PROCEEDINGS OF BIOMECHANICS OF SAFE ASCENTS WORKSHOP E ? 10 ft 30 ft TIME AMERICAN ACADEMY OF UNDERWATER SCIENCES September 25 - 27, 1989 Woods Hole, Massachusetts Proceedings of the AAUS Biomechanics of Safe Ascents Workshop Michael A. Lang and Glen H. Egstrom, (Editors) Copyright ? 1990 by AMERICAN ACADEMY OF UNDERWATER SCIENCES 947 Newhall Street Costa Mesa, CA 92627 All Rights Reserved No part of this book may be reproduced in any form by photostat, microfilm, or any other means, without written permission from the publishers Copies of these Proceedings can be purchased from AAUS at the above address This workshop was sponsored in part by the National Oceanic and Atmospheric Administration (NOAA), Department of Commerce, under grant number 40AANR902932, through the Office of Undersea Research, and in part by the Diving Equipment Manufacturers Association (DEMA), and in part by the American Academy of Underwater Sciences (AAUS). The U.S. Government is authorized to produce and distribute reprints for governmental purposes notwithstanding the copyright notation that appears above. Opinions presented at the Workshop and in the Proceedings are those of the contributors, and do not necessarily reflect those of the American Academy of Underwater Sciences PROCEEDINGS OF THE AMERICAN ACADEMY OF UNDERWATER SCIENCES BIOMECHANICS OF SAFE ASCENTS WORKSHOP WHOI/MBL Woods Hole, Massachusetts September 25 - 27, 1989 MICHAEL A. LANG GLEN H. EGSTROM Editors American Academy of Underwater Sciences 947 Newhall Street, Costa Mesa, California 92627 U.S.A. An American Academy of Underwater Sciences Diving Safety Publication AAUSDSP-BSA-01-90 CONTENTS Preface i About AAUS ii Executive Summary iii Acknowledgments v Session 1: Introductory Session Welcoming address - Michael A. Lang 1 Biomechanics of Safe Ascents Workshop introduction - Glen H. Egstrom 3 A historical look at ascent - Rev. Edward H. Lanphier 5 Introductory Session Discussion - Chair. Glen H. Egstrom 9 Session 2: Physics Session Phase dynamics and diving - Bruce R. Wienke 13 The physics of bubble formation ? David E. Yount 31 Physics Session Discussion - Chair: Glen H. Egstrom 45 Session 3: Physiology Session Growth of pre-existing bubbles in the body during ascent from depth - Hugh D. Van Liew 47 Ascent rate experiments and diver safety - Charles E. Lehner 55 Ascent and silent bubbles - Andrew A. Pilmanis 65 Physiology Session Discussion - Chair: Glen H. Egstrom 73 Session 4: Modeling Session Slow ascent rates: Beneficial, but a tradeoff- R.W. Hamilton 79 Ascent rates versus inert gas dynamics algorithms - Donald R. Short 83 Modeling Session Discussion - Chair Glen H. Egstrom 91 Session 5: Impact of Dive Equipment on Ascent Rate Dry suit buoyancy control - Richard Long 103 Dry suit valves and performance - Robert T. Stinton 111 Biomechanics of buoyancy compensation and ascent rate - Glen H. Egstrom 123 Dive computer monitored ascents - Panel: Lang, Walsh, Lewis, Coley, Huggins 127 Dive Equipment Session Discussion - Chain Michael A. Lang 137 Session 6: Impact of Training on Ascent Rate Chamber perspective of diving accident incidences - Andrew A. Pilmanis 139 The Divers Alert Network (DAN): Diving accident data and its implications - J.A. Dovenbarger, P.B. Bennett, and CJ. Wachholz 143 A review of ascent procedures for scientific and recreational diving - John E Lewis 153 Buoyancy control and ascent rates - Walter F. Hendrick, Sr. 163 Recreational training agencies' ascent training policy statements - NAUI, SSI, YMCA, PADI 169 Ascent Training Session Discussion - Chair: James R. Stewart 179 Session 7: SCUBA Equipment Standardization SCUBA equipment standardization discussion - M. A. Lang and G.H. Egstrom 187 Session 8: Individual Perspectives Insights gained: Diving accidents concerning ascents - Jon Hardy 197 Individual Perspectives Session Discussion - Chair: Michael A. Lang 201 Session 9: General Discussion, Concluding Remarks Workshop Co-Chairs: Michael A. Lang and Glen H. Egstrom 205 Appendices Participants list 207 Workshop program 211 Ascent rate comparisons 215 Preface The third major AAUS Workshop addresses the complexities of safe ascent rate. The information contained in this monograph is the result of the combined efforts of nearly fifty nationally recognized experts drawn from a variety of fields related to diving. The papers and discussions reflect some differences of opinion with regard to the options available to the diver when ascending from a dive. The message from these experts is, however, quite clear. There is a risk associated with ascending to the surface following a dive that can be minimized for the diver who will learn to exercise control over the buoyancy characteristics of the equipment in order to be able to make a stop 15-20 feet from the surface with ascent rates not in excess of 60 feet per minute. Once again, we are indebted to a group of dedicated professionals who gave of their time and energy to develop a position statement that represents the state of the art with regard to the understanding of the importance of controlling ascent rate. As a result of this workshop we have a clearer understanding of the known and the unknown that should provide guidance for our training programs and challenges for our researchers. A very special thanks to our hosts Terry Rioux at the Woods Hole Oceanographic Institution and Anne Giblin at the Marine Biological Laboratory who provided an outstanding facility for the workshop and to Mike Lang who has pulled mightily on the oars to insure that die proceedings are not delayed on their path to the diving public. Glen H. Egstrom, Ph.D. President, American Academy of Underwater Sciences About AAUS The American Academy of Underwater Sciences (AAUS) is a non-profit, self- regulating body dedicated to the establishment and maintenance of standards of practice for scientific diving. The AAUS is concerned with diving safety, state-of-the-art diving techniques, methodologies, and research diving expeditions. The Academy's goals are to promote the safety and welfare of its members who engage in underwater sciences. These goals include: * To provide a national forum for the exchange of information in scientific diving; * To advance the science and practice of scientific diving; * To collect, review and distribute exposure, incident and accident statistics related to scientific diving; * To promote just and uniform legislation relating to scientific diving; * To facilitate the exchange of information on scientific diving practices among members; * To engage in any or all activities which are in the general interest of the scientific diving community. Organized in 1977 and incorporated in 1983, the AAUS is governed by a Board of Directors. An Advisory Board of past Board of Directors members provides continuity and a core of expertise to the Academy. Individual membership in AAUS is granted at the Member, Associate Member, and Student Member categories. Organizational membership is open to organizations currently engaged in scientific diving activities. Maintenance of membership is dependent on a continued commitment to the purposes and goals of the Academy, compliance with the reporting requirements and payment of current fees and dues. * For the diving scientist, AAUS provides a forum to share information on diving research, methodologies and funding; * For the diving officer, AAUS provides an information base of the latest standards of practice for training, equipment, diving procedures and managerial and regulatory experience. * For the student, AAUS provides exposure to individuals, agencies and organizations with on-going programs in undersea research. Scientific diving means diving performed solely as a necessary part of a scientific activity by employees whose sole purpose for diving is to perform scientific research tasks. Scientific diving does not include tasks associated with commercial diving such as: rigging heavy objects underwater, inspection of pipelines, construction, demolition, cutting or welding, or the use of explosives. Scientific diving programs allow research diving teams to operate under the exemption from OSHA commercial diving regulations. This reduces the possibility of an OSHA fine and some concern regarding civil liability. Civil suits examine whether the "standards of practice of the community" have been met Diving programs which conform to AAUS standards reflect the standard of practice of the scientific diving community and allow divers from different institutions to perform underwater research together. This reciprocity between programs is the product of years of experience, trust and cooperation between underwater scientists. u EXECUTIVE SUMMARY The Biomechanics of Safe Ascents represents the combined effort of a group of selected experts in diving physics, physiology, equipment and training to address questions associated with diver ascent rates. There was consensus that there is a risk to the diver. In recent years the advent and increasingly wider use of dive computers, which require a variety of ascent rates, to assist divers in making safe ascents, has lead to a basic question. What is a safe and reasonable ascent rate? The traditional ascent rate of 60 ft/min is based upon the United Sates Navy tables. Presentations by formulators of the original United States Navy tables indicate that this rate was a operational compromise between the fastest rate a hard-hat diver could be physically hauled to the surface, and the fastest rate a free swimming diver could swim to the surface. It also represented an ascent rate of 1 ft/min which could easily be calculated by the diver and surface tenders. Dissolved and free gases within tissues do not behave in the same manner. Models indicate that bubble formation within tissues is initiated at micronuclei. The size and behavior of these bubbles is determined by the degree of saturation and the rate of ascent. A slow ascent rate has the advantage of maintaining the micronuclei under pressure, but has the disadvantage of slowing the diffusion of nitrogen from the tissue. The "staged" diver ascent - a relatively rapid ascent punctuated by stops at progressively shallower depths - approximates the ideal profile of a gradual but continuously decreasing pressure. The objective of such a protocol is to allow time for gasses to escape via the lungs and avoid supersaturated conditions which lead to the formation of bubbles in the blood or tissues. However, testing of human subjects has shown that dives conforming to U.S. Navy "no-decompression" limits produced bubble nuclei in all subjects after all dives. The occurrence of these "silent bubbles" was almost eliminated when divers stopped at depths of 20 to 10 feet for 1 to 2 minutes. All of the data presented indicated that slower ascent rates decreased the likelihood of bubble formation and that a shallow stop for a short period of time significantly decreased the risk of pressure related injury. Studies showed divers rarely ascend at rates as low as 60 ft/min. In practice, divers generally cannot recognize an ascent rate of 60 ft/min, and too frequently relied on equipment to replace adequate training in buoyancy control. The control of buoyancy is imperative in attaining and maintaining a predetermined rate of ascent. Tests of scuba divers with fully inflated buoyancy compensators showed rates of ascent ranging from 68 to 150 ft/min at depths of approximately 10 feet, and increased to a maximum of more than 250 ft/min in the last 4 feet of the ascent. The technique of buoyancy control in wet suits or dry suits is exactly the same, that is proper weighting and the adding or expelling of air to remain in neutral trim. Training is required to reach and maintain a degree of proficiency. In dry suits an automatic exhaust valve located in the upper portion of the torso is recommended. In wet suits added emphasis must be placed on training the individual diver to recognize the importance of proper weighting and maintenance of control of buoyancy. In addition buoyancy compensators should be equipped with a rapid exhaust valve that can be activated in the horizontal swimming position. iii In the examination of the records of hundreds of cases recompression treatment for pressure related injuries, approximately half were related to loss of buoyancy control. At present, it would appear that divers do not have adequate equipment or training to allow them to effectively monitor and control their ascent. In summary, it has long been the position of the American Academy of Underwater Sciences that the ultimate responsibility of diver safety rest with the individual diver. Divers are encouraged to slow their ascents. SAFE ASCENT RECOMMENDATIONS 1. Buoyancy compensation is a significant problem in the control of ascents. 2. Training in, and understanding of, proper ascent techniques is fundamental to safe diving practice. 3. Before certification, the diver is to demonstrate proper buoyancy, weighting and a controlled ascent, including a "hovering" stop. 4. Diver shall periodically review proper ascent techniques to maintain proficiency. 5. Ascent rates shall not exceed 60 fsw per minute. 6. A stop in the 10-30 fsw zone for 3-5 min is recommended on every dive. 7. When using a dive computer or tables, non-emergency ascents are to be at the rate specified for the system being used. 8. Each diver shall have instrumentation to monitor ascent rates. 9. Divers using dry suits shall have training in their use. 10. Dry suits shall have a hands-free exhaust valve. 11. BC's shall have a reliable rapid exhaust valve which can be operated in a horizontal swimming position. 12. A buoyancy compensator is required with dry suit use for ascent control and emergency flotation. 13. Breathing 100% oxygen above water is preferred to in-water air procedures for omitted decompression. IV Acknowledgments Michael A. Lang Workshop Co-Chair 1989 AAUS Symposium Chair I want to specifically thank a number of people right now. First, the speakers for preparing their presentations and sharing their knowledge and insight with the workshop. In addition, I extend an extra measure of appreciation to those speakers who provided me with a hard copy and floppy disk of their paper. It speeds up the compilation and editing of these workshop proceedings tremendously. We foresee a three months turn around time for this document, which should be available for distribution at the DEMA Trade Show in Orlando, Florida, January 18-21, 1990. I also thank the participants for their useful input and discussions. Very special thanks goes to the scuba equipment manufacturers representatives: Dick Long (DUI), Bill Oliver (SeaQuest), Mark Walsh (Dacor Corp.), John Lewis (DCs: US Divers, Oceanic), Doug Toth (ScubaPro), Ron Coley (Suunto/SeaQuest), Bob Stinton (DUI), Karl Huggins (ORCA-Edge). These companies and individuals have been very supportive over the years of the AAUS efforts to increase diving safety. Thanks to Terry Rioux (WHOI) and Anne Giblin (MBL) for making the local arrangements. Compiling these proceedings and transcribing and editing the recordings was a monumental, non-salaried effort. I wish to thank Maria, Michelle, Nicole and Sergio Lang for their patience and support, and understanding for the many hours spent away from them, locked up in the office. For this and other scientific diving projects, I very much appreciate the encouragement and support of Don Short, Bruce Wingerd and the SDSU Diving Control Board. The following sponsors of the Biomechanics of Safe Ascents Workshop had the foresight and support, and contributed funds to make this meeting possible: ? The American Academy of Underwater Sciences ? Diving Equipment Manufacturer's Association ? National Oceanic and Atmospheric Administration Finally, I thank Glen Egstrom, AAUS President and Workshop Co-Chair, for his efforts and thorough insight into the diving safety problems facing the diving community today. WELCOMING ADDRESS Michael A. Lang Biomechanics of Safe Ascents Workshop Co-Chair Department of Biology San Diego State University San Diego, CALIFORNIA 92182 U.S.A. On behalf of the American Academy of Underwater Sciences, I welcome you to Woods Hole, Massachusetts, the Woods Hole Oceanographic Institution, the Marine Biological Laboratory and the Biomechanics of Safe Ascents Workshop. This workshop is the third in the series of AAUS Diving Safety Workshops. The first workshop was held in November 1987 at the University of Washington, Seattle, and focused on cold water diving methods, equipment, physiology and specialized training considerations. The second workshop was convened in September 1988 at the USC Catalina Marine Science Center addressing dive computer procedures, guidelines for use and the underlying principles and algorithms. This year we aim to enhance our efforts to increase diving safety in general and specifically examine ascent rates: physics, physiology, training and equipment involved in bringing a diver to the surface. The self-introduction of invited speakers, workshop participants, and their affiliations acquainted the workshop with the workshop attendees. A brief program overview was followed by administrative comments regarding workshop logistics and proceedings. The following sponsoring agencies have made this workshop and the dissemination of the resulting information to the diving public possible: ? American Academy of Underwater Sciences (AAUS) ? Diving Equipment Manufacturers Association (DEMA) ? National Oceanic and Atmospheric Administration (NOAA). BIOMECHANICS OF SAFE ASCENTS WORKSHOP INTRODUCTION Glen H. Egstrom President, American Academy of Underwater Sciences Biomechanics of Safe Ascents Workshop Co-Chair 3440 Centinela Ave. Los Angeles, CALIFORNIA 90066 U.S.A. It is really a pleasure to be here and once again see that the American Academy of Underwater Sciences was able to mount an effort to deal with a problem that is both timely and important. I am reminded of a couple of things that have happened in the past. One is a quote that has become somewhat famous and is attributed to Jim Stewart who, when observing about meetings of this sort said that frequently you get more information over a cold beer in the dark of night than you do from the deliberations of the day. I hope you recognize that this is not a workshop that is limited just to the structure of this particular program, but that hopefully we will have an opportunity for people with similar interests to be able to discuss these topics at length and with all candor. I am also reminded of another quote where an individual made the observation that he had never encountered a problem, however complicated, which, when viewed in the proper perspective, didn't become more complicated. I really mink that is part of the problem of what we are running into, because when most of us in this room were trained as divers, life was really pretty simple. We had one set of dive tables to contend with and they came from the bible, the U.S. Navy Diving Manual. We had one ascent rate if you didn't read through the entire document too carefully. Reading more in-depth reveals that perhaps there were some considerations for some other ascent rates, but it was always "ASCEND NO FASTER THAN 60 FEET PER MINUTE", which was somehow equated with the small bubbles, smaller bubbles, smallest bubbles, or the person's best guess as to what that all amounted to. One of the other things I believe we need to be aware of is an observation that was made by Einstein who said: "you should always try to make things as simple as possible, never simpler". Our major concern at this meeting is that when we start to put all of this information together, that we are, in fact, not only going to try to make it as simple as possible, but are also going to have readily aware that what we are doing is probably going to have a significant impact on what will tal$e place within the instructional and possibly even the scuba equipment design communities as they are involved in our underwater activities. These are not simple issues. Regarding this whole notion of ascent rates, if we could just belt out a number and walk away from it, we wouldn't have to have this kind of a workshop. What has taken place then is that we have been charged over the next two and a half days with trying to clarify the issues regarding the rate of ascent, in order to determine if it makes a difference if we come up faster, slower or at the rates of speed that divers are currently using. We are going to become familiar to a degree with the mechanics of bubble growth and formation, and how these processes act, in a manner that we have not been exposed to before. Most of us have some generic sense of what bubbles are and what they do, but, in fact, when looked at by the people who really have that particular insight, it is not a simple issue. Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. We also are going to be pressed to consider rationally the risk factors that are involved because this is certainly where the game is being played today. We, as a group of scientific divers and scientists who are interested in the issue of health and safety, are hard pressed to be able to objectify all of the kinds of risks that are involved in our particular sport. I think we do a better job than most, but in fact I believe that sometimes we have not, perhaps, paid as close attention as we should to some topics. To other notions we have paid too much attention because there is a significant body of myths that is operational. I hope that we can factor out some of the myths, so that we can go away from Woods Hole with a perspective that is going to be helpful to us all. Basically, what we are charged to do is to try to quantify what we know and identify what we don't know so that we can start to make progress in that direction. We will, in this workshop, as I believe we did in the AAUS Dive Computer workshop last year, establish a state-of-the-art, if you will. In other words, at this point in time, this is what we know and understand and this is how we believe that it should be used in the best interests of our sport and our industry. Today we are going to have a rare opportunity to be able to get some historical perspective that I suspect could not be given by anyone other than Dr. Lanphier. We are going to have the opportunity to be able to get insight into the mechanics of bubbles, what they do and how they operate. We are going to be able to have discussions that will relate to the equipment issues that impinge on this particular type of phenomenon, as well as the training issues with which the majority of the people in this room are very concerned. I do make the observation again that when most of us started diving, life was really simpler. I recall fondly the resistance that Jim Stewart had to adding any kind of flotation to a diver. If you needed flotation, you would blow in your sleeve and catch the bubble up in between your shoulder blades, which actually works just fine as long as you stay in the horizontal position. The question was: "What are the tradeoffs associated with this additional equipment that you wear and is buoyancy compensation really necessary?" We have gone through a period of being concerned only with the business at hand, and as a result, we now have gotten to the point where the envelope that the diver occupies in the water column has grown larger and larger. A good portion of that envelope is associated with a variety of gas containing equipment items (i.e. BC's, thermal protective suits, etc.) Within this problem area we have seen a growing concern for the kinds of problems that are going to be associated with ascent. What I would also like to see come from this workshop is really an issue of some magnitude, which is: "What are the optimal ascent rates for people that are involved in our particular area of endeavor?" In other words, how fast should divers come up? "What are the tradeoffs if they come up at unacceptable rates of speed?" I believe that we are going to have a good deal of illumination in this area and for those of us who have been making some statements for years, we may have to change those as a result of the interface with facts. I would like to finish this little portion of the exercise by saying that we all have the opprotunity to deal with this topic in a framework where we will not have made up our minds to the point where we are not willing to be confused by the facts because I believe that there is still significant confusion and misinformation operational in the field today. We are going to take two and a half days and hopefully some of the evenings to educate ourselves on ascent rate facts. With that in mind, we have asked Dr. Lanphier if he would be willing to share with us some historical perspective and he was gracious enough to accept our invitation, so I would like to welcome as first speaker, the Rev. Ed Lanphier. A HISTORICAL LOOK AT ASCENT The Rev. Edward H. Lanphier, M.D. Department of Preventive Medicine U.W. Biotron, 2115 Observatory Drive University of Wisconsin Madison, WISCONSIN 53706 U.S.A. In considering a question like Safe Ascent, part of the process is understanding "how we got to where we are". Having been in this field since 1951, I hope to shed some light on this question from my own recollections and other sources not widely available. For example, I was part of the small but representative group that chose 60ftlmin as the rate of ascent for the 1958 USN air decompression tables. Only recently, re- reading parts of Sir Robert Davis' rare but famous book, I learned that 60 ftlmin had also been accepted long before. Introduction I believe that I am the second-oldest investigator still active in Diving Medicine and Underwater Physiology. That probably entitles me to tell sea stories and try to portray what diving was like back in the days when men were men. Here, however, I'll try hard to stick to relevant information. The main reason I'm pleased and grateful for being part of this Workshop is that the work Dr. Charlie Lehner and I have done with sheep and goats has focused our concern on the risk of central nervous system (CNS) injury from decompression sickness (DCS). This risk appears to be greatest in relatively short, relatively deep dives - clearly prevalent in both sport diving and scientific diving. It seems very likely that the pattern of ascent holds the key to reducing the risk of CNS DCS. In fact, we are on the verge of starting a study on this topic. This Workshop should help us decide just where to begin and what sorts of procedure to investigate. Ancient history I haven't tried to go back beyond the early 1900's, but it is interesting to note that ascent procedure was being argued even then. Prof. J.S. Haldane [1], whom we revere for his fundamental work on decompression tables, had a worthy rival: an equally-notable physiologist who was also deeply interested in decompression, Sir Leonard Hill [2]. Hill seriously questioned Haldane's stage decompression concept - especially for longer exposures - and advocated uniform decompression - the "slow bleed" approach, which indeed has prevailed in caisson and tunnel work and - much more recently - in very deep diving. Also, we know now that Haldane was off base in supposing that freedom from symptoms meant freedom from