Decompression (diving)

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For other uses, see Decompression (disambiguation).
Not to be confused with Decompression sickness. ‹See Tfd›
Divers decompressing in the water at the end of a dive
Basic deck decompression chamber

The decompression of a diver is the reduction in ambient pressure experienced by the diver during ascent, and also the process of elimination of dissolved inert gases from the diver's body, which occurs both during the actual ascent, during pauses in the ascent known as decompression stops, and after surfacing, until either the gas concentrations reach equilibrium, or another dive is started.

When a diver descends in the water the hydrostatic pressure, and therefore the ambient pressure, rises. Breathing gas is supplied at the same pressure as the surrounding water, and some of this gas dissolves into the diver's blood, and is transferred by the blood circulation to other tissues. Inert gas continues to be taken up until the gas dissolved in the diver is in a state of equilibrium with the breathing gas in the diver's lungs, (see: "Saturation diving"), or the diver moves up in the water and reduces the ambient pressure of the breathing gas until the inert gases dissolved in the tissues are at a higher concentration than the equilibrium state, and start diffusing out again.

Divers breathing gas at high pressure may need to do decompression stops, but a diver who only breathes gas at atmospheric pressure when free-diving, does not usually need to do decompression stops. However, it is possible to get taravana, thought to be a form of decompression sickness, from repetitive deep free-diving with short surface intervals.[1]

Divers who only use a snorkel near the surface or use an atmospheric diving suit do not need to decompress.

If the ambient pressure is reduced too quickly and to a pressure sufficiently low compared to the total concentration of dissolved gas, the dissolved inert gases such as nitrogen or helium can form bubbles in the blood and tissues of the diver in a manner similar to the fizzing of a carbonated beverage when opened.

The situation is similar when a diver or hyperbaric worker is compressed and decompressed in a diving chamber or airlock.

The symptoms of decompression sickness are known to be caused by damage resulting from the formation and growth of bubbles of inert gas within the tissues and by blockage of arterial blood supply to tissues by gas bubbles and other emboli consequential to bubble formation and tissue damage.

The precise mechanisms of bubble formation and the damage they cause has been the subject of medical research for a considerable time and several hypotheses have been advanced and tested. Tables and algorithms for predicting the outcome of decompression schedules for specified hyperbaric exposures have been proposed, tested, and used, and usually found to be of some use but not entirely reliable. Decompression remains a procedure with some risk, but this has been reduced and is generally considered acceptable for dives within the well tested range of commercial, military and recreational diving.

The immediate goal of controlled decompression is to avoid development of symptoms of bubble formation in the tissues of the diver, and the long term goal is to also avoid complications due to sub-clinical decompression injury.

During effective decompression, the asymptomatic venous microbubbles present after most dives are eliminated from the diver's body in the alveolar capillary beds of the lungs. If they are not given enough time, or more bubbles are created than can be eliminated safely, the bubbles grow in size and number causing the symptoms and injuries of decompression sickness.[2]

Decompression may be continuous or staged, where the ascent is interrupted by stops at regular depth intervals, but the entire ascent is part of the decompression, and ascent rate can be critical to harmless elimination of inert gas. What is commonly known as no-decompression diving, or more accurately no-stop decompression, relies on limiting ascent rate for avoidance of excessive bubble formation.

When diving with nitrogen-based breathing gases, decompression stops are typically carried out in the 3 to 21 metres (10 to 70 ft) depth range. With helium-based breathing gases the stop depths may start deeper.

The period at surface pressure immediately after dives is also an important part of decompression and can be thought of as the last decompression stop of a dive. It typically takes up to 24 hours for the body to return to its normal atmospheric levels of inert gas saturation after a dive.[3] When time is spent on the surface between dives this is known as the "surface interval" and is considered when calculating decompression requirements of the subsequent dive.

Decompression theory[edit]

Main article: Decompression theory
Recreational decompression tables printed on plastic cards

Decompression theory is the study and modelling of the transfer of the inert gas component of breathing gases from the gas in the lungs to the tissues of the diver and back during exposure to variations in ambient pressure. In the case of underwater diving and compressed air work, this mostly involves ambient pressures greater than the local surface pressure—but astronauts, high altitude mountaineers, and occupants of unpressurized aircraft, are exposed to ambient pressures less than standard sea level atmospheric pressure. In all cases, the symptoms of decompression occur during or within a relatively short period of hours, or occasionally days, after significant exposure to low pressure.

