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The Journal of Global Underwater Explorers Vol. 20, No. 1

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The Journal of Global Underwater Explorers Vol. 20, No. 1 The Journal of Global Underwater Explorers QuestVol. 20, No. 1 • A Different Light • The Ship That Changed History: The German Imperial Light Cruiser S.M.S. Breslau • The PBM Mariner Project • Bombs at Bikini: Operation Crossroads • The Glamorous World of Underwater Cave Exploration A Quarterly Journal Produced by Global Underwater Explorers QuestVol. 20, No. 1 EDITORS Kaitlin Kovacs Beth Murphy SENIOR EDITOR Panos Alexakos DESIGN EDITOR S.M.S. Breslau (Archive Dimitri Galon) Sheila D. Hardie PHOTOGRAPHERS Kathryn Arant Departments Kees Beemster Leverenz EQUIPMENT & TRAINING 4 JP Bresser Decompression: Revisiting Old Katy Fraser Assumptions Dimitri Galon S. Rhein Schirato Natalie Gibb John Kendall ENVIRONMENT 9 Jesper Kjøller The Sardinia Project Megan Lickliter-Mundon A. Marassich Claudio Provenzani ECOLOGY 13 Derk Remmers The Ecological Features of Valerie Wright Mediterranean Submarine Caves E. Romano, Ph.D. and L. Bergamin EXPLORATION 18 KTs: A Special Class of World War II Quest is published by: Cargo Ship Global Underwater Explorers 18487 High Springs Main Street C. Provenzani, E. Romano, Ph.D. and L. Zocca High Springs, Florida, 32643 Visit Quest on Facebook! www.facebook.com/ QuestJournal 2 Quest FeaturesContents A Different Light K. Fraser 22 The Ship That Changed 25 History: The German Imperial Light Cruiser S.M.S. Breslau D. Galon The PBM Mariner 33 Project K. Beemster Leverenz Bombs at Bikini: 39 Operation Crossroads J. Kjøller The Glamorous World of 46 Underwater Cave Exploration N. Gibb GUE AFFILIATES 32 GUE PARTNERS 56-58 THIS ISSUE'S CONTRIBUTORS 59 JP Bresser Vol. 20, No. 1 3 Equipment & Training Decompression: Revisiting Old Assumptions By Sergio Rhein Schirato D. Remmers Decmompression sickness is a complex condition that is still not entirely understood. HE first comprehensive attempt to understand the illness by Haldane are the same ones used in almost every computer related to the exposure to hyperbaric environments was or software available on the market today. Tled by John Scott Haldane in collaboration with Arthur Edwin Boycott and Guybon Chesney Castell Damant, and pub- Given the information that was available at the time, it is under- lished early in the 20th century as “The Prevention of standable that Haldane and his coworkers treated the matter as Compressed-air Illness.”1 In retrospect, the methodology used a physical (or mechanical) problem caused by bubbles forming in the study, the assumptions that different tissues would absorb during decompression. Having said that, it is worthwhile to note and eliminate gas at different rates and how he modeled it, and that in this study they specifically recognized that many of the the arguments used against the linear decompression (a method animals that died did not reveal signs of bubbles during nec- widely used at the time) are remarkable, especially if the knowl- ropsy and Haldane speculated that bubbles may have formed in edge and resources available at the time are taken into consid- parts of the body they did not study. eration. In many respects, most of Haldane’s conclusions remain the basis for many procedures still in use today. With a few Nevertheless, he laid the foundation for an idea that is still very improvements to supersaturation values, and other refinements much accepted: decompression sickness (DCS) is a mechanical (or “fit-to-reality adjustments”), the differential equations used problem caused by bubbles. 4 Quest D. Remmers It's long been thought that a lack of bubbles indicated a successful decompression. The purpose of this article is to discuss this and some other (1) Patent foramen ovale (PFO), a remnant of our fetal circula- assumptions widely accepted as true by the diving community tion, is found in approximately one-third of the population; (2) in light of recently published studies. pulmonary shunts are, among other things, a physiological response to handle the cardiac afterload, and different studies ASSUMPTION 1: VENOUS GAS EMBOLI AER FORMED DURING with high-performance athletes have shown that all subjects DECOMPRESSION ADN FILTERED BY THE LUNGS, WHILE studied presented some level of pulmonary shunting as the physi- BUBBLES FORMED IN OR TR ANSPORTED TO THE TISSUES AER cal effort to which they were submitted increased; (3) the cen- THE C AUSE OF DECOMPRESSION SICKNESS. tral nervous system has fast inert gas kinetics,2 meaning that bubbles eventually shunted through the heart to these tissues For many years it was believed that bubbles were related to tend to lose gas to the media, being reduced in size and quickly decompression sickness and that their absence would mean a collapsing. This assumption can be supported by the fact that successful decompression. However, with the development of the gold standard for PFO detection is the transesophageal echo- Doppler ultrasound technology late in the 1970s, it became clear cardiogram coupled with the injection of agitated (full of bub- that even mild exposures to