Decompression

"What it all boils down to, is that no one's really got it figured out just yet."
- Alanis Morissette -

The malady known as Decompression Sickness, or more commonly, the "bends", has been well-documented for many years. Starting with early caisson workers constructing bridges in pressurized chambers, it was soon evident that if people breathed compressed gas under elevated pressure for a period of time, and then returned to normal sea-level pressure, a wide variety of symptoms (including fatigue, mild to severe pain in the joints, rashes or itchy patches, dizziness, nausea, disorientation, numbness, mild to severe paralysis, loss of vision or hearing, unconsciousness, and even death) often ensued.

The U.S. Navy and other organizations spent a great deal of time and resources conducting experiments in order to better understand the physiological processes involved with this mysterious syndrome. It was soon learned by theory and empirical data that by slowing down the rate of ascent back to surface pressure after exposure to elevated pressure, the symptoms could be reduced or eliminated.

A set of "decompression tables" -- schedules that describe slow, staged ascent patterns back to the surface after exposures to various depths for various lengths of time (a process called "decompression") -- were eventually released for use by the general diving public. Unfortunately, no matter how "conservative" these schedules were, they were not perfect. In many cases, people following the schedules would suffer decompression sickness symptoms anyway.

Moreover, a great many dives that followed ascent patterns much less conservative than the schedules suggested, resulted in no decompression symptoms at all. Clearly, there were many other factors to the decompression "story" than simply depth and time. Thus began a long and continuing effort to understand all the actual factors involved, and produce a mathematical model that was better able to predict optimal ascent patterns (i.e, decompression schedules). As it turns out, this is an extraordinarily difficult undertaking.

If you ask a random, non-diving person on the street to explain what's really going on inside a diver's body that leads to decompression sickness, the answer is likely to be "I don't know".

If you ask the same question of a typical scuba diving instructor, the answer will likely be that nitrogen is absorbed by body under pressure (a result of Henry's Law); and that if a diver ascends too quickly, the excess dissolved nitrogen in the blood will "come out of solution" in the blood to form tiny bubbles; and that these bubbles will block blood flow to certain tissues, wreaking all sorts of havoc.

Pose the question to an experienced hyperbaric medical expert, and you will probably get an explanation of how "microbubbles" already exist in our blood before we even go underwater; and that ratios of gas partial pressures within these bubbles compared with dissolved partial pressures in the surrounding blood (in conjunction with a wide variety of other factors) determine whether or not these microbubbles will grow and by how much they will grow; and that if they grow large enough, they may damage the walls of blood vessels, which in turn invokes a complex cascade of biochemical processes called the "complement system" that leads to blood clotting around the bubbles and at sites of damaged blood vessels; and that this clotting will block blood flow to certain tissues, wreaking all sorts of havoc.

You will likely be further lectured that decompression sickness is an unpredictable phenomenon; and that a "perfect model" for calculating decompression schedules will never exist; and that the best way to calculate the best decompression schedules is by examining probabilistic patterns generated from reams of diving statistics.

If, however, you seek out the world's most learned scholars on the subject of decompression and decompression sickness, the top 5 or 6 most knowledgeable and experienced individuals on the subject, the ones who really know what they are talking about; the answer to the question of what causes decompression sickness will invariably be: "I don't know". As it turns out, the random non-diving person on the street apparently had the best answer all along.

What follows is a very coarse description of what seems to be going on, and what we think might have something to do with what causes decompression sickness.

We can probably assume that Henry's Law describes the nature of how gasses actually dissolve in our blood reasonably well. After that, however, things start to get complicated. To begin with, the rules that apply to oxygen are different from the rules that apply to other gas constituents. A lot of the oxygen that dissolves in our blood is immediately bound by hemoglobin, the important biomolecule that transports the all-important oxygen throughout our bodies. Furthermore, oxygen is constantly being "consumed" by metabolism, so that the dissolved concentrations are always somewhat lower than the inspired concentrations.

It is generally assumed among diving specialists that oxygen usually need not be considered in questions about decompression and decompression sickness, at least not when the inspired PO2 is within safe limits for CNS oxygen toxicity. Whether or not one could breathe 100% oxygen at great depths without risk of decompression sickness is moot, because risk of oxygen toxicity mandates that dives to depths in excess of about 20 feet (6 meters) should involve mixtures containing a gas or gases other than pure oxygen. For the purposes of this discussion on decompression, we will only consider the gases in the breathing mixture other than oxygen.