Physics and physiology of decompression[edit]

The absorption of gases in liquids depends on the solubility of the specific gas in the specific liquid, the concentration of gas, customarily measured by partial pressure, and temperature. The main variable in the study of decompression theory is pressure.

Once dissolved, distribution of the dissolved gas may be by diffusion, where there is no bulk flow of the solvent, or by perfusion where the solvent (in this case blood) is circulated around the diver's body, where gas can diffuse to local regions of lower concentration. Given sufficient time at a specific partial pressure in the breathing gas, the concentration in the tissues stabilises, or saturates, at a rate that depends on the solubility, diffusion rate and perfusion.

If the concentration of the inert gas in the breathing gas is reduced below that of any of the tissues, there is a tendency for gas to return from the tissues to the breathing gas. This is known as outgassing, and occurs during decompression, when the reduction in ambient pressure reduces the partial pressure of the inert gas in the lungs.

The combined concentrations of gases in any given tissue depend on the history of pressure and gas composition. Under equilibrium conditions, the total concentration of dissolved gases is less than the ambient pressure—as oxygen is metabolised in the tissues, and the carbon dioxide produced is much more soluble. However, during a reduction in ambient pressure, the rate of pressure reduction may exceed the rate at which gas is eliminated by diffusion and perfusion. If the concentration gets too high, it may reach a stage where bubble formation can occur in the supersaturated tissues. When the pressure of gases in a bubble exceed the combined external pressures of ambient pressure and the surface tension of the bubble-liquid interface, the bubbles grow, and this growth can damage tissue

Decompression models[edit]

Actual rates of diffusion and perfusion, and solubility of gases in specific tissues is not generally known, and vary considerably. However mathematical models have been proposed that approximate the real situation to a greater or lesser extent. These models predict whether symptomatic bubble formation is likely to occur for a given dive profile. Algorithms based on these models produce decompression tables. In personal dive computers, they produce a real-time estimate of decompression status and display it for the diver.

Two different concepts have been used for decompression modelling. The first assumes that dissolved gas is eliminated while in the dissolved phase, and that bubbles are not formed during asymptomatic decompression. The second, which is supported by experimental observation, assumes that bubbles are formed during most asymptomatic decompressions, and that gas elimination must consider both dissolved and bubble phases.

Early decompression models tended to use the dissolved phase models, and adjusted them by factors derived from experimental observations to reduce the risk of symptomatic bubble formation.

There are two main groups of dissolved phase models:

  • In parallel compartment models, several compartments with varying rates of gas absorption (half time), are considered to exist independently of each other, and the limiting condition is controlled by the compartment that shows the worst case for a specific exposure profile. These compartments represent conceptual tissues and don't represent specific organic tissues. They merely represent the range of possibilities for the organic tissues. The second group uses serial compartments, which assumes that gas diffuses through one compartment before it reaches the next.

More recent models attempt to model bubble dynamics, also usually by simplified models, to facilitate the computation of tables, and later to allow real time predictions during a dive. Models that approximate bubble dynamics are varied. They range from those that are not much more complex that the dissolved phase models, to those that require considerably greater computational power.

Decompression practice[edit]

Divers using the anchor cable as an aid to depth control during a decompression stop
Diver deploying a DSMB
Diver with bailout and decompression cylinders

The practice of decompression by divers comprises the planning and monitoring of the profile indicated by the algorithms or tables of the chosen decompression model, the equipment available and appropriate to the circumstances of the dive, and the procedures authorised for the equipment and profile to be used. There is a large range of options in all of these aspects.

Procedures[edit]

Decompression may be continuous or staged, where the ascent is interrupted by stops at regular depth intervals, but the entire ascent is part of the decompression, and ascent rate can be critical to harmless elimination of inert gas. What is commonly known as no-decompression diving, or more accurately no-stop decompression, relies on limiting ascent rate for avoidance of excessive bubble formation.

The procedures used for decompression depend on the mode of diving, the available equipment, the site and environment and the actual dive profile. Standardised procedures have been developed that provide an acceptable level of risk in appropriate circumstances. Different sets of procedures are used by commercial, military, scientific and recreational divers, though there is considerable overlap where similar equipment is used, and some concepts are common to all decompression procedures.

Normal diving decompression procedures range from continuous ascent for no-stop dives, where the necessary decompression occurs during the ascent, which is kept to a controlled rate for this purpose, through staged decompression in open water or in a bell, to decompression from saturation, which generally occurs in a decompression chamber that is part of a saturation system. Decompression may be accelerated by the use of breathing gases that provide an increased concentration differential of the inert gas components of the breathing mixture by maximising the acceptable oxygen content.

