![]() Inner ear disorders resulting from inadequate decompression-“vertigo bends”. Bethesda, MD: Undersea Medical Society, 1976, p. In: Development of Decompression Procedures for Depths in Excess of 400 Feet, edited by Hamilton RW. Philadelphia, PA: University of Pennsylvania, Institute of Environmental Medicine, 1978. Work capability and physiological effects in He-O2 excursions to pressures of 400, 800, 1200, and 1600 feet of sea water (Technical Report). Gas bubbles in the circulation of divers after ascending excursions from 300 to 250 msw. Brubakk AO, Peterson R, Grip A, Holand B, Onarheim J, Segadal K, Kunkle TD, Tonjum S. Medical aspects of a simulated dive to 1,500 feet (458 metres). In: Underwater Physiology V, edited by Lambertsen CJ. Fundamental studies in decompression from steady-state exposures. Development of unlimited duration excursion tables and procedures for helium-oxygen saturation diving. Spaur WH, Thalmann ED, Flynn ET, Zumrick JL, Reedy TW, Ringelberg JM. Testing of revised unlimited-duration upward excursions during helium-oxygen saturation dives. Correlation between decompression sickness and circulating bubbles in 232 divers. ![]() Houston, TX: Offshore Technology Conference, 1988. 20th Annual Offshore Technology Conference. Diving data bank: a unique tool for diving procedures development. Selective vulnerability of the inner ear to decompression sickness in divers with right to left shunt: the role of tissue gas supersaturation. Inner ear decompression sickness in scuba divers: a review of 115 cases. Biophysical basis for inner ear decompression sickness. Pathophysiology of inner ear decompression sickness: potential role of the persistent foramen ovale. Inner ear barotrauma and inner ear decompression sickness: a systematic review on differential diagnostics. Lindfors OH, Raisanen-Sokolowski AK, Hirvonen TP, Sinkkonen ST. This can explain why inner ear decompression sickness is more characteristic of rapid decompressions at great depths than of decompression at sea level. Bubbles in arterial blood have prolonged lifetimes at hyperbaric pressures compared with at sea level. NEW & NOTEWORTHY 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. 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. 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. 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. Previous data show that saturation excursions produce venous bubbles. 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 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. Inner ear decompression sickness (IEDCS) may occur after upward or downward excursions in saturation diving.
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