Department of Anaesthesiology, The University of Auckland, Auckland, New Zealand.
J Appl Physiol (1985). 2022 Sep 1;133(3):517-523. doi: 10.1152/japplphysiol.00121.2022. Epub 2022 Jul 14.
Inner ear decompression sickness (IEDCS) may occur after upward or downward excursions in saturation diving. Previous studies in nonsaturation diving strongly suggest that IEDCS is caused by arterialization of small venous bubbles across intracardiac or intrapulmonary right-to-left shunts and bubble growth through inward diffusion of supersaturated gas when they arrive in the inner ear. The present study used published saturation diving data and models of inner ear inert gas kinetics and bubble dynamics in arterial conditions to assess whether IEDCS after saturation excursions could also be explained by arterialization of venous bubbles and whether such bubbles might survive longer and be more likely to reach the inner ear under deep saturation diving conditions. Previous data show that saturation excursions produce venous bubbles. Modeling shows that gas supersaturation in the inner ear persists longer than in the brain after such excursions, explaining why the inner ear would be more vulnerable to injury by arriving bubbles. Estimated survival of arterialized bubbles is significantly prolonged at high ambient pressure such that bubbles large enough to be filtered by pulmonary capillaries but able to cross right-to-left shunts are more likely to survive transit to the inner ear than at the surface. IEDCS after saturation excursions is plausibly caused by arterialization of venous bubbles whose prolonged arterial survival at deep depths suggests that larger bubbles in greater numbers reach the inner ear. Inner ear decompression sickness that occurs during deep saturation diving is explained by arterialization of venous bubbles across intracardiac or intrapulmonary right-to-left shunts and growth of these bubbles if they arrive in the inner ear. Bubbles in arterial blood have prolonged lifetimes at hyperbaric pressures compared with at sea level. This can explain why inner ear decompression sickness is more characteristic of rapid decompressions at great depths than of decompression at sea level.
内耳减压病 (IEDCS) 可能发生在饱和潜水的上升或下降过程中。非饱和潜水的先前研究强烈表明，IEDCS 是由小静脉气泡通过心内或肺内右向左分流的动脉化以及当它们到达内耳时通过过饱和气体的内向扩散而导致的气泡生长引起的。本研究使用已发表的饱和潜水数据和内耳惰性气体动力学和动脉条件下气泡动力学模型来评估饱和潜水后的 IEDCS 是否也可以通过静脉气泡的动脉化来解释，以及这些气泡是否可能存活更长时间，并且在深饱和潜水条件下更有可能到达内耳。先前的数据表明，饱和潜水会产生静脉气泡。模型表明，这种潜水后，内耳中的气体过饱和度比大脑中的过饱和度持续时间更长，这解释了为什么内耳更容易受到到达气泡的伤害。在高环境压力下，动脉化气泡的估计存活时间明显延长，以至于能够通过肺毛细血管过滤但能够穿过右向左分流的大静脉气泡更有可能在到达内耳之前存活下来。饱和潜水后的 IEDCS 很可能是由静脉气泡的动脉化引起的，静脉气泡在深潜时的动脉化存活时间延长，表明更多数量的较大气泡到达内耳。内耳减压病是由心内或肺内右向左分流的静脉气泡动脉化以及这些气泡如果到达内耳而生长引起的。与海平面相比，高压下动脉血液中的气泡具有更长的寿命。这可以解释为什么内耳减压病在深潜时的快速减压比在海平面时更具特征性。
