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Te Future of Diving:

100 Years of Haldaneand Beyond

Michael A. Langand Alf. O. Brubakk

Editors

A Smithsonian Contribution to Knowledge

WASHINGTON, D.C.2009


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Tis publication of the proceedings of Te Future of Diving: 100 Years of Haldane and Beyond is co-sponsorby the Smithsonian Institution and rondheim University. Te symposium was convened by the Baromedical anEnvironmental Physiology Group of the Norwegian University of Science and echnology in rondheim, Norwon 1819 December 2008.

Published by SMI HSONIAN INS I U ION SCHOLARLY PRESS

PO Box 37012MRC 957 Washington, D.C. 20013-7012

www.scholarlypress.si.edu Compilation copyright Smithsonian Institution

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmin any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the ppermission of the publisher.

Cover image: Photo by Hans Wild// ime Life Pictures/Getty Images.

Library of Congress Cataloging-in-Publication Data [CIP data to come]

ISBN-13:978-0-9788460-5-3ISBN-10: 0-9788460-5-2

Te paper used in this publication meets the minimum requirements of the American National Standard fPermanence of Paper for Printed Library Materials Z39.481894.


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Content

FOREWORDby David H. Elliott vii ACKNOWLEDGMEN Sby Michael A. Lang and Alf O. Brubakk ixEXECU IVE SUMMARY xi

IN RODUC IONIntroductory Remarks Alf O. Brubakk 1 Welcoming Remarks Stig A. Slrdahl 3 J. S. Haldane, the First Environmental Physiologist Alf O. Brubakk and Michael A. Lang 5Environmental Physiology of the Future Richard E. Moon 11

DECOMPRESSION PHYSIOLOGY An Introduction to Clinical Aspects of Decompression Illness (DCI) Costantino Balestra 17Haldane Still Rules! David J. Doolette 29Biochemical Approach to Decompression Susan R. Kayar 33Exercise and Decompression Russell S. Richardson 41Diving Medicine and the Cellular Stress Response George A. Perdrizet 47Individual Risk of Decompression Sickness: Possible Effects of Genomic

or Epigenomic Variation Altering Gene Expression Andreas Mllerlkken and Ingrid Eftedal 53Inducing HSP for Protection against DCS: Heat Exposure before Diving

Reduces Bubble Formation in Man Jean-Eric Blatteau, Emmanuel Gempp, Jean-Michel Pontier, Costantin

Balestra, ony Mets, and Peter Germonpr 59


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Lack of Signs of Brain Injury in Rats on MRI after Decompression Marianne B. Havnes, Marius Widere, Marte Tuen, Andreas

Mllerlkken, and Alf O. Brubakk 65Exercise, Endothelium, and Diving Physiology eljko Duji 71 Animal Experiments for Evaluating Decompression: Development

of the Modern Submarine Escape Method Mikael Gennser 77

DECOMPRESSION ME HODOLOGY Ultrasound for Evaluating Decompression Olav S. Eftedal 83Current rends in Ultrasound Imaging echnology, SURF Imaging,

and Decompression Induced Microbubbles Lasse Lvstakken, Andreas Mllerlkken, and Svein-Erik Msy87Te Future of Dive Computers Michael A. Lang and Sergio Angelini 91

Discussion: Decompression Physiology and Methodology 101

S RA EGIC APPROACHESBreeding Diving Scientists: Cloning, Spawning, or Cultivation?

yvind Ellingsen 109National Centre for Hyperbaric and Diving Medicine Marit Grnning 111Baromedical and Environmental Physiology Group (BAREN) Alf O. Brubakk 113Physiopathology of Decompression (PHYPODE) Network Francois Guerrero, Jacek Kot, Peter Germonpr, Jean-Michel Pontier,

Alessandro Marroni, Adel aher, Frans Cronje, Bernard Gardette,D. Nicola, and Costantino Balestra 117

International Cooperation in Diving Research Matthew Swiergosz 119

Discussion: Diving Researcher Recruitment 123

ENVIRONMEN AL PHYSIOLOGY How Do Marine Mammals Avoid DCS? Andreas Fahlman 129Does Diving Destroy the Brain? Stephen Daniels 137Effects of Diving on the Lung Einar Torsen 145Te Limits of Breath-Hold Diving Peter Lindholm 147


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CON EN S v

Parameters of Extreme Environment Diving Michael A. Lang 153Creativity and Improvisation As Phenomena and Acting Potential

in Different ContextsBjrn Alterhaug 161

Discussion: Environmental Physiology and Strategiesfor the Next 100 Years 171

APPENDIX A:Te Prevention of Compressed-Air Illness (1908) 175 APPENDIX B: Syposium Speakers 281 APPENDIX C: Symposium Participants 285


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It was a disappointment for me not to be able to attend this conferencehonour to write its preface. While a postgraduate student in Oxford I h

of using the Lloyd-Haldane gas-analysis apparatus1

. My contribution to resptory research was negligible2 but some serious effects arose in a colleague froexposure to the mercury that had spilt from the apparatus and was trappthe laboratory oorboards. Mercury poisoning was noti able even in Haldbut while this incident introduced me to inhalation toxicology and health(another area in which Haldane excelled), it also shows that an importannot necessarily remain in the spotlight for a hundred years.

One hundred years ago John Scott Haldane was already a Fellow of NOxford, the Reader in Physiology at Oxford University and a Fellow of thety (FRS). In the opening review Michael Lang and Alf Brubakk illustratof his scienti c output and his philosophical criticisms. We should also remlike many other researchers, he was often his own subject and once aftecarbon monoxide mixture for nearly a half hour, he felt distinctly abnorm

Tis international meeting covers what has happened since Haldanes pand focuses on the hyperbaric aspect of his contributions to physiology.exposed to poison gas in the trenches and the coal miners exposed to afthe mines may still out-number divers as the bene ciaries of Haldanes ininto respiratory physiology and health protection, but these two major proHaldane solved, occur within an otherwise physiologically-normal body.

In contrast, there are additional factors in diving that arise from tha unique physiological variable, that of environmental pressure. Haldanethe decompression problems of deep air diving for the Admiralty and maprogress in providing a practical outcome for the diver and a foundationther development of decompression tables. Te additional complexity of thraised environmental pressure on the whole body affects many cellular ancal mechanisms, some of which in turn may in uence the bodys responseence of bubbles. All these developments and revelations have catalysed reviewed here and have inspired the convenors of this meeting to reprioriginal paper of 1908. Tis paper is the foundation of what follows in theings, more than a hundred years later.

Professor David H. Elliott O.B.E., D.Phil (Oxon), F.R.C.P

Forewor


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NOTES1Lloyd, B.B. J. Physiol . 1958; 143:5P.2Cunningham, D.J.C., Elliott D.H., Lloyd B.B., Miller J.P., Young J.M. A com-

parison of the effects of oscillating and steady alveolar partial pressures ofoxygen and carbon dioxide on the pulmonary ventilation. J. Physiol1966;179:498508.


