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KMID : 0356219990300010150
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Journal of the Korean Military Medical Association
1999 Volume.30 No. 1 p.150 ~ p.166
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The Effect of high Pressures on Physiological Function in vivo During deep Saturation Diving
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한진/Han, Jin
박세광/박인철/최병선/김희덕/Park, Sae Gwang/Park, In Cheol/--/Kim, Hee Duck
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Abstract
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When human divers or experimental animals are exposed to high presure, high pressure nervous syndrome(HPNS) and cardiovascular deconditioning(CD) has been observed. The HPNS occurs for pressure higher than 1.0 megapascal(MPa)[100 meter sea water(msw)] in a heliumoxygen mixture. Sign and symptoms of HPNS are factors that reduce diver´s ability to work at great depth. The CD has been reported to occur within 24-48 hour of exposure to 31 ATA environment and following decompression to sea level pressure. The CD was indicated by orthostatic intolerance, exaggerated cardiovascular response to a passive tilt, an elevated resting heart rate and a reduce stroke volume after diving.
Hyperbaric diving affects all parts of the human organism. Although much of the, research and development work has focused on the human factors of deep saturation diving such as thermal balance, breathing resistance and HPNS, there is little information on the physiological response to hyperbaric condition deep saturation diving. This study was designed to determine the possible effects of hyperbaric exposure on physiological function.
During the heliox saturation dives, P02 was maintained at 42 kilopascal(kPa) during_ the days of compression and for the bottom stay, 49.5 kPa during the days of decompression, and it was gradually decreased to 21 kPa for the last day of decompression. Multiple objective measurements of physiological function were made in seven divers by means of electrocardiograph(ECG), respiratory rate, electroculograph(EOG), electroencephalograph (EEG), and body temperature during a 14-day saturation diving to a pressure of 3.1 MPa, corresponding to a depth of 300 msw.
During compression there was a progressive decrease in heart rate(HR) and respiratory rate(RR). The greatest decrease in them was found at 2.1 MPa. The changes of HR and RR recovered to normal range, mostly before the end of the decompression. Little changes in EOG, EEG and body temperature were observed during the hyperbaric exposure. Clinical neurophysiological examination, including trail test, modified ball bearing test and sharpened Romberg test was also performed at the pressure of 0, 0.9, 2.1 and 3.1 MPa. No major neurophysiological problems arose during compression.
Our results suggest that hyperbaric exposure such as saturation diving may cause a decrease in HR and RR and also may facilitate some compensatory mechanisms from approximately 200 msw and deeper. We conclude that saturation diving to depth as great as 300 msw can be effective and safe. An attempt is made to assess the physiological significance of the principal findings.
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