Isobaric counterdiffusion

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This article refers to ICD as it relates to tissue diffusion. For other uses of the term ICD, see ICD (disambiguation)

Isobaric Counterdiffusion, Inert Gas Counterdiffusion (ICD) is the physiologic effect of diffusion of different gases occurring in opposite directions while under a constant ambient pressure.[1][2]

Background[edit]

Isobaric Counterdiffusion was first described by Graves, Idicula, Lambertsen, and Quinn in 1973 in subjects who breathed one inert gas mixture (nitrogen or neon) while being surrounded by another (helium).[3][4]

Clinical Relevance[edit]

In medicine, ICD is the diffusion of gases in different directions that can increase the pressure inside open air spaces of the body and surrounding equipment.[5]

An example of this would be a patient breathing nitrous oxide in an operating room (surrounded by air). Cuffs on the endotracheal tubes must be monitored as nitrous oxide will diffuse into the air filled space causing the volume to increase. In laparoscopic surgery, nitrous oxide is avoided since the gas will diffuse into the abdominal or pelvic cavities causing an increase in internal pressure. In the case of a tympanoplasty, the skin flap will not lay down as the nitrous oxide will be diffusing into the middle ear.

Diving Relevance[edit]

In diving, ICD is the diffusion of gases in different directions that can produce the formation of bubbles, without decompression and without changes in the environmental pressure. Two forms of this phenomenon have been described by Lambertsen:[1][6]

Superficial ICD[edit]

Superficial ICD occurs when the inert gas breathed by the diver diffuses more slowly into the body than the inert gas surrounding the body.[1][6][7]

An example of this would be breathing air in an heliox environment. The helium in the heliox diffuses into the skin quickly, while the nitrogen diffuses more slowly from the capillaries to the skin and out of the body. The resulting effect generates supersaturation in certain sites of the superficial tissues and the formation of inert gas bubbles.

Deep Tissue ICD[edit]

Deep Tissue ICD occurs when different inert gases are breathed by the diver in sequence.[1][6] The rapidly diffusing gas is transported into the tissue faster than the slower diffusing gas is transported out of the tissue.

An example of this was shown in the literature by Harvey in 1977 as divers switched from a nitrogen mixture to a helium mixture they quickly developed itching followed by joint pain.[8] Saturation divers breathing hydreliox switched to a heliox mixture and developed symptoms of decompression sickness during Hydra V.[9] More recently, Doolette and Mitchell have described ICD as the basis for inner ear decompression sickness and suggest "breathing-gas switches should be scheduled deep or shallow to avoid the period of maximum supersaturation resulting from decompression".[10]

ICD Prevention[edit]

Lambertsen made suggestions to help avoid ICD while diving.[1][6] If the diver is surrounded by or saturated with nitrogen, they should not breathe helium rich gases. Lambertson also proposed that gas switches that involve going from helium rich mixtures to nitrogen rich mixtures would be acceptable, but changes from nitrogen to helium should include recompression. However Doolette and Mitchell's more recent study of Inner Ear Decompression Sickness (IEDCS) now shows that the inner ear may not be well-modelled by common (e.g. Bühlmann) algorithms. Doolette and Mitchell propose that a switch from a helium-rich mix to a nitrogen-rich mix, as is common in technical diving when switching from trimix to nitrox on ascent, may cause a transient supersaturation of inert gas within the inner ear and result in IEDCS.[10] A similar hypothesis to explain the incidence of IEDCS when switching from trimix to nitrox was proposed by Steve Burton, who considered the effect of the much greater solubility of nitrogen than helium in producing transient increases in total inert gas pressure, which could lead to DCS under isobaric conditions.[11] Recompression with oxygen is effective for relief of symptoms resulting from ICD. However, Burton's model for IEDCS does not agree with Doolette and Mitchell's model of the inner ear. Doolette and Mitchell model the inner ear using solubility coefficients close to that of water.[10] Burton departs from this inner ear model and uses the solubility coefficients of lipids (fats) to model the inner ear. [11]

It is worth noting that now, at least one modern decompression planning software can predict ICD through modeling the inner ear as either water (Mitchell and Doolette's approach) or lipid tissue (Burton's approach). This software planning tool is called Ultimate Planner and could be found at http://www.techdivingmag.com/ultimateplanner.html

See also[edit]

References[edit]

  1. ^ a b c d e Hamilton, Robert W; Thalmann, Edward D (2003). "Decompression Practice". In Brubakk, Alf O; Neuman, Tom S. Bennett and Elliott's physiology and medicine of diving (5th ed.). United States: Saunders. pp. 477–8. ISBN 0-7020-2571-2. OCLC 51607923. 
  2. ^ Lambertson, Christian J; Bornmann, Robert C; Kent, MB, eds. (1979). "Isobaric Inert Gas Counterdiffusion". 22nd Undersea and Hyperbaric Medical Society Workshop. UHMS Publication Number 54WS(IC)1-11-82. Retrieved 10 January 2010. 
  3. ^ 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. Retrieved 10 January 2010. 
  4. ^ 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. Retrieved 10 January 2010. 
  5. ^ Barash, PG; Cullen, BF; Stoelting, RK (2005). Clinical Anesthesia (5th Rev ed.). United States: Lippincott Williams & Wilkins. ISBN 0-7817-5745-2. 
  6. ^ a b c d Lambertson, Christian J (1989). Vann, RD, ed. "The Physiological Basis of Decompression". 38th Undersea and Hyperbaric Medical Society Workshop. UHMS Publication Number 75(Phys)6-1-89. Retrieved 10 January 2010.  |chapter= ignored (help)
  7. ^ D'Aoust, BG; White, R; Swanson, H; Dunford, RG; Mahoney, J (1982). "Differences in Transient and Steady State Isobaric Counterdiffusion". Report to the Office of Naval Research. Retrieved 10 January 2010. 
  8. ^ Harvey, CA (1977). "Shallow saturation hyperbaric exposures to nitrogen-oxygen environments and isobaric switches to helium oxygen". Undersea Biomedical Research, Annual Meeting Abstract. Retrieved 10 January 2010. 
  9. ^ Rostain, JC; Lemaire, C; Gardette-Chauffour, MC; Naquet, R (1987). Bove; Bachrach; Greenbaum, eds. "Effect of the shift from hydrogen-helium-oxygen mixture to helium oxygen mixture during a 450 msw dive". Underwater and hyperbaric physiology IX (Bethesda, MD, USA: Undersea and Hyperbaric Medical Society). 
  10. ^ a b c Doolette, David J; Mitchell, Simon J (June 2003). "Biophysical basis for inner ear decompression sickness". Journal of Applied Physiology 94 (6): 2145–50. doi:10.1152/japplphysiol.01090.2002 (inactive 2010-01-09). PMID 12562679. Retrieved 10 January 2010. 
  11. ^ a b Burton, Steve (December 2004). "Isobaric Counter Diffusion". ScubaEngineer. Retrieved 10 January 2010. 

External resources[edit]

Lambertsen/ U Penn isobaric counterdiffusion references