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W elcome everyone. I am very pleased to see so many people ll utorium. I never expected that the idea of this Haldane symposi

catch on and encourage so many of you to attend. Our thoughtsorganizing a symposium to honor Haldane one hundred years after his secation in 1908 would be a good idea, because since that time we should grasp of what has happened in the eld of decompression and, more im what should happen in the future. We will try to discuss some of the isthink are important for the future and how we might approach them. Inhow can we get young people interested in this rather limited eld of sciare quite a lot of interesting biological and practical diving problems thaaddressed. Te interactions at this symposium are going to be important. Hopefpeople will take this opportunity to talk with each other and by making tbutions, lead to a useful result. We have asked all speakers to submit a mMarch 31, 2009 and we will hopefully not have to hound you about this scult to do after we have already paid for the airline tickets. Speaker formlled out and submitted to us for reimbursement. Te chairman of todays session is Otto Molvaer of Deep-X whom I hbecause of his excellent ability to keep speakers within their time limits.speakers may have a lot to say, we ask you to stay within your time limit bfull program schedule. Te discussions will be recorded because our goal is to publish this vgood friend Michael Lang from the Smithsonian has done a lot publishhas convinced me that, although this will be much work, this Haldane sysuch an event that we need to record it for posterity and disseminate thorder to do that, we have supplied two roving microphones. It is importanyou make a comment or ask a question you state your name in order to aremark to the appropriate speaker. Otherwise, we will not know who saidmight be an advantage in some cases. In others, some speaker might saythat for which we will have a video tape back up to prove that they diseveral N NU people in the audience and we will try to help you in any wI now welcome Stig Slrdahl, Dean of the N NU Medical Faculty, to s welcoming remarks. Once again, welcome to the Haldane Symposium.

Department of Circulation and Medical Imaging,Norwegian University of Science and echnology,N-7491, rondheim, Norway.

Introductory Rema Alf O. Bruba


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population participated, and in 2006, 56% of the populationshowed up to give blood samples, go through an examination,and provide other vital data on health and occupational back-ground. People working in the oil industry also participated.In total, over 100,000 individuals were invited to participatein the HUN 3 study, one of the worlds largest health stud-ies. Te Principal Investigator of the HUN projects has been Jostein Holmen, and the HUN 3 Project Director was SteinarKrokstad. Research related to diving has been an ever-increasing un-dertaking within our faculty. I came here as a research fellow in1987, working in the same Department as Alf, and I have, sincethen, been following the development of the diving researchactivities. I am quite impressed with the scope of Alf s work andhis creativity and success in this process.

Again, I wish you a warm welcome and I expect yohave two interesting symposium days. I also hope youhave an opportunity to see more of rondheim. We are crently building a new university hospital here on camp$2.5 billion dollar project. Te Faculty of Medicine wilhoused inside the hospital buildings and basic scientistbe moved to the academic oor within the new hospital interconnecting skywalks between the buildings. Our vis that more frequent interaction between basic scienclinical colleagues and engineers will stimulate excitinlaborative research. Te entire construction project shouldnalized by 2013. Hopefully we can reconvene the 200Haldane symposium in the new venue.


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INTRODUCTION

John Scott Haldane can be considered the rst environmental physiologi As suche was interested in how the human body functioned during normal lifthat, he took his physiological insight to various extreme environmemines, high altitudes, and under the ocean. Tus, using man as his subjecthow theoretical and experimental physiology could have direct applied usterms, it could be said that he was the rst to show the value of translationdemonstrating for instance that the sensitivity of canaries to carbon moncould be used to prevent CO toxicity in man. He was born in Edinburgh on 3 May, 1860, fourth son of Robert Haldsecond wife Mary Elizabeth and died March 16, 1936, of pneumonia. Fe J. S. Haldane actually exist. Haldane believed that the aim of the science of physis to deliver general principles which shall enable us to predict behaviourbody under various physiological conditions. He was also considered oxygen therapy: Te rst step in good practice is to know what the oxygeat, where it is going, and in what quantities. We know about Haldane from his work on developing decompressionhis contribution can only be understood if one considers his previous work First of all, Haldane was an observer and an experimentalist, who alwaythat careful observation and experiments had to be the basis of any theore

ABS RAC. John Scott Haldane was born in 1860 in Edinburgh, Scotland and can trthe rst environmental physiologist. He studied poisonous gases occurring in coal m

sunstroke, the physiological action of carbon monoxide and the use of a caged canadetection, the regulation of lung ventilation (with J. G. Priestley, 1905), and devisedbinometer, the apparatus for blood-gas analysis. He also described the effects of oand exercise on breathing. During the First World War he worked on effects of poisdesigned a portable oxygen administration apparatus. His work on hypoxia and theof the human body to high altitude revolutionized concepts in respiratory physiopublished some landmark books on his philosophical ideas about the true signi caMost importantly, however, Haldane investigated the problems of deep diving for miralty, developing the stage decompression method, a lasting contribution to thTis elaborate experimental investigation was conducted in part in a steel pressure Lister Institute and with divers in Scottish deep-water lochs. In 1908, J.S. Haldane results in his seminal paper Prevention of Compressed-Air Illness in the Journal Dr. A. E. Boycott and Lieutenant G. C. C. Damant. Stage decompression allowed dibrought to the surface and made it possible to conduct 120 fsw salvage operations onIC to recover over 5,000,000 of gold ingots without recordable incident.

Alf O. Brubakk, Norwegian University of Science andechnology, Department of Circulation and MedicalImaging, 7491, rondheim, Norway. Michael A.Lang , Smithsonian Institution, Offi ce of the UnderSecretary for Science, P.O. Box 37012, MRC 009,Washington, D.C. 20013-7012 U.S.A.

J. S. Haldane, the FEnvironmental Physiolo

Alf O. Brubakk and Michael A


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Why think when you can experiment and Exhaust experi-ments and then think. His passion for obtaining data was dem-onstrated by the fact that during his medical studies in Jena, hecarefully observed the amount of beer being drunk, noting thatthe students on the average drank about 20 pints per evening. Haldane received his education at the Edinburgh Academy,University of Edinburgh (1884), and University of Jena in cen-tral Germany, after which he was a Demonstrator at UniversityCollege, Dundee. From 1907-1913 he was a Reader in Physiol-ogy at Oxford University where his uncle, John Burdon-Sander-son, was Wayn ete Professor of Physiology. J. S. Haldane becamemember of the Royal Society in 1897 but had issues such as TeRoyal Society system of selecting papers and excluding specula-tive ones makes the meetings, Proceedings and ransactions asdull as ditch water and quite unrepresentative of the progress ofBritish Science (Goodman, 2007). Regardless, he was award-ed Royal Medallist of the Society in 1916, Copley Medallist in1934, and in 1928 he was appointed Companion of Honour for

his scienti c work in connection with industrial disease. J. S. Haldane was personally gifted with a unique powerof encouraging the faculty for research and his teaching wascharacterized by his efforts to make the students observe andthink for themselves. He had the great ability to add both forceand charm or character, the effect of which was securing the at-tachment of his pupils. Haldane had a profound sense of publicservice and he believed passionately that the world could bemade a better place through the application of science. Fromminers dying of carbon monoxide poisoning and soldiers beinggased like rats in the trenches, to mountaineers and aviatorscoping with high altitudes, Haldane showed that science couldbring light into the darkness. A friend described him as almost

quixotically anxious to do good to all mankind and to teachthem all a thing or two (Goodman, 2007). Haldane was also a philosopher of science and many of hislectures were published in books, such asTe Sciences and Phi-losophy in 1929,Te Philosophical Basis of Biology in 1931, andTe Philosophy of a Biologist in 1935.