Most divers breathe air when they go underwater. As already discussed, this results in increased concentrations of nitrogen dissolved in the blood and tissues of the diver. If a diver spends sufficient time at depth, the blood and tissues will have elevated concentrations of dissolved nitrogen in them.

These nitrogen molecules are "held" in the blood by the ambient pressure acting on the diver's body at depth (represented by the bottom of the figure at left). If the diver were to suddenly ascend to the surface, the pressure which "held" the nitrogen in solution would be greatly reduced. In this situation, the nitrogen molecules would either form bubbles, or (more likely) cause pre-existing and harmlessly small "microbubbles" in the blood to grow large enough to cause problems.

Whether these bubbles cause harm directly by blocking blood flow in capillaries, or by causing clotting via the complement system, it seems almost certain that the bubbles are ultimately what leads to decompression sickness.

The solution to avoiding decompression sickness, then, is to avoid bubble formation and/or growth. Nitrogen does not instantaneously "fill" a diver's body. The process of nitrogen diffusing into the blood and tissues takes some amount of time.

If a diver stays shallow enough, or keeps the time at depth short enough, the diver can usually ascend directly to the surface without experiencing symptoms of decompression sickness. Such dives are called "no-decompression" dives.

When divers remain at sufficient depth for sufficient time, however, enough nitrogen dissolves into the blood and tissues such that a direct return to the surface leads to a high probability of decompression sickness symptoms. When ascending from such dives, divers must spend time at shallower depths to allow the excess dissolved gas to escape. This is called "Decompression", and is illustrated in the figure at right.

As a diver ascends, the ambient pressure begins to decrease. This means that the pressure of the gas inside the lungs (and thus the partial pressure of nitrogen in the lungs) will also decrease. At this point, a reverse of Henry's Law occurs: nitrogen molecules will move from the blood and tissues into the lungs, and will be vented from the diver with the exhaled breath.

The depth at which this decompression is conducted is critical: it must be shallow enough such that the PN2 in the lungs is lower than the dissolved concentration of nitrogen in the blood, but deep enough such that the ambient pressure is sufficient to prevent significant bubble growth.

Usually decompression is performed in "stages" -- at 10-foot (3-meter) intervals. This allows the diver to incrementally return to the surface, allowing the excess dissolved nitrogen to escape from the body.

It should be noted that, even though a diver surfacing from a "no-decompression" dive will usually not experience symptoms of decompression sickness, it doesn't mean that bubbles are not being formed or are not growing in the blood. It simply means that the bubbles do not grow large enough to cause obvious symptoms.

Damage may still be occurring even in the absence of symptoms, so most divers are urged to spend some time returning to the surface, even after "no-decompression" dives. This practice is referred to as "safety decompression stops", or simply "safety stops".

The topic of decompression is much, much more complicated than this. Additional information can be obtained from some of the references listed below under "Further Reading".

Mixed-Gas Diving

Because of the problems associated with oxygen toxicity, nitrogen narcosis, and decompression sickness, the maximum safe limit for breathing air is about 200 feet (61 meters). To overcome these problems, gas mixtures other than air should be used.

Perhaps the most severe and potentially deadly of the limitations is CNS oxygen toxicity. Air contains about 21% oxygen. The maximum safe PO2 limit of 1.4 ATA is exceeded with air when the ambient pressure is about 7 ATA, or 198 feet (60 meters).

The nitrogen narcosis at this depth has been likened to drinking several Martinis; and, for each minute spent at this depth breathing air, about 3 to 8 minutes are required for decompression.

The first step is to solve the CNS oxygen toxicity problem. This is actually relatively easy: to increase the depth at which the PO2 limit of 1.4 ATA is reached, one need only reduce the fraction of oxygen in the breathing gas. For example, a mixture containing only 10% oxygen would reach a PO2 of 1.4 ATA when the ambient pressure is 14 ATA - over 400 feet (120 meters) deep!

The problem, however, is that if the removed oxygen was replaced by more nitrogen, the effects of nitrogen narcosis would be increased. Thus, to extend the maximum safe depth of diving, both the oxygen and the nitrogen must be reduced. The only was to do that is to introduce another constituent to the breathing gas mixture. That constituent is usually helium.