bubbles. It has even been suggested that Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Haldane's initial ascent produces bubbles that can slow the elimination of gas and cause problems later. We obviously need to keep an open mind. Early practice Sir Robert Davis1 classic book, Deep Diving and Submarine Operations [3] details Royal Navy practices as of 1962 and before. The main thing I gleaned there is that the rate of ascent to the first stop should not exceed 60 ft/min. The concern seemed to be less with the rate of ascent itself than with the chance that the diver would miss his first decompression stop if he were coming up too fast. A copy of the Royal Navy's The Diving Manual of 1943 [4] confirms this. It also has an excellent illustration of the contemporary hand-driven divers' air pump. The gauges on the front (one for each of two divers) are especially important since the reading is essentially equal to the diver's depth. The dive supervisor is instructed to consult the chart inside the pump cover to determine the gauge error, then use the gauge to determine the depth and rate of ascent. The 1950's I came on the scene at the Experimental Diving Unit (EDU) in 1951. At that time, it was located on the Anacostia River in the Washington, D.C. Navy Yard. Soon, and for some time thereafter, our "Bible" was a slender volume known as the Bureau of Ships Diving Manual, NAVSHIPS 250-880, issued in 1952 [5]. Ascent at "not over 25 ft/min" was firmly implanted there, and I have not been able to find out why that rate had been chosen - or when. The 25 ft/min rate was naturally reflected in Submarine Medicine Practice, NAVPERS 10838, issued in 1949 [6], and it never occurred to us to question that when we produced a revised Submarine Medicine Practice, issued in 1956 [7]. In 1954, EDU had a most interesting visit by French naval officers from "GERS" (Groupe d'Etudes et de Recherches Sous-Marines de la Marine Nationale). Most of them had been associated with Cousteau. Later, one of these officers kindly sent me a copy of a fine little book that they had produced: La Plongie, published in 1955 [8]. Going through La Plongie in preparation for this Workshop, I found some interesting things concerning ascent. Allowing for my ability to translate, one statement was that the duration of ascent to the first stop is an element in decompression. Another was that divers with self-contained equipment are capable of ascending as rapidly as 60 meters/min - roughly 180 ft/min - but that as the surface or first stop is approached, this speed should be considerably reduced. The section on ascent without stops presents depths and times resembling our "no- D" limits. (A curve of these depth/time limits elsewhere in the book suggests a maximum depth of 40 meters, where the allowable time is 15 min.). The text states that the diver should always take at least one minute to traverse the final 10 meters of ascent. If the dive was deeper than 40 meters, a short stop at 3 meters is indicated. "Negligence of these precautions in general tends toward illness." Lanphier: A historical look at ascent The 1958 USN air tables I remember one morning, probably in 1956 or 1957, when EDU personnel and a selected group from elsewhere met in a borrowed room in the nearby Naval Reserve Training building. The main topic concerned the proposed new USN Diving Manual; I'd been designated as editor of Part I; others were being consulted about suggested content, willingness to contribute, etc. Decompression was definitely not the primary topic of discussion, but the main reason for having a new diving manual at that point was to put forth the new air decompression tables that Officer-in-Charge Maino des Granges and his merry band had been working on. In any case, the proposed rate of ascent in the new tables became a hot topic of discussion. CDR Doug Fane, representing his West-coast Underwater Demolition Team, was adamant in saying that his frogmen couldn't possibly observe anything as slow as 25 ft/min. What they wanted was more like 100 ft/min - or even faster. The hard-hat types insisted that nothing of the sort would be practical for hauling up divers in suit and helmet. Those involved in calculating the tables insisted that ascent was an important element in decompression and that two complete sets of schedules would have to be produced for different rates of ascent - and that doing so would be utterly impractical. I'm quite sure nobody complicated matters further by asking for a variable rate. It was assumed that one constant rate would apply between the bottom and surface or the first stop. In that setting, the two sides decided to compromise on 60 ft/min. That had the merit of being one foot per second, and it seemed possible for a hard-hat diver to be hauled up that rapidly and for a scuba diver to come up that slowly. Anyhow, the group decided on 60 ft/min, and the calculations proceeded on that basis. I doubt that Doug Fane or anybody else realized quite how slow 60 ft/min would seem in practice. I suspect that Doug figured that coming up a little faster wouldn't really hur t . . . and the hard-hat contingent probably thought that coming up slower than 60 ft/min wouldn't matter much, either. In any event, the calculator - presumably Dr. Bob Workman at that stage - concluded that variations from 60 ft/min could make a real difference under some circumstances - a difference sufficient to warrant some rules. I seem to recall that, as editor, I had to squeeze those rules into the new Manual [9] in as intelligible a form as possible. I did my best, but I never got to the point where I could remember them from one day to the next myself. The basic ideas were that if a diver tarried close to the bottom, he would take up enough extra gas to require more time in decompression. On the other hand, if he came up too rapidly, he would miss some of the decompression time that ascent at 60 ft/min would have afforded. Adjustments were to be made accordingly. In the current (1985) USN Diving Manual [10], the rules are basically the same; but they are presented with examples that seem to help considerably in getting the ideas across. HI assume that most of you are familiar with more recent developments concerning ascent, so this concludes my excursion into history. Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCEWS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Current implications It will be both interesting and beneficial to hear what the participants in this Workshop believe and suggest concerning ascent. Basically, I'm most impressed by the lack of solid experimental data on this subject. We must try hard to avoid "determining the truth by voting on it in the absence of information" and setting up new procedures just because they sound good. At the same time, the need for better ascent procedures seems urgent, and there are things that surely can't hurt and might be of some help - like a stop at 30 ft or less on ascent. To my knowledge, only Dr. Lehner and I have actual plans for looking into this matter experimentally, and we will be doing so in sheep. This allows us to be more provocative than with human subjects, but our conclusions will have to be checked cautiously in humans. We hope that others will be able to undertake experimentation that will supplement and check what we can do. References [1] Boycott, A.E., G.C.C. Damant and J.S. Haldane. 1908. The prevention of compressed air illness. J. Hyg. Camb. 8: 342-443. [2] L. Hill. 1912. Caisson sickness and the physiology of work in compressed air. London: Edward Arnold. [3] R.H. Davis. 1962. Deep diving and submarine operations. Seventh Edition. London: The Saint Catherine Press. [4] Admiralty (Gunnery Branch). 1943. The diving manual, B.R. 155/1943. London: Her Majesty's Stationery Office. [5] US Navy Department (Bureau of Ships). 1952. Diving Manual, NAVSHIPS 250- 880. Washington: Superintendent of Documents. [6] US Navy Department (Bureau of Personnel). 1949. Submarine Medicine Practice, NAVPERS 10838. Washington: Bureau of Naval Personnel. [7] US Navy Department (Bureau of Medicine and Surgery). 1956. Submarine Medicine Practice. Washington: Bureau of Personnel - Superintendent of Documents. [8] Marine Nationale (Groupe D'Etudes et de Recherches Sous-Marines). 1955. La Plongee. Paris: Arthaud. [9] US Navy Department (Bureau of Ships). 1959. US Navy Diving Manual. Washington: Superintendent of Documents. [10] Navy Department. 1985. US Navy Diving Manual, NAVSEA 0994-LP-001-9010. Volume 1 Air Diving, Revision 1. Washington: Superintendent of Documents. Session 1: Introductory Session Discussion INTRODUCTORY SESSION DISCUSSION Discussion Leader: Glen H. Egstrom Hugh Van Liew asked if there was evidence from the tunnel work that the "slow bleed" really did work better than the stage decompression? Ed Lanphier responded that he really couldn't answer that. The next question inquired if there was a relationship of ascent rates and procedures in preventing bone necrosis at deeper depths/times? Ed Lanphier answered that Eric Kindwall would say that we didn't have procedures that would work for higher pressures or longer exposures to really prevent bone necrosis. Furthermore, Hills had some data on comparative approaches to decompression that he found quite convincing, but did not have time to analyze those. John Lewis wondered whether there was any testing that supported the Navy procedures for omitted decompression. Ed Lanphier couldn't remember, it was too long ago. "That is one disadvantage of being so old. I like to talk about my favorite vehicle, which is a 22 year old camper van. Everything that could possibly happen to a Dodge van has happened to Moby, but the problem is that I can't remember what a particular noise actually meant, so it doesn't help a lot to have known him for so long". Mike Emmerman asked if when the 60 fpm ascent rate came up, whether it was 25 fpm or 180 fpm and if there was any discussion or real data to determine whether it could have been 300 fpm or 5 fpm? Ed Lanphier didn't think so. The approach to reality came in the actual calculations where all they could say was that it made a difference what rate of ascent they assumed. The rate of ascent we adopted, 60 ft/min, was part of all of the Navy table testing that was done and we never really questioned whether that was a particular problem or not. Bill Hamilton noted that from the way Ed Lanphier described it, the 60 fpm ascent rate was for operational reasons, rather than for optimal decompression. Ed Lanphier: Yes, surely. If we had chosen something that sounded very fine from a physiological standpoint but it wouldn't work for either scuba divers or hardhat divers, it wouldn't have made a difference But I think it is very important to understand that these things did not come down from heaven. David Yount stated that it seemed like the only implications from the theoretician's point of view were that you'd have to add more or less time onto the stages. It wasn't that there was anything intrinsically wrong with the faster ascent or slower ascent. Ed Lanphier Well, we would have had misgivings about coming up much faster than 60 fpm, I think. David Yount rephrased: What I'm getting at is if the theoretician takes the ascent rate into account in calculating the tensions in these different tissues, then there is a particular reason. Ed Lanphier: As far as the theoretician can see, there isn't any particular reason, I think, especially since we were following Haldane in those days and at that point we really did not know. It took Spencer, quite a few years later, with his bubble detection to convince us that freedom from symptoms did not mean freedom from bubbles. It is hard to realize that this is fairly recent information. Ed Lanphier was asked to recall what kind of a repetitive schedule the Navy was testing. His response was that the schedules that were fairly well tested were in the diving manual. "One tiling a lot of people don't realize was the bind we were in for not doing as many exposures we would have liked. We just didn't have the manpower or the time to do it as thoroughly as we would have liked". Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Is there a myth around that the Navy tables were tested with only one, possibly two repetitive schedules? Ed Lanphier: I think that might be true because that was the main sort of thing that the Navy itself was concerned about, not about people diving time after time, day after day. Hugh Van Liew pointed out that when the tables were set up, there was a tremendous bias to be thinking about tissues and whether or not the gas was washing into them or out of them, and there wasn't any thought at all about bubbles. Ed Lanphier: That is correct, because we thought that if we did it right, there wouldn't be any bubbles. Now we know that they are probably there, at least in some of the schedules. Phil Sharkey: Did some of the foreign systems develop similarly, with different ascent rates applying to different tables which occurred in the same era, maybe also in an arbitrary fashion? Ed Lanphier: I think you can almost bet on it. I don't have proof, but how else could it have been done? Hugh Van Liew wondered if there was any information from non-written systems like the Polynesian divers that don't have tables but seem to be doing things right by experience? Ed Lanphier: I think David Yount is the best one to field that question. Hugh Van Liew: I wonder if primitive people who are diving successfully would favor a rapid ascent or a slow ascent? David Yount: They would go rapid. Ed Lanphier said that when you stopped to think about it, coming up at a specific, relatively slow rate like 60 fpm, which is relatively slow as far as he was concerned, it is extremely difficult. "How are you going to spend reliably and accurately 5 minutes at 10 feet unless you have a line with weight and float and can hang onto it and sit there. Of course, the dive computers help that now and if you have a good buoyancy compensator and are expert in using it, maybe you can, but it is still so much more difficult than just coming up". Glen Egstrom added that he had the opportunity to do some research with some of the Polynesian divers and it would be his observation that they come up slower if they're carrying a heavy load and faster if they are not. But the issue there, he believes, is that we don't know how many of those people were getting significant amounts of decompression sickness. In Polynesia, they have a malady called Taravana, which, as far as we could determine, really is acute decompression sickness from coming up too fast from depths in excess of 50 meters. Their bottom times are singularly short, but they make these rapid excursions to and from the bottom with working times on the bottom of maybe 50 seconds. Hugh Van Liew: So, that is breathhold diving which really is a different ball game. Ed Lanphier: Not totally. Glen Egstrom: I wonder if it is from the point of view of ongassing and bubble formation Hugh Van Liew: They have a terrible problem of getting oxygen into their lungs. Ed Lanphier summarized that the kind of diving they do was very clearly on the verge where breathhold diving can cause decompression sickness. Glen Egstrom: Remember Paulev? Ed Lanphier: "I sure do". He was a Dane who took a submarine crew up to the escape tank in Bergen, Norway, for training and in that setting, he and several others developed what almost had to be decompression sickness and they responded to recompression. They wrote an article for the Journal of Applied Physiology, describing this whole thing. I was called in as a referee editor. I recognized this paper as an extremely important first It was the first time that decompression sickness from breathhold diving had ever been reported. I assisted in rewriting the paper, it was published and is one of the monuments of decompression literature. Glen Egstrom added that the side issue to that was that Paulev described this experiment at the international physiological conference in 1965 in Tokyo and his observation was that they were making 30m drops into the tank and didn't seem to be having any kind of a problem. Finally, they were getting so tired they couldn't make it to the bottom and back up any more, so for the 10 Session 1: Introductory Session Discussion last dives of the series they were only getting down to about 20m. Everything seemed to be alright, he got out of the tank, started to walk, collapsed, lost bladder, bowl, etc. They rushed him to a chamber for treatment David Yount: One of the points you made was the "slow bleed". I'd like to make a remark about that. On a typical exposure, if you had only one tissue that was activated, then the ascent produces a certain delta p which is just barely enough not to produce any bubbles. In the one tissue, at one time constant, the ideal way to surface is a straight line, as you would get in a saturation dive. The saturation dive is characterized by one tissue because it is so long. Only the longest tissue comes into play. If you have two tissues, that would mean two different time constants where the first part of the dive is controlled by the fast tissue and the second part is controlled by the slower tissue. What really happens is you don't have a bunch of discrete tissues like ten different tissue compartments, but really nave a continuum of tissues and if you modeled it that way, you would have a smooth curve. That is the slow bleed. The slow bleed is really the best way to surface if you have an operational way of doing that, which you usually don't. Bill Hamilton commented that if you're doing this on a saturation, you're only operating in the last compartment and you do get a straight ascent. David Yount concurred. On a saturation dive where you have a continuous range of tissues, the step function, versus straight ascent, is only an operational artifact. It's only that way because it's hard in practice get the straight line. The slow bleed really is the way to do it if you have control. Ed Lanphier: One other thing to mention is that Ed Thalmann, in his calculations for the Navy, came up with the idea that once you had bubbles in more than one tissue, then the picture changed, and you ended up with a straight line. Bill Hamilton: Decompression is not necessarily a straight line, it's the outgassing. Ed Lanphier: It's the basic assumption that you no longer deal with an exponential curve. John Lewis: That presumes that the delta p (pressure change) is acceptable. David Yount: As you approach the surface when you're doing this, it's holding delta p constant. As long as you hold a fixed delta p in decompression, you're keeping the bubble number constant, or you're controlling the bubble volume. It's really delta p, it's not the ratio. John Lewis: You still have a ratio that's greater than it should be at depth, than on the surface. Bill Hamilton: In some cases the tolerable delta p expands as you go deeper, or it shrinks as you get towards the surface. John Lewis: The larger tension is not acceptable, and I think that's perfectly logical. Ed Lanphier: If I had said more about things we know are wrong with Haldane's concept, I would have emphasized the fact that this 2:1 ratio, while pretty true in shallower diving, does not hold when you go deeper. That is absolutely obvious. It is somewhere in between delta p and the ratio. The ratios have to be more conservative than 2:1 as you go deeper, but the delta p that you can get away with apparently gets a little bigger. David Yount: Basically, the delta p is the threshold for bubble formation. It is determined by the radius of the nucleus and the radius is connected to the delta p. Glen Egstrom: I want to thank Dr. Lanphier for getting us off to a flying start. 11 PHASE DYNAMICS IN DIVING Bruce R. Wienke Applied Theoretical Physics Division Los Alamos National Laboratory Los Alamos, NEW MEXICO 87545 U.S.A. Dissolved and free gases do not behave the same way in tissue under pressure, and their interaction is complex. Differences are highlighted, particularly with respect to time scales, gradients, and transport. Impacts of free phases on diving are described, contrasting increased off-gassing pressures, slower ascent rates, safety stops, and reduced repetitive exposures as consistent practical measures within traditional models (limited supersaturation) which can be played off against buildup of dissolved gas. Simple computations illustrate the points. Using critical volumes as trigger points lies between classical supersaturation models (tables and meters) and nucleation-modern bubble models, that is, a realistic limit point divorced from nucleation and stabilization for convenience. Such limit points can be substituted for matrices of critical tensions (M -values) in table or meter algorithms. Based on main concern of phase growth, we suggest that 60 ftlmin ascent rates be retained for nominal exposures, and that safety stops at 15-20 feet for 3-5 minutes are warranted, with stop time added to bottom time when using tables. The USN tables are the reference point. Introduction Diving sectors (military, sport, scientific, commercial) employ a modified supersaturation algorithm [1-11], often termed multi-tissue (different perfusion-dominated compartments) or M-value (critical tissue tensions), and therein an issue [12-31] has always been an incomplete treatment of gas dynamics. Concerns encompass all activity when recent investigations [26-29] conclude that living tissues are persistent storehouses of growth-excitable gas nuclei of sub-micron size, though problems surface more fully in repetitive cases. When supersaturation models do not address free phases, they are not optimal, nor global. As part fix-up, one might incorporate free phase limiters to make them more predictive when extended outside tested ranges, though full blown nucleation-bubble models appear preferable. Safety stops and slower ascent rates are other alternatives, along with reduced no-decompression time limits and critical tensions. We examine some possibilities, focusing on critical volumes, ascent rates, and safety stops, with a convenient program (DECOMP) [20], offering various combinations of gas transport models (perfusion-limited, diffusion-limited, both) and critical limiters (tissue tension, separated gas fraction, free-dissolved gradient, bubble number). Results are compared with the standard predictions of the multi-tissue algorithm. Safety stops and slower ascent rates in the context of the supersaturation model are consistent with free phase limiters, though perhaps less natural. For the future, we suggest that bubble models offer optimal bases for tables and meters, and that testing and further development are warranted. 13 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Some regard safety stops, slower ascent rates, and increased off-gassing pressures as consistent treatment practices for separated (free) gas phases, particularly near the surface where reduced pressure enhances growth. Nucleation theory and experiment tell us that on any given dive (compression-decompression), families of stabilized micronuclei larger than a critical minimum size are always excited into bubble growth, so we must pay attention to free phase development throughout the dive. Bubble growth criteria automatically address both issues, via allowable pressure gradients, and are more realistic, unlike critical gas tensions which the chemists tell us are ill-defined. We might think about replacing M-values with bubble criteria instead of patching time limits, ascent rates, and safety stops. Testing is central to diving, and much testing of bounce (single), no-decompression diving has transpired. Repetitive and multi-day exposures can neither claim, nor reap, the same benefits, and application of the algorithm in the latter cases has witnessed higher bends statistics than in the former one. Reasons appear tractable. The multi-tissue approach is a dissolved gas model, and so long as the bulk of tissue gas remains in the dissolved state, the more correct and useful such an approach will prove. But as increasing proportion of free phases grow, by direct excitation of critical micronuclei or more gradual bubble coalescing transitions, the multi-tissue algorithm can lose predictive capability. Invariably, such conditions attend diving activity extrapolated outside model and test ranges, sometimes as a surprise. The establishment and evolution of gas phases, and possible bubble troubles, involves a number of distinct, yet overlapping, steps: 1) nucleation and stabilization (free phase inception); 2) supersaturation (dissolved phase buildup); 3) excitation and growth (free-dissolved phase interaction); 4) coalescence (bubble aggregation); 5) deformation and occlusion (tissue damage and pain). In the past, much attention has focused on supersaturation. Recent studies have shed much light on nucleation and excitation. Bubble aggregation and tissue damage are difficult to quantify in any model, and remain more obscure. Complete elucidation of the interplay is presently asking too much. Yet, the development and implementation of better computational models is necessary to eliminate problems re-echoed in workshops, reports, meter disclaimers, publications, and even a very slanted segment of 20/20 on ABC last winter. History and background Origins of diving regimens at sea level are traced to a supersaturation model proposed by the eminent English physiologist, John Scott Haldane [1]. Observing that goats, saturated to depths of 165 feet of sea water (fsw), did not develop decompression sickness if subsequent decompression was limited to half the ambient pressure, Haldane constructed schedules that limited the critical saturation ratio to 1.58 in each of five hypothetical tissue compartments. The tissue compartments were characterized by their half-life, x, that is, the time required for the compartment to half, or double, existent nitrogen. The five original tissue compartments (5,10,20,40,75 minutes) were employed in diving calculations for fifty years. Later, in performing deep dives and expanding table ranges, workers, in particular the USN, advocated the use of six tissues (5, 10, 20, 40, 80, 120 minutes) in constructing diving tables, with each tissue compartment having its very own critical pressure (M-value). 