THE SELF-EXPERIMENTER

Haldane was himself such a coalmine canary, putting hisown health and life on the line to protect others (Goodman,2007). Haldanes own philosophy was All life is a physiologicalself experiment. Once, on his way home from his laboratoryafter such an experiment, he was stopped by an Oxford po-liceman who had observed the scientists stumbling progress.Haldane explained that it was not due to alcohol, but gas. Hishousekeeper offered her sympathies to his wife, Kathleen: Iknow how you feel, maam. My husbands just the same on aFriday night. Haldane liked nothing better than to explore dangerousmine shafts and sewers. But it was in the specially constructed,air-tight chamber in his lab that the effects of gases on people were revealed. In an age before risk assessments, Institutional

Review Boards and Human Subjects Ethics Committees,dane was a serial self-experimenter. He also thought nothexposing his own son Jack to dangerous doses of chlorinother noxious gases. His young daughter Naomi once t6-year-old friend outside their house: You come in. My wants your blood. Her friend screamed and ran away.

FIRST PAPER

Haldanes rst essay in 1883 with his brother Lord Halcontributed to Essays in Philosophical Criticism examinrelationship of philosophy to science and attempted to anthe questions: What is man; discover mans relationship environment; and, knowing mans relationship to his envment, determine his function, what is he most suited to do i world? His real interest was the study of the relationship bthe organism and the environment. Tis, as well as his deep fefor social issues, would determine the focus of his professio

FIRST STUDY

Haldane as Sherlock Holmes, environmental investiasked a) What is bad air? b) What makes air dangerous to brc) How can its bad effects be prevented? He proceeded bying the air in overcrowded Dundee slums, turning up wit warning in the middle of the night to collect air in bedr where eight people were sleeping. His results indicated thatof 180 cubic feet had 65% more carbon dioxide, twice as molds, 254% more organic matter, including hydrogen su(0.07% can be fatal), and 1000% more bacteria than norma

SELF EXPERIMENTS

Some of Haldanes rebreathing experiments revoaround the concept of the good air being used up. His ndincluded that oxygen was a gas that supported life longean equal amount of air; that carbon dioxide spoils pure airit was breathed; that after seven hours, O2 was down to 13%and CO2 was up to 6.5% accompanied by symptoms of hpanting, severe headache, and vomiting; and, that after bring O2 of 2%, he went unconscious after 40 seconds. Wof his propensity for experimentation got out promptingneighbor to knock on his door asking My wifes cat has

lost and we thought that possibly it might be here. Hainvented the haemoglobinometer, the apparatus for blooanalysis and also designed an apparatus for the accurate aanalysis of air or mixtures of gases (Snyder, 1937).

THE STINK

When a Select Committee called upon him to delve ithe lower depths of government and analyse the stink that beneath, Haldane ventured into the sewers below Westm


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mechanisms (lack of sunlight, poor ventilation, ladding, infections, smoke, high and low temperatures, uconditions and breathing of stone dust - silicosis). Acreferred to Haldane as the father of the salt tablet foommendation of salt replacement during excessive sw Haldanes altitude studies consisted of work at P(1911) and Mount Everest of which he said the highest pof the Earth could be reached without the help of oxyviding they had the right men and the right weather.further involved with the design of the rst prototype s(1921) and balloon ights to 90,000 feet (27,430 m) in Also, the identi cation of nitrite (NO2) as the active indient in red meat curing procedures dates to the late 1tury. J.S. Haldane was the rst to demonstrate that the of nitrite to hemoglobin produced a nitric oxide (NObond, called iron-nitrosyl-hemoglobin (HbFeIINO). Te reduction of nitrite to NO by bacteria or enzymatic reactiopresence of muscle myoglobin formed iron-nitrosyl-m

It is nitrosylated myoglobin that gives cured meat, hot dogs, their distinctive red color, and protects the moxidation and spoiling (Gladwin, 2004).

DECOMPRESSION STUDIESAND DIVING TABLES

Haldane found that it was not pressure that damabody, but differences in pressure. Paul Bert (1878) dogs to 290 fsw with rapid decompression, resultingby nitrogen bubbles. In his studies using goats (Figsthe Lister Institute of Preventive Medicine, Haldane uascent rates of 5 feet/min. Te decompression studie were published in the seminal paper by Boycott, DamHaldane (1908), one hundred years ago. Haldane made the important observation that no dthe bends after rapid decompression from 42 feet tface leading to the general principle that a 2 to 1 preference could be tolerated. A staged-decompression tech was developed and tables describing uptake and elimnitrogen were developed by his son Jack Haldane aTe body was divided into six compartments with diffetimes and the deepest dive tested to 210 fsw (64 msw) Haldane also suggested that oxygen should be useen decompression provided the pressure was kept lessbecause of the fear of oxygen toxicity. However, Haldlittle contribution to the therapy of decompression although he recognized that recompression was the tof choice. Haldane had doubts about the safety and euniform decompression practice. Haldanes experimconducted at the Lister Institute of Medicine in a recsion chamber and he assumed the following: a) for bform, the pressure of gas in the tissues must exceed thpressure; b) that body tissues will hold gas in a supestate unless a certain limit is reached; d) that any decois free from risk only if the degree of supersaturatio

Palace. A born iconoclast, he successfully challenged the ideathat sewer air was a cause of typhoid and other diseases.

COAL MINE CANARIES

Serinus canariais affected by gas 20 times faster than man,prompting Haldane to hold canaries in cages in the mines. Be-ing fundamentally a kind man and concerned about the animals well being, Haldane modi ed the cage so that only the front wasopen and could be o-ring sealed when closed. He had mounteda small oxygen bottle on top of the cage. When the canary felloff its perch from breathing toxic gas, he would shut the frontdoor and open the oxygen bottle, ensuring the canarys survival.

MINE ACCIDENT EXPERIMENTS

In 1896, a mine explosion occurred in ylorstown Colliery,Rhondda Valley, South Wales, with over 100 men below. Enter J. S. Haldane, medical detective. Te toxic gas after the ex-plosion (afterdamp) had not extinguished miners lamps, lead-ing Haldane to believe that oxygen was present and suffocationneeded to be ruled out. His diagnosis was accurate: 75% of thedeaths were attributed not to blast injuries, but to CO poison-ing as evidenced by pink and red skin coloration and carmine-red blood samples. Further re nement of Haldanes curiosity about why theminers died led to more self-experimentation. Breathing 0.2%CO for 71.5 minutes, Haldanes vision became dim, his limbs weak, he had some diffi culties in waking up or walking withoutassistance, and his movements were very uncertain. Afterwardshe confessed feeling confused, making spelling mistakes, ex-periencing indistinct vision, and not recognizing what he saw.Oxygen breathing made dramatic improvements. On anotheroccasion, after 29 minutes of breathing CO, Haldane calmlynoted that he felt distinctly abnormal: he was panting, breath-ing 18 times a minute, his limbs shook and his pulse was racing.Soon, he began to feel unsteady on his feet.

RESPIRATION STUDIES

Haldane and Priestly (1905) showed that the regulation ofthe breathing is normally determined by the tension of carbondioxide in the respiratory center in the brain, and that this ner-

vous center is sensitive to variations in the tension of carbondioxide supplied in the arterial blood. Since carbon dioxide isone of the principal products of the metabolism of the tissues,an explanation was afforded of the automatic changes in breath-ing rates which occur with alteration in bodily activity.