Therapeutic recompression is a medical procedure for treatment of decompression sickness, and is followed by decompression, usually to a relatively conservative schedule.

Equipment[edit]

Equipment directly associated with decompression includes:

History of decompression research and development[edit]

This painting, An Experiment on a Bird in the Air Pump by Joseph Wright of Derby, 1768, depicts an experiment performed by Robert Boyle in 1660.
Dry bell

The first recorded experimental work related to decompression was conducted by Robert Boyle, who subjected experimental animals to reduced ambient pressure by use of a primitive vacuum pump. In the earliest experiments the subjects died from asphyxiation, but in later experiments signs of what was later to become known as decompression sickness were observed.

Later, when technological advances allowed the use of pressurization of mines and caissons to exclude water ingress, miners were observed to present symptoms of what would become known as caisson disease, the bends, and decompression sickness.

Once it was recognized that the symptoms were caused by gas bubbles, and that re-compression could relieve the symptoms, further work showed that it was possible to avoid symptoms by slow decompression, and subsequently various theoretical models have been derived to predict safe decompression profiles and treatment of decompression sickness.

The symptoms of decompression sickness are caused by damage from the formation and growth of bubbles of inert gas within the tissues and by blockage of arterial blood supply to tissues by gas bubbles and other emboli consequential to bubble formation and tissue damage.

The precise mechanisms of bubble formation[4] and the damage they cause has been the subject of medical research for a considerable time and several hypotheses have been advanced and tested. Tables and algorithms for predicting the outcome of decompression schedules for specified hyperbaric exposures have been proposed, tested, and used, and usually found to be of some use but not entirely reliable. Decompression remains a procedure with some risk, but this has been reduced and is generally considered acceptable for dives within the well tested range of commercial, military and recreational diving.

Early developments[edit]

The first recorded experimental work related to decompression was conducted by Robert Boyle, who subjected experimental animals to reduced ambient pressure by use of a primitive vacuum pump. In the earliest experiments the subjects died from asphyxiation, but in later experiments[5] signs of what was later to become known as decompression sickness were observed.

Later, when technological advances allowed the use of pressurization of mines and caissons to exclude water ingress, miners were observed to present symptoms[5] of what would become known as caisson disease, compressed air illness,[6][7] the bends,[5] and decompression sickness.

Once it was recognized that the symptoms were caused by gas bubbles,[6] and that re-compression could relieve the symptoms.[5][8] In 1878 Paul Bert showed that decompression sickness is caused by nitrogen gas bubbles released from tissues and blood during or after decompression, and showed the advantages of breathing oxygen after developing decompression sickness.[9]

Further work showed that it was possible to avoid symptoms by slow decompression,[6] and subsequently various theoretical models[10] have been derived to predict safe decompression profiles and treatment of decompression sickness.

The start of systematic work on decompression models[edit]

In 1908 John Scott Haldane prepared the first recognized decompression table for the British Admiralty,[11] based on extensive experiments on goats using an end point of symptomatic DCS.[5][12]

George D. Stillson of the United States Navy tested and refined Haldane's tables in 1912,[13] and this research led to the first publication of the United States Navy Diving Manual and the establishment of a Navy Diving School in Newport, Rhode Island. At about the same time Leonard Erskine Hill was working on a system of continuous uniform decompression[5][8]

The Naval School, Diving and Salvage was re-established at the Washington Navy Yard in 1927, and the Navy Experimental Diving Unit (NEDU) was moved to the same venue. In the following years, the Experimental Diving Unit developed the US Navy Air Decompression Tables, which became the accepted world standard for diving with compressed air.[14]

During the 1930s, Hawkins, Schilling and Hansen conducted extensive experimental dives to determine allowable supersaturation ratios for different tissue compartments for Haldanean model,[15] Albert R. Behnke and others experimented with oxygen for re-compression therapy.[5] and the US Navy 1937 tables were published.[15]

In 1941, Altitude decompression sickness was first treated with hyperbaric oxygen.[16] and the revised US Navy Decompression Tables were published in 1956.