14 Wienke: Phase dynamics in diving Changes to the basic format were driven by increasing diving activity. New compartments and M-values were added as existing schedules failed extrapolations. Today, many slower compartments have been proposed in applications, with variable decompression ratios at 10 ft increments producing many degrees of freedom (fit parameters) to characterize the data. Yet, slower tissue compartments do not necessarily give the model proper physical signatures. While the concern is free phase growth and the hope is that slower compartments with smaller M-values will prevent growth, that hope is not physically realistic from different vantage points. Yet, though the M-value approach may not prevent bubble growth, it can represent an adequate treatment table for separated, but still asymptomatic, gas [2,8,23]. In such circumstance, treatment (elimination) of free phases tends to take place at shallower depths with present diving practice. Then, as elimination becomes less efficient with decreasing pressure, safety stops and slower ascent rates, tending to increase average pressure, appear qualitatively wiser practices. Further on, quantification will be presented. Certainly, any algorithm can be piecewise safe over tested ranges, but not always globally. Some implementations, as pointed out by Weathersby [7], may not be statistically rigorous, relying on much too small a set of exposure data to confidently predict outcome. Models not strongly correlated with tests can promulgate wide variation in predictive capability. Similarly, models can often interpolate within data, while failing to extrapolate outside the data. And then we must modify procedures to accommodate the extrapolation. A good point in question is the repetitive use of the USN tables. It is now clear [24, 25] that single, no-decompression dives, followed possibly by one more repetitive dive, form the test basis of the no-decompression parts of the schedules. Yet, we observe that multiple repetitive dives permitted by the tables incur higher bends statistics, particularly in the deeper categories. This results from both model shortcomings and less reliable statistics. Adequate testing of any algorithm is always requisite, that is, descent rate, exposure profile, ascent rate, surface interval, and repetitive loading. Supersaturation model and dissolved phase dynamics Multi-tissue computational algorithms are ultimately based on assumptions of limited supersaturation in tissues, with gas exchange controlled by blood flow rates (perfusion) in assumed homogeneous media. Tissue is first separated into intravascular (blood) and extravascular (tissue) regions for modeling. Blood containing dissolved inert and metabolic gases passes through the intravascular zone, providing both initial and boundary conditions for subsequent gas transport throughout the extravascular zone. Arterial blood tensions equilibrate rapidly with alveolar partial pressures, and venous tensions then equilibrate with arterial tensions at a somewhat slower rate. Tissue tensions fall somewhere between arterial and venous tensions during equilibration. Exchange of inert gas by random molecular motion across regions of varying concentration is driven by the gradient, that is, the difference between the arterial blood tension, pa, and the instantaneous tissue tension, p. That behavior can be modeled in time, t, by mathematical classes of exponential response functions, bounded by pa and the initial value of p, denoted pj. These multi-tissue functions are easily accessed with hand calculators, taking a very simple form, where \ is the tissue decay constant, P = Pa + (Pi - Pa) exp (-Xt), x (1) 15 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Ten compartments with 2.5, 5, 10, 20, 40, 80, 120, 240, 360, and sometimes 480 minute half-lives, T, are routinely employed in application, and half-lives are assumed to be independent of pressure. A one-to-one correspondence between the ten compartments and specific anatomical entities is neither established, nor implied. For very large values of x, tissue uptake and elimination of inert gas is relatively slow according to the response function. For small values of x, inert gas uptake and elimination proceed much more rapidly. An important assumption built into the supersaturation model requires intercellular diffusion of inert gas to occur rapidly compared to time scales of x, so as to not significantly limit, nor effect, the gradients driving gas exchange. The only controlling factor is assumed to be the perfusion rate. To maximize the rate of uptake or elimination of dissolved gases, the gradient, simply the difference between instantaneous tissue tension and ambient pressure, is maximized. Historically, maximization gives rise to a long (first) pull to the surface. Maximization of the gradient, however, must never permit gas buildup above empirical limits. Fits to the exposure data, mainly for no-decompression diving, limit degrees of compartment supersaturation by critical values, M, having a typical modern range, 122 < M < 36 fsw, notably of American origin. Critical gradient criteria require differences between the tissue tension and ambient pressure, P, to remain less than another critical trigger point, L. Gradient criteria can be linked to laboratory tests while critical tensions are empirical and not well defined. In decompressed gel experiments, Strauss [19] suggested that L ~ 14 fsw, for all pressure. Even in the early times of Haldane, Hill [9] opted for a fixed gradient near 24 fsw under nominal loadings as a realistic constraint. Thermodynamic tables [8] and recent bubble formation-regeneration tables [18] employ variants of L effectively. Critical gradients are more easily linked to bubble mechanics than critical tensions, but critical tensions enjoy widespread popularity in diving applications. Yet, T and M are not fundamental. Sets of half-lives and critical tensions evolved from self-consistent application of Equation (1) to sets of exposure data, that is, trial and error bootstrapping of model equations to observed exposure time limits. Newer compilations ultimately extend older ones in like manner. For instance, the sets of critical tensions, M, detailed by Workman [4] and Biihlmann [3] for arbitrary compartments at depth, as well as the later compilations of Schreiner [5] and Spencer [6], along with the response function, are popular realizations of the algorithm. The Workman (USN) critical tensions are plotted in Figure 1 as a function of ambient pressure for a chosen set of tissue half-lives. They are linearily increasing functions of pressure, and were tested at sea level (P = 33 fsw). Buhlmann, [3] and Bell and Borgwardt [10] extended (tested) the critical tensions at altitude (P < 33 fsw). The extension has not only been a study in itself, but also a reflection of the limitations of sea level compilations. Wienke [16] proposed exponential extrapolations of M-values back through zero absolute pressure, an intuitively conservative scheme. However, proposed extrapolations of critical parameters require testing, and altitude is no exception. Such is also the case for deep exposures. Based on reductions in Venous Gas Emboli (VGE) counts in select exposures, Spencer [6] and Pilmanis [32] pioneered a modern trend to reduce no-decompression time limits, and subsequent M- values extracted from them. These welcome conservative procedures must reduce bends incidence statistics, but central model issues remain. 16 Wienke: Phase dynamics in diving Figure 1. Critical Tensions (M-Values). Critical tensions are fitted linear functions of pressure, obviously increasing with ambient pressure. Faster compartments permit greater amounts of dissolved nitrogen, slower compartments less. During any dive, tensions in compartments must stay below the depicted curves in this modified Haldane approach. Wienke reduced them to an approximate form (fsw), M = 152.7 r 1 / 4 + 3.25 xAlA d, for depth d (ft). Dividing M-values by ambient pressure, P, yields the critical ratios, R. Extensions of the curves to altitude (P < 33 fsw) have been effected linearily and exponentially. In the linear case, the zero pressure intercepts are positive, while in the exponential case the intercepts are zero. Thus, in the former case, critical ratios become unbounded at zero ambient pressure, while in the latter case, they remain finite. These trigger points are artifacts of data fitting, and not necessarily physically tractable. Any set of no-decompression time limits can be plugged into Eq. (1) and ensuing sets of tensions for compartments can be scanned for maximum values (M-values) across all depths and half- lives. 33 66 99 PRESSURE (FSW) 17 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Bubble model and free gas phase dynamics Blood rich, well-perfused, aqueous tissues are usually thought to be fast (small T), while blood poorer, scarcely-perfused, lipid tissues are thought to be slow (large T). AS reflected in Figure 1, critical tensions are larger for faster tissues and increased pressures. The range is linear within tissue compartments. In the field, fast compartments control deep, short exposures, while slower tissue compartments contend with shallower, prolonged exposures. Additionally, near surfacing M-values are principal concerns, yet, as such, are somewhat shortsighted, probably contributing to ascent rate and safety stop concerns, among others. Algorithms tracking both dissolved and free phases offer broader perspectives and wider alternatives. Tracking the interplay of component gas phases throughout the dive automatically determines ascent rates and possible stops in modern bubble models, but with some changes from classical procedures. Free and dissolved gas dynamics differ. Since differences between free phase and ambient pressures increase with depth, the gradient for free phase elimination also increases with depth, directly opposite to the dissolved phase elimination gradient which decreases with depth. Then, changes in operational procedures become necessary for optimality. Impacts of this on decompression diving can be seen clearly in Figure 2, which contrasts supersaturation staging (USN and RN) against thermodynamic staging according to vintage Hills [8]. Similar profiles are seen in bubble models, such as the varying permeability approach [18]. Considerations of growth invariably require deeper staging procedures than supersaturation methods. Though not as dramatic, similar constraints remain operative in no-decompression exposures. The reason is linked to the interaction of free and dissolved phases in bubbles and tissue, as summarized in Figures 3 and 4. Internal pressures in bubbles exceed ambient pressures by amounts equal to the effective surface tensions of the bubbles, as seen in Figure 3. To eliminate bubbles or reduce growth, increasing ambient pressure is requisite not only to restrict size, but also to drive the gas by diffusion out of the bubble and across the tissue-bubble interface, as depicted in Figure 4. The shorter the desired time of elimination, the greater must be the ambient pressure. Experiments conducted in decompressed gels, notably by Yount and Strauss [12,19], Kunkle and Beckman [15], and others, bear testimony to this fact. Figure 5 contrasts experimental bubble dissolution time as a function of ambient overpressure for various small bubbles. The smaller the bubble, the shorter the dissolution time. Here, implication for diving is rather simple. In the presence of even threshold amounts of free phases, increased pressure is prudent. With any pressure, the length of time required to dissolve bubbles of 250 micron diameter is significantly shorter than that required to dissolve larger bubbles. Immediate recompression within less than 5 minutes is adequate treatment for bubbles less than 100 microns in diameter, and forms the basis for Hawaiian emergency in-water recompression procedures [22]. Such facts prop arguments for safety stops when conventional tables are pushed to limits, timewise or repetitively. There are other concerns with the presence of free phases in tissue. Use of just a supersaturation gradient to quantify elimination is not correct, because the free phase pressure is not the tissue tension, p. A split gradient [16] fractioning dissolved and free phases, is advisable. As recently discussed by Van Liew [30], the relative composition of gases in bubbles can also change upon decompression. Similarly, if inert breathing mixtures are changed, existing bubbles can grow or shrink, depending on relative gas solubilities and diffusivities [33]. Operational diving then becomes a complicated playoff against dominant phases. 18 Wienke: Phase dynamics in diving Figure 2. Phase And Supersaturation Decompression Profiles Decompression profiles for a dive to ISO ft for 40 minutes are depicted according to supersaturation and critical phase formats. The supersaturation schedules (USN and RN) obviously differ from the phase format (thermo). Such differences are generic to bubble models versus critical tension models and involve: 1. more time spent deeper to minimize bubble excitation and growth, and maximize the driving force to eliminate free phases, followed by; 2. possible drop out at 20-30 fsw to dump asymptomatic free gas, if phase separation has been minimized by the overall ascent procedure. In supersaturation formats, stops in the 10 to 30 ft range are thought to represent the treatment portion of the diving schedule. Computational analyses, some tests, and experiments have validated features of phase models, while work needs to continue on such approaches. Models extending biophysics can hopefully provide additional insights and optimal formats. 160 140 - 120 % too lA i ? 5u anM OO 40 20 0 1 1 1 1 1 1 1 1 1 1 1 - ? : i \ * * % ^ _ L i i i i i i i 1 t t | ? . i LEGEND usn _ rn mIHefmo " - . 1 . . i 10 20 30 40 50 60 70 80 90 100 110 120 TIME?minutes A free phase in tissue introduces another dimension to gas exchange models. But as a critical indicator, the free phase volume is noteworthy since it can be linked systematically to the mechanics of bubble formation, growth, and elimination, as probed in experiments and corroborated by theory. Bubbles, which are unstable, are thought to grow from stable, micron size, gas nuclei which resist collapse due to elastic skins of surface-activated molecules (surfactants), or possibly reduction in surface tension at tissue interfaces. Families of these micronuclei persist, varying in size and surfactant content. Large pressures (somewhere near 10 atm) are necessary to crush them. Micro-nuclei are small enough to pass through the pulmonary filters, yet dense enough not to float to the surfaces of their environments, with which they are in both hydrostatic (pressure) and diffusion (gas flow) equilibrium. According to Figures 3 and 4, when nuclei are stabilized, and not 19 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS. Costa Mesa, CA. 1990. activated to growth or contraction by external pressure changes, the skin (surfactant) tension offsets both the Laplacian (film) tension and any mechanical help from surrounding tissue (Y = 0). Then all pressures and gas tensions are equal. However, on decompression, the seed pockets are surrounded by dissolved gases at high tension and can subsequently grow (bubbles) as surrounding gas diffuses into them. The rate, r, at which bubbles of radius, r, grow (or contract) can be approximated, . 3r 1 DS f ? 2vlr [ p p \ with D the diffusivity, S the solubility, C the concentration, y the effective surface tension of the bubble, p t the total tissue tension, and P the usual ambient pressure. At some later point, a critical volume of separated gas is established and symptoms of decompression sickness become increasingly probable. On compression, the micronuclei are crunched down to smaller sizes across families, apparently stabilizing at a new reduced size. Bubbles are also crunched by increasing pressure because of Boyle's law, and then additionally shrink if gas diffuses out of them. As bubbles get smaller and smaller, they possibly re- stabilize as micronuclei. Figure 3. Pressure Balance. The total gas pressure, Pt, within a bubble equals the sum of ambient pressure, P, plus effective surface tension, 2y/r, according to, At small radii, surface tension effects are large, while at large radii effects of surface tension vanish. Effective surface tension is the difference between Laplacian (thin film) tension and skin (surfactant) tension. Stabilized nuclei exhibit zero effective surface tension, so that total gas pressures and tensions are equal. When nuclei are destabilized (bubbles), any gradients between free and dissolved gas phases will drive the system to different configurations, that is, expansion or contraction, until a new equilibrium is established. 20 Wienke: Phase dynamics in diving Figure 4. Gas Diffusion A bubble in hydrostatic equilibrium will grow or contract, depending on its size and any relative gradients between free gas in the bubble and dissolved gas in tissue. Gradients are inward if tensions exceed bubble gas pressures, and outward if free gas pressures exceed tensions. A critical radius, re, separates growing from contracting bubbles for a given set of pressures. The critical radius depends on the total tension, pt, ambient pressure, P, and effective surface tension, y. Pt = PN, + Po,+PHJO + Pco, ? where growth occurs for r > re, and contraction foT r < re. Some stabilized gas micronuclei in the body can always be excited into growth by pressure changes (compression- decompression). Nucleation theory is consistent with a number of diving observations [15, 19, 31]. Divers significantly increase tolerance against bubble formation, and therefore decompression sickness, by following three simple practices: 1) make the first dive a deep, short (crush) dive, thereby constricting the micronuclei down to a smaller, safer size; 2) make succeeding dives progressively more shallow, thus diving within the crush limits of the first dive and minimizing excitation of smaller micronuclei; 3) make frequent dives (like every other day), thus depleting the number of micronuclei available to form troublesome bubbles. An underlying point can be made here. If nucleation sites are extinguished, reduced in number, or ill-disposed to excitation, bubble formation and risk are commensurately reduced. Regeneration times for classes of micronuclei are estimated [18,26] to be near a week, underscoring physiological adaptation [IS, 31] to recurring pressure environments. The mechanics of nucleation, stabilization, and bubble growth are fairly complex, with stabilization mechanisms for micronuclei only having been recently elucidated [26-29]. Source and generation mechanisms before stabilization are not well understood. Some candidates include cosmic radiation and charged particles, dissolved gases in fluids we 21 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. drink, lymph draining tissues into veins, collisional coalescence, blood turbulence and vorticity, exercise, the stomach, and die thin air-blood endothelium in the lungs. Once formed, micronuclei apparently stabilize very rapidly with surfactant material [27, 28]. Passing through the pulmonary filters of the lungs, only sub-micron sizes survive. Figure 5. Dissolution Times For Graded Bubbles Bubbles develop and grow over longer time scales than nuclear stabilization. Yet, the rapid dissolution of bubbles in decompressed saturated gelatin (and the body proper) requires immediate and adequate repressurization. The absolute length of time required to dissolve bubbles with given overpressure is directly proportional to the size of the bubble. Obviously, the smaller the bubble, the shorter the time needed to dissolve that bubble at any overpressure. The bubbles studied in this experiment by Kunkle and Beckman grew to approximately lmm in 5 hrs, starting from stabilized micronuclei. Such experiments have provided vital information, and confirmation of nucleation and bubble theories. 400 i BRAIN SURVIVAL TIME PREDICTEO OATA oio. ButoM* MEASURED OATA 1.0-mm Oio. SuoMa 0.9-mn DM. BubMt 4 7 0 10 20 40 Timt to Dissolve Bubbles L (in minutes) 200 Introducing phase mechanics into decompression theory enhances our basic understanding, while maybe pushing numerical perseverance a little. Such perhaps is reason for slow integration into working algorithms. Testing and costs are important other reasons. Meter implementation appears timely, along the following lines. Critical volumes versus critical tensions In elegant experiments, Crocker [21] exposed goats to compressed air at one absolute pressure, Q, for 12 hours (saturation) and then decompressed the animals to another absolute pressure, P, for several hours, checking for bends development. A few days later, the same animals were exposed to the same pressure, Q, and decompressed to slightly higher or lower pressure, P, until a distribution of P, separating bends from no- 22 Wienke: Phase dynamics in diving bends points, was generated. The whole titration was then repeated for a new series of Q. Repetitive exposures are, of course, not included in the titration. Analyzing this data and others, Hills [8] proposed a complete separation of bends from no-bends points via a linear relationship between Q and P, redrawn in Figure 6 for the appropriate range, 0 < P < 200 fsw. Similar type constraint curves are demonstrable for saturation diving at great depth [34]. Over comparable pressure range, an exact one-to-one correspondence between the M- values in Figure 1 and the titration curve is not demonstrable. At most, only one correlation could be established anyway. Certainly, all linear representations of M-values must be broadly consistent with the titration trend of the experiment. Ambiguity arises, of course, because tissue compartments are assigned different critical tensions by design, and must differ from the curve. Actually, the original Haldane assignment of the same critical tension to all compartments is consistent with the titration line. With this in mind, it is worthwhile to now consider a more realistic trigger point for the bends, the critical volume. Figure 6. Decompression titration For simple bends (Type I and II), decompression derations have been performed. A linear relationship between the saturation pressure, Q, and permissible decompression, P, has been established over a range of exposures to depths less than 300 ft. While predictions of M-value models are close to the curve, only one compartment can match the curve. Models employing critical volumes recover the features (slope and intercept). The line is of the approximate form (fsw), Q = 1.37 P + 11.01, according to Hills, Hennessy and Hempleman, and Yount and Hoffman. Beyond 300 fsw the relationship becomes curvilinear. The original Haldane assignment of the same critical tension to all compartments is consistent with the titration experiment. One notes, however, that repetitive exposures are not cases in point here. Similar profiles apply to very deep saturation diving. 300 0 20 40 60 80 100 120 140 ambient P ? fsw 160 180 200 23 Lang and Egstrom (Eds.): B10MECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Hennessy and Hempleman [13] first established a linear titration curve for the data assuming that the same critical volume of released gas provokes mild attacks of decompression sickness. Their analyses also offer explanations for changes in signs and symptoms which follow changes in the nature of the exposure to pressure. Such findings question and press dissolved gas approaches. While the titration experiment is compatible with broad trends, it is clear that dissolved gas limiters, such as M-values, are often not the best critical flags. Indicators such as the volume fraction of free gas phases are not only more natural, but are also more strongly correlated with experiments. Computational algorithms, such as those suggested by Hills [8] and Hennessy [2] described by Wienke [16, 17] and, particularly, proposed by Yount [26-29] in coupling observed numbers of micronuclei in decompressed media to critical volumes, offer basic alternatives to the matrix of M-values. Fewer arbitrary parameters also attend those treatments. Some regard the zero-supersaturation approach of Behnke [11] whereby the inherent unsaturation is allowed to limit supersaturation on ascent, as the classical predecessor to phase algorithms. The interesting empirical practices of Hawaiian and Australian diving fishermen [22, 23] suggest a working cognizance of phase dynamics, and developed over many years of trial- and-error experimentation, albeit, with considerable trauma. Present diving practices, correlated with critical tensions, appear riskier [24,25] under increasing exposure time and pressure loading. Denoting the separated gas fraction per unit volume of tissue, x, and the solubility, S, as before, Hennessy and Hempleman [13] deduced for saturation exposures, f = .397, (3) from the titration curve (Figure 6).For lipid tissue, S = .069, while for aqueous tissue, S = .012. The ratio broadly represents a trigger point for bends, and can be employed in simple calculations to contrast effects against critical tensions. Under worst case conditions of zero gas elimination, the amount of free gas phase can be assumed to be the difference between the original amount in solution before a pressure excursion, and the amount remaining in solution. In terms of the above, this requires that, -PNl) (4) with PN2 the free (nitrogen) partial pressure, which can be estimated in models.[8,11,17]. Not important to discussion here, PN2 increases roughly with the ambient pressure, P. For given p, x. and S, Eq. (4) limits ascents through PN2, leading to deeper staging, as already seen in Figure 2. It appears to have some interesting implications for repetitve diving, particularly when compared to M-value approaches, and we hope to report results of calculations soon. The quantity, p - PN2, acts as a critical gradient, L, though not constant. Surfacing tensions will change with safety stops and slower ascent rates. The faster compartments will respond more quickly than the slower ones, and the relative change in tissue tensions will be greater in faster compartments. Similarly, bubbles will grow if conditions favor their expansion on ascent. Fast ascent rates (decreased average pressure) can maximize their growth rate, while slower ascents and safety stops (increased average pressure) can support their dissolution. Bubble growth and dissolved gas buildup compete. Table 1 contrasts relative changes in surfacing critical tensions, AMQ / MQ, critical volumes, Axo / Xo. and bubble radii, Aro / r0, for a dive to 120 feet for 12 minutes against the same dive with a stop at 15 feet for 3 minutes. Equations (1), (2), and (4) are employed, assuming an initial bubble radius of 1 micron, and an ascent rate of 60 ft/min. Clearly, relative effects are greater on free phase triggers than critical tensions. Calculations are typical for bounce exposures in the 40-150 feet range. 