Helium has two fundamental advantages over nitrogen for deep diving breathing mixtures. The first advantage is that it does not cause narcosis, even at very high inspired partial pressures. The second advantage is that it is a much smaller molecule, and therefore much less dense.

Because gas molecules are more closely packed together under higher pressures, the density of the gas is increased. For relatively large molecules, the increased gas density can lead to a significant increase in work of breathing. Helium is less dense at 300 feet (91 meters) than nitrogen is at sea level. These two advantages make helium the gas of choice for deep diving breathing mixtures.

Helium breathing mixtures generally come in two forms: heliox -- helium and oxygen without any nitrogen or other gas constituents; or trimix -- a combination of three primary gases, including helium, oxygen, and usually nitrogen.

Heliox is more often used by military and commercial divers, whereas trimix is more often used by civilian "technical" divers. Each has advantages and disadvantages, but both achieve the same basic result: reduce the concentration of oxygen, reduce or eliminate the nitrogen, and reduce the overall gas density.

Unfortunately, from the perspective of decompression, helium is not an ideal gas for the sorts of dive profiles most civilian deep divers do (i.e., less than one or two hours at depth). Because of its very small molecular size, helium dissolves into the blood and tissues much faster than nitrogen does.

More dissolved helium in less dive time means lower ratios of dive time to decompression time. If heliox or trimix were breathed for the entire duration of the dive, including the decompression, total dive times would be extremely long. The rate of decompression from deep dives using helium can be greatly increased if, during the ascent, the breathing mixture is changed to one that does not contain any helium.

Because most decompression time is spent at relatively shallow depths, narcosis is not a problem, so air would be adequate.

However, air is not an ideal decompression gas either, because it contains so much nitrogen. Even though the helium comes out of the body quickly when decompressing while breathing air, nitrogen is at the same time entering the blood and tissues. The amount of nitrogen added to the body can be reduced by reducing the fraction of nitrogen in the decompression breathing mixture.

Because oxygen does not factor in to decompression dynamics, the nitrogen can be replaced with oxygen. Mixtures containing only nitrogen and oxygen, with more than 21% oxygen, are popularly referred to as nitrox. More and more, recreational divers are using nitrox for dives to moderate depths, where CNS oxygen toxicity is not a major concern, and no-decompression times can be extended.

For deep diving, nitrox is used to accelerate decompression times.While nitrox is useful for decompression at intermediate depths, pure oxygen can be used at depths of 20 feet (6 meters) or shallower. Without any nitrogen or helium, pure oxygen maximizes the rate of decompression, cutting total decompression times down dramatically.

Thus, by using different gas mixtures during different portions of the dive, limits of conventional scuba can be extended and decompression can be optimized. A great deal of additional information on these and related topics is available in a wide variety of publications, some of which are listed below.

Divers who are interested in utilizing breathing gas mixtures other than air are encouraged to read as much material as possible, and to seek out proper training in mixed-gas diving techniques.

Further Reading

Note: This section is not yet complete. More references will be added later.

Bean, J.W. 1945. Effects of oxygen at increased pressure. Physiol. Rev. 25:1-147.

Bennett, P.B. 1982a. Inert gas narcosis. In: The Physiology and Medicine of Diving and Compressed Air Work. (P.B. Bennett and D.H. Elliot, eds), Balliere-Tindall, London. pp. 239-261.

Bennett, P.B. 1982b. The high pressure nervous syndrome in man. In: The Physiology and Medicine of Diving and Compressed Air Work. (P.B. Bennett and D.H. Elliot, eds), Balliere-Tindall, London. pp. 262-296.

Bennett, P.B. 1990. Inert gas narcosis and HPNS. In: Diving Medicine, Second Edition (A.A. Bove and J.C. Davis, eds.). W.B. Saunders Company, Philadelphia. pp. 69-81.

Bennett, P.B, R. Coggin, and J. Roby. 1981. Control of HPNS in humans during rapid compression with trimix to 650 m (2132 ft). Undersea Biomed. Res., 8(2): 85-100.

Bove, A.A. and J.M. Wells. 1990. Mixed gas diving. In: Diving Medicine, Second Edition (A.A. Bove and J.C. Davis, eds.). W.B. Saunders Company, Philadelphia. pp. 50-58.