The beginnings of alternative models[edit]

In 1965 LeMessurier and Hills published A thermodynamic approach arising from a study on Torres Strait diving techniques, which suggests that decompression by conventional models forms bubbles that are then eliminated by re-dissolving at the decompression stops—which is slower than elimination while still in solution. This indicates the importance of minimizing bubble phase for efficient gas elimination,[17][18] Groupe d'Etudes et Recherches Sous-marines published the French Navy MN65 decompression tables, and Goodman and Workman introduced re-compression tables using oxygen to accelerate elimination of inert gas[19][20]

The Royal Navy Physiological Laboratory published tables based on Hempleman's tissue slab diffusion model in 1972,[21] Isobaric counterdiffusion in subjects who breathed one inert gas mixture while being surrounded by another was first described by Graves, Idicula, Lambertsen, and Quinn in 1973,[22][23] and the French government published the MT74 Tables du Ministère du Travail in 1974.

From 1976, decompression testing sensitivity was improved by ultrasonic methods that can detect mobile venous bubbles before symptoms of DCS become apparent.[24]

Several more approaches are developed[edit]

Paul K Weathersby, Louis D Homer and Edward T Flynn introduce survival analysis into the study of decompression sickness in 1982.[25]

Albert A. Bühlmann publishes Decompression–Decompression sickness in 1984.[26] Bühlmann recognized the problems associated with altitude diving, and proposed a method that calculated maximum nitrogen loading in the tissues at a particular ambient pressure. In 1984 DCIEM (Defence and Civil Institution of Environmental Medicine, Canada) release No-Decompression and Decompression Tables based on the Kidd/Stubbs serial compartment model and extensive ultrasonic testing,[27] and Edward D. Thalmann published the USN E-L algorithm and tables for constant PO2 Nitrox closed circuit rebreather applications, and extends use of the E-L model for constant PO2 Heliox CCR in 1985. The E-L model may be interpreted as a bubble model. The 1986 Swiss Sport Diving Tables were based on the Haldanean Bühlmann model.[28]

Bubble models start to become prevalent[edit]

D. E. Yount and D. C. Hoffman proposed a bubble model in 1986, and the BSAC'88 tables were based on Hennessy's bubble model.[29]

The 1990 DCIEM sport diving tables were based on fitting experimental data, rather than a physiological model, and the 1990 French Navy Marine Nationale 90 (MN90) decompression tables were a development of the earlier Haldanean model of the MN65 tables.

In 1991 D.E. Yount described a development of his earlier bubble model, the Varied Permeability Model, and the 1992 French civilian Tables du Ministère du Travail (MT92) also have a bubble model interpretation.

NAUI published Trimix and Nitrox tables based on the Wienke RGBM model in 1999, followed by recreational air tables based on the RGBM model in 2001.

In 2007 Gerth & Doolette publish VVal 18 and VVal 18M parameter sets for tables and programmes based on the Thalmann E-L algorithm, and produce an internally compatible set of decompression tables for open circuit and CCR on air and Nitrox, including in water air/oxygen decompression and surface decompression on oxygen, and in 2008 the US Navy Diving Manual Revision 6 includes a version of the 2007 tables by Gerth & Doolette.

See also[edit]

References[edit]