24 Wienke: Phase dynamics in diving Table 1. Relative Decrease In Critical Parameters After Safety Stop t(min) half-life 5 10 20 40 80 120 critical tension relative change .21 .11 .06 .02 -.01 -.02 critical volume relative change .34 J2A .11 .08 -.03 -.04 bubble radius relative change .68 .39 .24 .18 .02 -.01 If stop time is added to bottom time, exposures in Table 1 will exhibit higher tensions, as seen in Table 2, contrasting tensions after the safety stop with an actual dive to 120 feet for 15 minutes. Big differences occur in the fastest compartments, but the procedure is conservative. A small table penalty in the slowest compartment, incurred by adding stop time to bottom time, is offset by free phase reduction after the stop. Table 2. Comparative Surfacing Tissue Tensions x(min) half-life 5 10 20 40 80 120 surfacing tension (fsw) 120///15 min 101.5 87.5 66.9 49.9 39.0 34.9 surfacing tension (fsw) 120/J/12 mia/l5ft/3 min 77.0 73.0 59.0 45.7 36.9 33.5 25 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Suggestions The computational issues of dual phases, bubble formation, growth, and elimination are seen to be outside traditional framework, but get folded into specifications in terms of M-values. Very slow tissue compartments with small M-values can be treatment compartments, tracking both free and dissolved gas exchange in poorly perfused regions. Attempts to track free phases within patently dissolved phase models are not optimal, but still can be mocked up to be more consistent with phase dynamics. One approach is to slow ascent rates and/or introduce safety stops strategically. As far as net gas exchange is concerned, most combinations of stops and rates can be equated to almost any other set at given pressure, so there is always some leeway. Growth minimization and free phase elimination favor slow ascents, but very slow ascent rates are difficult maneuvers at best, and most divers pay lip service to 60 ft/min. Additionally, ascent rates of 60 ft/min are part of tested schedules. Therefore, we suggest maintaining the present rate of 60 ft/min, while introducing safety stops instead. Based on results similar to Table 1, a safety stop for 3 minutes at 15 feet is recommended, with the stop time added to bottom time. Such procedure helps to restrict bubble growth, while having relatively small impact on buildup in the slow tissue compartments. A stop at 15 feet for 3 minutes is roughly equivalent to more than halving the standard ascent rate at depths in excess of 120 ft Adding the stop time to bottom time is conservative, without much penalty. Procedures such as this, as well as reduced no- decompression time limits, appear beneficial in repetitive cases, and we are checking possibilities more completely. A safety stop near 15 ft is easier than 10 ft in adverse water conditions, such as surge and surface disturbances. At altitude, the same procedures are suggested, with depths, ascent rates, and stops scaled [16,20] by correction factors, a a = exp(-.038119z), (5) for z measured in multiples of 1000 ft, when using the USN tables, or any set for which M-values need extrapolation at reduced ambient pressure. Tables with M-values fitted to altitude data [3,10] have their own rules. Summary We presently do not possess a totally first-principles decompression theory, but we suspect shortcomings of approaches and how to enhance their effective implementation. In the case of the multi-tissue algorithm, there are two problem areas, free phase dynamics and bends trigger points. Fundamentally, tissue tensions are not the same as gas pressures in bubbles and elimination gradients for dissolved phases are not the same as gradients for free phases. Alone, M-value trigger points cannot optimally address the most probable cause of decompression sickness (Type I and II) symptomatic phase levels. With increased exposure, one deduces lower tolerance levels to free phases. With successively deeper profiles, one expects to excite greater numbers of micronuclei into troublesome growth, exceeding body capacity for elimination. These considerations appear at the root of higher bends statistics for divers embarking on multi-day, repetitive, and multi-level excursions, in that order of decreasing risk.[24, 25]. Bounce (non-repetitive) dives appear relatively risk free these days, especially algorithms employing reduced time limits ostensibly restricting growth. And the presence of only small proportions of free phases bootstraps 26 Wienke: Phase dynamics in diving any supersaturation treatment. Overall, such issues might best be left to nucleation and bubble models. Safety stops and slower ascent rates are useful, and correlate in principle with bubble models. Further reduction in no-decompression time limits appears a zero-sum game between safety and optimality. Acknowledgements We thank Tom Kunkle (LANL) for discussions of many bubble experiments and the Yount-Hoffman-Kunkle-Beckman nucleation approach to decompression, Dave Yount (University of Hawaii) for many of his references, Paul Weathersby (NMRI) for comments on maximum-likelihood USN approaches to tables, and Val Hempleman, (Alverstoke) for elucidation of experiments probing critical volumes. Bibliography [I] Boycott A.E., G.C.C. Damant and J.S. Haldane. 1908. The Prevention Of Compressed-Air Illness. J. Hyg. 8: 342-443. [2] Hennessy, T.R. 1974. The Interaction Of Diffusion And Perfusion In Homogeneous Tissue. Bull. Math. Biol. 36: 505-527. [3] Biihlmann, A.A. 1984. Decompression/Decompression Sickness, Berlin: Springer- Verlag. [4] Workman, R.D. 1965. Calculation Of Decompression Schedules For Nitrogen- Oxygen And Helium-Oxygen Dives, USN Experimental Diving Unit Research Report, NEDU 6-65, Washington, D.C. [5] Schreiner, H.R. and P.L. Kelley. 1971. A Pragmatic View Of Decompression, Proc. Fourth Symp. Underwater Physiol. New York: Academic Press : 205-219. [6] Spencer, M.P. 1976. Decompression Limits For Compressed Air Determined By Ultrasonically Detected Blood Bubbles. J. Appl. Physiol. 40: 229-235. [7] Weathersby, P.K., L.D. Homer, and E.T. Flynn. 1984. On The Likelihood Of Decompression Sickness. J. Appl. Physiol. 57: 815-825. [8] Hills, B.A. 1977. Decompression Sickness, New York: John Wiley And Sons Inc. [9] Hempleman, H.V. 1957. Further Basic Facts On Decompression Sickness. Investigation Into The Decompression Tables, Medical Research Council Report, UPS 168, London. [10] Bell, R.L. and R.E. Borgwardt. 1976. The Theory Of High Altitude Correction To The US Navy Standard Decompression Tables: I. The Cross Corrections, Undersea Biomed. Res. 3: 1-23. II1] Behnke* A.R. 1967. The Isobaric Oxygen Window Principle Of Decompression, Trans. Third Annual Conf. Marine Tech. Soc, Washington, D.C: Marine Technology Society: 213-228. 27 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. [12] Yount, D.E. and R.H. Strauss. 1976. Bubble Formation In Gelatin: A Model For Decompression Sickness. J. Appl. Phys. 47: 5081-5089. [13] Hennessy, T.R. and H.V. Hempleman.1977. An Examination Of The Critical Released Gas Concept In Decompression Sickness, Proc. Roy. Soc. London (B) 197: 299-313. [14] Epstein, P.S. and M.S. Plesset.1950. On The Stability Of Gas Bubbles In Liquid- Gas Solutions. J. Chem. Phys. 18: 1505-1509. [15] Kunkle, T.D. and E.L. Beckman.1983. Bubble Dissolution Physics And The Treatment Of Decompression Sickness. Med. Phys. 10: 184-190. [16] Wienke, B.R. 1987. Computational Decompression Models. Int. J. Bio-Med. Comp. 21: 205-221. [17] Wienke, B.R. 1989. Tissue Gas Exchange Models And Decompression Computations: A Review. Undersea Biomed. Res. 16: 53-89. [ 18] Yount, D.E. and D.C. Hoffman. 1986. On The Use Of A Bubble Formation Model To Calculate Diving Tables. Aviat Space Environ. Med. 57:149-156. [19] Strauss, R.H. 1974. Bubble Formation In Gelatin: Implications For Prevention Of Decompression Sickness. Undersea Biomed. Res. 1: 169-174. [20] Wienke, B.R. 1986. DECOMP: Computational Package For Nitrogen Transport Modeling In Tissues. Comp. Phys. Comm. 40: 327-336. [21] Crocker, W.E., F.C. Goodenough and W.M. Davidson. 1951. Investigation Into The Decompression Tables: Progress Report On The First Series Of Human Exposures. Medical Research Council Report, UPS 118, London. [22] Farm, F.P., E.M. Hayashi and E.L.Beckman. 1986. Diving And Decompression Sickness Treatment Practices Among Hawaii's Diving Fisherman", University of Hawaii Sea Grant Report UNIHI-SEAGRANT-TP-86-01, Honolulu. [23] LeMessurier, D.H. and B.A. Hills. 1965. Decompression Sickness: A Study Of Diving Techniques In The Torres Strait. Hvaldradets Skrifter 48: 54-84. [24] Lang M.A. and R.W. Hamilton (Eds.). 1989. Proceedings Of The American Academy Of Underwater Sciences Dive Computer Workshop", University Of Southern California Sea Grant Publication, USCSG-TR-01-89, Los Angeles, CA. [25] Vann, R.D., J. Dovenbarger, C. Wachholz and P.B. Bennett. 1989. Decompression Sickness In Dive Computer And Table Use. DAN Newsletter 3-6. [26] Yount, D.E. 1982. On The Evolution, Generation, And Regeneration Of Gas Cavitation Nuclei. J. Acoust. Soc. 71: 1473-1481. [27] Yount D.E., CM. Yeung and F.W. Ingle. 1979. Determination Of The Radii Of Gas Cavitation Nuclei By Filtering Gelatin. J. Acoust. Soc. Am. 65: 1440-1450. [28] Yount, D.E. 1979. Skins Of Varying Permeability: A Stabilization Mechanism For Gas Cavitation Nuclei. J. Acoust Soc. Am. 65: 1431-1439. 28 Wienke: Phase dynamics in diving [29] Yount, D.E. 1981. Application Of A Bubble Formation Model To Decompression Sickness In Fingerling Salmon. Undersea Biomed. Res. 8:199-208. [30] Van Liew, H.D. 1989. Readjustment Of O2, CO2, and H2O In Bubbles After A Decompression. Undersea Biomed. Res. 16: 32. [31] Walder, D.N. 1968. Adaptation To Decompression Sickness In Caisson Work. Biometeor. 11: 350-359. [32] Pilmanis, A.A. 1976. Intravenous Gas Emboli In Man After Compressed Air Ocean Diving. Office Of Naval Research Contract Report, N00014-67-A-0269- 0026, Washington, D.C. [33] Hyldegaard, O. and J. Madsen. 1989. Influence Of Heliox, Oxygen, And N2O - O2 Breathing On N2 Bubbles In Adipose Tissue. Undersea Biomed. Res. 185-194. [34] Thalmann, E.D. 1989. Testing Of Revised Unlimited-Duration Upward Excursions During Helium-Oxygen Saturation Dives. Undersea Biomed. Res. 16: 195-218. 29 THE PHYSICS OF BUBBLE FORMATION: IMPLICATIONS FOR SAFE ASCENT RATES IN DIVERS David E. Yount Department of Physics and Astronomy University of Hawaii Honolulu, HAWAII 96822 U.S.A. A typical decompression schedule for divers consists of a series of relatively rapid ascents interspersed with appropriate safety stops at progressively shallower depths. This is a convenient way of approximating, in practical situations, a theoretically more ideal profile, which would be a smooth curve describing a gradual but continuous pressure reduction. The objective of such a profile or schedule is to allow time for gas dissolved in the body to exit through the lung, thereby avoiding excessive supersaturation, the formation of bubbles in blood or tissue, and the onset of decompression sickness. In the past, attention has been focused mainly on the stops, their depths, and their durations; and the ascent rates between stops varied widely from one set of tables to another with no apparent justification. This paper focuses on the rate of ascent between safety stops and addresses the question of whether there are any limits on that rate that can be deduced from a theory of decompression sickness based on the physics of bubble formation. Introduction The topic of this workshop is the biomechanics of safe ascents. The particular issue examined in this paper is whether there are any limits on ascent rates that can be deduced from a theory of decompression sickness based on the physics of bubble formation. To lay a proper foundation for such an inquiry, the paper begins with some observations about decompression sickness. These are followed by a discussion of bubble nucleation and a description of the use of a bubble formation model to calculate diving tables. Finally, with this foundation and all of this scaffolding in place, the more specific subject of ascent rates is addressed. Decompression Sickness Decompression sickness is caused by a reduction in ambient pressure which results in supersaturation and the formation of gas bubbles in blood or tissue. This well-known disease, often called "the bends," is associated with such modern-day activities as deep-sea diving, working in pressurized tunnels and caissons, flying at high altitudes in unpressurized aircraft, and EVA excursions from spacecraft. A striking feature of decompression sickness is that almost any body part, organ, or fluid can be affected, including skin, muscle, brain and nervous tissue, the vitreous humor of the eye, tendon sheath, and bone. Medical signs and symptoms range from itching and 31 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. mild tingling sensations to crippling bone necrosis, permanent paralysis, and death. There are cases in which bubbles have been found in a diver who died more than 30 days after surfacing. Similarly, bone necrosis can show up months or even years after a single exposure, and often there is no other indication of hyperbaric stress. Evidently, decompression sickness is a syndrome, rather than a single sign or symptom. It is also a series of events, rather than a single incident. In spite of this complexity and variability, safe decompression can usually be achieved. The key is to reduce the ambient pressure gradually, allowing sufficient time for gas elimination. The word "safe" really means "relatively safe," implying, for example, that the incidence rate for decompression sickness is on the order of 1% of less. The expression "gas elimination" refers to the transport of dissolved gas from blood and tissue to the lung, where it can be expired before bubble formation occurs. Previous strategies for decompressing humans have been based mainly on trial-and- error informed by past mistakes as well as by a set of unsupported algorithms and assumptions, some of which are now known to hie wrong (Yount, 1978). Given the shortcomings of the standard model, it is appropriate to consider a new theory based on verifiable physical principles and especially on the physics of bubble formation. Bubble Nucleation Ordinary samples of sea water, tap water, or even distilled water form visible bubbles when subjected to tensile, ultrasonic, or supersaturation pressures as small as 1 atm. This is several orders of magnitude below the theoretical tensile strength of pure water, and it implies that cavitation must be initiated by processes other than modest changes in pressure and the random motion of water and gas molecules. Numerous experiments have demonstrated that thresholds for bubble formation can be significantly raised by degassing or by a preliminary application of static pressure. These are specific tests for gas nuclei, and it is therefore evident that the precocious onset of cavitation in water and in aqueous media generally must be due mainly to the presence of such nuclei, even though their origins and the mechanisms stabilizing them are still poorly understood. The existence of stable gas nuclei is at first rather surprising. Gas phases larger than 1 micron in radius should float to the surface of a standing liquid, whereas smaller ones should dissolve within a few seconds due to surface tension. The various proposals for coping with this dilemma are critically reviewed in an earlier paper (Yount, 1979b), and a new model, called the varying-permeability or VP model, is introduced. The essence of the VP model is that cavitation nuclei consist of spherical gas phases small enough to remain in solution and strong enough to resist collapse, their mechanical compression strength being provided by an elastic skin or membrane composed of surface- active molecules. VP skins are ordinarily permeable to gas, but they can become impermeable if the ambient pressure is increased rapidly by a sufficiently large amount, typically exceeding 8 atm. Fig. 1 is a photomontage of microbubble nuclei found in agarose gelatin (Yount et al., 1984). Moving clockwise from upper left are phase-contrast, Nomarsky or interference-contrast, dark field, and transmission electron micrographs. The largest nuclei 32 Yount: The physics of bubble formation in each case have radii on the order of 1 micron. The structures identified as nuclei with phase-contrast and Nomarsky optics resemble ordinary gas bubbles. In the Nomarsky micrographs, the shadowing of the nuclei is opposite that of the surrounding gelatin, implying that nuclei are spherical cavities rather than solid or liquid inclusions. Fig. 1. Candidate nuclei found in agarose gelatin. Moving clockwise from upper left are phase-contrast, Nomarsky, dark-field, and transmission electron micrographs. 33 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Near the center of the phase-contrast micrograph in the montage are two osculating nuclei, that is, two nuclei that are just barely touching and appear to be spherical in shape at the point of contact. Fig. 2 shows a similar binary nucleus photographed in distilled water with ordinary bright-field illumination (Yount et al., 1984). Fig. 2. Two osculating nuclei photographed in distilled water with ordinary bright-field illumination. The larger member of this stable binary has a radius of 1.5 microns. The facts that there are binary nuclei in nature and that binary nuclei are stable provide further evidence that individual nuclei are enclosed in gas-permeable skins. The idea is that permeable skins allow each nucleus to reach diffusion equilibrium with the gas dissolved in the surrounding liquid. Since both members of a binary configuration are in diffusion equilibrium with the same liquid, they are in diffusion equilibrium with one another and retain their gas contents and relative size. This situation does not hold for binary soap bubbles in air, where it is well-known that the smaller member of the pair will lose its gas to the larger. The fact that nuclei occur in distilled water suggests that they probably can be found in almost any aqueous medium including blood and tissue. Fig. 3 shows four microbubbles injected into blood plasma (Yount, 1988). The largest radius in the first micrograph is about 5 microns. Moving left to right and top to bottom, the pressures are 1.0,0.75,0.5, and 0.25 atm abs. If these microbubbles were not stabilized by some mechanism, presumably by a skin of surface-active molecules, they would have dissolved within a few seconds. It is an important feature of the VP model that a given nucleus can reach equilibrium at different pressures and that a given pressure can support nuclei having widely different radii. 34 Yount: The physics of bubble formation Fig. 3. Four microbubbles injected into blood. The largest radius in the first micrograph Is 5 microns. The respective pressures are 1.0, 0.75, 0.S, and 0.25 atm abs. fe-.O 35 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Theoretical curves are calculated in the VP model by tracking the changes in nuclear radius that are caused by increases or decreases in ambient pressure. This is facilitated by the "ordering hypothesis" which states that nuclei are neither created nor extinguished by a pressure schedule and the initial ordering according to size is preserved. It follows that each bubble count is determined by the properties of a single critical nucleus since all nuclei with larger than critical radii will form bubbles and all those with smaller than critical radii will not. Obviously one of the properties of a VP nucleus is its radius; another is the crumbling compression of its skin. Typical results of a bubble counting experiment carried out in supersaturated gelatin are shown in Fig. 4 (Yount et al., 1979). The test schedule illustrates how the supersaturation pressure pss = ps - pf and crushing pressure Pcrush = Pm - Po are defined in terms of the initial pressure po, the maximum pressure and supersaturation pressure pm = ps , and the final pressure pf. The impermeability threshold (p* - p0) is that value of Pcrush beyond which the nuclear skin becomes effectively impermeable to gas; this is regarded as another property of the nucleus, yielding a total of three nuclear parameters altogether. The experimental points in Fig. 4 were determined by finding combinations of pss and Pcrush that give a fixed bubble number: N = 0.1, 1.0, 10, 30, 100, and 200 per 0.4 ml sample. The dashed lines were calculated from the VP model. Below the impermeability threshold, the lines are straight with a slope determined primarily by the crumbling compression and with an intercept determined primarily by the radius. At higher crushing pressures where the nuclear skins are impermeable to gas, the pressure inside the nucleus increases as the volume decreases. This makes the nucleus more resistant to further crushing and thereby reduces the slope in a manner rigorously determined by Boyle's law. Calculating Diving Tables In the earliest applications of the VP model to decompression sickness (Yount, 1979a, Yount, 1981), one additional assumption was made, namely, that isopleths of constant bubble number N are also lines of constant physiological stress. This idea is tested in Fig. 5 (Yount, 1981) using data from a paper by D'Aoust et al. (1980). The new variable Pj = pm is just pcrush displaced by po = 1 atm abs to the right, and Pj - Pf is the pressure reduction and hence the supersaturation pss. Since the pressure excursions are entirely within the permeable region of the VP model, the individual dive scores map out another family of straight lines. Comparison with Fig. 4 suggests that for saturation dives at least, there is a close correlation between physiological outcome and bubble number, as was originally assumed. An in vivo test of the VP model in the impermeable region is shown in Fig. 6 (Yount, 1979a; Yount and Lally, 1980), where ED-50 is the pressure reduction required to produce signs of decompression sickness in 50% of the subject rats (Berghage et al., 1976; Berghage and McCracken, 1979a; Berghage and McCracken, 1979b). In this case, the permeable region extends up to an exposure pressure of about 10 atm abs (pcrush = 9 atm), and the VP model continues to provide an excellent description of the rat data all the way out to 40 atm abs. Similar comparisons have been made with decompression results for humans, and although the data for humans are sparse and highly variable, the agreement with the VP model appears to be satisfactory (Yount, 1979a). Can it be that diving tables are just protocols for producing a constant bubble number in divers? The answer is no. Fig. 7 illustrates what goes wrong (Yount and 36 Yount: The physics of bubble formation Hoffman, 1986). Shown here are the US Navy (1977) and Royal Naval Physiological Laboratory (1968) no-stop decompressions along with various practical observations - combinations of depth and bottom time which yield no symptoms or only the mildest symptoms - compiled by Leitch and Barnard (1982). When one tries to describe these "data" with a line that yields a constant bubble number, the result is always too flat. Fig. 4. Supersaturatlon pressure p s s versus the initial crushing pressure Pcrush f?r various numbers of bubbles N per sample. Dashed lines were calculated from the VP model. SATURATION TIME = 5.25 HOURS Q. I CO CL I I (0 LJ cn if)(/) LJ : Surface Tension A * J ? l ? Alveolar gas was hi n, washout Fig. 1. Diagram of the main factors that determine whether a bubble grows or shrinks. In what follows, specific examples of bubbles or bubble nuclei will be described. A broader perspective can be achieved by remembering that other bubbles or nuclei in the body may differ from the cases shown in size or in washout characteristics of their surroundings. Tissues with slow washin may still be taking up N2 when the ascent occurs, so they may have relatively low N2, and they will be slow in giving off N2 after ascent. pressure ATA 1 - amb r in bubble ~ in tissue 0 10 20 30 time, minutes Fig. 2. Ambient pressure (dashed), and partial pressures of N2 in a bubble and in the surrounding tissue in an ascent from 33 fsw to surface. Decompression from 33 fsw to surface Figure 2 is a diagram of events which occur during a simple ascent, at a rate of 1 fsw/sec, from an ambient pressure of 2 ATA to 1 ATA. When ambient pressure falls during the ascent, N2 in a bubble falls too. If it is assumed that the sum of partial pressures equals ambient pressure, PN2 inside (labeled "in bubble") is always a little lower than ambient pressure because the bubble contains O2, CO2, and water vapor as well as N2, but if the tissue exerts significant pressure on the bubble, the PN2 inside the bubble could actually be above the ambient pressure. The hatched region in Fig. 2 emphasizes the time when PN2 in the tissue (labeled "in tissue") is temporarily above PN2 in the bubble because dissolved gas in the tissue awaits washout by the circulation. The phenomenon can be called a "crossover"; it is crucial for causing bubble growth or transformation of a nucleus into a bubble. In steady states before and after the ascent, the PN2 is higher in a bubble than in the tissue because of what is known as the "oxygen window", or "inherent unsaturation" (1). The two heavy arrows in Fig. 2 show the magnitude of the oxygen window before and after the ascent. 48 Van Liew: Growth of pre-existing bubbles and gas nuclei during ascent The author has developed a computer program in the BASIC language to predict size of a bubble, as a function of time, under various circumstances (Van Liew, 1989); the program includes the important aspects of dynamics of bubbles (Van Liew and Hlastala, 1969). The program assumes that bubbles are always spheres, which may be adequate for small bubbles, but bigger ones are probably distorted into cylinders or sheets by tissue or blood vessels. Figure 3 shows the calculated radius of a bubble subjected to the pressures discussed in connection with Fig. 2. At first the bubble shrank from its original radius of about 80 micrometers due to the oxygen window. When the ascent occurred, the bubble enlarged because of simple decompression of the gas (Boyle's law), but there was a crossover of N2 , so the bubble also grew by diffusion of N2 molecules. The Boyle's law effect alone would have increased the bubble from 50 micrometers to 63 micrometers, whereas it actually grew to 100 micrometers. When tissue N2 became lower than bubble N2 at 11 minutes, the bubble shrank again. When the radius became very small, at 27 minutes, surface tension became the overriding component, so total pressure inside the bubble rose precipitously, which led to an abrupt rise in N2 partial pressure in the bubble. v / i n bubble | radi us urn 100H 1 ^ ^ - ? - ? ? ^ ^ s in tissue 0 -L - | 1 1 1 r 0 10 20 30 time, minutes Fig. 3. Radius of a pre-existing bubble which is subjected to an ascent from 2 ATA to the surface. When a bubble is very small, surface tension pressure inside is very large, so the tendency for diffusion out of N2 is very large. Thus a simplistic interpretation of the physical rules indicates that bubbles cannot be small and therefore cannot exist in the body, where the oxygen window always tends to cause bubbles to shrink. This logical problem has led to the idea that the simple physical rules do not apply, or that something else is happening. The popular way around the problem is to assume that there are "gas nuclei", which do not obey the rules of surface tension for free bubbles in a liquid medium. When the circumstances are right, the very small entities of gas which persist as nuclei can grow into real bubbles that do obey the physical laws. Nuclei Gas nuclei were simulated with the abovementioned computer program by not allowing a very small initial bubble to become smaller, but allowing it to grow larger by Boyle's law and by N2 diffusion. Figure 4 illustrates some issues about nuclei. A large bubble would have PN2 inside it of about 1.9 ATA as in Figs. 2 and 3 (light dotted line at the left in Fig. 4), whereas a nucleus of 1.57 micrometers radius has a PN2 of almost 2.5 ATA as shown - the difference is caused by the high surface tension pressure consequent to the small radius of the 49 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. nucleus. When the ambient pressure fell from 2 ATA to 1 ATA, the PN2 in the nucleus fell in parallel so that after ascent, at the right, the nucleus would have a PN2 of about 1.5 ATA whereas a bubble would have a PN2 of about 0.9 ATA. At no time was nucleus PN2 less than tissue PN2 in Fig. 4; a crossover was narrowly avoided (at the big arrow). When the nucleus was just one one-hundredth of a micrometer larger, a different picture emerged (Fig. 5). There was a tiny crossover at the arrow which allowed the nucleus to grow, and the growth caused a rapid decrease of surface tension pressure so that PN2 inside fell (from the level of the arrow to 0.9 ATA). The nucleus became a bubble. When the bubble decayed to a nucleus again, the PN2 inside was again high because of the surface tension pressure. 