MORE ENVIRONMENTAL STUDIES

Haldane conducted other environmental studies on the ef-fects of hyperthermia, nutrition, and in particular lung disease


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borne with safety; and, d) that tissue perfusion was the limitingfactor in inert gas uptake (Boycott et al., 1908). His decompression experiments examined the depth andpressure exposure, its duration, and the mode and decompres-sion rate. Initially, a few experiments were conducted on rab-bits, guinea pigs, rats and mice but it was diffi cult to detectsymptoms in these smaller animals. Te goat (Figs. 1a,b) waschosen as the experimental model because they were the larg-est animals which could be conveniently dealt with and those who are familiar with them can detect slight abnormalities witha fair degree of certainty. Te dog was rejected because they hadnoted that Heller et al. (1900) had previously used them to pro-duce safe decompression pro les that had failed in humans. Goats were excluded from the experiments if they were ill.Only 5-8 goats were used per experiment. Te chamber was notventilated because they believed CO2 to have a minimal effecton the susceptibility to decompression sickness. Te chambertemperature was not controlled and no allowance was made for

any variation in atmospheric pressure. Large pressure variations were used to produce minor to severe symptoms. Te compres-sion time of 6 minutes was neglected in short exposures butincluded in longer, deeper exposures. At the time of the experiments, Haldane knew from Navaldiving data that decompression from 2 bar produced no symp-toms irrespective of the time of exposure. However, decompres-sion from 2.25 bar produced the occasional slight case henceHaldanes assumption that halving the pressure would not pro-duce symptoms. He used a perfusion mathematical model ofgas uptake, the half lives of which were calculated from dataavailable at that time (Acott, 1999). Te most common bends symptoms in goats were limb

pain where the affected limb, often the foreleg, was raised(Fig. 1a); pain was detected by urgent bleating and continual

restlessness with the goat often gnawing at the affectesuch as the testicles; temporary paralysis noted about 1after decompression with improvement within 30 minthe animal being quite well the next day; permanent decompression paralysis where the hind legs were notedparalyzed immediately with any spontaneous improvemelowed by a permanent relapse (urinary retention and an gut distension were also noted); obviously ill goats wereto be apathetic and ill, refused to move or to be temptedcorn (of which goats are inordinately fond); dyspnoea, ister symptom usually occurring just before the animal and, death. Importantly, Haldanes data showed that goatsan individual variability and susceptibility to decompresickness.

Diving tables were published in 1907, the Royal Navy ad-opted them for military divers in 1908, and the U.S. Nav1912. Tey became the Blue Book for civilian divers whono discomfort from working at 210 feet. Referring to ap

physiology, Richard Haldane, John Scotts brother, statedHaldane has shown yet one more instance of the applicatiscience to practical work. Haldane continued to think athe decompression problem for the rest of his life, considhow to extend and extrapolate the tables. Te S.S. LAUREN IC (White Star Lines), built by Haland & Wolff at their Belfast yard, went down the slipw29 April 1909 at the time that construction on the I ANIstarted. Captain Reginald Norton was chosen to carry 43of gold bullion from Great Britain to Canada. On 25 Jan1917, she struck a mine and sank within an hour in 40 m water in Lough Swilly, Donegal, Ireland, with a huge lossand all the gold bullion. In 1906, Commander Guybon C

Damant had set a world diving record of 210 feet during Nendurance diving tests. His experiences as a salvage dive

FIGURE 1. Bends in the foreleg of a goat (a) and goat chamber dives (b). Both gures from Boycott et al. (1908) and reprinted wision from Cambridge University Press.


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well known to the Admiralty. In 1917, the 36-year-old Dam-ant and his team included Augustus Dent, a diver and aboardS.S. LAUREN IC when she sank, who knew where the bul-lion room was. An incredible salvage feat between 1917 and1924 recovered 3,186 gold bars of the missing 3,211 with afurther 5 being recovered in 1932 by another salvage opera-tion, leaving 20 gold bars still unaccounted for at the bottom ofLough Swilly worth some 10 million at current prices. Over5,000 salvage dives were conducted using Haldanes tables in a200 square-yard working area at 120 feet with no loss of life orserious problems.

HALDANES ENDURING LEGACY

Apart from his many important contributions to physiolo-gy, where perhaps the description of the principles of breathingcontrol is the most signi cant, Haldane demonstrated that envi-ronmental physiology was a scienti c discipline of considerable

theoretical and practical value. By studying the intact organ-ism in various extreme environments, he was able to determinehow the environment in uenced normal physiological variablesas well as disease processes. Tis approach is still controversial,even in our own eld, diving, where there is considerable sup-port for focusing on what works, works and where studiesof basic mechanisms are considered more of academic ratherthan practical value. Haldane, with his strong focus on scienceas the basis for his practical approach, demonstrated that realprogress for improving health can only be achieved by combin-ing the two. Tis is even clearer today as we increasingly areunderstanding how the environment may even in uence geneexpression.

A CKNOWLEDGMENTS

We wish to thank the Haldanes and their endurinthe Baromedical and Environmental Physiology GroNorwegian University of Science and echnology inheim, and the Smithsonian Offi ce of the Under Secr

Science.

LITERATURE CITED

Acott, C. J. 1999. J. S. Haldane, J. B. S. Haldane, L. Hill, and Abrief resume of their lives.South Paci c Undersea Medical Societ29(3):161165.

Bert, P. 1878.Barometric pressure.ranslation by Hitchcock, M. A. and Hitchcock. Columbus, Ohio: College Book Company, 1943. RBethesda, Maryland: Undersea Medical Society, 1978

Boycott, A. E., G. C. C. Damant, and J. S. Haldane. 1908. Preventipressed air illness. Journal of Hygiene, Cambridge 8:342425.

Gladwin, M. . 2004. Haldane, hot dogs, halitosis, and hypoxic vathe emerging biology of the nitrite anion. Journal of Clinical Investi

113(1):1921.Goodman, M. 2007.Suffer and Survive. Gas Attacks, Miners Canasuits and the Bends: Te Extreme Life of J. S. Haldane . London: Simon Schuster. 320 pp.

Haldane, J. S, and J. G. Priestley. 1905. Te regulation of the lung-ventilati Journal of Physiology32:225266.

Heller, R., W. Mager, and H. von Schrtter. 1900.LuftdruckerkrankungenBesonderer Bercksichtigung der Sogenannten Caissonkran. ViennHlder.

