In a recent interesting study (), arterial PO2 was measured while diving to 15 m and 42 m of freshwater (mfw). It was explored whether calculation of arterial PO2 at depth could use the arterial/alveolar [partial pressures of oxygen ratio (a:A ratio)] at 1 ATA, as suggested by . The a:A ratio calculated from the baseline arterial blood gases obtained at rest, out of the water, adequately predicted the PaO2 at depth. However, at the greater depth of 22 mfw, the calculation proved to be inaccurate. In addition, presented higher PaO2 than that predicted by the a:A ratio.
Although the slower diffusion while breathing dense gas should increase the alveolar–arterial difference in PO2 (A-a)DO2, it is well documented that breathing dense gas begets an opposite result and reduces the (A-a)DO2. During the breathing cycle, pressure reduction at inspiration causes an increase in venous return. Thus, during normal breathing, lung perfusion increases by 18% at inspiration. With the increase in gas density, breathing resistance is increased, and so there is an increase in pressure swings during the breathing cycle. This would cause an increase in tidal perfusion in the lung. When the increase in alveolar PO2 during inspiration meets an increased perfusion, higher oxygenation is expected. Thus, the decrease in (A-a)DO2 can be related to better timing between perfusion and elevated PAO2. Modeling this assumption in a single-compartment lung, presented that at dense gas breathing, (A-a)DO2 was reduced by 2 torr. Expanding the model to nine vertical differently perfused lung compartments, calculated a decreased (A-a)DO2 by 4–5 torr. The increase in cycling perfusion of the lung at a high pressure would explain why the a:A prediction would be inaccurate at the high pressure. Therefore, I claim that in any discussion of arterial PO2 at high pressure, cycling perfusion in the lung must be considered.
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RA: Writing – original draft, Writing – review & editing.
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References
1
ArieliR. (1992). Cyclic perfusion of the lung by dense gas breathing may reduce the (A- a)DO2. J. Basic Clin. Physiol. Pharmacol.3, 207–221. doi: 10.1515/jbcpp.1992.3.3.207
2
ArieliR.FarhiL. E. (1985). Gas exchange in tidally ventilated and non-steadily perfused lung model. Respir. Physiol.60, 297–309. doi: 10.1016/0034-5687(85)90059-3
3
MoonR.CamporesiE.SheltonD. (1987). “Prediction of arterial PO2 during hyperbaric treatment,” in Proceedings of the Ninth International Symposium on Underwater and Hyperbaric Physiology (Undersea & Hyperbaric Medical Society, Bethesda, MD), 1127–1131.
4
PaganiniM.ZucchiL.GiaconT. A.MartaniL.Mrakic-SpostaS.GarettoG.et al. (2024). Arterial blood gases in SCUBA divers at depth. Front. Mar. Sci.11. doi: 10.3389/fmars.2024.144569
5
WeaverL. K.HoweS. (1992). Normobaric measurement of arterial oxygen tension in subjects exposed to hyperbaric oxygen. Chest102, 1175–1181. doi: 10.1378/chest.102.4.1175
Summary
Keywords
high pressure, diving, arterial oxygen, dense gas, depth
Citation
Arieli R (2025) Commentary: Arterial blood gases in SCUBA divers at depth. Front. Mar. Sci. 12:1557303. doi: 10.3389/fmars.2025.1557303
Received
09 January 2025
Accepted
03 February 2025
Published
05 March 2025
Volume
12 - 2025
Edited by
Pieter-Jan A.M. Van Ooij, Royal Netherlands Navy, Netherlands
Reviewed by
Ingrid Eftedal, Norwegian University of Science and Technology, Norway
Updates
Copyright
© 2025 Arieli.
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*Correspondence: Ran Arieli, arieli1940@gmail.com
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.