2 - pressure ATA 1 - 0 - ... t nucleus V in nucleus s in tissue I I I 0 10 20 30 time, minutes Fig. 4. A bubble nucleus subjected to the same ascent as in Figs. 2 and 3. r adi us jjm 1 2 ? pressure ATA 0 0 - n ? U u ^ c in nucleus y? \ in bubble X. \ 1 1 10 time J s radi us 1 1 20 , minutes n nucleus in tissue 30 Fig. 5. In a nucleus slightly larger than the one of Fig. 4, a crossover allowed transformation into a bubble. Several variables can be critical in the transformation of a nucleus into a bubble. One of these is initial size of the nucleus, as evidenced by the finding that an increase of less than 1% (from 1.57 to 1.58 micrometers) changed the situation from no-growth to growth. In a much smaller nucleus, the PN2 inside would be much higher, so crossover would not occur unless PN2 in tissue was also much higher than in the Fig. 5 case. 50 Van Liew: Growth of pre-existing bubbles and gas nuclei during ascent A second critical variable is tissue washout rate, as characterized by the washout halftime that would be observed after an instantaneous decompression. If the washout had been faster in Fig. 5, the tissue PN2 would have fallen more steeply so the PN2 crossover might not have occurred. The slower the washout, the higher the "in tissue" curve, and the more likely a crossover and bubble growth. A third critical issue is the ascent rate. If ascent had been faster, the PN2 in the bubble would have fallen more steeply and crossover would have been more likely. If ascent were slower, the fall of PN2 in the nucleus would have been slower, but also the removal of N2 from the tissue would have been slower. The relation between these competing influences is shown in Figs. 6 and 7. When washout halftime is held constant, decrease of ascent rate by factors of 10 and 20 from the usual 1 fsw/sec delays the removal of N2 by factors of just 3 or 4 (Fig. 6). Only very slow ascent has an appreciable effect. PN2 in tissue. ATA 1 . 0 - 0 - \ 1 1 .0 i fsw/sec \0.05 " ? o.iN. 1 1 1 1 1 0 10 20 30 time, minutes Fig. 6. Effect of various ascent rates on removal of N2 from a tissue having a washout halftime of 2.5 minutes. 2-\ pressure ATA 1 H 1 fsw/sec 0.05 fsw/sec in bubble in bubble in tissue - in tissue 10 20 time, minutes 10 20 30 time, minutes Fig. 7. Relation of tissue N2 removal to PN2 in the bubble when washout halftime is 2.5 minutes. Figure 7 illustrates the relation between PN2 in a bubble and in the tissue for the .05 and 1.0 fsw/sec profiles of Fig. 6. When ascent is fast, the N2 removal has an essentially exponential form but with the slower ascent, the tissue PN2 tends to be parallel to the bubble PN2, which of course follows the ambient pressure. The fast ascent gave a big crossover region, whereas the slow ascent had almost no crossover. One could conclude from this comparison that the high ambient pressure (and high bubble PN2) in the slow 51 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. ascent is more of an advantage than the more rapid N2 removal with the fast ascent. When washout is slow, such as in tissues with a halftime of 30 minutes, bubbles comparable to those shown in Fig. 7 have long-lasting crossovers for both 1 and .05 fsw/sec ascents, but for nuclei there would still be an appreciable advantage of a slow ascent. Slow ascents may have an additional disadvantage: slow tissues which are not yet equilibrated may take on additional gas. Two-stage decompression The rectangular-appearing profile in Fig. 8 is PN2 in a nucleus which became a bubble when the diver followed U.S. Navy table decompression for a dive to 60 fsw for two hours. Ascent is 1 fsw/sec in two stages; the diver goes from 60 fsw to 10 fsw, remains 26 min, then ascends to the surface. In the case shown, tissue washout halftime is 5 min. The transformation to a bubble occurred during the first ascent and the second decompression caused a small additional phase of growth. When the ascent rate in this particular case was decreased by a factor of 6, the nucleus did not become a bubble until near the end of the ascent. The PN2 in the nucleus decreased along with the decrease of ambient pressure, but the nucleus PN2 eventually was less than tissue PN2, so the drastic decrease of PN2 inside occurred, which allowed a drastic influx of N2 by diffusion. Decrease of the ascent rate by a factor of 10 prevented the nucleus of Fig. 8 from becoming a bubble. 3 - pre$$ure ATA 2-\ radius 100- in bubble ,? intissuej 20 40 time, minutes Fig. 8. Behavior of a nucleus during a two-stage decompression. An alternative to the two-stage decompression shown in Fig. 8 would be a very slow linear ascent which would allow the diver to arrive at the surface in the same time, but without stops (Fig. 9). Ascent is .04 fsw/sec, or 2.4 fsw/min. Tissue N2 removal is slower. A bubble would have a crossover, but PN2 in the nucleus would not reach the PN2 in the tissue. However, note that if tissue washout halftime had been so slow that tissue PN2 remained almost level during the ascent, there could have been a PN2 crossover and consequent nucleus growth in the region to the right of the big arrow. 52 Van Liew: Growth of pre-existing bubbles and gas nuclei during ascent 3 - pressure ATA 2 - 1 - ? ^ in i I i / i n nucleus tissue ' ^ ^ ^ ^ i ? i i i i i i 0 20 40 time, minutes Fig. 9. Partial pressure of N2 in a nucleus and the surrounding tissue during a very slow ascent from 60 fsw to surface. The simulations above all indicate that the slowest possible ascent is desirable. However, a note of caution is advisable; only certain of the many possible combinations of dive profile, ascent rate, and tissue washout characteristics have been examined; other combinations of variables might modify the conclusions reached. References Van Liew, H.D. 1989. Gas exchanges of bubbles in tissues and blood. In: R.D. Vann (ed.). The Physiological Basis of Decompression. Thirty-eighth UHMS Workshop. Bethesda, MD: Undersea and Hyperbaric Medical Society Inc. pp. 73- 83. Van Liew, H.D. and M.P. Hlastala. 1969. Influence of bubble size and blood perfusion on absorption of gas bubbles in tissues. Respir Physiol 7: 111-121. 53 ASCENT RATE EXPERIMENTS AND DIVER SAFETY Charles E. Lehner Department of Preventive Medicine University of Wisconsin-Madison 2115 Observatory Drive Madison, WISCONSIN 53706 U.S.A. Submarine escape experiments in goats conducted by the Royal Navy offer an animal model of physiological responses to rapid ascent rate and decompression. Rapid ascents in submarine escape involve insults of rapid decompression, but these are usually tolerated by animals and humans. In those cases where injuries do result, arterial gas embolism and decompression sickness, frequently with CNS manifestations, characterize the injuries from such maneuvers. While tissue Afe uptake and the incidence of decompression sickness decrease in submarine escapes with shortened compression and ascent times, such rapid ascents increase the risk of pulmonary barotrauma and arterial gas embolism. Ascent rates up to 2.6 mlsec (8J5ftlsec) are tolerated in humans with a comparatively low risk of serious injury or death. However, recreational and scientific diving with compressed air require an even lower risk of serious outcome. This paper reviews ascent rate outcomes in animals and humans with the goal of improving diver safety. "A life without adventure is likely to be unsatisfying, but a life in which adventure is allowed to take whatever form it will is likely to be short". ~ Bertrand Russell Introduction Submarine escapes represent examples of extremely rapid decompressions and as such they can provide valuable insights about human physiological responses with extremely rapid ascent. Both animal and human findings in submarine escape experiments that sometimes provoke decompression sickness (DCS) and arterial gas embolism will be reviewed with most attention focused on the Royal Navy's submarine escape outcomes. Previous findings reported in the submarine escape literature are re-examined to determine if conventional ascent rates (60 ft/sec) and somewhat faster ascents pose a significant risk for the diver. Several implications that such findings have for recommendations of ascent rates with acceptable risk for recreational and scientific diving with scuba will be evaluated. Risk in ascent: Pulmonary barotrauma and decompression sickness The primary risks in scuba diving ascent are DCS and pulmonary barotrauma which causes arterial gas embolism (Elliott and Kindwall, 1982). Arterial gas embolism and some forms of DCS can seriously imperil the diver (Shilling, Carlston and Mathias, 1984), and these will be briefly described. 55 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Pulmonary barotrauma from overinflation of the lungs during ascent is the usual cause of arterial gas embolism in the brain, heart and other organs. Lung dissection from overinflation during ascent can also result in pneumothorax, mediastinal emphysema, and subcutaneous emphysema (Shilling and Faiman, 1984). Pulmonary barotrauma can occur with a low intrapulmonary overpressure compared to ambient pressure. With the lungs fully inflated (at total lung capacity), pulmonary barotrauma would be expected with a 0.9- 1.8m (3-6 ft) ascent to surface accompanied by overinflation pressures in the lungs as low as 80mm Hg (Lanphier, 1965; Elliott and Kindwall, 1982; Anthonisen, 1984). Decompression sickness has three major manifestations caused by bubble formation and embolization in the body's tissues (Elliott and Kindwall, 1982). Central nervous system DCS (CNS-DCS) usually involves the spinal cord, often resulting in limb paralysis or numbness, and less frequently there are signs of cerebral involvement. The "chokes" is a respiratory form of DCS (Atkins et al., 1988). It occurs when decompression generates massive quantities of circulating venous bubbles that transit the right heart and embolize the pulmonary arterial vasculature. Extensive pulmonary embolization causes the insidious symptoms of fatigue, coughing, dyspnea and labored breathing that are characteristic of chokes. The obstructive pulmonary hypertension that develops in chokes may lead to fulminant pulmonary edema with pleural effusion (Atkins et al., 1988). Both CNS-DCS and the chokes can be fatal. By contrast, limb bends represents an often painful, but not life-threatening, form of DCS which is focused in the joint regions. Animal and human responses to decompression A classic paper in decompression physiology by Boycott, Damant and Haldane (1908) developed the early theoretical basis for practical decompression procedures to avoid DCS. Much of their work was based on decompression studies using goats as an animal model of human responses to decompression. The traditional use of experimental goats by the Royal Navy has continued in recent studies that tested various dive profiles, including submarine escape maneuvers characterized by extremely rapid ascent rates. Human and goat responses to decompression appear similar. This fact is probably due to their similar tissue metabolisms and comparable tissue blood flows (perfusion rates) which result in corresponding rates of inert gas exchange (Lehner, Palta and Lanphier, 1987). Species' metabolisms and blood flow rates appear correlated to the 3/4 power of body weight (Lightfoot, 1974) so that smaller species have higher perfusion rates than larger species. Such relationships between species, based on body mass, are examples of allometric scaling (Schmidt-Nielsen, 1984). Decompression studies at the University of Wisconsin-Madison used sheep and pygmy goats to simulate no-stop (without decompression stops) air dives (Lehner et al., 1985). All no-stop ascents were at a 60 ft/min ascent rate to surface, often followed by a simulated altitude exposure at 570mm Hg (8000 ft) to provoke DCS signs. There were relatively few CNS-DCS cases after "long," 4-h and 24-h, dives. Most DCS cases in these long exposures involved limb bends and transient chokes. Interestingly, no-stop ascents from relatively deep, 1/2-h dives provoked a high proportion of CNS-DCS cases with transient signs of paraplegia or quadriplegia indicating spinal cord DCS. In sheep, the proportion of CNS-DCS in DCS cases went from less than 10% in the "long," shallow dives to 68% in the 1/2-h dives. In pygmy goats, CNS-DCS increased from less than 5% in the "long" dives to more than 30% in the 1/2-h dives. Both the long and short duration dives generated a similar incidence of DCS cases, but the manifestations of DCS varied according to dive profile. These findings indicate that no-stop ascents from short, relatively 56 Lehner: Ascent rate experiments and diver safety deep air dives provoke a higher proportion of CNS-DCS than ascents from longer dives at shallow depths. In humans, the reported incidence of CNS involvement in sport diving accidents has increasingly gained the attention of the diving community (Dick and Massey, 1985). In some areas where relatively deep scuba diving predominates, a high percentage of CNS- DCS points to the importance of re-examining diving procedures to improve diving safety. Recent findings reported from the Royal Navy treatment of civilian and military divers as well as submarine escape trainees indicate that CNS-DCS and cerebral air embolism accidents may result in chronic cerebral perfusion deficits (Adkisson et al., 1989). Chronic cerebral perfusion deficits occurred in all patients with Type II DCS, even those limited to classic spinal cord DCS presentations. These findings suggest that chronic brain dysfunction may be more widespread than previously recognized in DCS victims. Goats in submarine escape simulations Submarine escape experiments by the Royal Navy with goats and humans provide a rich source of information on extremely rapid ascents which is germane to an understanding of the risk involved in diving ascent rates. Goats were commonly used by the Royal Navy to test profiles for subsequent human experiments. First, we will examine goat decompression experiments conducted by the Royal Navy at Alverstoke. A 1984 paper by Bell and associates on goat responses to simulated submarine escapes drew our attention because more CNS-DCS than limb bends occurred in deeper submarine escape profiles. As previously mentioned, we had observed a greater proportion of CNS-DCS cases in sheep and pygmy goats after relatively short, deep, no- stop ascent profiles. Bell et al. (1984) observed similarly high percentages of CNS-DCS in DCS cases provoked by submarine escape maneuvers. Importantly, they also demonstrated a comparatively low risk of serious injury in very rapid ascents. Their simulated submarine escape profile using goats involved a mild 16-h "pre-escape" hyperbaric exposure followed by a quick simulated submarine escape. Abrupt submarine escapes involved a rapid exponential compression phase, a 4 sec hold at maximum pressure, and a linear ascent rate of 2.75 m/sec to surface pressure. Such escape maneuvers increased the CNS-DCS incidence compared to that of limb bends as the maximum escape depth increased: CNS- DCS in goat DCS rose from less than 20% to greater than 60% of the DCS cases as the depth changed from 135m to 280m. The Bell et al. (1984) observations in goat "escapes" on air are remarkably similar to the sheep responses in our 1/2-h "deep" dives. A shift from limb bends to CNS-DCS in goats as well as sheep with profiles of decreasing time and increasing depth suggests a relationship between tissue blood flows and the manifestation of DCS. Presumably, CNS-DCS in the spinal cord occurs with bubble injury to those tissues characterized by relatively high blood flows and correspondingly fast washin and washout rates of nitrogen. It follows that limb bends affects tissues in the joint regions with presumably slower washin and washout rates which are largely controlled by lower rates of tissue blood flow. Moreover, sufficient bubble formation or embolization in those tissues susceptible to DCS injury appears necessary for the tissue injury mechanisms that produce the signs and symptoms of DCS. A rapid ascent from a brief deep dive tends to provoke more CNS-DCS manifestations than an equally rapid ascent rate from a shallow dive of long duration. Therefore, the risk of DCS, whether chokes, CNS-DCS or limb bends, would appear to depend on adequate decompression time rather than ascent rates per se. 57 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Much of the information gained from Royal Navy studies in submarine escapes appears in Royal Navy reports with limited circulation. Eaton (1971) provides a particularly interesting account of the extreme depths that can be tolerated by goats in submarine escape. His experiments involved extremely rapid compression and decompression rates to minimize tissue gas loading. Decreased tissue gas loading, accomplished by rapid compression and ascent phases in submarine escape, prevented a high incidence of serious DCS and C^-induced convulsions while the goats were briefly exposed to very high pressures of air. Hyperoxic seizures result from relatively short exposures to high partial pressures of O2 (Clark, 1982; Shilling and Faiman, 1984). Ascent rates of 2.6 m/sec (8.5 feet/sec) and decompression from brief exposures at 200m (650ft) and 290m (950ft) were tolerated by most goats. In the 200m series, there were no adverse signs observed in any of the 12 goats. However, in the deeper 290m series, two of the twelve goats died. Rates of ascent tolerated by goats were also explored by Eaton (1967) in earlier submarine escape experiments. From the goat responses, he concluded that faster rates of ascent were safer than slower rates in submarine escapes. Enhanced safety from faster ascents in submarine escapes may initially appear to represent a paradox. In submarine escapes on air, exceptionally brief pressure "spikes" reduce tissue gas loading that would otherwise cause DCS and obligate the "diver" to significant additional decompression time. In Eaton's study, ascent rates ranged from 1.8 m/sec (6 ft/sec) to 4.6 m/sec (15 ft/sec). Indeed, the conventional ascent rate of 60 ft/min or 1 ft/sec (0.3 m/sec) recommended by the U.S. Navy (1978) is remarkably slow by comparison. Submarine escape in humans: Rapid compression and ascent Submarine escape offers a practical basis for evaluating human risk in extremely rapid ascents. Submarine escape procedures were reviewed in an international workshop on this subject (Gell and Parker, 1974). Data of human responses to submarine escape maneuvers encompass numerous training outcomes in simulated submarine escapes as well as chamber and field trials. Rapid compression and ascent in submarine escape maneuvers focus on the lung's ability to withstand rapid pressure reduction without pulmonary barotrauma and on minimizing tissue gas loading and DCS risk. Sir Robert Davis' insightful book on deep diving and submarine operations (1962) offers a useful historical perspective to submarine escape. Davis points out the simple but essential maneuvers required of those who engage in submarine escapes. Avoidance of breath-holding during ascents in both submarine escapes and scuba diving is essential. Davis states, "There is a natural tendency in men escaping from submarines to hold their breath, whether they are wearing apparatus or not. This is a fundamental protective reflex under water.... The act of venting easily, and suppressing the desire to hold one's breath is acquired by training practice." By inference, inadequate training appears strongly implicated in diving accidents that involve arterial gas embolism, except for those cases where lung defects predisposed the diver to pulmonary barotrauma (Elliott and Kindwall, 1982; Saywell, 1989). Another factor in submarine escape and diving involves the psychological condition of the individual (Biersner, 1984). Inadequate training can set the stage for inappropriate, life-threatening behavior in certain divers susceptible to panic. The personality of the diver appears to play a crucial role in panic behavior that may lead to breath-holding and a pulmonary barotrauma accident upon ascent (Morgan, in press). 58 Lehner: Ascent rate experiments and diver safety In a Royal Navy report, Barnard, Eaton and Snow (1971) described 112 submarine escapes simulated by 20 men during chamber experiments. Men tolerated compression to 150m in 20 sec at a compression rate of 7.5 m/sec (24.6 ft/sec) and an ascent rate of 2.6 m/sec (8.5 ft/sec) to the surface. Somewhat deeper exposures were also simulated in an exposure to a maximum depth of 191m (625 ft). No cases or air embolism or DCS were reported. Mild itching was provoked in a few instances, but the symptoms were usually slight, transient and restricted to the ears. The ears have a large surface to tissue mass ratio and probably become vulnerable to bubble formation by a significant transcutaneous flux of N2 at high pressure and by cooling upon rapid decompression. Five cases of otitic barotrauma or "ear squeeze" occurred; one resulted in a perforated tympanic membrane. Much of the submarine escape research conducted by the Royal Navy has been comprehensively reviewed by Donald (1979). His review summarizes many of the human and some of the animal experiments that led to submarine escape procedures adopted by the Royal Navy. Chamber-simulated and sea trial data found in Table 1 of Donald's paper are summarized in Fig. 1 that plots submarine escape maneuvers at various ascent rates and depths. Donald reported 295 decompression outcomes. Most were uneventful, but two escapes provoked Type II CNS-DCS. There were no reported cases of gas embolism in these experimental escapes despite many 2.6 m/sec ascents. We have grouped the same data from Donald by ascent rate (Fig. 2), and they indicate no correlation between ascent rate and CNS-DCS. Despite such rapid ascent rates, decompressions were generally well- tolerated in these trained subjects. Figure 1. Submarine escape ascents from various depths. Two of 295 individual ascent trials provoked CNS-DCS, but no pulmonary barotrauma and arterial embolism cases were reported (Data from Table 1, Donald 1979) . E LU Q 200 -i 160- 120 - 8 0 - 4 0 - o O o o <5 5-10 >10-20 >20 ? Type II DCS 8 o o oC O o o o o O 8 o o O 8 O % o O oo O ?o o O ooQ O N = 295 0.0 0.4 0.8 1.2 1.6 2.0 2.4 2.8 ASCENT RATE, m/sec 59 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCEWS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Figure 2. Histogram of ascent rates and number of individual trials represented in Fig. 1. All submarine escapes were uneventful outcomes except for two cases of Type II DCS (cross-hatch and stars). 120 -i CO LU SC AP LU cr LU m 2 1 W V 8 0 - 6 0 - 40 - 20 - < 1.5 1.5-2.0 > 2.0-2.5 > 2.5 ASCENT RATE, m/sec Although there were no reported cases of pulmonary barotrauma or cerebral air embolism in Donald's studies, these conditions pose grave risks to individuals practicing submarine escapes. Brooks et al. (1986) reviewed the submarine escape outcomes from an extensive series of training exercises. The Royal Navy's training protocol for submarine escapes involved ascents from shallow depths that achieved a terminal velocity of 2-3 m/sec. In 232,000 tabulated submarine escapes, there were 84 reported cases of arterial gas embolism. This represents an incidence of 1 in 2771 decompressions or a 0.036% incidence of arterial gas embolism. In this series, there were 4 mortalities with a mortality rate of 1 in 58,211 decompressions or 0.0017%. Rapid ascent and acceptable risk in diving With submarine escapes we face a dilemma: shortened compression times and faster ascents lower the incidence of DCS, but faster ascent rates also increase the risk of pulmonary barotrauma and arterial gas embolism. In a well-instructed population such as submariner trainees, the risk of a pulmonary barotrauma accident and arterial gas embolism is comparatively low. Rapid ascents are routinely tolerated in this setting with relatively few accidents. Based on the experience gained from animal decompression experiments, we may begin to answer the question: How important is the dive profile in determining the risk of DCS and the manifestations provoked? It appears that certain pressure profiles will provoke a high incidence of CNS-DCS. Such profiles are comparatively deep air dives (>100 ft) with rapid ascents, typically with no-stop rapid decompression. 60 Lehner: Ascent rate experiments and diver safety With the submarine escape model, extremely rapid rates of ascent are routinely tolerated by animals and humans, and the risk of arterial gas embolism is relatively low. Based on the submarine escape experience, currently recommended rates of ascent, as high as 60 ft/min (18.3 m/min) or 1 ft/sec (0.3 m/sec), should be well within the bounds for a comparatively low risk of cerebral arterial gas embolism. Factors other than small differences in recommended ascent rates, particularly the diver's training, physical condition, personality type, and dive profiles with a significant DCS risk, largely determine risk in scientific and sport diving. Any endeavor that we undertake, including diving, involves some risk. Informed choices appear to offer a useful approach towards answering two questions which are important for both the diver and those asked to provide diving recommendations: What is a voluntary acceptable risk in diving, and are the risks of pulmonary barotrauma and CNS- DCS voluntarily assumed by sport and scientific divers too high? A comprehensive body of literature now exists on risk analysis (Waller and Covello, 1984; National Research Council, 1982; Shrader-Frechette, 1985) and acceptable risk (Lowrance, 1976; Fischoff et al., 1981). In this context, risk assessment can provide a decision-making approach for determining what is acceptable risk in diving. Current information about diving risk has improved with the gathering of epidemiological data from scuba diving accidents by organizations such as DAN (Diver's Alert Network, Duke University). Other sources of information include well-controlled decompression experiments in bom animals and humans. With additional information about risk, we can then make informed choices about dive profiles. Clearly, the risk voluntarily assumed by certain divers is not necessarily the same that would be freely chosen by informed individuals in other diving populations. Acknowledgments The author thanks Mr. Blair A. Rhode, Cdr. Gregory H. Adkisson, and Dr. Edward H. Lanphier for their assistance in the preparation of this paper. This work was funded by the University of Wisconsin Sea Grant Institute under grants from the National Sea Grant College Program, National Oceanic and Atmospheric Administration, U.S. Department of Commerce, and from the State of Wisconsin. Federal grant NA84AA-D- 00065, project R/DP3. Literature cited Adkisson, G.H., M. Hodgson, F. Smith, Z. Torak, M.A. Macleod, J.J.W. Sykes, C. Strack, and R.R. Pearson. 