Snyder, J. C. 1937. A note on the use of the Haldane apparatus for of gases containing ether vapor. Journal of Biological Chemistry 122:212


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INTRODUCTION

Environmental physiology can be de ned as the study of adaptation tmental conditions, which are often adverse. Tese include the followtions: altitude, hyperbaria, immersion, extremes of temperature, dand altered G force: microgravity or increased G. Environmental physiology is worthy of study for at least two reasonthat because humans and other animals live in, or voluntarily expose thsuch adverse conditions, an understanding of the biological effects is of iest and importance. Te second is that for those interested in understandiphysiology, environmental physiology in the eld consists of an experimpeople willingly expose themselves for fun to the kind of condition that msic experimental purposes, be considered unethical. Like most areas of science, environmental physiology received its mthe 19th century. An example is the series of observations that were madealtitude balloon ights. Glaisher, in 1871, reported that the number of heaminute increases with the altitude at 10,000 feet, certain persons are

ABS RAC. Environmental physiology consists of the varied responses and adaptatisms to environmental stresses. Tese include cold, heat, water immersion, high an

pressure and microgravity. Why should environmental physiology be studied? Firstanding of the human response to the environment can lead to protective strateconditions. A second reason is that humans often voluntarily expose themselves the eld that would never be allowed by any human ethics committee. Studying peocircumstances can elucidate and lead to understanding of basic mechanisms. Systhumans under different environmental conditions began in earnest in the 19th cenemplary experiments were conducted in hypo- and hyperbaria. Hypoxia, hyperoxiG, and high ambient pressure have been extensively studied. However, much remaiFor instance, exposure to altitude hypoxia is known to cause several clinical syndroegies to prevent and treat these conditions are well known, their etiologies are obscfor compressing and decompressing divers have also been worked out, at least to athat is acceptable. We know that bubbles instigate decompression illness. Howeveabout the biochemical connections between bubbles and syndromes. Te almost excbubble formation, growth, and resolution has blinkered investigators to moleculabubbles may trigger, the understanding of which could lead to improved preventionI propose two approaches that need greater emphasis. (1) Most physiology is basof the steady state, but there is much to be learned by studying physiological transstudies of macro-physiology are crucial, they alone will not lead to a complete uenvironmental physiology, which can only be achieved by parallel study of cellulamechanisms.

Center for Hyperbaric Medicine and EnvironmentalPhysiology, Duke University Medical Center,Durham, North Carolina, 27710, USA.

Environmental Physiology of the FRichard E. Mo


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purplish red, while others are hardly affected. At 17,000 feet mylips were blue (Doherty, 2003). Amongst other things, Glaish-ers observations pointed out the variability of the biological re-sponse to hypoxia.

ALTITUDE PHYSIOLOGY:FROM THE FIELD TO THE LAB

An understanding of the effects of varying degrees of hy-poxia on oxidative capacity has been obtained from eld mea-surements by Pugh et al. (1964). Field observations then led tolaboratory studies of acclimatization in a hypobaric chamber, where sophisticated measurements can be obtained such as arte-rial and mixed venous blood gases, cardiac output, and ventila-tion-perfusion relationships using the multiple inert-gas elimi-nation technique (Sutton et al., 1988). Exposure to extremelevels of hypoxia and hyperoxia in a laboratory setting has alsogiven us an understanding of vasoregulation in the pulmonary

circulation. While hypoxia causes an increase in pulmonary vas-cular resistance, hyperoxia at 3 atmospheres absolute (A A) ac-tually reduces pulmonary vascular resistance (McMahon et al.,2002). It has been pointed out that the warm, comfortable envi-ronment in the laboratory setting does not accurately representconditions in the eld. Tis has led to application of monitor-ing techniques previously available only in the lab to the moun-tain environment with often spectacular results (Scherrer et al.,1996; Maggiorini, 2006). Ear oximetry under eld conditionshas revealed evidence of exceptionally low hemoglobin-oxygensaturations (Hackett and Roach, 1987) (see Fig. 1). End-tidalPCO2 measurements atop Mount Everest revealed values lowerthan expected from the laboratory environment (Sutton et al.,

1988; Malconian et al., 1993). More recently, arterial blooanalysis has been obtained from climbers very close to thmit of Mount Everest, with yet different values (Grocott 2009). Of course, arterial and mixed venous blood gas analysresents only surrogate measurements of processes at the lthe cell (see Fig. 2). We have learned from near infrared ation that there is variability in the response of tissue to theof changes that occur during altitude exposure. For exaHampson and Piantadosi (1990) observed measurable chin cytochrome a,a 3 redox level in the brain during manipution of arterial PCO2. During hypocapnia cytochrome a,a 3 re-dox in the brain moves towards a reduced state, presumdue to a reduction in cerebral blood ow and oxygen deli At the same time, only minimal changes occur in musclFig. 3). Tis may explain how the profound hypocapnia occurs during high altitude exposure may adversely affecoxygenation while muscle oxygenation is maintained with

ceptable limits. As yet, estimates of tissue oxygenationneedle electrodes or near infrared optical techniques havlimited eld use. Te clinical conditions associated with prolonged hyphave been well described from eld observations. Acute mtain sickness (AMS) consists of nausea, headache, and m While this disorder is poorly understood, the time courits spontaneous resolution even when hypoxia is maint(Sampson and Kobrick, 1980) and development of approprophylactic measures have also been developed from obtions in the eld. Headache and progressive encephalopare the hallmarks of high altitude cerebral edema (HACE which, despite its name, there is scant evidence for sign

cerebral edema (see below).High altitude pulmonary edema (HAPE) is a conditiogenerally healthy people, which became well-known duriIndia-China border con ict of 1962, where the incidencHAPE was noted to be 13-15% among Indian army rectransported rapidly from sea level to altitudes above 3,3(Menon, 1965; Singh et al., 1965). Te condition was initibelieved to be due to acute left heart failure induced by hya hypothesis that was quickly dismissed by right heart catization measurements. Pulmonary artery wedge pressure tients affl icted with HAPE was shown to be normal, alth

FIGURE 1. Ear oximeter in a sleep study of a climber at 4,400 mon Mt. McKinley. When he attempted to climb to a higher altitudehe developed severe AMS. Te severe degree of his hypoxemia mayhave been explained by a negligible increase in ventilation whenexposed to hypoxia (absent hypoxic ventilatory response). Re-drawn from Hackett and Roach (1987), with permission.

FIGURE 2. Oxygen transport cascade from atmosphere to michondrion. From Moon and Camporesi (2004), with permission


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than low altitude US residents, yet during hypoxia theblood ow is twice as high (Erzurum et al., 2007).

DIVING PHYSIOLOGY AND MEDICINE

As in altitude physiology, high pressure physioloas a result of the adverse effects of large numbers and tunnel workers during and after exposure to comair. Musculoskeletal and neurological syndromes occudecompression from high pressure were initially not uand not treatable. In 1878, Bert (1978) provided the as to pathophysiology by demonstrating that decompanimals after a hyperbaric exposure produced bubbblood, and that administration of oxygen would reso We now know that bubble formation in tissues can ocviade novo formation of bubblesin situ due to supersaturatof inert gas (usually N2 or He) in tissue or due to pulmobarotrauma during decompression. reatment of so-ca

compression illness (DCI) was developed entirely eon the basis of men experiencing relief of symptomsentering the compressed air environment during a fshift. Tis was eventually systematized by Ernest Moigineer, who instituted regular recompression for affl working in the Hudson River tunnel project in New YMoirs approach of recompression using air reduced rate from 25% per annum to 2 deaths of 120 men at wmonths (1.3%) (Moir, 1896). Tis therapeutic success lowed by successful strategies to prevent compressedin which staged decompression was proposed by Boy(1908).

