Decompression Sickness – Decompression Physiology
Decompression Sickness (DCS) is an illness caused by the effects of gas coming out of solution to form bubbles in the body after diving. It is due to the effect of Henry’s Law following diving exposures. Understanding decompression theories is difficult if not impossible, so the average diver may well bypass most of this blog post, if he is not technically inclined.
In sport divers the main gas formed in bubbles is nitrogen (N2) because these divers almost always breathe air. However, the same principles apply to other inert gases, such as helium (He), which may be breathed by deep commercial and technical divers.
When a diver breaths air from scuba equipment at depth, N2 is breathed at an increased partial pressure. Because gas diffuses from areas of high concentration (high partial pressure) to areas of lower concentration, N2 is taken up from the lungs by the blood and transported around the body and into the tissues. The greater the depth, the greater the partial pressure of N2, and therefore the amount of N2 absorbed. Early in the 20th century, John Scott Haldane applied this concept to develop the first ever decompression tables.
The speed of N2 distributing to the tissues depends on the their blood flow. Tissues with high metabolic needs such as the brain, heart, kidneys and liver receive most of the blood pumped from the heart. They will also receive most of the N2 carried in the blood and will have a rapid N2 uptake. Such tissues are termed “fast tissues” because of their fast N2 uptake.
Because blood passing through the lungs immediately equilibrates with any change in inspired N2 partial pressure, blood is the fastest tissue of all.
Other tissues such as ligaments, tendons and fat, with a relatively small blood flow, have a relatively slow N2 uptake. These tissues are termed “slow tissues”. Between the two are tissues of intermediate blood flow such as muscle. Some organs, such as the spinal cord, have both fast and slow tissue components. The rate of uptake of N2 in a tissue is exponential i.e. it varies depending on the amount of gas already taken up by the tissue. As the tissue takes on gas, the uptake slows because the partial pressure gradient decreases.
The filling of a scuba cylinder is an example of an exponential process. When an empty cylinder is connected to a high-pressure source, the cylinder initially fills quickly, but the flow slows as the pressure in the cylinder increases and approaches that of the gas source.
The uptake of gas in any tissue is initially rapid but slows with time. Accordingly, it may take a long time for a tissue to become fully saturated with gas, but fast tissues become saturated sooner than slow tissues.
Since the exponential uptake takes a long time to reach completion, even if it starts rapidly, the concept of tissue “half times” is used to compare tissues. The half time is the time taken
for a tissue to reach half its saturation level. A fast tissue may have a half time as little as a few minutes, while a slow tissue may have a half time of some hours.
N2 is eliminated in a reverse of the uptake process. As the diver ascends there is a reduction in the partial pressure of N2 in the air he breathes, allowing blood to release N2 into the lungs. The decrease in the blood level of N2 causes N2 to diffuse into the blood from the tissues. Fast tissues naturally unload N2 quicker than slow tissues.
Theoretically, tissues should lose N2 exponentially, and most decompression tables are calculated on this assumption. While large amounts of N2 are lost initially, the process slows with time and it may take 24 hours or longer for all the N2 taken up during a dive to be released. Diving again during the time of N2 elimination will mean that the diver will start his second dive with a N2 retention in some tissues. Adjustments are provided in the decompression schedule to allow for this and are incorporated as the repetitive dive tables.
If there is diminished circulation to a tissue during decompression, gas elimination will be reduced and thus bubble formation will be more likely.
In practice, even during routine conservative dives, bubbles of N2 frequently form in the blood and tissues, interfering with N2 elimination. It has been estimated that as much as 5% of N2 taken up by the body after some dives is transformed into bubbles on decompression. These are often termed “silent bubbles” since they usually do not produce any symptoms. They do however have a profound and unpredictable influence on the decompression requirements for repetitive diving, because it takes much longer to eliminate gas bubbles in tissues than it does gas in solution.
When tissues are subjected to an increased partial pressure of inert gas during a dive, they take up dissolved gas in accordance with Henry’s Law. However, there is a limit to the amount of gas which can be dissolved by a tissue exposed to any given partial pressure of gas (i.e. depth of dive). When this limit is reached the tissue is said to be saturated.
Our bodies are normally saturated with N2 at atmospheric pressure and contain about one liter of dissolved N2. If a diver were to descend to 20 meters (3 ATA) and remain there for a day or more, his body would take up the maximum amount of N2 possible at that pressure and would then be saturated at that depth. His body would now have about 3 liters of N2 dissolved in it.
Once the body is saturated with inert gas at a given depth, it will not take up more of that gas, no matter how long the diver spends at that depth. Consequently, once the diver is saturated the decompression requirement does not increase with time. This economy of time is exploited in saturation diving, when the diver is kept at depth for very long periods of time (days, weeks, months) but then needs only the same lengthy decompression.or more, his body would take up the maximum amount of N2 possible at that pressure and would then be saturated at that depth. His body would now have about 3 liters of N2 dissolved in it.