1989. Cerebral perfusion deficits in dysbaric illness. Lancet 15 July: 119-122. Anthonisen, N.R. 1984. Respiration. Lung volumes: effects of gas compression and expansion. The Physician's Guide to Diving Medicine. C.W. Shilling, C.B. Carlston, and R.A. Mathias (Eds.). Plenum Press, New York, Ch. 3:71-85. Atkins, C.E., C.E. Lehner, K.A. Beck, R.R. Dubielzig, E.V. Nordheim, and E.H. Lanphier. 1988. Experimental respiratory decompression sickness in sheep. J. Appl. Physiol. 65: 1163-1171. 61 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Barnard, E.E.P., WJ. Eaton, and R.E. Snow. 1971. Experiments in submarine escape. Rapid compression of men to 625 feet (191 metres). Royal Naval Physiological Laboratory, Alverstoke, United Kingdom, RNPL Report 10/71:1-8. Bell, P.Y., D.W. Burgess, M. Summerfield, and EJ. Towse. 1984. The effect of presaturation on the maximum submarine escape depth of goats and the implications for human research. Underwater Physiology VIII, Proceedings of the Eighth Symposium on Underwater Physiology. A.J. Bachrach and MM. Matzen (Eds.). Undersea Medical Society, Bethesda, MD. pp. 241-248. Biersner, R.J. 1984. Psychological standards for diving, Physical and psychological examination for diving. The Physician's Guide to Diving Medicine. C.W. Shilling, C.B. Carlston, and R.A. Mathias (Eds.). Plenum Press, New York. pp. 520-529. Boycott, A.E., G.C.C. Damant, and J.S. Haldane. 1908. Prevention of compressed air illness. J. Hyg., London 8: 342-443. Brooks, G.J., R.D. Green, D.R. Leitch. 1986. Pulmonary barotrauma in submarine escape trainees and the treatment of cerebral arterial air embolism. Aviat. Space Environ. Med. 57: 1201-1207. Clark, J.M. 1982. Oxygen toxicity. The Physiology and Medicine of Diving, 3rd Edition, Bennett, P.B., and D.H. Elliott, (Eds.). Bailliere Tindall, London, Ch 9: 200-238. Davis, R.H. 1962. Deep Diving and Submarine Operations. A Manual for Deep Sea Divers and Compressed Air Workers. Saint Catherine Press Ltd., London. Dick, A.P.K., and E.W. Massey. 1985. Neurologic presentation of decompression sickness and air embolism in sport divers. Neurology 35: 667-671. Donald, K.W. 1979. Submarine escape breathing air. A review and analysis of animal and human experiments by the Royal Navy. Bull. Europ. Physiolpath. Resp. 15: 739- 754. Eaton, W.J. 1967. Experiment in submarine escape. 1. Goat experiments with fast decompression from pressures equivalent to depths of from 300 to 500 feet of sea- water. 2. Extension of the maximum safe depth of escape for goats by increased rates of ascent. Royal Naval Physiological Laboratory, Alverstoke, United Kingdom, RNPL Report 1/67: 1-9. Eaton, W.J. 1971. Depth limitations of the buoyant (hooded) ascent submarine escape procedure. Royal Naval Physiological Laboratory, Alverstoke, United Kingdom, RNPL Report 9/71: 1-12. Elliott, D.H., and E.P. Kindwall. 1982. Manifestations of the decompression disorders. The Physiology and Medicine of Diving, 3rd Edition. P.B. Bennett and D.H. Elliott, (Eds.). Bailliere Tindall, London, Ch 18: 461-472. Fischoff, B., S. Lichtenstein, P. Slovic, S.L. Derby, and R.L. Keeney. 1981. Acceptable Risk. Cambridge University Press, Cambridge. Gell, C.F., and J.W. Parker (Eds.) 1974. International Workshop on Escape and Survival. U.S. Navy Submar. Med. Res. Lab. Rep. (NSMLR 794). 62 Lehner: Ascent rate experiments and diver safety Lanphier, E.H. 1965. Overinflation of the lungs. Handbook of Physiology. Respiration II. W.O. Fenn and H. Rahn (Eds.). American Physiological Society, Washington, D.C. Sect. 3, Vol. 2: 1189-1193. Lehner, C.E., G.G. Adler, T.M. Kanikula, M. Palta, E.H. Lanphier. 1985. 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Low-probability/High-Consequence Risk Analysis. Plenum Press, New York. 63 ASCENT AND SILENT BUBBLES Andrew A. Pilmanis USAF/SAM/VNBD Brooks AFB, TEXAS 78235-5301 U.S.A. In 1971, when the Doppler "Bubble Detector" became readily available to research, studies were initiated at the University of Southern California's Catalina Marine Science Center to document the degree of "silent bubble" occurrence after open ocean scuba dives. One hundred ten Doppler monitored subject-dives were done. Dives conformed to the limits of the U.S. Navy Standard Air Decompression Tables. Exact bottom times, depths and ascent rates were adhered to. No symptoms of DCS were seen. However, venous gas emboli (vge) were found to some degree in all subjects after all dives. It was found that with small increases in decompression times, vge scores could be greatly reduced. Thus, short "safety stops" could be beneficial in reducing the occurrence of "silent bubbles" in divers using the limits of the U.S. Navy Tables. Preface This paper is a summary of one part of a 3-year study done by the author between May, 1972 and June 1975. The complete report has the following reference: Pilmanis, Andrew A. 1975. "Intravenous Gas Emboli in Man After Compressed Air Ocean Diving." USN Office of Naval Research, Final Technical Report, Contract No. N00014-67-A-0269-0026, May 1, 1972 to June 30, 1975. Background The condition of decompression sickness stems from the inert gas partial pressure gradients developed after hyperbaric exposure between the ambient breathing gas and the body tissues. The degree and rates of various tissue inert gas saturation and desaturation determine if, and to what extent, tissue gas emboli formation and growth occurs. Specifically, the primary variables associated with the evolution of gas bubbles in the body during and/or after hyperbaric exposure are: 1. ambient pressure (depth of water) 2. bottom time 3. decompression time. In addition, under actual open ocean diving conditions, there are other factors that influence inert gas uptake and elimination, including: 1. degree of exercise 2. water temperature 65 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. 3. water immersion 4. constrictive equipment worn 5. psychological factors. The development of non-invasive methods of detecting in vivo intravascular gas emboli opened a relatively objective field of study for the problems of decompression sickness in man. Through the use of the Doppler ultrasonic flow-meter, modified for use as a bubble detector, definitive evidence has been obtained that circulating non-symptomatic venous gas emboli (vge) exist after certain dive profiles previously considered "safe". These non-symptomatic gas emboli have been termed "silent bubbles". Despite the lack of apparent symptoms from these vge, it is highly probable that there is some degree of tissue damage associated with frequent "silent bubble" foundation. Most of the Doppler studies have been done in hyperbaric chambers under very controlled conditions. Thus, many of the inert gas uptake/elimination variables listed above for open ocean diving were not considered in these studies. The task of bubble detection in an immobile man in a hyperbaric chamber is much less complex than the task of bubble detection in a working diver in the ocean environment where pressure change is but one of the influencing factors. The overall purpose of this study was to attempt to define the occurrence and extent of decompression "silent bubble" formation in man after ocean diving to the limits of the U.S. Navy Standard Air Decompression Tables (USN Tables). The initial objective was to demonstrate the feasibility of in vivo intravascular bubble detection during the post-dive period of open ocean air scuba dives. This was immediately followed by a characterization of the post-dive time course of vge occurrence. Methodology All experimental work was done at the University of Southern California Catalina Marine Science Center, located at Big Fisherman Cove, Santa Catalina Island. The diving site for these studies was approximately 300 yards from the dock in 100 to 200 feet of water. A powered diving platform was always anchored over the site during the diving operations. A model A 5 MHz Precordial Doppler Ultrasonic Bubble Detector was acquired from the Institute for Environmental Medicine and Physiology, Seattle; Washington. This was replaced with a Model B in the second year. These units were successfully used during the project for the detection of venous gas emboli. The large precordial transducer consisted of two 1/2 inch square piezoelectric crystals separated 1.3 cm. and tilted at a 13? angle so that the ultrasonic transmitter and receiver beams cross in a region 3 to 4 cm. distant. The advantage of this unit was that it covered a large tissue volume at its focus and, thus, positioning was less critical and there was higher probability of detecting vge in the pulmonary blood. During the course of the 3-year study, 18 resident scientific divers of the U.S.C. Catalina Marine Science Center were used as subjects. These people routinely perform working dives and are thoroughly familiar with the diving station. All dives were free- swimming air scuba dives. After extensive experience with several brands of depth gauges (in a test chamber and in the ocean) it was concluded that none of them had the reliability and accuracy required for these experiments. Thus, a steel cable lead-line was used as the primary depth sounder and was dropped and left suspended during all dives. Markers on 66 Pilmanis: Ascent and silent bubbles this line every ten ft. permitted accurate ascent rates. Horizontal visibility was between 40 and 80 ft. Water temperature was between 11 and 13?C. The subjects' descents were totally passive. During the resting dives, the subject knelt motionless on the bottom for the full bottom time. The ascents were at 60 ft./min., were passive, and controlled through buoyancy regulation. The Doppler recordings were made on the diving platform. Two- minute control recordings were made prior to each dive. Due to the time required for boarding the dive platform and the removal of diving gear, the earliest bubble detection recordings were made 3-5 minutes after the point of surfacing. Eight two-minute post-dive recordings were made at 5, 15, 30, 45, 60, 90, 120, and 180 minutes after surfacing. The data was simultaneously recorded on tape and monitored with earphones. Subjects were seated and motionless during the recordings. The following 3 dive profiles were used: 1. 2. 3. Depth (ft.) 100 100 190 ?(decompression was Bottom time (nun.) Decomoression Cmin./ft.1) 25 30 10 added to USN none 3/10* 2-3/20' 4-5/101* requirements for safety reasons) Animal studies were done to verify the electronic characteristics of the intravascular bubbles as recorded by the bubble detector. The animals and human data were subjected to audio and oscillograph analysis and a method was then developed for quantification of the data. It is important to note that these signals are termed "events", not bubbles, because occasionally, there are cardiac events which also elicit above-control level characteristics. However, the majority of these electronic events are interpreted to represent gas emboli passing through the right heart. The events are tabulated for each 2-minute period and compared with the audio counts made for the same period (Figure 1). There were two problems encountered with this method of bubble quantification. The sensor placement had to be very critical, since it was found that signals produced by valve closures and/or peak flow were sometimes as high as those produced by bubbles and, thus, masked the bubble data. Secondly, a substantial portion of the bubbles that were audible in the earphones did not display above control frequencies. Because of these problems, the human ear continued to be considered the most accurate method. Figure 1. Brush recording from the "Bubble Counter" SUBZEC7:A.R 3 Minutes - EVENTS ABOVE 1110 H * .' CONTROL RECORDING DIVE # 3 0 CUT-OFF FREQUENCY: 1110 Hx 5M.We POST-DIVE RECORDING Depth: HO Ft. Bott.wTVme: \0Hin. Decompression: DOPPLER SIGNALS 67 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. C O N T R O L = 15 3 0 4 5 b o Figure 2. Averaged vge data from 3 dive profiles Average from 14 Dives (to Subjects) Depth- I00F+. Bottom Time: 25h in . Decompress ion: Nione Water Temp-. |2-I3"C. I Events Above Control { D Audio Even+s izo Average from*} Dives ( 5 Subjecls) DeP+h: 100 R. Bo4-tomTime: 30 Hln. Decompression: 3-5(5) 10 Wa+erTemp: I2-|3'C. I Even-is Above Con+ro\ B Audio Events 40- 30- 20- 0 CONTROL* 5 A 5 30 45 l 4,0 Average -from (o Dives ( 3 Subjec+s.) Dep^n: HOFT. Bo-Hom Time: 10 Mm Decompression. 2-Xa)2O 4O Water Temp: I PC I Events Above Con+rol Frequency 0 Aud.o Events no ?IBr Time Pos-t-Dive- 68 Pilmanis: Ascent and silent bubbles Results One hundred ten subject-dives were made in the open ocean. No symptoms of decompression sickness were seen as a result of any of the diving. Intravascular "silent bubbles" were present, to some degree, after all of the dives reported. The averaged vge occurrence time-courses of the three dive profiles are seen in Figure 2. "Silent bubbles" were present within a few minutes after surfacing from the dives. The number of events generally peaked within an hour post-dive, declined and was close to control levels by three hours post-dive. Table I gives the levels of significance of each averaged recording to the control levels. Significant differences occurred at the 5, 15, 30, and 45 minute post-dive recordings. A great range of individual variability was seen. Furthermore, each individual showed a relatively consistent degree of bubble formation on various dive profiles and repeated dives. In particular, the subject in Figure 3 consistently produced large numbers of events, even after a relatively "safe" dive profile. A bottom time of 25 minutes is the "no- decompression limit" for a depth of 100 feet according to the USN Tables. Yet, this subject always exhibited large numbers of events after such an exposure. However, when relatively short decompression periods were added to the dive profile, the number of post-dive events was drastically reduced. Table 1 Punnet's t Statistic Dive Profiles Recordings Post-Dive (minutes) 1. 100ft/25min 5 15 30 45 60 90 120 180 No decompression Audio ** ** ** ** NS NS NS NS Electronic ** NS NS NS NS NS NS NS 2. 100ft/30min 3 min @ 10 ft Audio NS * ** NS NS NS NS NS Electronic NS NS * NS NS NS NS NS 3. 190 ft/10 min 2 min @ 20 ft 4 min @ 10 ft Audio ** * NS NS NS NS NS NS Electronic ** NS NS NS NS NS NS NS NS = Not Significant * = P less than 0.05 ** = P less than 0.01 69 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Figure 3. Vge data from subject A.P. after 3 dive profiles; depth and bottom times were identical, only tbe decompression was changed. 10- to- 50 HO 30 20- (0 o CONTHOC s i ?i . s i n 1 D * 5 Dive # 3 f Subject: A.R Depth: 100 Ft. Bo* torn Time : ?5 Mm. Decompression: NJone Water Temp-. IZ?C, 1 Events Above. Con+rol 0 Aud'O Events i 6 I ii 6 iBo 40 3? 20 10 COMTHH. ? j 3 IS 1 ? 1 r 1,1 Dive#37 Subject: A.P. Depth 100 Ft. Bottom Time: 25 Min. Decompression: 2 ? 10 Water Temp: IZ'C. 1 Events Atove Control Frequency 0 Audio Enen-ts .B 1 20- OWTML 'ft ?-ii iX l y j ? J ? i ^ i 5 15 3O 45 *O 90 5? Time Post-Dive Dive#38 Subject: Depth: Bottom Time: Decompression: Water Temp: |Events Above Frequency I Audio Events IZO (Minutes) 100 25 1(5) 4? 10 Cont A.R Ft 20 10 ?c. -ol 70 Pilmanis: Ascent and silent bubbles Discussion The full extent of the pathophysiological complexity of decompression sickness has recently become more and more apparent At the same time, many of the basic mechanisms of action that lead to the varied and interrelated clinical manifestations of decompression sickness remain elusive. The existence of asymptomatic venous gas emboli is now generally accepted. However, the pathophysiological significance of these bubbles has still not been adequately defined. It is clear from this study, as well as others, that man can tolerate and eliminate at the lungs relatively large quantities of gas emboli from the venous system without developing clinical symptoms of decompression sickness. It is also clear that pre- symptomatic bubbles are present in large numbers after open ocean dives which strictly adhere to the limits of the USN Tables. It is suggested that silent bubble formation and clinically symptomatic bubble formation are not two distinct conditions, but rather, the same condition at various levels of gradation. In addition, the point of development of obvious symptoms is not necessarily synonymous with the start of tissue damage. The pathology from vge may simply be a milder form of "symptomatic" tissue damage. Any gas emboli in the tissues are potentially harmful. It should be noted that the bubbles detected by the Precordial Doppler are, physiologically, relatively unimportant. These venous bubbles funnel into the right heart, pass to the pulmonary circulation and dissipate. It is unlikely that they cause any tissue damage, except perhaps for hematological alterations. Pathophysiologically, the stationary bubbles in the various tissues are the prime contributors to the disease. However, we cannot detect stationary bubbles. The circulating gas emboli may only be detectable indicators of the presence of bubbles in other tissues. In conclusion, these data suggest that by increasing decompression times by a few minutes over those required by the USN Tables, "silent bubble" formation into the venous system can be significantly reduced. Thus, the routine use of "short safety stops" when diving the U.S. Navy Tables to the "no-decompression" limits is strongly encouraged. However, it is also emphasized that this conclusion is based on an N of 1, and additional research is needed to confirm these findings. 71 Session 3: Physiology Session Discussion PHYSIOLOGY SESSION DISCUSSION Discussion Leader: Glen H. Egstrom Andy Pilmanis answered what safety stop was instituted at his facility by saying that it was a historical question and that the stops were arbitrary. Andy: When we still used the Navy tables, first of all we didn't go to the limit; Secondly, we stopped at 10 feet for whatever air we had left; Ultimately we stopped for 5 minutes and then we said stop at 15 feet for whatever time you have left. This evolved gradually. When the Huggins tables came out we shifted to them as a better solution and then to the Canadian tables after that. Glen Egstrom wondered: If when you say symptom free in that circumstance with an N of 1, you had no symptoms whatsoever? Andy: Anybody who has worked with the Doppler close to the limits, I think, will probably bear out that you can get individuals that bubble a lot and still don't bend. One thing we did not do were objective neurological examinations and, remember, this is back in the early 1970's before we had the chamber experience. At this point what I would do is a serious examination of every subject after the dive, because one of the things we found in patients is we don't see type I limb pains in the chamber. Mainly, this is because if somebody walks in complaining of a shoulder pain, you give him a thorough neurological exam and almost always you find a neurological finding that they are not aware of. Therefore, I would always do an examination in a grade 4 bubbler before I would say they were symptom free. Dennis Graver asked what the physical characteristics of the bent diver were? Andy: About 6'3", 200 lbs, male Caucasian, young man, good-looking, initials A.P! Woody Sutherland remarked that there was a lot of variation between individuals, but that within individuals, it was fairly consistent. Given that, and assuming that there is some sort of correlation between silent bubbles and the risk of DCS, is there any prophylactic use in using the Doppler and adjusting tables for individuals? Andy: Theoretically, you probably could, but practically I don't quite know how to do that. You would practically have to push every one of your subjects to a clinical bends case to find out. You're talking about screening exams and that becomes a whole world in itself, with large populations especially. Bob Stinton reported on a French Navy experiment where they were doing a 300m dive and trying to establish decompression profiles using Doppler devices. The interesting aspect was that during the first two days of decompression there were no bubbles. The second day, when the divers started walking around a little more, there were all kinds of bubbles. Then they realized that listening to people who were laying on bunks were quiet, versus the people walking around who sounded like "fizzies". Next, they had the people on bunks walk around and they too sounded like "fizzies". I never heard the final discussion, but they stopped doing that method of schedule development. Andy responded that they should have controlled for that, it was a bad experimental design. The way you elicit bubbles if you want to find them, is to have people move around. There is no consistency though in the field and I believe a workshop is convening in October just on that point, to try to standardize Doppler measurements. How can you otherwise compare data between still and exercising subjects? That's just one of the problems. Phil Sharkey asked about the length of bubble life on Andy's Doppler versus Hugh's model. Hugh Van Liew: I did the models on short halftimes, just because it showed up in my picture a little better. I do believe that what I was saying would also pertain to longer halftimes. The 1 foot per second is almost like an instantaneous, explosive decompression as far as the time of the bubbles and the tissue washout are concerned. I found that out when I brought the ascent rate towards the timeframe of the bubbles and the 73 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. tissue washout, then it seemed as if things were getting better. Phil continued that his concern was how long we had to sit between the pending dives? Andy clarified a major point that the bubbles seen by the Doppler were meaningless in themselves. They tell you nothing about the damaging bubbles. All they tell you is that a bubble passed through this field and went on to wherever it goes in the lung. It doesn't tell you when they disappear. John Lewis wondered if it wouldn't be reasonable to presume that the population number of bubbles equated with a probability of DCS. Andy stated that wasn't a reasonable assumption at all. John then asked what the proper conclusion of Doppler work was? Andy: This is just a window into the body, because it's the only one we have and it tells us yes, there are bubbles occurring, they pass through, go on to the lungs, they are no longer being broken free from the tissues. But it says nothing about stationary, extravascular bubbles and nothing about when bubbles go away. John then inquired if Andy wouldn't be willing to go back to Spencer's work and correlate the gap between bubbles and decompression sickness? Andy: No, because symptoms are a gross manifestation of the existence of bubbles also. What we need is a device to measure stationary bubbles. Hugh Van Liew observed that Andy's talk changed the ball game a little bit because some of us have been talking about avoiding bubbles and the transformation of nuclei into bubbles. Andy is essentially telling us that there are always bubbles there so the problem gets to be what kind of bubbles are going to give you trouble, rather than avoiding bubbles. Andy responded that there are only bubbles there when you go to the limit of the U.S. Navy tables, but if you back off, they are not there. I believe I was preventing bubbles from forming by slowing the ascent Bill Hamilton amplified two points that Andy made about the bubbles you hear going by the Doppler being on their way out. That is indeed true, but they're not necessarily innocuous and I have heard this from you also. Those bubbles represent foreign bodies in the blood stream and they do have measurable effects. It's curious though that these people who bubble a lot, don't seem to have more symptoms than anyone else who doesn't bubble very much. Andy felt that was a point to be determined yet. Bill *thought this got into biochemistry and lung pathology and other things. Bill further pointed out that there seemed to be occasionally cases of decompression sickness that aren't explained. They don't fit any pattern in the profile and the patients don't get just pain in the knee, they get a debilitating embolism type effect The investigation going on in that today is that it is possibly due to a defect between the right and left heart. This is congenital in some people and everybody has it as a fetus, but sometimes the opening between the right and left heart does not close completely: the patent foramen ovale. It may not ever have any physiological effect on their normal lifestyle, but bubbles can get through from the venous side, instead of going to the lungs and being trapped, they may go to the brain. We aren't sure that is the case though. There are still ongoing studies investigating that phenomenon, to build more evidence. There are several reasons why the hypothesis is good. The point is, a lot of bubbles, even in an asymptomatic person, are to be discouraged. Unanimous agreement Charlie Lehner observed that he and Ed Lanphier had done a whole series of experiments involving sheep as animal models in decompression sickness. In that series they had animals under pressure for 24 hours and brought them to altitude and produced chokes in all of the sheep. Charlie: We had extraordinary numbers of bubbles detectable by Doppler and in that situation, where there were such excessive numbers of bubbles, we had a very serious manifestation developing with the chokes and, in fact, approximately half of the animals would have been fatally affected, we feel, by that. More recently, we found even with short, deep dives or half hour profiles, in some instances, extraordinary numbers of bubbles in the pulmonary artery. Usually associated with that are early signs of chokes, mainly mild, labored breathing in the animals. Obviously, fatigue is a symptom which 74 Session 3: Physiology Session Discussion would be correlated with that. We presented this in the Journal of Applied Physiology in 1988. Glen Egstrom asked what the characteristic of the lungs as a filter was, what kind of loads it could handle before you started seeing respiratory manifestations? Charlie responded that typically, in sheep at least, the respiratory manifestations in those animals scored 4 with the Spencer grades. We start seeing signs of labored breathing. At Spencer levels 1 and 2 we rarely see anything that would be indicative of labored breathing. Chokes is very bad decompression sickness. Most recently, we had a dive where we were modelling the Japanese diving fishermen profile reported by Kawashima and had disastrous results. The animals died of chokes. In fact, in that series I didn't even go to the maximum pressure reported by Kawashima, so all those Japanese fishermen are undergoing extraordinary exposures, certainly from the standpoint of potential chokes development. In this instance, I think our animals probably had a higher fat composition in the