While it is generally agreed that bubbles are the iof decompression illness, little is known about the doevents that produce decompression sickness. One mfor which there is some evidence is related to bubbledamage to the endothelium. Once believed to be noththan the lining of blood vessels, the endothelium is nostood to play a major role in maintenance of uid homand regulation of vascular tone. In the endotheliumzyme nitric-oxide synthase catalyzes the reaction of oL-arginine to produce nitric oxide (NO) and citrullinoxide can then diffuse into the bloodstream where it cadhesion of platelets and leucocytes. It can also diffuadjacent smooth muscle cell. Tere, it activates the enzynylyl cyclase, which facilitates the conversion of G PGMP (cGMP). Tis initiates a series of reactions that relaxation of vascular smooth muscle. Tis mechanism the effect of agonists that interact with receptors on tthelium cell, such as catecholamines. It has been demthat vascular bubbles can injure the endothelium and rvasoactive effects of compounds such as substance Ptylcholine (Nossum et al., 1999). Nitric oxide producbe up-regulated by exercise. Indeed, studies in animalet al., 2004) and humans (Dujic et al., 2004) have ppreliminary evidence that appropriately timed exercis

pulmonary artery pressure was high (Fred et al., 1962; Hultgrenet al., 1964). Tis provided a clue, since the previously described in-crease in pulmonary artery pressure with hypoxia (hypoxic pul-monary vasoconstriction, HPV) tends to be greater in peoplesusceptible to HAPE (Hultgren et al., 1971). Furthermore,reducing PA pressure with vasodilators can prevent and treatHAPE (Scherrer et al., 1996; Maggiorini et al., 2006; Anand,1998). Observations using the balloon occlusion method toestimate pulmonary capillary pressure have further implicatedhigh intravascular pressure as a cause of HAPE (Maggiorini etal., 2001). A genetic predisposition to HAPE has been suggest-ed by evidence implicating polymorphisms of the eNOS gene(Dehnert et al., 2007).

While the mechanisms of HPV are incompletely under-stood, recent advances have been based upon molecular evi-dence implicating nitric oxide as a mediator. Observations byMcMahon et al. (2002) have demonstrated the relationshipbetween blood PO2 and S-nitrosohemoglobin. In low PO2 situ-ations, NO is released from its binding to reactive thiols (Cys

93) of hemoglobin. A genetic factor is suggested by racial dif-ferences in the degree of HPV. Te rise in pulmonary arterypressure in response to hypoxia is greatest in North Americans,somewhat attenuated in South Americans, and signi cantly lessin ibetans, a population adapted to high altitude (Groves etal., 1993). Recently it has been observed that ibetans have asigni cant higher concentration of nitroso proteins in the blood

FIGURE 3. Muscle and brain redox as a function of PCO2. Duringhypocapnia cytochrome a,a 3 redox in the brain becomes more re-duced, presumably due to reduced cerebral blood ow and oxygendelivery. Hypocapnia induces only minimal changes in muscle.Redrawn from Hampson and Piantadosi (1990), with permission.


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a decompression stress may reduce the number of intravascularbubbles. Similarly, administration of nitroglycerine to animalsprior to decompression stress can reduce venous gas embolism(Mllerlkken et al., 2006). Whether either of these interven-tions will reduce decompression sickness in humans remains tobe investigated.

FROM BODY TO MOLECULE:ORTHOSTATIC INTOLERANCE AFTER

SPACE FLIGHT

Orthostatic intolerance is commonly experienced afterspace ight (Buckey et al., 1996). Tis was initially believedto be mostly caused by relative hypovolemia induced in spaceby diuresis due to central translocation of blood from the ex-tremities (Blomqvist and Stone, 1983). If this were the solemechanism the syndrome should be preventable by volumeloading prior to re-entry and landing. However, evidence hasaccumulated suggesting impaired vasoconstrictive response tostanding (Buckey et al., 1996). Using a rat model designed tosimulate weightlessness (hind limb unloading with head downposition) impairment of the arterial vasoconstrictor response tonorepinephrine was observed (Delp et al., 1993; Purdy et al.,1998). Another possible mechanism involves up-regulation ofeNOS (Nyhan et al., 2002). Such observations not only pro-vide a more complete understanding of the problem, but willundoubtedly lead to more effective pharmacological or physi-ological countermeasures.

STEADY STATE MEASUREMENTS:

BLINDERS ON While advanced technology is facilitating increasingly so-phisticated measurements in environmental physiology, ourunderstanding is thus far largely built on steady state measure-ments. However, signi cant transients can be missed by steadystate techniques. For example, in primary pulmonary hyperten-sion, indwelling pulmonary artery catheters have shown thatmean pulmonary artery pressure and pulmonary vascular resis-tance may change substantially from hour to hour (Rich et al.,1985). Similarly, during acute immersion in cold water, quitelarge transient changes occur in both systemic and pulmonaryartery pressure (Wester et al., 2009). Another example is nor-

mal pressure hydrocephalus, a condition consisting of gait dis-turbance, cognitive decline and incontinence. In this conditionenlarged ventricles suggest that intracranial pressure (ICP) is el-evated. Static measurements of ICP in this condition are usuallynormal, however long term observations of intracranial pressurein these patients reveal cyclical variations, with periodic eleva-tions to high levels (McGirt et al., 2005).

Te pathophysiology of high altitude headache is un-known, but the possibility has been raised that it may be dueto increased intracranial pressure, although with some contrary

evidence. For example, a study in which normal volunbreathed 12% oxygen for 18 hours induced either severe ache or clinical acute mountain sickness (AMS) (Bailey2006). However, there was neither MRI evidence of brainma nor elevation of lumbar CSF pressure. Te possibilitytransients may be important has been suggested by a remaeld study, in which ICP was directly measured in three subduring an expedition to Hagshu Peak in the Himalayas tude 6,330 m) (Wilson and Milledge, 2008). While undering conditions CSF pressure was normal, intermittent preelevations occurred in two of three subjects studied. Of three subjects the only one to develop headaches was a sin whom elevated CSF pressure was observed.

SUMMARY

Measurements at the level of the whole organism prfundamental observations and remain the bedrock of ou

scriptions of environmental physiology. Whole human oimal studies should provide the impetus to look beyondoriginal observations into the cellular and molecular mnisms. By so doing, we may gain an understanding of nophenomena of immediate interest, but of physiology in geFurther advances will require widening of the scope of re(traditionally based on steady state methods) to include niques that can detect and measure transients. By implemea wider array of investigative techniques to include tranphenomena and cellular and molecular methodologies, a cunderstanding might be obtained of hitherto elusive phenena such as high altitude pulmonary edema and decompresickness.

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Blomqvist, C.G., and H.L. Stone. 1983. Cardiovascular adjustments to gtional stress. In Shepher, J. ., and F.M. Abboud, eds.Te CardiovascularSystem. Bethesda, MD: American Physiological Society. pp. 10251

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Hackett, P.H., and R.C. Roach. 1987. Medical therapy of altitude i llness. Annals

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Maggiorini, M., C. Melot, S. Pierre, F. Pfeiffer, I. Greve, C. Sartori, M. Lepori,M. Hauser, U. Scherrer, and R. Naeije. 2001. High-altitude pulmonaryedema is initially caused by an increase in capillary pressure.Circulation103:20782083.

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Bartsch, and H. Mairbaurl. 2006. Both tadala l and dexamethasone mayreduce the incidence of high-altitude pulmonary edema: a randomizedtrial. Annals of Internal Medicine 145:497506.

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INTRODUCTION

Decompression Illness (DCI) is a complex condition that can appearvariety of signs and symptoms. Any signi cant organic or functiment in individuals who have been exposed to a reduction in envpressure must be considered as possibly being DCI until proven otherwiseto acute, sub-acute and chronic changes related to decompression and mayacute clinical symptoms or to situations that may develop subclinically anIt is in fact generally accepted that subclinical forms of DCI, with little osymptoms, may cause changes in the bones, the central nervous system a(Kelemen, 1983; Shinoda et al., 1997; Wilmshurst and Ross, 1998).