hyperbaric environments and sub- bles) saline solution, in which gas serves as a contrasting media sequent decompression would lead to bubble formation in the to the ultrasound. There are no known cases of decompression venous circulation. Though bubbles were commonly found in sickness-like symptoms related to the use of such contrast, even the right chambers of the heart, Doppler echocardiograms when bubbles are clearly shunted to the left atrium. showed that most of them were filtered by the lungs and were not observed in the left chambers of the heart. In theory, bub- Additionally, post-dive bubbles detected by Doppler have diam- bles would be pumped from the left chambers into the systemic eters larger than 30 µm. A recent study using contrast-enhanced circulation, which would send them to the central nervous sys- imaging techniques capable of detecting bubbles with diameters tem, causing the neurological symptoms of decompression sick- smaller than 10 µm indicated the presence of smaller emboli in ness. This finding led to the endless discussion about the role of both sides of the heart, demonstrating that: (1) there are small cardiac or pulmonary shunts in decompression sickness since bubbles in humans that are not filtered by the lungs; (2) there the existence of a shunt would allow the migration of bubbles are small bubbles even in the absence of larger venous gas emboli; from the venous to the arterial (i.e., systemic) circulation, bypass- and (3) smaller bubbles follow a different timeline than larger ing the filtering effect of the lungs. venous gas emboli.3 Bubbles forming in the arterial circulation have also been identified in previous studies though their role While this statement might hold true for large venous gas emboli in decompression sickness, especially in the presence of neuro- most of the time, there are other facts that must be considered: logical symptoms, is yet to be understood. Vascular bubble Vol. 20, No. 1 5 models, designed to study nucleation on a flat hydro- phobic surface and how they expand to form bubbles after decompression, hold great promise for the improvement of decompression procedures in the future.4 ASSUMPTION 2: MECH ANICAL DE AMAG C AUSED BY BUBBLES IS DUE TO DECOMPRESSION SICKNESS. Several studies over the past two decades have shown that decompression has many physiological implications, D. Remmers ranging from reduction in Decompression sickness is not just a physical or mechanical issue. endothelial function to acti- vation of the immune sys- tem. As discussed above, formation of bubbles is a common finding in subjects exposed ASSUMPTION 3: DECOMPRESSION PROFILES WITH D EEP to hyperbaric environments and subsequent decompression. The STOPS AER S AFER. causal relationship between bubbles and physiological altera- tions, however, is yet to be proven. In recent years, the endothe- With divers pushing the boundaries of deeper diving beyond lial dysfunction hypothesis, which postulates that microparticles military and commercial diving, and the introduction of helium associated with endothelial damage act as nucleation sites for in the breathing mixes in the 1990s, different decompression bubble formation, has drawn attention and gained support. This techniques for bounce (non-saturation) dives started to be tested. has resulted in decompression sickness being seen not as merely Richard Pyle, an American ichthyologist from Hawaii, was prob- a physical or mechanical problem, but instead as a result of a ably one of the first to publicly advocate for decompression stops complex biochemical process. deeper than those calculated by algorithms derived from Haldane´s theory. On dives ranging in depth from 40 to 70 m, Recent studies have shown that the exposure to high-pressure he correlated catching fishes with his overall feeling after div- environments is sufficient to increase the production of IL-1β, ing, and attributed feeling better to the fact that when a fish was an interleukin that belongs to cytokines, which is an important caught, he had to stop much deeper than determined by decom- mediator in inflammatory responses.5 The mechanism behind pression algorithms to release gas out the fish´s swim bladder. the formation of such microparticles is related to high inert gas Decompression algorithms based on the control of bubble for- pressure through a mechanism that causes singlet oxygen for- mation and growth including the Varying Permeability Model mation, a potentially toxic free radical initiated by a cycle of developed by David Yount, which is the most well-known algo- actin S-nitrosylation, nitric oxide synthase-2, and NADPH oxi- rithm based on this strategy (probably because it is open code dase activation ultimately leading to microparticle formation.6 software), require decompression stops at greater depths, cor- Despite their harmful effects to the host, the production of reac- roborating Richard Pyle´s conclusions. At some point, it became tive oxygen species (ROS) is part of an orchestrated physiologi- well-established within the diving community that deeper stops cal response of the immune system to stop bacteria and fungus.
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