Decompression Sickness 

  • Author: Stephen A Pulley, MS, DO, FACOEP; Chief Editor: Barry E Brenner, MD, PhD, FACEP   more...
 
Updated: Sep 17, 2009
 

Background

Although decompression sickness (DCS), a complex resulting from changed barometric pressure, includes high-altitude–related and aerospace-related events, this article focuses on decompression associated with the sudden decrease in pressures during underwater ascent, usually occurring during free or assisted dives. People involved with tunneling projects, in submarines during emergencies, and in breath-hold free diving may also experience the physiologic effects of decreased pressure brought on by such ascents.

Since 4500 BCE, humans have engaged in free (breath-hold) diving to obtain food and substances from shallow ocean floors at depths of 100 ft or more. The 2007 record-setting breath-hold unlimited dive of Herbert Nitsch to 702 ft (214 m) attests to this human feat. Humans began experimenting with crude diving bells as early as 330 BCE. These bells were submerged containing only air. In 1690, the first diving bell with a replenishing air supply was tested. The first crude underwater suit dates back to 1837, and helium was first used in place of nitrogen in 1939.

All these early diving methods required a physical connection to a support platform or boat. The Aqua-Lung, developed by Cousteau and Gagnon, and the submarine escape appliances, developed by Momsen and Davis in the 1930s, were forerunners of the self-contained underwater breathing apparatus (SCUBA), which frees divers from the limitations of tethering.

The increasing popularity of scuba diving and the growth of commercial diving have increased the frequency of deep-pressure injuries. Even in regions far from coasts, individuals are diving in quarries, lakes, rivers, and caves. In addition, the ability to travel rapidly between areas of disparate altitudes in a matter of hours (including the exacerbation caused by decreased pressures in flight) increases the chance of experiencing decompression injuries. Emergency physicians worldwide should know the physiologic effects and management of decompression sickness.

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Pathophysiology

Changes in pressure affect only compressible substances in the body. The human body is made primarily of water, which is noncompressible; however, the gases of hollow spaces and viscous organs and those dissolved in the blood are subject to pressure changes. Physical characteristics of gases are described by the following 4 gas laws, which quantify the physics and problems involved in descending under water.

Boyle law

For an in-depth discussion on the Boyle law, please see the article on Dysbarism.

Dalton law

Pt = PO2 + PN2 + Px

(Pt = total pressure, PO2 = partial pressure of oxygen, PN2 = partial pressure of nitrogen, Px = partial pressure of remaining gases)

In a mixture of gases, the pressure exerted by any given gas is the same as the pressure the gas would exert if it alone occupied the same volume. Thus, the ratio of gases does not change, even though the overall pressure does. The individual partial pressures, however, change proportionally.

Dalton's problem (see the image below): As an individual descends, the total pressure of breathing air increases; therefore, the partial pressures of the individual components of breathing air have to increase proportionally. As the individual descends under water, an increasing amount of nitrogen dissolves in the blood. Nitrogen at higher partial pressures alters the electrical properties of cerebral cellular membranes, causing an anesthetic effect termed nitrogen narcosis. Every 50 ft of depth is equivalent in its effects to one alcoholic drink. Thus, at 150 ft, divers may experience alterations in reasoning, memory, response time, and other problems such as idea fixation, overconfidence, and calculation errors. Even when no signs of nitrogen narcosis are noted, divers may significantly overestimate diving time during deep dives.

Illustration of Dalton gas law. As an individual dIllustration of Dalton gas law. As an individual descends, the total pressure of breathing air increases and the partial pressures of the individual components have to increase proportionally. Nitrogen at higher partial pressures alters the electrical properties of cerebral cellular membranes, causing an anesthetic effect. Oxygen at higher partial pressures can cause CNS oxygen toxicity.

Descending also increases the amount of dissolved oxygen. Breathing 100% oxygen at 2 atm (33 ft) may cause CNS oxygen toxicity in as few as 30-60 minutes. At 300 ft, the normal 21% oxygen in compressed air can become toxic because the partial pressure of oxygen is approximately equal to 100% at 33 ft. For these reasons, deep divers (usually professional or military but increasingly sport divers as well) use specialized mixtures that replace nitrogen with helium and allow for varying percentages of oxygen depending on depth.

Henry law

%X = (PX / Pt) X 100

(%X = amount of gas dissolved in a liquid, PX = pressure of gas X, Pt = total atmospheric pressure)

At a constant temperature, the amount of gas that dissolves in a liquid with which it is in contact is proportional to the partial pressure of that gas (ie, a gas diffuses across a gas-fluid interface until the partial pressure is the same on both sides).

Henry's problem (see the image below): With increasing depth, nitrogen in compressed air equilibrates through the alveoli into the blood. Over time, increasing amounts of nitrogen dissolve and accumulate in the lipid component of tissues. As an individual ascends, a lag occurs before saturated tissues start to release nitrogen back into the blood. This delay creates problems.

Illustration of Henry gas law. If nitrogen is addeIllustration of Henry gas law. If nitrogen is added to a bottle, it diffuses into and equilibrates with the fluid. If pressure is suddenly released (decreased), such as when an individual ascends rapidly, a lag occurs before nitrogen can diffuse back to the nonfluid space. This delay causes nitrogen to bubble while still in the fluid.

When a critical amount of nitrogen is dissolved in the tissues, ascending too quickly causes the dissolved nitrogen to return to its gas form while still in the blood or tissues, causing bubbles to form. Further reductions in pressure while flying or ascending to a higher altitude also contribute to bubble formation. The average airline cabin is pressurized to only 8000 ft to save fuel costs. If a person flies too soon after diving, this additional decrease in pressure may be enough to precipitate bubbling. If the bubbles are still in the tissue, they can cause local problems; if they are in the blood, embolization may result. (See the discussion under Deterrence/Prevention for more information.)

Charles law

For an in-depth discussion on the Charles law, please see the article on Dysbarism.

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Organ involvement associated with decompression sickness

As discussed in the section describing the Henry law, a reduction in pressure while ascending at the end of a dive can release dissolved gas (principally nitrogen) from solution in the tissues and blood, consequently forming bubbles in the body.

DCS results from the effects of these bubbles on organ systems. The bubbles may disrupt cells and cause a loss of function. They may act as emboli and block circulation, as well as cause mechanical compression and stretching of the blood vessels and nerves. The blood-bubble interface may act as a foreign surface, activating the early phases of blood coagulation and the release of vasoactive substances from the cells lining the blood vessels.[1] DCS may be divided into 3 categories: (1) type I (mild), (2) type II (serious), and (3) arterial gas embolization (AGE).

Type I decompression sickness

Type I DCS is characterized by one or a combination of the following: (1) mild pains that begin to resolve within 10 minutes of onset (niggles); (2) pruritus, or "skin bends," that causes itching or burning sensations of the skin; and (3) skin rash, which generally is a mottling or marbling of the skin or a papular or plaquelike violaceous rash. On rare occasions, skin has an orange-peel appearance.

Lymphatic involvement is uncommon and is usually signaled by painless pitting edema. The mildest cases involve only the skin or the lymphatics. Some authorities consider anorexia and excessive fatigue after a dive as manifestations of type I DCS.

Pain (the bends) occurs in most (70-85%) patients with type I DCS. Pain is the most common symptom of this mild type of DCS and is often described as a dull, deep, throbbing, toothache-type pain, usually in a joint or tendon area but also in tissue. The shoulder is the most commonly affected joint. The pain is initially mild and slowly becomes more intense. Because of this, many divers attribute early DCS symptoms to overexertion or a pulled muscle.

Muscle splinting causes decreased function. Upper limbs are affected about 3 times as often as lower limbs. The pain caused by type I DCS may mask neurologic signs that are hallmarks of the more serious type II DCS. Dysbaric osteonecrosis is a phenomenon that occurs in divers with high numbers of dives. This is a persistent problem, suggesting that the mechanisms involved in the disorder are not yet understood.

Type II decompression sickness

Type II DCS is characterized by the following: (1) pulmonary symptoms, (2) hypovolemic shock, or (3) nervous system involvement. Pain is reported in only about 30% of cases. Because of the anatomic complexity of the central and peripheral nervous systems, signs and symptoms are variable and diverse. Symptom onset is usually immediate but may be delayed as long as 36 hours.