Generally, a disorder is a physical derangement, frequently slight and nature. A disease is considered a condition of an organ, part, structure, or body in which there is abnormal function resulting from genetic predispoor environmental factors. A disease is typically a more serious, active, pdeep-rooted condition. DCI should be considered a disorder due to a physcause that can transform into a disease unless adequate and timely action ito abort or to minimize the pathophysiological effects of bubbles on the b Te predominant physical cause of DCI is the separation of gas in thesues, due to inadequate decompression, leading to an excessive degree saturation (Kumar et al., 1990). Rapid decompression (rate of ascent or decompression stops) is a primary cause of gas separation in tissues (Figu Te most obvious prevention strategy for DCI is, therefore, determininserving appropriate ascent and decompression procedures (Marroni and Za

ABS RAC. Decompression Illness (DCI), Decompression Sickness (DCS), Dysbaridisorder, syndrome are terms associated with the clinical signs or symptoms origina

a reduction of absolute pressure surrounding the patient. For 100 years the de nitioease is a matter of disputes or consensi. We understand nowadays that it is not how to cure evident clinical manifestations, but also to reduce or virtually eliminphysical cause for the physiological damages: the gas separation phase from saturationary or circulating bubbles. o achieve this goal, research is more oriented on the procedures or the diver pre-conditioning (heat exposure, physical activity, whole antioxidant medication, oxygen breathing, hyperbaric oxygen therapy, hydration oand post-conditioning (different decompression procedures or models, deep stopfollowed by a deeper one, post exposure hydration, speed of ascent, exercise dusion). Some factors that were believed to be crucial, such as patency of the cardiacor gender, are considered less important than modi ed decompression procedures ttoday with sharper technology.

Haute Ecole Paul Henri Spaak, Environmental andOccupational Physiology Laboratory, 91, Avenue C.Schaller, 1160 Auderghem, Belgium.

An Introduction to Clinical Asof Decompression Illness (D

Costantino Bale


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Marroni et al., 2001). Unfortunately, the recommendations for

decompression are largely empirical and not always reliable. Tisis con rmed by the nding that more than half of the DCI casesmanaged by Divers Alert Network (DAN) worldwide over thepast several years have not been associated with an obvious viola-tion of decompression procedures, dive table or dive computerlimits; they have been unpredictable. Tis has led to a searchfor other contributing factors to the development of DCI, suchas a Patent Foramen Ovale, in an effort to explain the wide varia-tion in individual susceptibility to DCI. Other factors includecomplement activation in the presence of gas bubbles as well as anuncertain relationship between gas bubbles, blood cells, and thecapillary endothelial lining in response to bubble presence anddevelopment of DCI.

Te manifestations of DCI are sometimes trivial and subtle.Tese are likely to be ignored or denied by individual divers,training organizations, and emergency physicians unless theyare made aware of them and offered speci c information on themanifestations of DCI. However, there appears to be growing ev-idence that under-reported, under-estimated and under-treatedsigns and symptoms of DCI may result in permanent organic orfunctional damage so that raising the level of suspicion amongstdivers and physicians alike becomes increasingly important. Although the presence of Doppler-detectable gas bubblesin the blood is not necessarily predictive of clinically evidentDCI, the appearance of DCI in the absence of detectable pul-monary artery and venous bubbles is rare. Tere is even grow-ing experimental and clinical evidence that suggests that asymp-tomatic silent bubbles in the body may be causing cellular andbiological reactions that release secondary potentially damagingbiochemical substances in the blood.

DEFINING DCI

Te previously adopted classi cation criteria, i.e., ype Ior ype II DCS (decompression sickness) and AGE (ArterialGas Embolism), are inadequate in that they presume that the

underlying pathophysiology is fully appreciated. Unfortuthere is great disparity in the application of this classi cof DCI amongst specialists when asked to de ne similar of decompression disorders using this traditional classi cConsequently, a descriptive form of classi cation has appthat uses the common term DCI, followed by a descriof the clinical signs and symptoms and their onset and devment characteristics. Te latter has been considered both muniversally understandable and simpler to teach. It also shmuch higher degree of correlation among specialists descthe same DCI cases. For purposes of clarity and consisDCI refers to disorders of decompression that are clearlto DCS or where the origin or embolized gas cannot be dtively attributed to pulmonary barotrauma. Where the cauarterial embolization is the direct consequence of pulmooverexpansion, the term AGE is used. Epidemiologically, there is universal consensus amoninternational diving medical community that the incid

of DCI is generally very low and that there is no signigender-related susceptibility. Tere is also consensus that nlogical manifestations are by far the most common form oamongst recreational divers. Many yet unknown aspects of DCI are the subject ogoing international studies. Tese include: the relationshiptween gas separation and DCI injury, the relationship betclinical symptoms and the severity of the disease, the relship between initial clinical onset, treatment results, andmanent sequelae, the reason for the large variation in indivsusceptibility to DCI, the lifespan of gas bubbles; and thincidence of DCI.

DCI HISTORY

Boyle (1670) demonstrated that DCI could be produin a reptile by a sudden lowering of atmospheric pressurrst clinical recording of DCI was in compressed-air worriger (1845) reported that two men had suffered very spain in the left arm and another had pain in the knees andshoulder 30 minutes after emerging from a seven-hour expat pressure (the pressure could have ranged between 2.4 anatm). Although not knowing what it was, riger also repothe clinical treatment for DCI as rubbing with spirits of soon relieved this pain in both men and they kept workinthe following days. Pol and Watelle (1854) wrote that theyjusti ed in hoping that a sure and prompt means of relief wbe to recompress immediately, then decompress very care Yet it was only many years later that their advice was hee In 1878, Paul Bert demonstrated that the cause of D was dissolved nitrogen going into gas phase in body tissuthat this bubble formation was responsible for symptomsalso highlighted the existence of silent bubbles in the vblood. He understood that recompression was the key treatof value and that it should be applied promptly. He also oxygen at one atmosphere following very rapid decompr

FIGURE 1. Intravascular bubbles in rodent submaxillary capillar-ies (Courtesy of Divers Alert Network)


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medical personnel), caisson work and tunneling under

P REDISPOSING F ACTORS

Whereas the primary factor causing DCI is undithe reduction in ambient pressure causing a rapid inesaturation of tissues, several factors have been idencan increase an individuals susceptibility to DCI.

E XERCISE

Exercise during exposure to increased ambient (during the bottom phase of the dive) appears to incincidence of DCI. Te probable explanation is that inperfusion during exercise leads to a corresponding iinert gas uptake, which must be subsequently eliminatdecompression. Exercise during ascent has differential effects. D

compression stops, mild exercise appears to be helpfother hand, increased activity during pressure changto increase the DCI risk. At least three mechanisms mexplain this effect:

1. Te formation of gas micronuclei. Rapidly owingespecially in the area of vessel bifurcation, may cof relative negative pressure through a venturi effecules of gas from the surrounding supersaturatemay then diffuse into these foci down a partial-gradient. Te resulting localized collections of smabers of gas molecules called micronuclei are thouas a nidus for further bubble growth formation;

2. Increased local CO2 production by exercising musclplay a role since CO2 is a highly diffusible gas thatcontribute to the formation of gas micronuclei. Evincreases in FiCO2 seem to increase the incidence ofTe mechanism of this effect is not clearly understo

3. Increases in core body temperature due to increasactivity may reduce the solubility of gas in bodleading to bubble formation.

