On feeling any ear pain, the diver should stop his descent, ascend a few feet, and try to equalize ear pressure. If the ears cannot be equalized, the dive should be terminated. Diving should be avoided when respiratory infection or allergy is present. Squeeze can affect any gas space that does not equilibrate with ambient pressure. Eye goggles are not worn because they can result in conjunctival hemorrhage. The diver's face mask encloses
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his nose as well as eyes so that compressed air can reach the mask. Sinus squeeze causes pain over the affected sinus and sometimes results in extravasation of blood, which may be observed in the face mask on surfacing. Many divers can equalize ear pressure without conscious effort, but others use maneuvers such as trying to exhale forcefully against the pinched nose to force air through the eustachian tubes. This maneuver is occasionally associated with sudden deafness and tinnitus, usually in one ear. A probable mechanism is that increased pressure in the thorax and abdomen is transmitted to the cerebrospinal fluid as blood engorges veins within the spinal column. The increased pressure is in turn transmitted from the cerebrospinal fluid, via the endolymphatic and cochlear ducts, to the fluid of the inner ear (figure 8). The increased perilymphatic pressure tends to rupture the round or oval window of the inner ear with loss of fluid into the middle ear, which is at a lower pressure. T h e neural portion of the inner ear is damaged in the process (46,47). Many experienced divers assimilate a method of equalizing ear pressure that may well be safer (Frenzel maneuver). They increase pressure within the pharynx by occluding the nose, closing the glottis, and then contracting the pharyngeal muscles. Air is thus forced through the eustachian tubes without altering thoracic pressure. This can be performed with the mouth open or with a regulator in place because the tongue and soft palate occlude the posterior oral cavity. Barotrauma rarely affects the ears during ascent because the eustachian tube acts somewhat like a one-way valve. Air escapes from the middle ear with relative ease, although it may enter with difficulty. Still, occasional divers become vertiginous during ascent (alternobaric vertigo). It is believed that this occurs when the pressure within one or both middle ears exceeds ambient pressure by a critical amount (48, 49). Symptoms usually stop when the surface is reached. Transient vertigo has also been observed in divers during descent. Barotrauma of Ascent
As ambient pressure is decreased during ascent, gas within the lungs tends to expand in accordance with Boyle's law. This effect becomes especially important at shallow depths where a relatively small change in depth can lead to a
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RICHARD H. STRAUSS
large change in gas volume. Thus, a 33-foot ascent from 99 feet (4 ATA) to 66 feet (3 ATA) changes gas volume by the ratio 4/3, an increase of 33 per cent. However, ascent from a depth of 33 feet (2 ATA) to the surface (1 ATA) leads to a doubling of gas volume. Pulmonary Barotrauma The ascending scuba diver must permit expanding gas to escape from his lungs, either by breathing normally or, in case of an equipment problem, by exhaling continuously. Failure to do this can lead to overdistension of the lungs, tearing of lung tissue, and escape of air from alveoli. The extra-alveolar air may travel to any of several locations: (1) small amounts may dissect no farther than the interstitial tissue of the lung, (2) dissection may occur along vessels to the mediastinum and then to subcutaneous tissue or elsewhere (50, 51), (3) air may enter pulmonary vessels and be carried to distant parts of the body as arterial emboli; and (4) pneumothorax may occur. Extra-alveolar air is sometimes asymptomatic (52). Overdistension of the lungs, not merely the difference between alveolar pressure and that outside the chest, is responsible for damage to lung tissue. In experiments with anesthetized dogs, lung rupture occurred when intrapulmonic pressure exceeded ambient pressure by 80 mm Hg. Yet much higher pressures could be tolerated without damage when the thorax and abdomen were bound in order to limit expansion (53). Comparable findings have been noted in fresh cadavers. Coughing results in high intraalveolar pressures, but generally does not cause lung rupture. Air embolism has occurred under conditions in which observers were sure that breath holding had not occurred. It is hypothesized that local obstruction to egress of air may be responsible for barotrauma to lung tissue. Potential causes of obstruction include broncholiths, gas-filled cysts, active asthma, and viscous secretions. Persons with obstruction to egress of air should not dive. Occasional persons suffer from air embolism without any apparent cause. Air Embolism The mechanism by which air enters pulmonary vessels is not entirely clear. It is believed that small vessels rupture as lung tissue is overstretched. Air may not enter the circulatory system until the high intra-pulmonic pressure is relieved by the resumption of breathing and
pulmonary circulation is restored. Bubbles are carried quickly to the heart and then by the arterial system to various parts of the body. The bubbles lodge in small arterial vessels, occluding circulation beyond that point. They are stabilized by surface tension; loss of gas by diffusion is slow. Air embolism to the brain generally becomes apparent within seconds as a stroke-like syndrome. A typical history is that of a scuba diver who ascends rapidly, often under emergency conditions, reaches the surface, gasps, and sinks unconscious into the water. If not rescued, the diver drowns. Almost any sign of cerebral damage may appear, including focal paralysis, paresthesias, or visual disturbances. Hemoptysis sometimes occurs. Trainees should remember that cerebral air embolism has occurred on several occasions during scuba practice in a standard swimming pool. (Decompression sickness does not occur under such shallow conditions.) Cerebral air embolism is a medical emergency and treatment in a hyperbaric chamber should be initiated as soon as possible. The patient should be transported in the Trendelenberg position, lying on his left side. This position is believed to decrease the chances of additional gas emboli reaching the brain and may possibly improve cerebral circulation impaired by gas emboli. T h e patient should breathe 0 2 continuously through a mask with a seal that assures a high inspired Po 2 . In the presure chamber, an often used treatment schedule is similar to that used for decompression sickness (figure 5), except that initial pressurization is to 165 fsw (6 ATA) with air breathing for 15 to 30 min (28). This initial high pressure is believed to decrease the size of bubbles sufficiently to permit them to be carried to smaller vessels, thus decreasing the size of the affected area (54). Bubble absorption also begins. Chamber pressure is subsequently decreased to 60 fsw so that 0 2 may be breathed with only a small risk of convulsions. Corticosteroids are administered to minimize cerebral edema. Although massive cerebral air embolism leads to death within minutes, those victims who reach a hyperbaric chamber while still alive have an excellent chance for full recovery. Cerebral air embolism is often accompanied by mediastinal emphysema sufficient to be visible on roentgenograms. Subcutaneous emphysema, palpable particularly in the supraclavicular fossae, may also be present. Mediastinal and subcutaneous emphysema do not require treatment in
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a pressure chamber if they occur without manifestations of air embolism and if they are asymptomatic or cause only mild symptoms such as substernal discomfort or voice change. The breathing of 0 2 by mask is usually sufficient treatment. Pneumothorax occurs infrequently as a result of pulmonary overdistension in diving. In contrast, during the use of positive pressure breathing in patients, pneumothorax is well known and cerebral gas embolism is rare. Uncomplicated pneumothorax in a diver is treated in the usual manner. If it accompanies cerebral air embolism, the latter must be treated in a chamber. As ambient pressure increases, additional air may enter the pneumothorax. When ambient pressure is subsequently decreased, a tension pneumothorax may result and require treatment. A chest tube may be inserted prophylactically before decompression. Breath-hold Diving
Many of the interesting forms of sea life that can be viewed by a scuba diver can also be seen by a breath-hold diver. The abundance of life decreases as water becomes deeper because sun light is the foundation of the food chain, and water acts as a filter for light. Breath-hold diving is simpler, cheaper, and safer than scuba diving, but often requires more exertion in the water. Basic equipment consists of a face mask for clear vision under water, fins to aid propulsion, and a snorkel (breathing tube) so that the diver can breathe at the surface without lifting his or her face from the water (figure 3). Persons who merely wish to swim at the surface and look at the bottom can do so with little expenditure of energy, given calm water conditions. Anyone who performs breath-hold dives should be aware of the danger associated with hyperventilation. Breath-hold Blackout Each year, a number of persons die from loss of consciousness (blackout) under water and subsequent drowning. Breath-hold blackout occurs almost exclusively in young males who are demonstrating how far they can swim under water or how long they can remain submerged. Many such incidents occur in guarded swimming pools (55). Swimmers often learn through experience that, by hyperventilating immediately before submerging, they can extend their time under water. However, unless alerted to the danger, they fail to realize that this maneuver can lead to loss of consciousness without warning. The mechanism of breath-hold blackout be-
comes clear when alveolar gases are examined during breath holding (56-58). Such measurements have been made using a rebreathing technique. That alveolar Po 2 decreases steadily during breath holding and that Pco 2 increases more slowly is shown in figure 9. These changes are more pronounced during exercise (56-58). When a person tries to hold his or her breath as long as possible, he or she is forced to terminate breath holding at a time (the breaking point) when the urge to breathe can no longer be suppressed. The breaking point is determined primarily by alveolar (arterial) Pco 2 , but other factors such as arterial Po 2 , attention, motivation, and lung volume play a role (59). Greater lung volumes permit longer breath holding, and sport divers usually inspire to nearly maximal lung volume before diving. Voluntary breath holding without hyperventilation (figure 9) is terminated even in highly motivated adults before alveolar Po 2 is sufficiently low to cause unconsciousness. (Small children may prolong breath holding to the point of cyanosis, unconsciousness, and convulsions [60]). However, hyperventilation can significantly decrease alveolar Pco 2 and body stores of C 0 2 so that the urge to breathe is delayed during subsequent breath holding. Unfortunately, hyperventilation increases body stores of 0 2 only slightly; alveolar Po 2 may approach 140 mm Hg, but the quantity of 0 2 in the blood is little increased because arterial hemoglobin is normally almost fully saturated with 0 2 . As a result, after hyperventilation arterial Po 2 may
l i m e , Seconds
Fig. 9. Alveolar Po2 and Pco2 during breath holding with air. Resting consumption of 0 2 (Vo2) = 320 ml/min. Work was mild: Vo2 = 580 ml/min (from Lanphier, E. H., and Rahn, H.: Alveolar gas exchange during breath holding with air, J Appl Physiol, 1963, 18, 478; used by permission).
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RICHARD H. STRAUSS
decrease to the point that consciousness is lost before arterial Pco 2 is sufficiently increased to result in a strong urge to breathe. The stimulus to breathing furnished by low arterial Po 2 is weak enough to be ignored by a highly motivated person. A practical guideline for divers is to take only one or 2 deep breaths before submerging. Pressure changes during diving can increase further the chances for unconsciousness. As water pressure increases, lung volume decreases and both alveolar Po 2 and Pco 2 increase (figure 10) (61). During submergence, alveolar Po 2 may become quite low. Upon ascent, the ambient pressure decreases and gas within the lung expands. Alveolar Po 2 then decreases even further and may result in loss of consciousness. During ascent, alveolar Pco 2 also decreases and the urge to breathe diminishes—a paradoxic event in terms of survival. Diving Reflex When whales, seals, or other aquatic mammals dive, cardiovascular changes occur that result in the conservation of 0 2 . Seals can swim underwater for 20 min (62), and some whales can remain submerged for one hour. During a dive by such an animal, the circulation of blood is essentially restricted to the heart, lungs, and brain. Vasoconstriction severely limits blood flow to the remainder of the body, including the working muscles (63, 64). Cardiac output decreases and heart rate decreases—to 16 beats per min in freeswimming seals (62). This response is known as the diving reflex. When the animal returns to the surface and breathes, peripheral circulation is restored and lactic acid, which has accumulated in the anaerobic muscle, enters the blood stream and is subsequently metabolized. After a long dive, the whale must remain at the surface for several minutes, a fact that whalers have long used to their advantage. Some humans exhibit bradycardia and vasoconstriction during breath-hold diving. These changes result in part from breath holding itself, but are augmented by exposure of skin, especially the face, to cool water (65-67). There is no clear evidence that the bradycardia response significantly conserves 0 2 in human divers. Negative Intrapulmonic Pressure In a person who breathes surface air while immersed to the neck in water, external chest pressure exceeds intrapulmonic (intra-alveolar) pressure by the weight of the column of water at a given point on the chest. This hydrostatic
(H 0
.
1
.
1
20 40 T i m e , Seconds
.
!(>0
Fig. 10. Po2 and Pco2 during 80-sec simulated dives (in a pressure chamber) preceded by hyperventilation (from Lanphier, E. H., and Rahn, H.: Alveolar gas exchange during breath-hold diving, J Appl Physiol, 1963, 18, 471; used by permission).
pressure causes a moderate decrease in expiratory reserve volume and a small decrease in vital capacity. Such changes are comparable to those found during negative pressure breathing in air. During immersion to the neck in the sitting position, approximately one fourth of the decrease in expiratory reserve volume is accounted for by the hydrostatic pressure of the water on the abdomen and most of the remainder by the pressure on the thorax (68). (The scuba diver swimming in the horizontal position with a good regulator at his mouth must generate a slightly negative intrapulmonic pressure for inhalation and a slightly positive pressure for exhalation. If he assumes an upright position, the pressure differences become similar to those during immersion to the neck.) Swimmers and divers have long noted a tendency for increased production of urine after they enter the water. Such diuresis has been documented and is believed to be caused by an increase in thoracic blood volume that results from negative intrapulmonic pressure, as well as from loss of the effect of gravity on the circulation. Stimulation of stretch receptors in the left atrium of the heart results in decreased secretion of antidiuretic hormone and associated diuresis (69, 70). Water temperature may also play a role. For many years, a breath-hold diver's maximal depth was believed to be determined by the point
DIVING MEDICINE
at which his total lung capacity was compressed to his residual volume (RV). If a subject's RV were 20 per cent of his total lung capacity, the depth limit would be 5 ATA (132 feet). It was predicted that further descent would rapidly result in negative intrapulmonic pressures leading to lung squeeze: rupture of vessels with extravasation of blood as seen in ear squeeze. However, one extensively studied subject dived to 240 feet (71), and even deeper breath-hold dives have been recorded. Although external pressure can compress the rib cage and raise the diaphragm to decrease residual volume, an important factor may be the shift of blood from the peripheral to thoracic blood vessels as intrapulmonic pressure becomes negative. A shift of 600 ml of blood has been estimated experimentally (72). Such blood shifts would lead to additional compression of the gas in the lungs and would permit diving to depths greater than those previously predicted. Among sport divers, lung squeeze has rarely proved to be a problem. A possible case has been reported in a diver who apparently lost consciousness and then sank while apneic (73). Those divers who attempt breath-holding depth records may yet be able to demonstrate the syndrome. Deep Diving (Commercial and Military) Military uses of deep diving include salvage and rescue operations. However, the major impetus for extending the depth at which divers can work is the recovery of undersea oil. Whenever possible, the oil industry avoids using divers in deep water because such operations are time-consuming and expensive. Decompression after even a brief deep dive may require several days at a cost of thousands of dollars per day. It is not surprising that undersea robots and armored diving suits, within which the operator remains at one atmosphere, are used increasingly. Still, some jobs are done most effectively by divers, who currently work as deep as 1,000 feet. Much of the present research in diving medicine focuses on the practical problems of extending divers' working depth in the sea and increasing safety at all depths. In dives greater than approximately 150 feet, helium is used as the main inert breathing gas to avoid narcosis. Sufficient 0 2 is added to result in an inspired Po 2 slightly greater than normal. At a depth of 500 feet, a gas mixture with a Po 2 of 200 mm Hg is 1.63 per cent 0 2 . This is insufficient to support a flame, but respiration proceeds well. The breathing of helium causes the voice to
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sound like "Donald Duck." This occurs because helium conducts sound more rapidly than does air, resulting in an upward shift in resonance frequency components in the vocal tract (74, 75). The effect becomes more pronounced as depth increases so that direct conversations are unintelligible. Electronic unscramblers are used to alter voice characteristics so that speech can be understood. Exposure of persons to great pressures is associated with tremors and decreased manual dexterity. This problem is termed the high pressure nervous syndrome and may result from a decrease in the lipid volume of nerves. (Lipids are more compressible than water.) Adding a small amount of N 2 to the breathing mixture helps to counteract the high pressure nervous syndrome (76), possibly by increasing lipid volume. Rapid compression makes the symptoms worse. Avoidance of decompression sickness is the most time-consuming problem. Because decompression from high pressures requires several days, "saturation diving" is frequently used. After 12 to 24 hours at a given pressure, the diver's body has absorbed as much inert gas as it can and is said to be saturated with that gas. Additional time under pressure does not add to decompression time. Thus, the diver can remain for many days at the pressure at which he must work, generally living in a pressure chamber within a ship or surface rig. He is lowered to the work site in a diving bell, which can be detached from the larger chamber. When water pressure equals the gas pressure within the bell, the hatch in the floor is opened and the diver enters the water. When the job is finished the diver is decompressed in the larger chamber at a rate of approximately 100 feet of seawater pressure per day. Faster methods of decompression are sought continually. Increasing the Po 2 of the inspired gas speeds the loss of inert gas from the body, but is limited by pulmonary 0 2 toxicity. Inspired Po 2 that is to be maintained for several days generally does not exceed 0.5 atmosphere. Helium, N 2 , or any mixture of inert gases can cause decompression sickness. However, differences in solubility and diffusivity between gases can sometimes be used to advantage. During decompression from a dive in which helium was breathed, the inert gas can be changed to N 2 as the surface is approached. After the change, helium leaves the body more rapidly than N 2 enters it, and the total inert gas load is decreased. Decompression time can thus be shortened (77). What is the ultimate depth limit for divers?
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RICHARD H. STRAUSS
The answer is unknown and research continues. Humans have worked within a chamber at a pressure equivalent to 2,001 feet (61 ATA) (78). It has been suggested that alveolar ventilation may be the limiting factor. Gases become more dense when compressed, and concomitantly, resistance to flow within airways increases. The ability to perform moderate exercise is required under water, and increased ventilation is therefore necessary. One group of persons in a dry chamber was able to exercise at heavy work loads while breathing a neon-helium-0 2 mixture with a density of 25 g per liter (79). This density is approximately 22 times that of air at sea level and is equivalent to that of a helium-0 2 mixture at 5,000 feet of seawater. In contrast, persons exercising under water within a wet chamber while breathing a less dense gas mixture (helium-0 2 , 7.3 g per liter) were forced to stop exercise at lighter work loads because of severe dyspnea (80). The differences may be due to factors related to the underwater versus dry pressure environment. As gas density increases, diffusion of one gas through another (binary diffusion) becomes slower. It has been suggested that diffusion of 0 2 or C 0 2 through the layer of unmixed gas within the alveoli might be impaired sufficiently, increasing stratified inhomogeneity, to create problems in gas exchange at great depths (81, 82). This effect may be opposed, at least initially, by increased intrapulmonary gas mixing or by improved ventilation/perfusion matching (83) as gas density increases. If humans could breathe liquid rather than gas, many of the problems associated with diving, including decompression requirements, would be eliminated. Anesthetized dogs have been ventilated successfully with a fluorocarbon liquid for one hour (84). The solubility of 0 2 and CO a in this liquid is sufficiently high to support the dogs' resting respiratory needs. In humans, however, maximal ventilation with a liquid has been estimated at 4 liter per min (85). This would apply even if ventilation were assisted externally because airways would collapse during expiration. Given so small a ventilatory limit, the quantity of gas transported by a volume of liquid must be large. Sufficient 0 2 could be dissolved in fluorocarbon liquid by exposing it to 0 2 under hyperbaric conditions. However, at present, insufficient C 0 2 can be dissolved in the liquid at Pco 2 values compatible with life to support human respiration during exercise or even at rest. If such problems were solved, the ultimate depth limit would probably be determined by
hydrostatic pressure. Many biologic processes are affected adversely by altered pressures (86). Whales are believed to dive to 3,000 feet. However, when liquid-breathing mice are subjected to a pressure equal to 5,400 feet of seawater (166 atmospheres), they stop breathing (87). Humans' hydrostatic pressure limit could well be within such a range. Selection of Divers: Examination and Physical Standards*
The type of diving planned and the diving background of the candidate must be considered (28, 88-93). In general, standards are more strict for a beginning student than for experienced divers. Some conditions (e.g., subpleural blebs or aircontaining pulmonary cysts) are clearly disqualifying for all diving. It may be seen, however, that commercial and naval diving standards are more rigid than those for a sport diver who can select the conditions and timing of his pleasure dives. For commercial divers, the legal liability of a diving school or diving company and the relative remoteness of most commercial diving operations—in time as well as distance—from definitive medical care facilities are additional considerations. A diver in saturation at 1,000 fsw in a chamber may require 6 to 10 days of decompression before evacuation to a hospital intensive care unit. Even after an ill or injured diver has been decompressed, adverse weather conditions can halt helicopter operations or preclude safe transfer at sea to rescue vessels for days at a time. Freedom from musculoskeletal or other disabilities that impair efficiency or job longevity is an important consideration in commercial diving. Skin conditions that might be insignificant in sport divers (e.g., chronic furunculosis) would be disqualifying for scientific or commercial saturation diving. Conditions that could cause alteration of consciousness underwater (e.g., seizure disorders, insulin-dependept diabetes mellitus, and cardiac arrhythmias) are always disqualifying for any type of diving. Responsibility to other divers is a consideration. A diver may be willing to take a calculated risk with regard to his own safety, but if an acci* This section is reprinted from Davis, J. C, Kindwall, E. P., and Youngblood, D. A.: Selection of divers: Examination and physical standards, in Weekly Update: Hyperbaric and Undersea Medicine, Jefferson ,C. Davis, ed., Biomedia Inc., Princeton, 1978, pp. 1-7. Reprinted by permission.
DIVING MEDICINE
dent occurred, other divers could be injured or killed in rescue attempts. T h e decisions of the examining physician must include this possibility and not be clouded by the candidate's willingness to take a chance. With the infinite array of borderline decisions that must be considered, the examining physician must know the diving environment. T h e best way to acquire this knowledge is for the physician to be a diver. Physical Standards Specific physical standards have been established and published by various agencies—the U.S. Navy, the Occupational Safety and Health Administration (OSHA), the National Oceanic and Atmospheric Administration (NOAA), scuba certifying organizations, and commercial diving companies.* It is not our intent to review the provisions of these references but rather to draw on our personal experiences to comment on rationale in key areas. Some conditions are obviously always disqualifying for any type of diving, so we will dispense with those first, then move on to the controversial areas. T h e standard disqualifying conditions are the following: (1) Any history of seizure disorder (except febrile convulsions in infancy) or during the period after a head injury when a neurologist believes the patient is at risk for post-traumatic epilepsy. (2) Recurrent or unexplained episodes of syncope, whether cardiovascular or neurogenic. (3) Insulin-dependent diabetes mellitus. T h e risk of an insulin reaction under water is increased by the ever present possibility of the need for sudden bursts of energy expenditure in emergencies or the need for unexpected hard swimming against current. Diabetes mellitus that is well controlled by diet alone might be waived for sport divers. In some regulations, however, diabetes of any degree is a disqualification for diving. (4) Coronary artery disease. Heavy exertion in the water as well as topside work—carrying and donning diving equipment and climbing into boats—must be added to the risk of sudden incapacitation under water. A history of myocardial infarction is always disqualifying in the opinion * Many American commercial divers work in places subject to the regulations of other nations (e.g., United Kingdom, Norway, and Australia), and U.S. physicians certifying such divers "fit to dive" may have to be "approved" to do so by the government of the particular country.
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of most physicians but possible exceptions in sport diving will be discussed subsequently. (5) Sickle-cell disease or trait. Heavy exertion in cold water increases the risk of sickling, and if blood flow were compromised in decompression sickness, the local areas of hypoxia could cause sickling and compound the problem. Moreover, aseptic bone necrosis has been associated with sickle-cell disorders. (6) Middle ear surgery with placement of a prosthesis in the conduction chain. Displacement during pressure changes could cause permanent derangement of the surgical repair. (7) Persistent inability to equalize pressure in the middle ear by the Valsalva or Frenzel maneuvers. Re-examination after correction of a deviated nasal septum, removal of nasal polyps, desensitization in allergk rhinitis, or clearing of acute coryza may remove this disqualification. (8) Meniere's disease. (?) History of pulmonary overpressure accident. Aside from those cases which occur because of panic and a breath-holding ascent or the presence of air-containing pulmonary cysts or blebs, cases have occurred o n normal ascent in which no pulmonary pathology is detectable. T h e potentially fatal consequences of arterial gas embolism make any risk of a recurrence unacceptable. Despite normal results of pulmonary function testing, a candidate cannot be cleared for diving because small areas of local pulmonary gas trapping cannot be detected. These areas may have caused the original event, or, in the case of breath-holding ascent, residual damage may make recurrence more likely. (10) Air-containing pulmonary cysts or blebs are always disqualifying for any type of diving. In this, as well as all forms of barotrauma, the physician should remember that Boyle's law dictates the greatest volume changes in trapped gas at shallow depths. Thus, clearing a patient to do only shallow, compressed-gas diving would be especially dangerous. (11) Significant obstructive pulmonary disease. Minimal pulmonary function values that have been suggested are vital capacity, forced expiratory volume in one second, and maximal voluntary ventilation 75% of predicted. It must be reemphasized, however, that the usual pulmonary function tests cannot detect potentially dangerous local air-trapping areas. (12) Chronic alcoholism. Besides errors in judgment during periods of intoxication or hangover, aseptic bone necrosis is a known concomitant of alcoholism per se. Roentgenographically, it is
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RICHARD H. STRAUSS
not possible to distinguish this etiology from that of dysbaric osteonecrosis. Conditions in which there is significant disagreement among authorities or in which answers are not based on studies or extensive experience are more difficult. In the following discussion, we will try to summarize both sides of each issue and give our own opinions. Pulmonary Asthma. Because of the increased risk of local air trapping and pulmonary overpressure accidents on ascent with exertion or cold-induced bronchospasm, one recommendation is disqualification for any history of asthma beyond early childhood. At the other extreme are those who believe that the filtered, clean air used in diving should not cause bronchospasm; hence, except during periods of asthmatic attacks, diving can be approved. In our experience, a history of bronchial asthma is disqualifying if there have been any attacks within 2 years, if medication is needed for control, or if bronchospasm has ever been associated with exertion or inhalation of cold air. Pneumothorax. Some authorities advise against diving after any pneumothorax—spontaneous, traumatic, or surgical. They believe the risk of undetectable local air trapping by scarring and adhesive bands is too great. Others argue that with traumatic pneumothorax, chest surgery, or hemopneumothorax, the pleural scarring induced is protective; after a chamber pressure test, experienced divers with normal pulmonary functions and chest roentgenograms may be requalified. Our own view of this most difficult decision revolves around these 2 divergent opinions. Any history of chest surgery or pneumothorax should disqualify a candidate for any type of diving training. There is no need to assume any risk. In the case of an experienced scientific or commercial diver whose livelihood depends on diving, some people recommend the more liberal approach, except in the case of spontaneous pneumothorax with its established high recurrence rate even at sea level. Some regulations, however, strictly forbid diving after any perforating chest injury or open chest surgery. Neurologic Migraine. Many affected people take part in sport diving with no evidence of any effect. We could make a case for disqualification by citing the changes in vascular tone caused by C 0 2 im-
balance and so forth, but in sport diving, we recognize only one significant problem. Severe migraine-intensity headache with scintillating scotomata is seen as decompression sickness or arterial gas embolism symptoms. A migraine attack after diving may require compression therapy to ensure that a case of decompression sickness or gas embolism is not masquerading as a migraine attack. Frankly, we do not see this as a valid contraindication to sport diving. Commercial diving poses a quite different problem, so migraine is totally disqualifying. Whereas the sport diver can easily avoid diving during attacks, unpredictable periods of incapacitation make commercial diving with migraine unacceptable. History of neurologic decompression sickness with residual deficit. This condition is disqualifying. The precise microcirculatory status at the involved site of the spinal cord or brain has not been defined. The possibility that such areas may be less well perfused and susceptible to further decompression insult must be considered. Paraplegia. Paraplegia after traumatic transection of the cord is not a contraindication to sport diving, provided the subject has sufficient pulmonary function to breath-hold to the bottom of a pool. The Participating Pioneer of Sport for the Disabled advises the use of a buddy, however, to guard the trailing legs against injury, particularly over coral. Psychiatric. Psychiatric considerations are complex. However, one criterion is whether or not you would trust the candidate with your life. Cardiovascular Myocardial infarction. A history of myocardial infarction is an absolute disqualification for further diving under most circumstances. A possible exception has been suggested in the case of an experienced sport scuba diver who will not accept a blanket disqualification. If the patient is more than one year postinfarction, has no angina or arrhythmias, has normal exercise tolerance, and is re-evaluated by a cardiologist at 6month intervals, some authorities have reluctantly agreed to permit such a patient to return to sport diving after the patient fully understands the risk. Both the patient and fellow divers must understand the risk of drowning due to a recurrence under water. Hypertension. Diving itself has no effect on hypertension, but good medical practice requires drug control at some point. If more than a mild diuretic and dietary and weight controls is re-
DIVING MEDICINE
quired in the form of antihypertensive drugs, diving must be discontinued. Vision In commercial diving, the established standards for acuity correctable to 20/20 and normal color vision are for topside and chamber work. Most underwater work is in such low visibility that most tasks are performed mainly by touch. In fact, one current study has demonstrated an advantage to blind divers doing mechanical underwater tasks in zero-visibility water. In sport diving, corrective lenses can be mounted in scuba face masks, or contact lenses can be worn. Soft contact lenses are permissible. Musculoskeletal For commercial diving, there is great sensitivity to the need to reject all candidates with conditions that might predispose to aseptic bone necrosis. Besides alcoholism and sickle-cell disorders, a major disqualifying factor is a history of systemic corticosteroid administration for a prolonged period. It is not known whether the steroids themselves or the underlying disorder (e.g., lupus) represent the cause of the increased risk of aseptic necrosis. Jones (90) has pointed out, however, that only patients who have received the steroid equivalent of 500 mg of prednisone appear to be at increased risk because of steroids. Otolaryngology Hearing acuity. Hearing acuity is of no concern in sport diving. In commercial diving, however, it is vital to understand communications from topside. An on-the-job test may be required to make this determination despite audiometric findings. Labyrinthine window rupture after successful repair. Opinions are divided on this condition because our experience base is so small. Perforation of the tympanic membrane. Until fully healed, this condition is disqualifying for scuba diving. An exception might be an experienced helmet diver, caisson worker, or hyperbaric chamber worker whose tympanic membrane is not exposed to water. Temporary Disqualifications Upper or lower respiratory infection. Upper or lower respiratory infection that causes inability to equalize pressure in the ears, sinuses, or lungs due to mucous plugs or bronchospasm is a temporary disqualification.
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Pregnancy. Studies in animals have shown significant species variation in the susceptibility for bubble formation in fetal circulation. Much more experimental work will be required before we can exclude the risk of intra- or extravascular gas separation in the fetus during decompression from a dive that is safe for the mother. Recent fractures or sprains. Recent fractures or sprains that interfere with local tissue perfusion for normal inert gas uptake and elimination are disqualifies. Some studies have shown an increased risk of bends at such sites. Drugs. Besides the obvious dangers of diving under the influence of alcohol or psychotropic drugs, prescribed medications must be considered. In general, it is not only the side effects of the drug with the unknown potentiating effect of nitrogen narcosis that represent hazards, but also the underlying disorder requiring medication. Even acute coryza requiring antihistamines or decongestants may not only cause difficulty equalizing ears and sinuses, but may represent a risk because of distraction. Tranquilizers not only dull alertness, but if anxiety is of such a degree to require their use, the patient should not dive. Inguinal hernia. Until successfully repaired, inguinal hernia provides the possibility of trapped gastrointestinal gas expansion and strangulation on ascent. Furthermore, various phases of all types of diving require lifting and other forms of exertion. Physical fitness. Most commercial diving requires adequate strength and endurance to perform heavy manual labor. Sport scuba diving is deceptively easy—until an emergency occurs or unexpected currents require long, hard swims in heavy surface action or against a current. The sport diver should be capable of such activity before embarking on any dive. The high N 2 content and poor perfusion of adipose tissue predispose the truly obese person to decompression sickness, besides having an effect on endurance. Skin-fold measurements below the scapula and over the triceps, or body composition studies, are a better guide to disqualifying obesity than height-weight tables. Increased skin-fold thickness in other areas (e.g., abdomen) does not seem to be correlated with an increased risk of decompression sickness. Examination Required The agency or company to which the diver is applying will provide a form calling for specific tests. In general, an examination should be adequate to discover any of the factors discussed.
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For any form of diving, the m i n i m u m components of an e x a m i n a t i o n are the following: (i) a history a n d review of systems, (2) a complete physical e x a m i n a t i o n with emphasis o n the otorhinolaryngeal, p u l m o n a r y , a n d cardiovascular systems, (3) inspiratory chest roentgenograms (posteroanterior a n d lateral), (4) baseline electrocardiogram (desirable for all applicants a n d m a n d a t o r y for those m o r e t h a n 40 years of age), stress electrocardiography a n d special studies as indicated, (5) complete neurologic e x a m i n a t i o n to establish a baseline in case of decompression sickness or gas embolism, (6) complete blood count, urinalysis, serology, a n d sickle-cell studies in susceptible p o p u l a t i o n s .
Further Reading I n t r o d u c t o r y books i n t e n d e d for the practicing physician include Diving Medicine, R. H . Strauss, ed. (94); Diving and Subaquatic Medicine, by C. E d m o n d s , C. Lowry, a n d J. P e n n e father (95); and Underwater Medicine, by S. Miles a n d D . E. Mackay (96). A m o r e complete, research-oriented text is The Physiology and Medicine of Diving, P. B. B e n n e t t a n d D. H . Elliott, eds. (97). Diving techniques are described in detail in the U.S. Navy Diving Manual (28) a n d t h e NO A A Diving Manual (93). A book popularly used in t h e t r a i n i n g of recreational divers is The New Science of Skin and Scuba Diving (98). Acknowledgment T h e writer wishes to thank the following persons for reviewing and commenting on this paper: Albert B. Craig, Jr., M.D., Jefferson C. Davis, M.D., Eric P. Kindwall, M.D., Herbert A. Saltzman, M.D., and Michael E. Whitcomb, M.D.
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