  • Nervous system
    • The spinal cord is the most common site affected by type II DCS; symptoms mimic spinal cord trauma. Low back pain may start within a few minutes to hours after the dive and may progress to paresis, paralysis, paresthesia, loss of sphincter control, and girdle pain of the lower trunk. Vertebral back pain after a dive is a poor prognostic sign and can be a hall mark of spinal DCS with anticipated poor long-term outcome.[2]
    • Dysbaric myelitis occurs in half of the cases of neurological DCS. Venous ischemia is the most likely cause. Bladder problems, such as neurogenic bladder, may be common in the acute phase of DCS, may be the primary presentation, and may be prolonged.
    • DCS can be dynamic and does not follow typical peripheral nerve distribution patterns. This strange shifting of symptoms confuses the diagnosis, differentiating DCS from traumatic nerve injuries.
    • Pulmonary filtration protects the nervous system by stopping bubbles at the lungs, unless a bypass such as a patent foramen ovale or atrial septal defect is present. This filtration is size dependent. Tiny bubbles, or microemboli, that escape entrapment and continue to the brain do not cause infarction. Normal cerebral circulation starts with the highly oxygenated arterial blood flowing through the gray matter where much of the oxygen is extracted. This less oxygenated blood then flows to the long draining veins that supply the white matter of both the cerebral medulla and the spinal cord. At this level, even small additional decreases of oxygen content by embolization can be enough to damage the blood-brain barrier and initiate a cascade that ends with axonal damage. The result can be perivenous syndrome.[3]
    • Neurological deficits after a spinal cord injury can be multifocal. Sensory and motor disturbances can present independently, often resulting in a situation of "dissociation." This dissociation is found in most cases of spinal cord DCS.
  • Eyes
    • When DCS affects the brain, many symptoms can result. Negative scotomata, devoid of any lights or shapes, are the earliest symptom. Negative scotomata become positive after a few minutes.
    • Other common symptoms include headaches or visual disturbances, dizziness, tunnel vision, and changes in mental status. However, isolated diplopia, without other neurologic or ocular symptoms, is not consistent with decompression sickness. Mask barotrauma has been reported to cause an orbital hematoma in one diver. Physical examination and CT scan of the orbits confirmed the diagnosis.[4]
  • Ears
    • Labyrinthine DCS (the staggers) causes a combination of nausea, vomiting, vertigo, and nystagmus, in addition to tinnitus and partial deafness. This alternobaric vertigo can be difficult to differentiate from dysbaric eustachian tube dysfunction.[5] A history of eustachian tube problems depicted by past otitis media, past eustachian tube dysfunction, and problems equalizing pressure in the ears during the dive is associated with an increased prevalence of alternobaric vertigo.[6, 7] In inner ear DCS, vertigo was the major presenting complaint. In contrast to this, in dysbaric barotrauma, vertigo was not found to be the presenting complaint, or a significant problem. Instead, those patients complained of tinnitus and hearing loss. For more on dysbarism in the ear, please see the article on Dysbarism.
    • A study of offshore professional divers found higher incidence of dizziness, vertigo, and ataxia than nondiver controls. With an incidence range from 14-28%, 61% of the divers had prior DCS, mostly type I, which was found to correlate more than the total number of dives.[8]
    • The pathophysiology for inner ear DCS is believed related to a left to right shunt in the labyrinthine artery.[6] However, such a shunt should also cause cerebral symptoms that do not happen. The reason may lay with a difference in nitrogen washout in the inner ear compared to the brain. Experimental models suggest that the washout time for the inner ear is about 8 times as long compared to the brain (half-times of 8.8 and 1.2 minutes, respectively).[9]
  • Lungs
    • Pulmonary DCS (the chokes) is characterized by the following: (1) burning substernal discomfort on inspiration, (2) nonproductive coughing that can become paroxysmal, and (3) severe respiratory distress.
    • This occurs in about 2% of all DCS cases and can cause death. Symptoms can start up to 12 hours after a dive and persist for 12-48 hours.
  • Circulatory system
    • Hydration status appears to be affected by scuba diving. A number of influences play a role. First, many scuba divers engage in their sport in hot tropical environments. This naturally increases fluid requirements as the body works harder to keep itself cool. The same effect can even be found in colder climates where the diver uses a heated dry suit. Scuba diving is a physically demanding activity and thus utilizes more fluids. The breathing gases, whether they are compressed air or technical gas mixtures, are also dry, thus robbing the body of moisture in the exhaled gases. Most people underestimate their fluid requirements in these situations. Add to this, the drying effect of commercial airliner altitude pressures and the vacationer's preferred beverages being alcoholic. The average diver is thus set up for the possibility of significant dehydration.
    • A study of simple hematocrits after a single tropical dive found increases that were statistically significant and greater with the depth of the dive.[10] While the changes were overall small, they do highlight the drying effect of diving. Another study found significant increases in hematocrit with a median of 43 (the range was up to 60). They attempted to correlate more significant increases (to above 48) with neurological DCS. They did find this association in women but not in men.[11] In addition, a swine study found that dehydration significantly increased the risk of severe cardiopulmonary and CNS DCS and of overall death.[12] A human study also found a significant decrease in venous bubble formation with predive hydration.[13]
    • Hypovolemic shock is commonly associated with other symptoms. For reasons not yet fully understood, fluid shifts from the intravascular spaces to the extravascular spaces. The signs of tachycardia and postural hypotension are treated via oral rehydration if the patient is conscious or intravenously if the patient is unconscious. The treatment of DCS is less effective if dehydration is not corrected.
    • Thrombi may form because of the activation of the early phases of blood coagulation and the release of vasoactive substances from cells lining the blood vessels.[1] The blood-bubble interface may act as a foreign surface, causing this effect. Bubble formation in DCS has been believed not only to cause mechanical stretch or damage and blockage of blood flow by embolization but also to act as a foreign body and to activate the complement and coagulation pathways creating a thrombus.[14, 15, 16] Recent studies appear to leave this concept unresolved. Some of the studies' authors indicate that they have supported this hypothesis, while others could not find a correlation with degree of injury.
    • To assist with studying of DCS, it has been classified as type A for the more serious neurologic DCS (stroke-like). Type B is for the mild, or doubtful, neurologic symptoms. Studies suggest that the etiology is different for the two types and not explained by patent foramen ovale with left to right shunting.[17, 18]
    • Patent foramen ovale (PFO) or congenital atrial septal defect (ASD) also comes into play in DCS.[19, 20] These defects allow bubbles to pass from right to left circulation, bypassing the screening effects of the pulmonary circulation. This has been found to correlate with a higher prevalence of high spinal cord and head (brain)/neck DCS injury, which was more profound when a procedural violation during the dive led to DCS. Patients with only a large patent foramen ovale had an increased risk of DCS when decompression rules were not violated.
    • Although the overall prevalence of patent foramen ovale in the general population is significant (about 15-30%),[21, 22, 23] the prevalence of serious type II DCS is very low. Therefore, routine screening of divers for patent foramen ovale is not recommended. However, in the face of a serious DCS episode, it could be considered in evaluation of the patient for future diving. Serious active divers and professionals might consider routine screening for either atrial defect.[24] There are two reported cases of women with breast pain after diving that were found to have PFO.[25]
    • In a small sample of divers of which about one half experienced DCS on ascent, a PFO was found in 53% of those with DCS. In all of these symptomatic divers, they had the neurological form of DCS due to paradoxical embolization. In the other half, which did not experience DCS, only 1 (statistically 8%) was found to have a PFO. In addition, the complaint of breast pain in women who were found to have PFOs has been reported. All divers who experience neurological DCS or expect to push the limits of the diving tables should consider screening echocardiographic evaluations for PFO or ASD. In addition, serious active divers and professionals might consider routine screening for either atrial defect.
    • In a two samples of divers of which about one-half suffered significant DCS on ascent, a PFO was found in 50-53% of those with DCS. In all of these symptomatic divers they had the neurological form of DCS from paradoxical embolization. In the other half, which did not suffer DCS, only 1 (statistically 8%) was found to have a PFO. Of note is that only 1 out of 4 divers with serious DCS received any PFO screening. All divers who suffer neurological DCS, and frequent divers in general, should be considered for screening for PFO. This should be done with agitated saline contrast echocardiogram testing.[26, 23]
    • Another interesting feature of PFO is the relationship with migraines, in particular those with aura. In limited studies, approximately 48% of migraine patients with aura were found to have PFO. Interestingly, for many years, HBO physicians had noted that many patients with neurologic DCS had a prior history of recurrent migraines. When a group of divers was specifically studied for this condition, results showed that 47.5% of divers with a large right to left shunt at rest from PFO who had been victims of DCS had a history or migraines with aura.[27, 28]
    • The diagnosis of the shunt from an atrial defect is made through transcranial Doppler after an injection of agitated NSS through the antecubital vein to create minute bubbles and scanning at rest and with Valsalva. This was found more sensitive than transesophageal echocardiography using similar provocative maneuvers.[29] Therefore, a reasonable conclusion is that individuals with a history of migraine, especially those with aura, should consider specific screening for a PFA or ASD.

Arterial gas embolization

Pulmonary overpressurization (see article on Dysbarism) can cause large gas emboli when a rupture into the pulmonary vein allows alveolar gas to enter systemic circulation. Gas emboli can lodge in coronary, cerebral, and other systemic arterioles. These gas bubbles continue to expand as ascending pressure decreases, thus increasing the severity of clinical signs. Symptoms and signs depend on where the emboli travel. Coronary artery embolization can lead to myocardial infarction or dysrhythmia. Cerebral artery emboli can cause stroke or seizures.

Differentiating cerebral AGE from type II neurologic DCS is usually based on the suddenness of symptoms. AGE symptoms typically occur within 10-20 minutes after surfacing. Multiple systems may be involved. Clinical features may occur suddenly or gradually, beginning with dizziness, headache, and profound anxiousness. More severe symptoms, such as unresponsiveness, shock, and seizures, can quickly occur. Neurologic symptoms vary, and death can result. DCS of the CNS is clinically similar to AGE. Since the treatment of either requires recompression, differentiating between them is not of great importance. During the numerous dives involved in the recovery of wreckage from TWA Flight 800, rapid ascents resulting in AGE were uncommon even under stressful conditions.[30]

Acclimatization

Research is showing that experiencing DCS initiates a stress response in the body. The bubble formation causes the release of a stress protein (HSP70). The presence and preconditioning of HSP70 decreases the likelihood of developing DCS during a subsequent dive. This mechanism may be the cause for observed acclimatization with continued diving.[31, 32]

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Epidemiology

Frequency

United States

Between 1987 and 2003, the Sporting Goods Manufacturers Association estimated the number of scuba divers who dive at least once a year in the United States to have risen 32.1% from 2.4 to 3.2 million participants. However, over the past 6 years (2000-2006), a decrease of 23% to 3.2 million has occurred. The peak year was 1998 at 3.5 million. Of equal importance is the breakdown of those divers. Only about one third of divers were active or regular participants. Approximately two thirds of divers were casual divers, with many as little as a single dive in a year.[33, 34, 35] Experience yields a safer diver, though at the other extreme, over confidence can lead to pushing too close to limits.

Due to variability in reporting and collection of information, there is inconsistency in the mainstream medical journal publication of diving-related injury statistics. To improve statistical collection of information, the Divers Alert Network (DAN), based in North Carolina in the United States, acts as a medical information and referral service for diving-related injuries. In addition to this role, it provides education, acts as a clearinghouse for reports of diving-related injuries from around the world, and participates in studies related to diving injuries and illnesses. Their efforts to be the clearinghouse and repository of injury reports has been hampered in recent years, from 2003 and on, in the United States due to a change in federal law that makes medical confidentiality more stringent and thus their abilities to obtain reports and follow-up that much more difficult. They also have sponsored an ongoing long-term research study entitled Project Dive Exploration (PDE). According to DAN, fewer than 1% of divers experience DCS.[36] See the next section for details from a number of sources.

International

See Morbidity and Mortality below.

Mortality/Morbidity

  • Separating mortality data for DCS from those for barotrauma is impossible. Pathologists demonstrated little knowledge of diving accidents while performing autopsies and missed the more subtle diving injuries.[37, 38]
  • In 1995, 590 cases of DCS were analyzed (of a total 1132) by DAN.[36]
    • Of these, 27.3% were type I (pain-only DCS) and 64.9% were type II (neurologic DCS).
    • The remaining 7.8% were AGE cases.
  • A study from the US military in Okinawa reported 94 cases of DCS over 7 years.[39]
    • The annual incidence of DCS was 13.4 per 100,000 dives or 1 per 7400 dives.
  • Another study from Britain 1992-1996 found that the annual incidence of diving accidents increased from 4 per 100,000 dives to 15.4 per 100,000 dives during that time.
  • In another study, the lifetime incidence of DCS was 1 per 5463 dives. For severe DCS, it was 1 in 20,291 dives. It was also found that the more experienced divers were less likely to get DCS, presumably through more meticulous adherence to safety concerns and safer diving profiles.[40]
  • The DAN PDE study has followed about 8,000 divers for around 100,000 dives since 1995.[41]
    • The incidence of DCS in this population is 3.6 per 10,000 dives (or about 36,000 cases since the study began).
    • Through the PGE study, two groups were specifically observed. One is for divers in the colder North Sea and the other for divers in temperate regions, primarily the Caribbean.
    • The colder water group has seen a dramatic decrease in DCS from 400 to 100 cases per 10,000 dives over the most recent 3-year data period.
    • For the warmer water group, the yearly incidence is 50 per 10,000 or less.
  • DAN also participates in a diver's insurance program for injuries while traveling in general (though most of the travel is diving related).[42]
    • The incidence of diving-related injuries, though not just DCS, is around 55 claims per 10,000 insured.
  • DAN Project PGE data for 2004 based upon almost 24,000 dives.[41]
    • In this group, about 1300 reported an incident during the dive that could have been equipment, procedural, or equalization issues.
    • Twelve non-DCS injuries (of which some were dysbarism related) were reported.
    • Two cases of type I DCS, 3 cases of type II, none of AGE (see article on Dysbarism), and 2 cases that were undetermined.
    • DAN has analyzed their data in a very detailed manner.
  • Mortality rates are as follows:
    • In South Africa, the mortality rate was found to be as low as 0.016%.[43]
    • The US military in Okinawa reported fatalities at 0.0013% (1.3 per 100,000 dives).[39]
    • A New Zealand report states that the most common cause of death was drowning, but pathologists were frequently imprecise.[38]
    • In the United States, 3-9 deaths per 100,000 dives annually occur. The most common cause of dive-related death is drowning (60%), followed by pulmonary-related illnesses.
    • Diving fatalities in the United States and Canada have fluctuated year to year but have averaged around 83 over the past two decades.
    • The mortality rate is around 10-20 diving fatalities per 100,000 DAN members and increases by about one case per year.
    • In the breath-hold free-diving group, fatalities have steadily increased worldwide over the past decade to 22 in 2004. Note that only 5 or less were related to free-diving competitive activities, either training or competition. Most fatalities were during snorkeling, spear fishing, or collecting of marine specimens.
    • Divers Alert Network (DAN) studied mortalities over an 11-year period (1992-2003) to try and identify causes. Not surprisingly, asphyxia was a common cause for death, with entrapment and insufficient gases as the two most common in this category. Arterial gas embolism (AGE), also a common cause of death, was caused overwhelmingly by emergency ascent with insufficient gases as a key contributing factor. For those older than 40 years, there was an association with cardiovascular disease.[44] In AGE, mortality and morbidity is directly related to time to hyperbaric oxygen (HBO) treatment. If recompression with HBO occurs within 5 minutes, the death rate is only 5% with little residual morbidity in the survivors. If delayed 5 hours, mortality increases to 10% with residual symptoms in half of the survivors.[45]

Age

Many scuba divers start out in the sport young and relatively healthy. With time, they develop medical conditions. Likewise, other divers have significant medical issues upon entering the sport. An Australian study identified that a significant prevalence of medical conditions existed in experienced divers. Many conditions would be considered to disqualify these divers from future participation in scuba diving.[46]

DAN data also notes a steadily aging trend in their data.[41, 42]

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Contributor Information and Disclosures
Author

Stephen A Pulley, MS, DO, FACOEP  Assistant Professor, Department of Emergency Medicine, Philadelphia College of Osteopathic Medicine; Attending Faculty, Emergency Medicine Residency, Albert Einstein Healthcare Network; Attending Physician, Montgomery Hospital Medical Center

Stephen A Pulley, MS, DO, FACOEP, is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Eric M Kardon, MD, FACEP  Attending Emergency Physician, Georgia Emergency Medicine Specialists; Physician, Division of Emergency Medicine, Athens Regional Medical Center

Eric M Kardon, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

James Steven Walker, DO, MS  Clinical Professor of Surgery, Department of Surgery, University of Oklahoma College of Medicine

James Steven Walker, DO, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP  Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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Illustration of Dalton gas law. As an individual descends, the total pressure of breathing air increases and the partial pressures of the individual components have to increase proportionally. Nitrogen at higher partial pressures alters the electrical properties of cerebral cellular membranes, causing an anesthetic effect. Oxygen at higher partial pressures can cause CNS oxygen toxicity.
Illustration of Henry gas law. If nitrogen is added to a bottle, it diffuses into and equilibrates with the fluid. If pressure is suddenly released (decreased), such as when an individual ascends rapidly, a lag occurs before nitrogen can diffuse back to the nonfluid space. This delay causes nitrogen to bubble while still in the fluid.
 
 
 
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