However, very recent research results are question

of these assumptions regarding exercise and diving, ilar that of exercise prior to diving. Te latter appears DCI incidence depending on when the exercise is peTe explanation of these ndings is still hypothetical, anitrous oxide seems to be protective when it is proan increase in physical exercise 20 hours before divinand Brubakk, 2001; Wisloff et al., 2003; Dujic et a Wisloff et al., 2004). Tere is an association between rcal musculoskeletal injuries and an increased incidenat or near the site of the injury. Te mechanism respfor this phenomenon is unclear. Changes in local perfincreased gas micronuclei formation in injured tissue lated mechanisms.

and observed that cardiopulmonary symptoms, but not spinalcord paralysis, could be relieved by normobaric oxygen breath-ing (Bert et al., 1943). Moir (1896) published his work on the 1889 excavationsof the Hudson River tunnel. Facing a tragic fatality rate of 25%of the employed workers due to DCI, he installed a recompres-sion chamber at the work site. Following this intervention there were only a further two deaths out of 120 men employed overthe following 15 months. Moir wrote:

With a view to remedying the state of things an air compartmentlike a boiler was made in which the men could be treated homeo-pathically, or reimmersed in compressed air. It was erected nearthe top of the shaft, and when a man was overcome or paralyzed,as I have seen them often, completely unconscious and unable touse their limbs, they were carried into the compartment and theair pressure raised to about 1/2 or 2/3 of that in which they hadbeen working, with immediate improvement. Te pressure wasthen lowered at the very slow rate of one pound per minute or

even less. Te time allowed for equalization being from 25 to 30minutes, and even in severe cases the men went away quite cured.

Unknowingly, Moir was recording both the means of pre-vention and treatment of DCI. Variations of his techniques,now called surface decompression, are currently still used. Even though few subsequent publications appeared on re-compression treatment for the next 30 years, it was the widelyaccepted notion that, to be effective, recompression shouldcommence promptly followed by slow decompression. Teseprinciples remain in effect to this day even though the pres-sures used, breathing gases applied, and rates of decompressionobserved, have undergone much modi cation.

ETIOLOGY ANDPATHOPHYSIOLOGY OF DCI

DCI is a disease with protean clinical manifestations. It fol-lows the appearance of gas bubbles produced by the excessivelyrapid lowering of ambient pressure. Tis reduction enables inertgas dissolved in tissue to enter the gas phase causing the forma-tion of gas bubbles in tissues and body uids. Te clinical syndrome is known by a multitude of namesincluding decompression sickness, DCI, decompression injury,caisson disease, bends, chokes, staggers, dysbarism and gas bub-ble injury. Although arterial gas embolism is usually associated with pulmonary barotraumas, decompression bubbles can alsolead to embolization if there is shunting between the venousdrainage and systemic circulation (e.g., intracardiac and intra-pulmonary shunting). Tis blurs the boundaries between de-compression sickness and arterial gas embolism, which is whythe term DCI was created. Many languages do not differentiatebetween sickness and illness so that the terms dysbarism,dysbaric illness, or dysbaric injury have become equivalentterms for DCI. Clinical settings of DCI include diving, aviation,hyperbaric oxygen therapy (i.e., nurses, chamber assistants, and


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COLD W ATER

Diving in cold water tends to increase the incidence ofDCI. Inert gas uptake is generally not affected because the ex-ercising diver is usually warm and has increased tissue perfu-sion due to exercise (Martini et al., 1989; Gerriets et al., 2000).However, as the diver cools during the dive and at the safety ordecompression stops, the divers tissues experience a reductionin blood ow due to the cold and an increase in solubility tendsto retain more gas. As the diver rewarms after the dive, the ex-cess gas may be released as bubbles.

A GE

Advancing age increases the incidence of DCI for reasonsthat are not yet clearly known but may be related to the re-duction in pulmonary function or the reduction of tissuemicrovascularization.

DEHYDRATION

Dehydration was reported as a factor that increases the riskof DCI during studies on aviators during World War II. Temechanism is again unclear. Changes in the surface tension inserum favoring bubble formation have been postulated. Anec-dotal reports suggest that prior alcohol ingestion increases theincidence of DCI, possibly through this mechanism. Some re-cent papers add insight on the mechanism and advocate new ap-proaches, considering hydration of the tissues more importantthan plasmatic volume or surface tension (Gempp et al., 2009).

F ATIGUE

As with alcohol, there is anecdotal evidence suggesting thatsigni cant fatigue preceding a dive increases the incidence ofDCI. It is uncertain whether the fatigue is a subtle indicator ofsome unidenti ed biochemical factor or a non-speci c warningof general hemodynamic factors.

PATHOGENESIS OF DCI

V ASCULAR O BSTRUCTION

Vascular obstruction by bubbles or bubble-formed com-plexes may occur in the systemic or pulmonary circulation, amost important element in the pathogenesis of DCI. Vascularobstruction may occur as bubbles enter the circulation fromsupersaturated tissues and slow down venous return or due toembolization of vascular beds by bubbles formed elsewhere.Such disturbances may be clinically invisible in non-critical ar-eas such as fatty tissue, but may be life-threatening in criticalorgans such as the central nervous system and heart. Diffuse peripheral vascular obstruction and stasis with re-sultant tissue hypoxia or anoxia may lead to metabolic acidosis

and hypovolemia due to increased capillary permeabilitydosis and hypovolemia may considerably impair cardiovafunction. Vascular obstruction of pulmonary capillariesondary to embolization of bubbles or bubble-formed compin venous blood, results in increased pulmonary vasculartance, bronchiolar constriction and peribronchiolar oedTese changes may lead to alterations in ventilation-perfuratios with resultant arterial hypoxemia, a condition callechokes.

BLOOD -BUBBLE INTERACTIONS : C OAGULATION

Much attention has been devoted to the possible coquences of blood-bubble interaction. Bubbles are thougbe capable of activating Hageman Factor (Factor XII) witivation of coagulation, contributing to vascular obstrucBubbles constitute a foreign element in the blood and acthe complement and coagulation cascades. Tey may even c

denaturation of lipoproteins with the release of large tities of lipid. Electron-micrographic studies in animalsshown vascular obstruction by a complex that appears composed of a gas bubble surrounded by a layer of lip which platelets are agglutinated. Tis and similar observahave given rise to a variety of experimental work investiinter alia the possible usefulness of anticoagulants in DCIdate there is no rm experimental evidence to indicate thatseminated intravascular coagulation occurs in DCI, norroutine anti-coagulation is therapeutically useful. Enhacoagulation at local sites in tissue, however, may contribthe pathogenesis of DCI. Coagulation Factor XIIa is, howcapable of triggering the reaction of the complement syTe sequence of reactions of this system produces factorsincrease capillary permeability and factors that are chemtic to leukocytes. Factor XIIa is also capable of activatiKinin-Bradykinin System with liberation of bradykininhistamine. Bradykinin may cause local pain. Both are caof increasing capillary permeability.

LOCAL VERSUS V ASCULAR B UBBLES

Tere is little reason to doubt that the localized pain i joint is the result of local gas formation. Webb et al. (11944b) and Ferris and Engel (1951) showed that gas couseen in periarticular and perivascular tissue spaces. