Introduction to the physiology of Diving - part 5

Decompression

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

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.

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