body. I think in chokes the fat composition in the body is extremely important. It may not be as important in spinal cord decompression sickness, but I think with chokes it is a very high risk factor. Andy remarked that in 15 years of a total of 600 patients at the Catalina Chamber, we've seen two questionable cases of chokes and they were very minor, very questionable, if they were chokes at all. Charlie added that the interesting thing about chokes is that oftentimes you see manifestations of labored breathing and these tend to remiss, so we don't see any manifestations later. In the more severe cases, we'll see early manifestations, apparent recovery and then a catastrophic relapse that sometimes will occur 3 or 4 hours after the animal has reached the surface. I think one has to be extremely careful with chokes. In that instance, it may be blood factors that are involved in terms of coagulation and so forth as mentioned by Bill. Ray Rogers made the point to Hugh that it was unclear if nuclei that became bubbles "lay in wait" or revert back to nuclei. Hugh: That is the way I fixed the model up, but it may not necessarily be true, but that's all we need. I don't see any reason why a nucleus shouldn't revert back to being a nucleus after it's been a bubble, but on the other hand I don't have any information about it John Lewis: With respect to the animal experiments, what is the role of acclimization to hyperbaric exposures like the Japanese fishermen? Have you ever tried acclimization experiments with animals to reduce bends incidences? Charlie answered that they typically run two experiments with an animal per week and most of the exposures in the Japanese fishermen involve 6 exposures per week, they take out 1 day. If the information I've received is true, they're doing extraordinary exposures, similar to the caisson work acclimatization. John: Have you ever tried to simulate a gradient to that? Charlie: It might have been some mild acclimatization, but given the span between exposures, it is largely one dive per weekend. I would suspect that in the case of what Ed talked about, our animals have a body fat composition that is greater than 25%, which is obviously very high and I would suspect that the Japanese fishermen probably have a body fat composition less than 8% and therefore probably get away with what they're doing. David Yount: Regarding the discussion of whether bubbles become nuclei again, I have observed this with gelatin. You find bubbles occurring at certain points and then we'll dissolve those bubbles by raising the pressure, decompressing, then getting the same number of bubbles as before in the same location, so that does happen. Bubbles can become nuclei again and bubbles again. On the other hand, the acclimatization suggests that some of the nuclei can, after repeated exposures, offer some resistance. Hugh Van Liew added that the body was much more complex than gelatin so that it could be that the bubbles migrated some place else. If there are surfactants, other possibilities arise. But I 75 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. guess if there are plenty of nuclei, it doesn't matter whether one nucleus becomes a bubble and then goes back to being a nucleus or not Steve Blair questioned if with the formation of the nuclei it were possible that it were the structure per se serving as the nucleus or source or point of nucleus formation rather than actually a bubble itself being present. David Yount disagreed because the fact that you can get rid of nuclei by high pressure means there is gas present. When we see nuclei with microscopes, there is gas present. The structure might be a crevice in some cases or surfactant skin, but in either case there will be gas present. David pointed out a very nice paper by Johnson and Cooke in which they injected air bubbles into sea water and observed these bubbles rise, but then they were under a glass plate and although some bubbles dissolved completely, others stopped decreasing in size abruptly and remained as microbubbles apparently stabilized by films. Originally, the radial distribution ranged up to 7 microns and peaked at around 2 microns. During the first 4 hours, there was little change in this distribution. After 22 hours, although there was little reduction in the number, the microbubbles were generally smaller, and the radial distribution resembled a decaying exponential cut off at the microscope resolution, about 0.3 microns. It appears, therefore, that Johnson and Cooke observed the creation of stable microbubble nuclei in sea water. There is some question about whether bubble formation nuclei are always present in plant and animal systems. It seems very likely that they are. For example, we have carried out an experiment in Hawaii and we see bubbles in hen's eggs, which is even more pristine than an embryo and yet it has the bends. Walt Hendrick asked Andy if the incidences of symptoms were correlated with grades of bubbles? Andy: All patients that we monitored had grade 4 bubbles. The consensus currently in the field is that there is no correlation between Doppler bubbles and the bends. I personally don't agree with that. Walt: Is it possible that you could, on a single dive, not looking at multiple dives where you would have secondary problems like the offloading of gas, have less problems if you have any symptoms because you had silent bubbles as opposed to being more prone because you had silent bubbles? Andy: Dumping nitrogen with silent bubbles? More efficiently eliminating nitrogen through bubbles? The other side of it is that some people believe bubbles are superfat and take on more gas, thereby making it worse. Again, we are looking at one small window in the body, only at moving bubbles, only in the right heart and they're going on their merry way. We don't know anything about what's going on elsewhere in the body in the damage areas, in the spinal cord, the brain, the bone, etc. Walt: Andy, from your own diving experience, would you include a safety stop because you feel that is a positive way to reduce the probability of bends? Of course I do, but only in situations where you're approaching some kind of limit. If I dive 5 minutes at 20 feet, I don't stop at 10 feet for 15 minutes. So, yes, if I'm approaching any limit or if I'm diving anywhere below 100 feet, I always do just as a general practice. It doesn't hurt. Mark Walsh: Charlie, some of the data that you showed on the studies of what the various ascent rates looked like, it seemed all of them had zero bottom time. Did any of the studies you looked at show rapid ascent rates after longer bottom times?.Charlie: In the literature it became obvious based on the experiments that the Royal Navy was doing that if the bottom time, for example, lasted 15 or 20 seconds, there was a high incidence of decompression sickness. When they decreased the amount of bottom time ascents, the time that the maximum pressure was held, then the frequency of decompression sickness dropped dramatically. There is a very strong correlation in terms of the amount of time for gas to wash in and the occurrence of decompression sickness in those subjects, both in the animals as well as the humans. These were extremely short times we're talking about, from the standpoint of maximum pressure, in terms of seconds. 76 Session 3: Physiology Session Discussion Walt Jaap: Andy, is there new technology coming on line for better detection of bubbles and better confidence in terms of what they mean? Andy: The only new technology I know of is in our own lab where we have echoimaging simultaneously with the Doppler. We actually see the bubble as you hear it on the headset. That's one more parameter mat is helpful. But again, those are still moving bubbles that are going out, they are not the important ones. Mark Walsh: Andy, I wish that Tom were hear to make this statement concerning the critical size, not the existence of the bubbles being the factor. I'm not sure whether he's talking about stationary bubbles or trapped bubbles. Andy: I'm sure critical size has a lot to do with it, but what that critical size is, I don't know. Mark: Now that you've brought up echoimaging, you're still talking about stationary bubbles? Andy: If you watch that movie that Hallenbeck made about spinal cord decompression sickness, where you actually see in a living system bubbles going through the epidural venous system, you'll see all bubbles of the same size. It's like marbles all the same size going through. Now, once it becomes cold, they coalesce and it looks like foam. They all appear to be the same size initially in the cardiovascular system, I don't know about tissues. Hugh Van Liew: The bubble that is moving along like it was a red cell, isn't going to do any damage probably unless it does damage by reacting with blood elements. Andy: Well, that and in the epidural venous system they do cause occlusion there. Hugh: Eventually, when they're bigger than a red cell. Andy: When the volume reaches a critical load, when enough of them get together. 77 SLOW ASCENT RATE: BENEFICIAL, BUT A TRADEOFF R.W. Hamilton Hamilton Research Ltd. 80 Grove Street Tarrytown, NEW YORK 10591-4138 U.S.A. It should be obvious that the key to avoiding decompression sickness (DCS) is to ascend slowly. What this means specifically depends heavily on the profile of the dive (or pressure exposure) and the gases breathed. A "slow ascent" may be managed by doing stops for a standard commercial or military dive, or perhaps may be a linear ascent taking several days for a saturation dive. Short scientific and recreational dives regarded as "no- decompression" dives are no different in type, only in degree. All dives except perhaps the most trivial breathhold dives involve decompression to some extent., and proper management of the ascent rate can greatly reduce the risk of DCS. Computational models, although they should not be regarded as true pictures of gas biophysics, nevertheless can afford a means of comparing profiles with enough validity to be enlightening. Analyses show in general that for a given exposure it is better to ascend slowly, and that there is an optimal linear ascent rate that will result in the lowest theoretical gas loading and hence the lowest risk of DCS. They show further that it is possible to go too slowly, and that ascent at two or more rates can be even more beneficial. An additional benefit of a slow, controlled ascent is that it is also less likely to result in embolism. Some years ago it was my good fortune to work with a laboratory whose objective was to develop decompression tables for deep mixed gas bell diving. We were working in the range 500 to 650 fsw (150 to 200 msw). We had our algorithms, but a lot of what we did was still cut and try. One thing we decided on early was that the 60 fsw/min ascent rate used by the US Navy (and as we are hearing today, the recreational diving community) was too fast. We did not have any data to justify a slower ascent, really, but we rationalized that when one ascends, an unstable state exists, and this could and should promote bubble formation. It is like a champagne bottle. If one pops the cork, one can shoot the cork at a nearby stuffed moose head and spray everyone nearby, but if one opens the bottle slowly the entire bottle is available for drinking. Recognizing my self-classification as a "decom- pression expert" I now make it a practice to open champagne gently, and it rarely fizzes when it is done slowly. The difference is impressive. Without the sophisticated bubble dynamics modeling of a Yount or Wienke, the champagne bottle approach led us to try to avoid jumps or abrupt ascents. Again, I acknowledge no real data, but we implemented the slower ascent and we think it helped. In addition to the 30 fsw/min for travel from the bottom to the first stop, we also kept the travel between 10 fsw stops slow, making it take at least one minute (Hamilton and Kenyon, 1976). 79 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. If your diver is so "fizzy" that he has to be decompressed as one might handle explosives, it suggests the entire decompression is probably inadequate, and in retrospect we feel that was true about our early deep heliox decompressions. But if one gets better results by moving slowly with a fizzy diver, then the same approach should reduce the risk in a more routine ascent. This is perhaps an extreme example, but it should make the point. This reflects a long standing prejudice against fast ascents. However, another story shows there is another aspect to this. I had the dubious good fortune to be asked to help Sheck Exley, a Florida schoolteacher and recordsetting cave diver, to plan a dive to 800 fsw in a Mexican spring. The philosophy behind this is beyond the scope of this meeting, but can be summarized that if I would not help him, he was going to go ahead and calculate the tables himself. Not really confident I could do it better than he could, I nevertheless gave it a try. His descent was fixed at about 25 fsw/min due to an upwelling current, and the bottom time was to be no more than a minute. I tried the calculation using the Tonawanda II (Haldane-type) algorithm, and the first try required an unacceptably long decompression (approx. 16 hr). This used the 30 fsw/min ascent I had become so comfortable with. It made the decompression a lot longer that die dive Exley had done the year before, successfully. Again without much confidence, I asked him if he could ascend faster during the travel to the first stop, which was at about 500 fsw. He agreed he could, so we recalculated it at an ascent rate of 120 fsw/min. The total decompression time dropped to about 11 hr, and a version of this approach was the dive that was done. I felt that with such a short bottom time and being so deep, this would be all right. For an N of 1, it worked. Actually, it is an N of 2 now, because he did the same dive, but a bit deeper, this year, again without incident. The lesson is that a rapid ascent early in a dive with a short bottom time worked well. I feel the faster dive involved less risk overall than would a slower ascent which would effectively be a longer bottom time. Again, these are impressions, but the message seems clear enough. So, we have a strong feeling with limited evidence that a slow ascent rate is beneficial, and a case, again with limited data, that says the rate can be fast at first, especially when deep and after a short bottom time. These judgements were based on vague guesses of what might be happening physiologically. This caused me to have the obvious curiosity as to the effect of ascent rate as seen by the computer, the neo-Haldanian algorithm based on hypothetical halftime compartments and limiting M-values of exponential gas loading and unloading. This example uses a conservative air matrix that is close to the relatively reliable USN rates in the no-stop range but is more conservative for deeper and longer dives. The results are as you might guess (Fig. 1 and Table 1). Initially, decreases in ascent rate improve the decompression and allow (for example) longer no-stop times when everything else is equal. Further decreases reduce the allowable time. The example shows that reducing from an ascent rate of 60 to 30 fsw/min gives one more minute of no-stop time at 130 fsw (11 to 12 min). An additional decrease from 30 to 10 fsw/min gives still another minute of no-stop bottom time. An additional decrease to 5 fsw/min now reduces the allowable no-stop time back to 11 min. This is not unexpected. Eventually, when the rate gets slow enough, the "no-stop" bottom time will increase again. 80 Hamilton: Slow ascent rate: Beneficial, but a tradeoff Table 1. Times from sample dive with various ascent rates. GAS: Air BasecaseD99NA0.H01 DEPTH: 130 fsw Matrix MF11F6.DCP RATES: 60 to 5 No-stop time Ascent rate Ascent time, min Run time, min 11. 12. 13. 11. 60 30 10 05 2. 4. 13. 26. 13. 16. 26. 37. From a practical point of view, however, this does not make a case against a short stop at say 10 fsw, and in fact that is easier to perform and is theoretically more beneficial. Three min at 10 fsw, with travel at 60 fsw/min, allows 15 min at 130 fsw. Again, the effect is in the expected direction, but perhaps it is not as great as one might expect (Table 2). Figure 1. No-stop times for various ascent rates FSW 125 IBB 75 59 25 0 v\ ? AAUS ASCENT DEMO D99HA0.H01 HF11F6.DCP ? fcpth ?i Depth 12 ? Depth n ? D e p t h 14 8 I T ' - I B " ' !ib Tine dun) 2 b ' ' ' ' 3 b 1 ' ' "3b 1 89Octl9 15:17 Table 2. Times from sample dives with various 10 fsw stops GAS: Air Basecasc D99NA0.H03 DEPTH: 130 fsw Matrix MF11F6.DCP STOPS: 1 to 4 min No-stop time 12. 13. 15. 16. Ascent rate 60 60 60 60 10 fsw stop time, min Run time, min 1. 2. 3. 4.* 15. 17. 20. 22. * Includes 1 min at 20 fsw 81 Lang and Egstrom (Eds.): BI0MECHAN1CS OF SAFE ASCEATS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Thus we can conclude that as far as hypothetical gas loadings are concerned, slightly slower rates improve the decompression, but when still slower ascent rates are used, the result is a penalty in bottom time. Over the range which could reasonably be done by a scuba diver, however, the effect is not prominent and slow ascents can be regarded as beneficial. A short stop is slightly more beneficial than a slow rate and does not increase the dive time as much. Reference Hamilton, R.W. and D.J. Kenyon. 1976. Decompression work at Tarrytown. In: R.W. Hamilton (Ed.) Development of decompression procedures for depths in excess of 400 feet. WS: 2-28-76. Undersea Hyperbaric and Medical Society, Bethesda, MD. 82 ASCENT RATES VERSUS INERT GAS DYNAMICS ALGORITHMS Donald R. Short College of Sciences San Diego State University San Diego. CALIFORNIA 92182 U.S.A The bulk diffusion model of Haldane and the diffusion-perfusion model of Krogh are developed For a representative set of dive profiles and ascent procedures the gas tension in excess of ambient pressure is calculated. Based on these calculations, it is recommended that for all dives to a depth in excess of 60 feet, that a three minute stop at 20 feet be taken, the "no- bubble" no-decompression limits be used, and that the standard 60 foot per minute ascent rate be used. Following this recommendation will result in an approximately 30% reduction in the calculated peak gas tensions in the most highly perfused tissues Introduction The bulk diffusion model of Haldane, which has been the standard model for controlling diving hyperbaric exposures, does not have the time scale resolution for detailed evaluation of an ascent procedure Typically, the ascent is a small fraction of the total dive time. However, this model being the standard is well calibrated to determine the limits of safe exposure. For improved time resolution the Krogh Model was chosen. This model is a contemporary of the bulk diffusion model of Haldane and has been used by physiologists for detailed analysis of uptake and release of various substances by the capillaries for the last seventy years. The major disadvantage of the Krogh Model is the computational effort required for the solution of the equations. From this study, the gross properties of the two models are in agreement However, as expected, the time courses are usually quite different. Krogh Model Krogh (1919a , 1919b) first introduced this model in 1919 for the study of oxygen supply to tissue. Subsequently, many investigators (Levitt, 1972; Tepper et al., 1979) have used this model to study the transport of various substances by the capillaries. A very good description of the assumptions of this model can be found in a paper by Hennessy (1974) The model consists of two co-axial cylinders of length L with inner radius a and outer radius b. The inner cylinder represents the capillary which is perfusing the surrounding tissue annulus. The blood flow in the capillary is assumed Newtonian with a uniform velocity of v. Radial diffusion within the blood is assumed instantaneous. Thus, the blood is well stirred in the radial direction. The surrounding tissue annulus is assumed to consist of only cellular material. Roughton (1952) has shown that the saturation time of any interstitial matter is very rapid, on the order of one second. Thus, this material can be thought of as incorporated within the capillary cylinder. 83 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Figure 1. Krogh capillary model The outer boundary and the ends of the tissue compartment are assumed impermeable by symmetry. If the diffusion equation describes the inert gas dynamics within the tissue compartment, and the mass balance equation on a disk of blood within the capillary compartment describes the inert gas transport down the capillary and into the tissue, then the following equations and boundary conditions apply. dt = D 2 gt 2 gt = -V-sr-^ + r = a dgt = 0 , r = b , , t >0 t = 0, z = 0,L, , t > 0 gb = g t , r = The gas tension in the blood is denoted by gb and the gas tension in the tissue is denoted by gt. The diffusion coefficient in the tissue compartment is given by D. The inert gas tension in the blood on the arterial side is assumed to be in equilibrium with the breathing mixture, which is delivered at the ambient pressure. An approximate solution of this set of equations can be found numerically using the implicit method of Crank and Nicholson as found in the book by Ames (1972). The resulting linear system is solved for a transition matrix which describes the change in inert gas tension for each time step. An implicit method of discretizing was chosen to avoid the usual stability problems associated with the numerical solution of the diffusion equation. Even with this choice, the time step required for stability was .01 seconds. Various powers 84 Short: Ascent rates versus inert gas dynamics algorithms of this transition matrix were calculated to provide time steps of 10 seconds, 1 minute and 10 minutes. These longer time steps provide for the rapid calculation of models for any dive profile without sacrificing accuracy. For the current application the physiological parameters were set to the following values: a = .0005cm (.0004 - .0005cm - Krogh, 1936) b = .003cm (.0015 - .003cm - Krogh, 1936) L = . lcm (.04 - . lcm - Krogh, 1936) D = 10"5cm2/sec (.4xlO5 - 1.3xl0-5cm2/sec - Homer and Weathersby, 1980) The blood velocity v was calculated from the perfusion rate P and is the critical variable in this model. The velocity was expressed in terms of capillary transit times T for the blood. From the physiology book of Bell et al (1961) we find that the perfusion rate varies as .01 ? P ? 5.6 ml of blood/ml tissue per minute. Active muscle and central nervous system tissue have perfusion rates near the upper end and tissues subject to vascular constriction would have perfusion rates near the low end. Using these values and the chosen values for the capillary geometry, one obtains, .00058 < v < .33 cm/sec for the capillary velocity, or a range for the capillary transit time of .3 < T ^ 170 seconds. It is possible that under environmental conditions of cold or exertion, the perfusion rate could change during the course of a dive profile. However, for the purpose of this investigation transit times of 1/5, 1, 5, 10 and 50 seconds were chosen and were considered constant throughout each dive. The very short transit times would correlate with highly perfused tissue such as the central nervous system and the long transit times with tissue subject to vascular constriction. While one can calculate from this model the inert gas tension at each point within the cylinder, only the venous side gas tension in the capillary will be used. The rationale for this choice was based on the work of Hemmingsen and Hemmingsen (1979), where it was shown that cells seemed to withstand large differences between internal and external inert gas tensions. Thus, any potentially damaging bubbles should occur in either the blood or in the interstitial areas. Since both of these areas are lumped together in the inner cylinder of this model and since the blood pressure is at a minimum on the venous side, it follows that this should be the site for the first formation of damaging bubbles. Haldane Model The Haldanian Model assumes that the change in the internal pressure of inert gas is proportional to the difference between the external and internal pressures. Thus, the equation governing the Haldanian decompression model is the rate equation: ? ? ? = C(P ft)-Rt(t)) If we define the half time T as the time required for the change in the internal pressure to reduce the difference between a constant external and the internal pressure by half, then r - ln<2> 85 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Assume that all pressures are gage pressures which we measure in feet of sea water (fswg). Since a scuba regulator delivers compressed air at ambient pressure and the inert gas component of air constitutes 79%, the external pressure of the inert component is given by: Pext(t) = 0.79d(t) where d(t) is the depth measured in feet of seawater at the time t. Then the solution of the rate equation can be conveniently expressed as the following integral: t 0 J 9 C Je"C(tr)d(r)dr 0 In the model for the Navy Tables, six different half times were used namely; 5,10, 20, 40, 80, and 120 minutes. The solution of the rate equation, the internal pressure for each of the six compartments, can be calculated for any time t, given any dive profile d as a function of time The final component of the Haldanian model assumes that at all times during the dive the internal pressure of the inert gas will not exceed a preset maximum amount denoted by M(d) which can depend on the depth and which differs for each half time compartment. While descending, the internal pressure is always less than M(d) so the problem of exceeding an M-value is never encountered. However, on ascent the reverse is usually true. This condition in practice leads to limited bottom times, controlled ascent rates, and decompression stops. For the implementation in the Navy model, the formula for the M-values which depends on depth is determined by two constants for each compartment, denoted by Mo, the maximum allowed at the surface, and AM, the increment allowed for each foot of depth in sea water. Mo is usually measured in feet of sea water absolute. r?. I - 26.1 + AMd For the Navy Model these values are given in Table 1. For latter use MQ is given in feet of sea water gage. Halftime(min) 5 10 20 40 80 120 Mo (fswg) 78 62 46 32 26 25 AM(fsw) 2.27 2.0 1.71 1.4 1.29 1.27 Table 1. Navy model Mo values Based on this model, if at each point in time, Pint(0), 5 cfm min/max opening pressure SI-TECH 117 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. The flow rates of the A2OP valves were tested in the manual modes. The valves were first tested in the fully closed modes, then in the fully open mode (fig. 7). The interesting thing is that only two of the valves, the Whites and the GSD, have the same pressure drop at the fully closed and open positions. The Apeks valve experienced a drop in pressure from the closed to open position. For some reason not determined at this time, the SI-Tech valve showed an increase in the pressure drop from the closed to the open position. The pressure drop across the four A2OP valves were compared in two modes: In the automatic mode (fully open) and the manual mode. The results are presented in fig. 8. The most interesting result is that in all A2OP valves except the GSD, the fully open automatic setting produced a lower pressure drop than when the valves were operated in the manual mode. Figure 8. Pressure drop (I11H2O), 5 cfm auto and manual operation o CM I WHITES APEKS W\ AUTO SI-TECH A comparison of the four A2OP valves and the two MPD valves was also made figure 9. The A2OP valves were fully open and the flow rate was 5 cfm. As one would expect from the previously reviewed data, the two MPD valves have a much lower pressure drop. The question has always been asked what effect the underwear has on the operation of the valve. In the case of the A2OP valves in the automatic mode of operation, it is believed that the underwear will have less impact on the performance of the valve. This is because the valve in the automatic mode floats up off the underwear. Because the MPD valve must be pushed in to activate the valve, the valve is pressed into the underwear. At this point we have only evaluated the MPD valves. Figure 10 shows the performance of the Delphi valve with (pile) and without underwear at 1, 2 and 5 cfm. As can be seen in fig. 118 Stinton: Dry suit exhaust valve performance: Effect on buoyancy control and rate of ascent 10, the underwear has a major impact on the performance of the valve. Additional testing will have to be performed to fully determine the impact the different types of underwear have on the performance of the dry suit valves. Figure 9. Pressure drop O11H2O), 5 cfm 6 - 5 - 4- - o CM I 2 - 1 - 0 - 1 I V '*, 'A- / i WHITES APEKS GSD SI-TECH DELPHI POSEIDON The force that is required to activate the valves is shown in figure 11. The two manual push to dump valves required the greatest force to activate. Although all the valves are grouped in a close range, I think we may consider that the MPD valves are near the upper limit for the force required to activate them. In the case of the MPD's being mounted on the upper arm, a 112 lb. small female experienced some difficulty in activating the valves. This difficulty was not experienced when the valves were mounted on the front chest area. This shows that the force required to activated the MPD valves and the positioning of the valve should be taken into consideration in the layout of a suit. The last item examined was the flow rate of all of the inlet valves. This is of interest because some manufacturers claim the inlets and exhausts are of a balanced design and that the flow rate of the inlet valve is less than that of the exhaust valve. The flow rates were determined using a flow restricted auxiliary hose (most auxiliary hoses in the diving market have flow restricting mechanisms). As can be seen, the flow capacities of the inlet valves are grouped in a small range (fig. 12). 119 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Figure 10. Pressure drop (In H2O), Delphi valve with and w/o underwear behind valve o CM X 1 .9 - 1.8 1 .7 - 1 .6 - 1 .5 - 1 A - 1 .3 - 1 .2 - 1 .1 - 1 - 0.9 - o.a - 0.7 - 0.6 - 0.5 - CM- - 0.3 - 0.2 - 0.1 - 0 WITHOUT cf rn (2 ) ,2 140 fsw 28 22 48 4 2 2 1 TOTAL 107 The remaining 19 divers were single day, single or repetitive divers and within the limits of the Navy tables. Thirteen of these 19 divers had at least three of the risk factors shown in Table 1 involved in their dive day. Additional frequent risk factors also included diving at 80 fsw or greater, pushing the no stop limits to within one letter group of a decompression dive, diving repetitively, using alcohol, or a medical history of spinal cord surgery. Seven divers had 4 or 5 risk factors involved and one had 6 risk factors on the causative day of diving. Environmental and physical conditions are the most commonly associated factors in a diving injury even in this small population of 19 divers where one would expect to find the safest group of DCS victims. This is further evidence that divers do not make appropriate adjustments in their dive schedule based on the conditions at the time of their dives and this is most likely due to the relative lack of information that divers have concerning the nature of dive accidents. Individual susceptibility in DCS cannot be ruled out, but as cases are looked at more carefully, there seems to be very little chance occurrence of recreational decompression sickness. Only 6 divers (2.7%) had 2, 1, or no risk factors at all in our DCS study population. In this group of six divers, four were diving at 80 fsw or greater and two of these were unduly extending their time at depth. Rapid ascent The 1987 and 1988 National Divers Alert Network reports on diving injuries contained a total of 538 non-fatal injuries. One hundred fifty-three or 28.4% of these injured divers experienced a rapid ascent. The breakdown of these rapid ascent injuries were 49 arterial gas embolisms, 81 Type II decompression sickness, and 23 Type I decompression sickness. Arterial gas embolisms are the dive injury most often associated with rapid ascent In 1987 48% of all embolisms studied involved a rapid ascent. The 1988 figures show that 54% of all gas embolisms stated they had a rapid ascent. One of the most common reasons for rapid ascent is equipment failure. In 1987, 29 rapid ascents were made because of equipment problems. Seventy percent of equipment problems involved rapid ascent. Equipment problems and rapid ascent combined resulted in 8 air embolisms. In the 1988 population, 32 equipment problems were associated with 16 rapid ascents and 8 arterial gas embolisms. 147 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. New divers are particularly at risk for rapid ascent because they are still developing skills in buoyancy and ascent control and do not yet have the appropriate responses for sudden underwater problems. Lack of experience may lead new divers into having a rapid ascent. In the total population of 538 studied divers, 163 had one year or less experience. There were 60 divers (37% of the total inexperienced divers who had an injury) who experienced a rapid ascent problem. There is a direct relationship between rapid ascent which causes over-expansion of the lungs and arterial gas embolism. The relationship between rapid ascent and decompression sickness is not clear. In 1987, 23% of the decompression sickness cases involved a rapid ascent. The 1988 figures show 24% of all DCS injured divers had a rapid ascent. Rapid ascent often occurs in combination with other events. The most common conditions occurring in the population of 153 divers are listed below in the table. Some of these conditions were present during the dive and others may have initiated the rapid ascent. Table 3. Rapid ascent risk factors Condition Dive 80' or greater Single dive Buoyancy problem Experience equal to 1 year or less Low or no air Equipment problem Diver experience Percentage 56 51 40.5 39 31 29 Diver experience is a difficult quality to determine. It involves more than just the number of dives or the number of years a person has been diving. Experience also involves the understanding and practice of safety habits. Time and experience is important in developing both of these traits. The 1987 Report on Dive Accidents provides some clues as to the role of inexperience in diver accidents. Suppose a diver is arbitrarily assigned an inexperienced status if the number of dives is less than 20 times a year or if the number of years diving is 1 year or less. Fifty-five percent of all diver injuries fall into this one year or less, twenty dives or less category. Fifty-two percent of all males and sixty-six percent of all females are inexperienced by these standards. This is the only area where women seem to be more susceptible than men, but this could just be an artifact of the small female population size. Lack of experience is a factor in diver injuries because (1) it is the principle reason for the information gap, and (2) inexperience can lead to a loss of control in the diving environment resulting in panic, a rapid ascent and possible injury. Sixty percent (31) of the gas embolism cases fit the inexperience criteria (20) or were injured in training (11). Inexperience may also have played a role in the more experienced divers because 12 (57%) of 21 more experienced divers were involved in spearfishing or photography which focus the diver's attention away from maintaining depth or an open airway. We do not know how experienced the divers were in these activities. 148 Dovenbarger, Bennett and Wachholz: DAN: Diving accident data and its implications Dive computers One of the latest technologies in diving is the use of dive computers (DCs). The use of DCs is becoming more popular and more cases are showing up in the accident reports. In 1987 there were 41 computer cases in 270 total injuries (15%) and in 1988 there were 83 dive computer cases in 268 total injuries (31%). Some of the cases from both years were the result of misuse of the DCs and some injuries such as gas embolism were unrelated to the use of the dive computer. It is not yet clear if the increase in dive computer accidents is due to a more aggressive diving population buying computers, by divers justifying the purchase of an expensive dive accessory with maximum use or by the simple increase in total dive computer purchases (Scheer, 1988). It is clear from the 1987 DAN Report that most DC divers who are injured dive more often, start their dive day deeper and do more decompression diving than table divers who are injured. Repetitive multi-day diving was a common associated risk factor for divers using both computers and the U.S. Navy decompression tables (Vann et al., 1989). The risk of injury with dive computers may be no greater than with the use of the Navy tables, but their ease of use allows a higher risk style of diving. Delay to call for assistance The signs and symptoms of gas bubble disease are perhaps the most misunderstood aspect of diving injuries by divers in general. The lack of information adds to the validity of myths and anecdotal stories which are told as fact to the inexperienced. Very few divers or instructors actually come in contact with DCS or AGE. Divers learn about DCS or AGE from a list of potential signs and symptoms, but few remember more than pain, paralysis, and seizures. Anything less than what a diver may feel represents DCS symptoms is subjectively dismissed as "something else". The gradual onset of pain and numbness, or a light tingling sensation are overlooked because these symptoms are quite tolerable and do not match the diver's perception of what a dive injury should be. This subjective view of symptoms and lack of information results in an average delay to calling for assistance of 15 hours after symptoms have started. Not only do the divers not realize they are hurt, but the subsequent delay to treatment lessens the chance of a complete recovery after therapy. Only 56% of the treated divers had symptom resolution after a single hyperbaric treatment It is interesting to note that only 56% of the accident population received any first aid at all. Only thirty-six percent of all divers received oxygen as a first aid measure. In a review of the combined DCS cases for 1987 and 1988 some interesting data on recreational DCS signs and symptoms are noted. In 70% of all cases, the first recognized symptom of DCS was reported by the diver to have occurred in 2 hours or less after the last dive. Another 23.5% of die total population reported the occurrence of their first symptoms between 2 and 23 hours post-dive. This means that 93.5 percent of the total accident population had a recognized symptom occurring within the first day post-dive. 149 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP AAUS, Costa Mesa, CA. 1990. The most prominent first symptom is pain; this supports military data which suggests that most DCS is pain only (Elliott and Kindwall, 1982). The most prominent second symptom is also pain, but nervous system signs and symptoms such as numbness/tingling, weakness, and fatigue are more frequent as a secondary symptom. This may account for the fact that recreational divers have more Type II DCS than pain only Type I. They wait much longer to seek help, giving time for secondary symptoms to arise. Conclusions The systematic collection of diver data by DAN and its network of volunteers is creating a great deal of information for analysis on recreational diving injuries. Many conditions exist within a diver accident profile that may be factors which contribute to an individual injury. A causal relationship between these conditions and diving injuries has not yet been established and the relationship remains statistical, but the DAN data indicates a strong relationship. Even though this data remains associated with diving injuries, it is a better basis for safe diving practices than the use of anecdotal information. In order to validate the DAN data, a prospective study was begun in May 1989. This study will follow a randomly selected group of divers in an attempt to determine the individual diver demographics, physical health, abilities and experience. It will also attempt to establish the risk associated with recreational diving and to determine if there is individual susceptibility. Such actual information will eventually form the basis of scuba diving safety education. "The most severe injuries occurred during or shortly after training" (Dick and Massey, 1985) reported one retrospective study of neurological decompression sickness. The recent DAN data also reflects a similar finding, but would add the infrequent diver to this group. The evidence of a relationship between dive accidents and the lack of experience is strong, but difficult to define. The inexperienced diver has accidents for many different reasons. Individual susceptibility to dive injuries may be influenced by a diver's physical ability, behavior, and response to the physical risk and stress present in diving (Dembert, 1987). Stress, and the diver's response to stress play an important role in new diver accidents (Bachrach and Egstrom, 1987). The analysis of inexperienced diver accidents can prove to be of short and long term value in the prevention of dive accidents. Accident avoidance is a strong incentive for the new diver to develop safety habits that take dive day conditions into consideration. These safety habits will carry over into a continuing dive career. The more information gained by accident reporting, the more accurate the safety recommendations will be in the future. The presentation of gas bubble disease represents a broad spectrum of disease symptomatology. This is one reason why a more intensive study of symptomatology was begun by DAN. A severity code classification scheme was devised by DAN to generate data on symptomatology for research purposes. The six level coding system classifies divers by the severity of their symptoms. Severity code 1 would be a pain only, limb DCS, while a cerebral embolism would be classified as a code 6. The presentation of peripheral and central nervous system symptoms are represented by codes two through six. This coding system has proved beneficial in determining the extent of diver injury in our accident population and provides a basis for comparison in cases with residual 150 Dovenbarger, Bennett and Wachholz: DAN: Diving accident data and its Implications symptoms (Bond et al., 1989). It has also pinpointed symptoms which require greater diver awareness. Summary Recreational scuba diving is evolving as a leisure activity and there is still much to learn about safety and accident prevention. In order to obtain an accurate database on recreational diving accidents, a wide variety of information must be analyzed. It is impossible to get a clear picture of this problem if study is confined to limited or single aspects of dive accidents. It appears from this study that dive accidents are the result of die interaction of many factors and in general are not caused by a single condition. There are approximately 600 treated dive injuries a year, making it difficult to convince a diver in a population of one to two million divers that he may be hurt. Divers rely on their traditional diving habits until they stop diving, are injured, or better information comes their way. The first step in unraveling the speculation and myths associated with recreational diving is to establish solid information based on the accumulation of actual statistics. This data will be the basis for safer diving habits in the future. DAN is indebted to the treatment facilities and many physicians who assist in the collection of accident data. This paper would not be possible without their efforts and cooperation. References Bachrach, A.J. and G.H. Egstrom. 1987. Stress Indicators (Chapter 2). In: Bachrach, AJ. and G.H. Egstrom (Eds.). Stress and Performance in Diving. Best Publishing Co., San Pedro, CA. pp 11-22. Berghage, T.E. and D. Durman. 1980. U.S. Navy Air Recompression Schedule Risk Analysis. Naval Medical Research Institute, Bethesda, MD. Bond, J.G., R.E. Moon and D.L. Morris. In press. Initial Table Treatment of Decompression Sickness and Arterial Gas Embolism. Submitted to Aviation, Space and Environmental Medicine. 1989. DAN Emergency Line Use. May, 1988. A Review of DAN Emergency Calls on Pagers. From: Divers Alert Network Preliminary Report on Diving Accidents. Dembert, M.L. 1987. Individual Factors Affecting Decompression Sickness. In: Symposium on Decompression Sickness, Duke University. November 1987. Sponsored by Duke Medical Center, NOAA and UHMS. Dick, A.P. and E.W. Massey. 1985. Neurologic Presentation of Decompression Sickness and Air Embolism in Sports Divers. Neurology, Vol. 35, No. 5, pp. 667-671. Divers Alert Network. December, 1988. "Report on 1987 Diving Accidents", Elliott, D.H. and E.P. Kindwall. 1982. Manifestations of the Decompression Disorders. In: The Physiology and Medicine of Diving, 3rd edition. Bennett, P.B. and D.H. Elliott (Eds.). Bailliere Tindall, London, pp. 461-471. 151 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Scheer, T. 1988. Computer Diving Style - Diving into the 1990's. In: DAN In-House News, Vol. 1, No. 1. Vann, R.D., J. Dovenbarger, J. Bond, B. Bond, J. Rust, C. Wachholz, R.E. Moon, E.M. Camporesi and P.B. Bennett. 1989. DAN's Results and Perspective of Dive Computer Use. In: M.A Lang and R.W. Hamilton (Eds.) Proceedings of AAUS Dive Computer Workshop, USC Catalina Marine Science Center, September 26- 28, 1988. USCSG-TR-01-892. USC Sea Grant Publication. Wachholz, C. 1988. What Is the Incidence of Nonfatal Diving Injuries? In: Alert Diver, Vol. 4, No. 3. Wachholz, C.J., J.A. Dovenbarger, G.P. Fowler, III, J.S. Rust, and L.D. Thompson. 1989. Comparison of Accident Data vs Survey Data of Uninjured Divers of DAN Membership June 1988. (Abstract). UHMS Annual Meeting, June 7-11, 1989. Hawaii. Williams, J., R.E. Moon, E.M. Camporesi, G.Y. Mebane, J. Dovenbarger, C. Wachholz and P.B. Bennett. 1989. Utility of Divers' Alert Network Non-Emergency Telephone Information Service. From: Diving Accident Network Preliminary Report. Hyperbaric Center, Duke University, Durham, NC. 152 A REVIEW OF ASCENT PROCEDURES FOR SCIENTIFIC AND RECREATIONAL DIVERS John E. Lewis 4524 Palos Verdes Drive E. Rancho Palos Verdes, CALIFORNIA 90274 U.S.A. An ascent procedure consists of three distinct elements. It has a beginning, which for most scientific and recreational divers occurs when a no- decompression limit has been reached. It progresses at some defined rate or rates of ascent, and if a safety stop is included, it ends with a stop at a shallow depth for a prescribed period of time. The issues are the prevention of air embolism and decompression sickness. The options are reduced no- decompression limits, a safety stop, and a reduced ascent rate. The test data of Spencer and Powell are referred to as a basis for reduced no- decompression limits, and the tests ofPilmanis are presented in support of a safety stop. The absence of experimental evidence that a reduced ascent rate is necessary for the prevention of air embolism is noted, and calculations are are presented that quantify its effectiveness as a means of decompression. These calculations demonstrate that the maximum effect of reducing the present rate of ascent by a factor of wo is equivalent to a safety stop of less than 0.6 min at 15 ft. Introduction The Underwater Diving Manual published by DAN describes two "life-threatening conditions" that are directly related to ascent: air embolism and decompression sickness. Both are a result of gas bubbles but with differing origins. Air embolism is caused by "ruptured lung tissue releasing bubbles into the circulation", whereas decompression sickness occurs when "(absorbed) nitrogen comes out of solution and forms bubbles in the tissues and blood stream." The purpose of this paper is to quantify the net benefit of differing ascent procedures in order that an informed decision can be made by the American Academy of Underwater Sciences (AAUS) as to what ascent procedure is best suited for both scientific and recreational divers. What are the issues and options? As illustrated in Figure 1, an ascent procedure consists of three distinct elements. It has a beginning, which for most scientific and virtually all recreational divers occurs when a no-decompression limit has been reached. It progresses at some defined rate or rates of ascent, and, if a stop is included, it ends with a stop at a shallow depth for a prescribed period of time. The issues are as stated previously: the prevention of air embolism and decompression sickness. The options under consideration are reduced no-decompression limits, a safety stop, and a reduced ascent rate. 153 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. Figure 1. Basic elements of an ascent procedure -SO DEPTH (FT) ?100 END-SAFETY STOP MIDDLE-ASCENT RATE BEGINNING -NOD LIMIT -150 4- 10 20 30 40 TIME (MIN) No-Decompression Limits There are three relatively recent experiments that deal with no-decompression (NoD) limits that are relevant to our discussion: Thalmann (1984), Spencer (1976), and Powell (1987). Thalmann attempted to increase the Navy NoD limits, and he tested a total of 107 exposures without any occurrences of decompression sickness (DCS) to the following limits: ? 60 feet for 66 minutes ? 100 feet for 30 minutes ? 120 feet for 24 minutes ? 150 feet for 14 minutes However, a careful reading of his report indicates that these experiments actually included a short decompression stop at 10 feet, although the actual time spent at 10 feet is not documented. More important is that during a second trial of 100 feet for 30 minutes, 4 cases of DCS occurred out of 20 exposures. Thalmann did not use Doppler monitoring of his test subjects, and this result leads me to conclude that if clinical symptoms of DCS is the only diagnostic, what does not work is far more important than what may work on occasion. Spencer performed tests to the Navy limits. He also Doppler monitored his test subjects for nitrogen bubbles as well as recorded clinical symptoms of DCS. Each of the following examples produced high grade bubbles and at least one case of DCS: ? 60 feet for 60 minutes ? 70 feet for 50 minutes ? 25 feet for 720 minutes 154 Lewis: A review of ascent procedures for scientific and recreational divers The one example of a bottom time he tested that did successfully exceed U.S. Navy NoD limits was 150 feet for 10 minutes. Powell tested reduced NoD limits that closely resemble Spencer's empirical formulae for 15% VGE. These bottom times closely resemble the U.S. Navy Dive Tables with the addition of 10 feet to the actual depth of a dive, and thus they do not differ greatly from the admonition in the U.S. Navy Diving Manual to "always select the next depth greater than the actual depth". Powell also Doppler monitored his test subjects. These experiments produced no DCS and at most low grade bubbles. DEPTH 50 hi 60 70 80 90 100 110 120 130 140 150 B(jiiOMJiiivik 100 MIN 60 50 40 30 25 20 15 10 10 5 DECOMPRESSION TIME 7.9 MIN 3.2 6.5 5.3 3.5 3.3 1.8 0.7 NoD 0.3 NoD Table 1. Decompression required by Oceanic DataMax Sport when diving to U.S. Navy NoD limits. It seems probable that diving to the U.S. Navy NoD limits has worked so well for so long because a large percentage of diving was performed well within these limits. Lately, the diving community seems to be besieged with well meaning but poorly founded new rules. Reduced NoD limits do not fit into this category. They are well documented and, in my judgment, should be adopted by scientific divers as well as recreational divers. For scientific divers that have a need for bottom times closer to those of the U.S. Navy, most dive computers can still be used for this purpose, despite the fact that they are based on reduced NoD limits. They will require a decompression stop, but as can be seen in Table 1, the required decompression stops are quite modest and are not unlike a "Pilmanis safety stop", which is discussed in the next section. While we are on the subject of NoD limits and dive computers, presently available dive computers seem to fit into three distinct groups (Table 2). We have already discussed the Spencer NoD limits. The so-called "Biihlmann limits" are considerably more conservative for intermediate depths, e.g., allowing as little as 12 minutes at 100 feet. In view of Powell's extensive testing of 20 minutes at 100 feet, Group 3 would appear to be unnecessarily restrictive, particularly for scientific divers. The Pilmanis Safety Stop The effectiveness and importance of a safety stop, i.e., a decompression stop that is not required by either a dive table or dive computer, was dramatically demonstrated by Pilmanis (1976). As can be seen in Figure 2, following a dive to 100 feet for 25 minutes, as little as 2 minutes at 10 feet was shown to reduce the Doppler monitored bubble count by a factor of 5, and a 5 minute stop virtually eliminated any trace of measurable bubbles. No 155 Lang and Egstrom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. one who has seen these data can seriously argue with the decision to include a stop in the ascent procedure recommended for both scientific and recreational divers. Group 1. Group 2. Group 3. U.S. Navy limits Spencer 15% VGE "Biihlmann limits" Suunto USN Oceanic Datamaster II Oceanic Datamaster Sport Oceanic DataMax Sport ORCAEDGE ORCA Skinny Dipper Suunto SME-ML U.S. Divers Datascan 2 U.S. Divers Datascan 3 Beuchat Aladin DACOR Microbrain DACOR Microbrain Pro U.S. Divers Monitor Table 2. NoD Limits of Presently Available Dive Computers. Figure 2. Pilmanis experiments on ascent procedures 120- BUBBLE COUNT DIRECT ASCENT 2 MN AT 10 FT 1 MM AT 20 AND 4 MM AT 10 FT Following 0i en ^1 Cn to b I I I I I I I I I I M l o O J ^ U i c n v J C n i O Q I I I I I I I I s O CD o CD O M O O 218 Lang and Egstrom (Eds.): B10MECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Costa Mesa, CA. 1990. TIME-TO-SURFACE (minutes) M o " o = m I u> 5 CO i ?i mI o o CO o 219 Lang and Egstiom (Eds.): BIOMECHANICS OF SAFE ASCENTS WORKSHOP. AAUS, Cosu Mesa, CA. 1990. TIME-TO-SURFACE (minutes) cn m o i cn = o 1 a 1 ? j CO : O 1 O _ O 3 O = Cn O cn a CD o o MOO m o 89 m 9: O O ~D 00 O K) 220