Decompression sickness (DCS, also called the bends) can occur when gas that dissolved in your body at depth comes out of solution as bubbles, in the wrong place or in too great a number. Symptoms range from an aching shoulder to paralysis.
No model can guarantee that DCS will not happen. A decompression model keeps the conditions for bubble formation below a limit that, over many thousands of dives, has kept the rate of DCS low.
- Planned: GF 30/70, 9 m/min
On the bottom
On the bottom, the nitrogen you breathe is at a higher pressure than the nitrogen in your tissues, so nitrogen diffuses into them. Every tissue holds less gas than the ambient pressure could keep dissolved.
Bubbles cannot form in this state. The line on the chart is the tissue nearest its limit, and it stays below zero for the whole bottom time.
Supersaturation during the ascent
As you ascend, the ambient pressure falls faster than your tissues can release their gas. A tissue soon holds more gas than the ambient pressure can keep in solution: it is supersaturated.
Supersaturation occurs on every ascent, and it is what drives gas out of the tissues. Most of the gas is carried away in the blood and breathed out. Supersaturation is also the condition in which bubbles can grow, probably starting from microscopic gas nuclei already present in the body.
Decompression stops
A decompression plan limits supersaturation. At each stop the ascent pauses while the leading tissue releases gas. The next few metres of ascent raise its supersaturation again, which produces the sawtooth pattern on the chart.
This plan uses gradient factors of 30/70, so the model never lets the leading tissue exceed 70% of its limit, and on surfacing it is lower still.
A rushed ascent
The red line is the same dive with an ascent twice as fast and only the stops the model’s raw limit requires. It rises almost to the M-value, 100% on the chart.
The M-value does not separate safe dives from harmful ones. Divers have been bent below it, and others have exceeded it with no symptoms. The risk increases closer to it, so most divers plan to stay well below it.
Where bubbles form and travel
Supersaturation determines when bubbles can form. Where they form, and where the blood carries them, determines the symptoms.
- Venous side
- Arterial side
Bubbles in the tissues
Bubbles can form in the tissues themselves: around joints, in muscle and under the skin. There they press on nerves and block small blood vessels.
For this reason the most common symptom of DCS is pain, usually a deep ache in or near a joint, often the shoulder or elbow. Itching, a blotchy rash and swelling are other signs that start near where the gas is.
Venous bubbles and the lungs
Bubbles that enter the blood do so on the venous side, returning to the heart. The right side of the heart pumps them to the lungs. The fine blood vessels of the lungs filter them out: the gas passes into the airways and is breathed out.
Ultrasound often detects venous bubbles after dives that cause no symptoms. In most cases the lungs remove them without harm.
Bubbles in the arteries
Serious symptoms start when bubbles reach the arteries, which supply the brain, spinal cord and inner ear. One route is a patent foramen ovale (PFO), a flap-like opening between the upper chambers of the heart that about 1 in 4 adults have. Another is a larger number of bubbles than the lungs can filter.
A third route does not involve supersaturation. A breath held during the ascent can rupture lung tissue and force gas directly into the arteries. This is an arterial gas embolism, caused by the expansion described by Boyle’s law. Doctors group it with DCS under the term decompression illness.
Type I and Type II
The traditional classification is by where the symptoms appear. Type I covers pain, skin and lymphatic symptoms: less serious, but still a reason to get medical help. Type II involves the nervous system, the inner ear or the lungs (the “chokes”), with numbness, weakness, tingling, vertigo, breathlessness or confusion. It is more serious.
Symptoms are often mixed, and a mild symptom can be the first sign of a serious one. Many clinicians now describe the diver’s symptoms instead of assigning a type.
Risk factors
A plan controls the dive profile. It does not control the diver’s physiology. DCS is a matter of probability: the same profile can cause DCS in one diver and not in another, or in the same diver on different days. The factors below are those identified by reviews of the evidence, strongest first.
- The dive profile. Greater depth, longer bottom time, faster ascents and missed stops increase the risk more than any other factor.
- Repetitive and multi-day diving. The slow tissues carry residual gas from one dive into the next.
- Altitude after diving. Flying or driving over high ground soon after diving reduces the ambient pressure further.
- A patent foramen ovale. Associated with a higher risk of the neurological, inner-ear and skin forms, especially when the opening is large.
- Exercise and cold. Hard exercise soon after diving and being cold during decompression are both thought to increase the risk; the evidence is weaker.
- Individual factors. Fitness, fatigue, dehydration and age have all been studied, with less consistent results.
Try it
Choose a dive. The engine plans it twice: once with gradient factors 30/70 and normal ascent rates, and once rushed. The chart shows how close each ascent takes the leading tissue to its limit, and the caption shows how little time the rushed ascent saves.
- Planned
- Rushed
What to remember
- DCS starts with supersaturation: during the ascent, tissues hold more gas than the ambient pressure can keep in solution.
- Most of the gas leaves through the lungs without harm. Bubbles cause harm where they form, or when they reach the arteries.
- Type I covers pain, skin and lymphatic symptoms; Type II involves the nervous system, inner ear or lungs, and is more serious. Any symptom after a dive needs oxygen and medical help.
- Stops and slow ascents keep supersaturation well below the model’s limit. Diving to the limit still carries risk, and some divers are bent below it.
Supersaturation in the planner
Every DiveLogic plan shows each tissue’s supersaturation at every stop, as in the figures above. Plan the same 30 m dive, change the gradient factors, and compare how the margin and the run time change.
Sources
- Vann R. D., Butler F. K., Mitchell S. J., Moon R. E. (2011). Decompression illness. The Lancet 377(9760): 153-164.
- Golding F. C., Griffiths P., Hempleman H. V., Paton W. D. M., Walder D. N. (1960). Decompression sickness during construction of the Dartford Tunnel. British Journal of Industrial Medicine 17: 167-180. (The Type I and Type II classification.)
- Brubakk A. O., Neuman T. S., eds (2003). Bennett and Elliott’s Physiology and Medicine of Diving, 5th edition. Saunders, London.
- Hagen P. T., Scholz D. G., Edwards W. D. (1984). Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clinic Proceedings 59(1): 17-20.
- Torti S. R., Billinger M., Schwerzmann M., et al. (2004). Risk of decompression illness among 230 divers in relation to the presence and size of patent foramen ovale. European Heart Journal 25(12): 1014-1020.
- Baker E. C. (1998). Understanding M-values. Immersed 3(3): 23-27.