The process of bubble formation can be demonstrated easily by opening a bottle of beer (or champagne, depending on taste and income). In a carbonated beverage CO2 is dissolved in the liquid at a high pressure, which is then maintained by the lid. When the lid is opened, the pressure over the liquid becomes atmospheric and the partial pressure of CO2 in solution exceeds the critical limit for bubble formation, causing bubbles to form. This could be avoided if the pressure was reduced slowly (decompressed).
During ascent, the pressure surrounding the diver (the environmental pressure) is reduced. Eventually, the pressure of N2 dissolved in the tissues may become greater than the environmental pressure. The tissue is then said to be supersaturated.
The tissues are able to tolerate a certain degree of gas supersaturation. Nevertheless, Haldane explained that if the pressure of N2 in the tissues exceeds the environmental pressure by a critical amount, then bubble formation is likely. The pressure differential needed to cause this varies between tissues but with most scuba diving it equals or exceeds 2 : 1 (i.e. the partial pressure of inert gas in the tissues should not be more than twice the environmental pressure). This explains why DCS under recreational diving conditions is unlikely after an isolated dive to less than 10 meters — the pressure at 10 meters is 2 ATA, while the pressure at the surface is 1ATA – a 2:1 ratio.
Gas bubbles in the tissue and blood are the cause of DCS. The exact mechanism of bubble formation is complex. It is likely that microscopic gas spaces (bubble nuclei) exist in all body fluids and that these form a nucleus for bubble formation during decompression.
Bubbles can form in any tissue in the body including blood. The pressure in each bubble will be the same as the environmental pressure (if it was not, the bubble would expand or contract until it was) and the bubble size is governed by Boyle’s Law as the pressure changes.
At the onset of DCS, the pressure of N2 in the tissues is supersaturated (greater than the environmental pressure) so there is an immediate diffusion (pressure) gradient of N2 which then diffuses into any bubbles (or nuclei) present, causing them to expand.
Once a bubble has formed its behavior depends on several factors. Any increase in pressure such as diving or re-compression will reduce its size while any decrease in pressure such as ascent in the water, over mountains or in aircraft, will expand it. The bubble will continue to grow in any tissue until the N2 excess in that tissue has been eliminated. Once this has occurred (which may take hours or days) the bubble will begin to decrease in size but it may take hours, days or weeks to disappear. In the meantime the bubble can damage the tissues around it.
There is good evidence that bubbles frequently form in tissues and blood of recreational divers after routine no-decompression dives, even when the tables have been faithfully followed. These bubbles do not usually cause symptoms but certainly cause doubt about the validity of the tables.
Tissue damage by a bubble results from several factors. Bubbles in the blood obstruct blood vessels in vital organs such as the brain, while bubbles forming in the tissues may press on blood vessels and capillaries obstructing their blood flow. Bubbles in the blood can also stimulate the clotting process causing the blood to clot in the blood vessels, obstructing blood flow to vital organs, and reducing the ability of the remainder of the blood to clot adequately. In the brain, spinal cord and other tissues, bubble pressure in or on nerves may interfere with nervous system function.
The type of dive has a significant bearing on where and when bubble formation takes place. Short deep dives (i.e. deeper than 30 meters) tend to cause bubbles in the fast tissues (blood, brain and spinal cord) while long shallow dives tend to produce bubbles in the slow tissues (like the joints). Long deep dives cause bubbles everywhere.
This distribution occurs because:
- in short dives, only the fast tissues take up enough N2 to form bubbles on ascent and
- after shallow dives, fast tissues eliminate their relatively modest N2 excess before a critical pressure differential develops.
It can thus be seen why it is important to ascend slowly. The slower the ascent, the longer the time for fast tissues to eliminate N2 through the lungs, before a critical N2 pressure differential develops.
Diving folklore contains a myth that a diver using a single 2000 liters (72 cu. ft) tank cannot develop DCS. The air supply available was said to limit the diver to safe dive profiles. This is only true at very shallow depths and even then only partly so, e.g. for a dive to 20 meters, the average endurance may be about 30 minutes, which is within the no-decompression time given by most tables. Remember though, as mentioned previously, that any dive in excess of 10 meters can produce DCS.
The myth may become more apparent for deeper dives. For example, a single 2000 liter tank will give around 10 minutes duration for a 50 meter dive. According to most decompression tables, a 10 minute dive to 50 meters will require 10 minutes of decompression — but there will be no air remaining to complete these stops. Even if there was sufficient air, dives to this depth have a significant risk of DCS despite the tables being followed correctly.