Clark, J.M.. 1982. Oxygen toxicity. In: The Physiology and Medicine of Diving and Compressed Air Work. (P.B. Bennett and D.H. Elliot, eds), Balliere-Tindall, London. pp. 200-238.

Clark, J.M. and C.J. Lambertsen. 1971. Pulmonary oxygen toxicity: a review. Pharmacol. Rev. 23:37-133.

Hamilton, R.W. 1992a. Understanding special tables: Some things you should know. aquaCorps 3(1):28-31.

Hamilton, R.W. 1992b. Rethinking oxygen limits. technicalDIVER, v.3.2., pp. 16-19.

Hamilton, R.W. and J.T. Crea. 1993. Desktop decompression review. aquaCorps no. 6: 11-17.

Hamilton, R.W. and D.J. Kenyon. 1990. DCAP Plus: New concepts in decompression table research. In: MTS: Science and Technology for a New Ocean's Decade, Vol. 3., Marine Technology Society, Washington, D.C.

Kindwall, E.P. 1990. A short history of diving and diving medicine. In: Diving Medicine, Second Edition (A.A. Bove and J.C. Davis, eds.). W.B. Saunders Company, Philadelphia. pp. 1-8.

Lambertsen, C.J. 1978. Effects of hyperoxia on organs and their tissues. In: Extrapulmonary Manifestations of Respiratory Disease. Lung Biology in Health and Disease. Vol. 8. (E.D. Robin, ed.). Marcel Dekker, New York. pp. 239-303.

Lambertsen, C.J., J.M. Clark, R. Gelfand, et al. 1987. Definition of tolerance to continuous hyperoxia in man. An abstract report of Predictive Studies. In: Underwater and Hyperbaric Physiology IX (A.A. Bove, A.J. Bacherach, and L.J. Greenbaum, eds), Undersea and Hyperbaric Medical Society, Bethesda. pp. 717-735.

Menduno, M. 1992. Set theory: a look at rigging options. aquaCorps 3(1):22-23.

Mount, T. 1993. Chapter 13. Operational practices: Equipment configurations. In: Mixed Gas Diving: The Ultimate Challange for Technical Divers. (T. Mount and B. Gilliam, eds) Watersports Publishing, Inc., San Dieago, California. pp. 233-248.

Mount, T. and B. Gilliam (eds). 1993. Mixed Gas Diving: The Ultimate Challange for Technical Divers. Watersports Publishing, Inc., San Dieago, California. 392 pp.

National Oceanic and Atmospheric Administration (NOAA). 1991. NOAA Diving Manual: Diving for Science and Technology. Office of Undersea Research, National Oceanic and Atmospheric Administration, U.S. Department of Commerce, Washington, D.C.

Pyle, R.L. 1996. Section 7.9. Multiple gas mixture diving, Tri-mix. In: Flemming, N.C. and M.D. Max (Eds.) Scientific Diving: a general code of practice, Second Edition. United Nations Educational, Scientific and Cultural Organization (UNESCO), Paris; and Scientific Committee of the World Underwater Federation (CMAS), Paris, pp. 77-80.

Sharkey, P. and R.L. Pyle. 1992. The Twilight Zone: The potential, problems, and theory behind using mixed gas, surface-based scuba for research diving between 200 and 500 feet. In: Diving for Science...1992, proceedings of the American Academy of Underwater Sciences Twelfth Annual Scientific Diving Symposium. American Academy of Underwater Sciences, Costa Mesa, CA.

Stone, W.C. 1989a. Deep cave diving: Physiological factors. In: The Wakulla Springs Project (W.C. Stone, ed.), U.S. Deep Caving Team, Derwood, Maryland. pp. 25-53.

Stone, W.C. 1992. The case for heliox: a matter of narcosis and economics. aquaCorps 3(1):11-16.

Thom, S.R. and J.M. Clark. 1990. The toxicity of oxygen, carbon monoxide, and carbon dioxide. In: Diving Medicine, Second Edition (A.A. Bove and J.C. Davis, eds.). W.B. Saunders Company, Philadelphia. pp. 82-94.

Yarbrough, O.D., W. Welham, E.J. Brinton and A.R. Behnke. 1947. Symptoms of oxygen poisoning and limits of tolerance at rest and at work. Nav. Exp. Diving Unit Rep. 01-47.

By Richard Pyle Copyright © 1997, by Bishop Museum