  1. ^ Wong, R. M. (1999). "Taravana revisited: Decompression illness after breath-hold diving". South Pacific Underwater Medicine Society Journal 29 (3). ISSN 0813-1988. OCLC 16986801. Retrieved 2008-04-08. 
  2. ^ Sport Diving, British Sub Aqua Club, ISBN 0-09-163831-3, page 104
  3. ^ BSAC '88 Decompression Tables Levels 1 to 4
  4. ^ http://www.sciencedirect.com/science/article/pii/S0001868613000146#!
  5. ^ a b c d e f g Acott, C. (1999). "A brief history of diving and decompression illness". South Pacific Underwater Medicine Society Journal 29 (2). ISSN 0813-1988. OCLC 16986801. Retrieved 2012-01-10. 
  6. ^ a b c Huggins 1992, chpt. 1 page 8
  7. ^ Butler, WP (2004). "Caisson disease during the construction of the Eads and Brooklyn Bridges: A review". Undersea and Hyperbaric Medicine 31 (4): 445–59. PMID 15686275. Retrieved 2012-01-10. 
  8. ^ a b Hill, L (1912). Caisson sickness, and the physiology of work in compressed air. London E. Arnold. Retrieved 2011-10-31. 
  9. ^ Bert, P. (originally published 1878). "Barometric Pressure: researches in experimental physiology". Translated by: Hitchcock MA and Hitchcock FA. College Book Company; 1943. 
  10. ^ Zuntz, N. (1897); Zur Pathogenese und Therapie der durch rasche Luftdruck-änderungen erzeugten Krankheiten, Fortschr, d. Med. 15, 532–639
  11. ^ Boycott, AE; Damant, GCC; Haldane, John Scott (1908). "Prevention of compressed air illness". Journal of Hygiene 8 (3): 342–443. doi:10.1017/S0022172400003399. PMC 2167126. PMID 20474365. Retrieved 30 May 2010. 
  12. ^ Boycott, A. E.; G. C. C. Damant, J. S. Haldane. (1908). "The Prevention of Compressed-air Illness". J. Hygiene 8 (3): 342–443. doi:10.1017/S0022172400003399. PMC 2167126. PMID 20474365. Retrieved 2008-08-06. 
  13. ^ Stillson, GD (1915). "Report in Deep Diving Tests". US Bureau of Construction and Repair, Navy Department. Technical Report. Retrieved 2008-08-06. 
  14. ^ US Navy. "Diving in the U.S. Navy: A Brief History". Retrieved 2008-08-06. 
  15. ^ a b Huggins 1992, chpt. 3 page 2
  16. ^ Davis Jefferson C, Sheffield Paul J, Schuknecht L, Heimbach RD, Dunn JM, Douglas G, Anderson GK (August 1977). "Altitude decompression sickness: hyperbaric therapy results in 145 cases". Aviation, Space, and Environmental Medicine 48 (8): 722–30. PMID 889546. 
  17. ^ LeMessurier and Hills. (1965) Decompression Sickness. A thermodynamic approach arising from a study on Torres Strait diving techniques. Hvalradets Skrifter, Nr. 48, 54–84.
  18. ^ Hills, BA (1978). "A fundamental approach to the prevention of decompression sickness". South Pacific Underwater Medicine Society Journal 8 (2). Retrieved 2012-01-10. 
  19. ^ How, J., West, D. and Edmonds, C. (1976); Decompression sickness and diving, Singapore Medical Journal, Vol. 17, No. 2, June 1976.
  20. ^ Goodman, MW; Workman, RD (1965). "Minimal-recompression, oxygen-breathing approach to treatment of decompression sickness in divers and aviators". United States Navy Experimental Diving Unit Technical Report. NEDU-RR-5-65. Retrieved 2012-01-10. 
  21. ^ Huggins 1992, chpt. 4 page 3
  22. ^ Graves, DJ; Idicula, J; Lambertsen, Christian J; Quinn, JA (February 1973). "Bubble formation in physical and biological systems: a manifestation of counterdiffusion in composite media". Science 179 (4073): 582–584. doi:10.1126/science.179.4073.582. PMID 4686464. http://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=4686464. Retrieved 10 January 2010.
  23. ^ Graves, DJ; Idicula, J; Lambertsen, Christian J; Quinn, JA (March 1973). "Bubble formation resulting from counterdiffusion supersaturation: a possible explanation for isobaric inert gas 'urticaria' and vertigo". Physics in medicine and biology 18 (2): 256–264. doi:10.1088/0031-9155/18/2/009. PMID 4805115. http://stacks.iop.org/0031-9155/18/256. Retrieved 10 January 2010.
  24. ^ Spencer MP (February 1976). "Decompression limits for compressed air determined by ultrasonically detected blood bubbles". Journal of Applied Physiology 40 (2): 229–35. PMID 1249001. Retrieved 2012-01-10. 
  25. ^ Weathersby, Paul K; Homer, Louis D; Flynn, Edward T (September 1984). "On the likelihood of decompression sickness". Journal of Applied Physiology 57 (3): 815–25. PMID 6490468. Retrieved 2009-04-27. 
  26. ^ Bühlmann Albert A. (1984). Decompression–Decompression Sickness. Berlin New York: Springer-Verlag. ISBN 0-387-13308-9. 
  27. ^ Huggins 1992, chpt. 4 page 6
  28. ^ Huggins 1992, chpt. 4 page 11
  29. ^ Huggins 1992, chpt. 4 page 4

Sources[edit]

Further reading[edit]

  1. Powell, Mark (2008). Deco for Divers. Southend-on-Sea: Aquapress. ISBN 1-905492-07-3. 
  2. Hills. B. (1966); A thermodynamic and kinetic approach to decompression sickness. Thesis
  3. Gribble, M. de G. (1960); A comparison of the High-Altitude and High-Pressure syndromes of decompression sickness, Brit. J. industr. Med., 1960, 17, 181.
  4. Lippmann, John; Mitchell, Simon (2005). Deeper into Diving (2nd ed.). Melbourne, Australia: J L Publications. ISBN 0-9752290-1-X.  Section 2 chapters 13–24 pages 181–350

External links[edit]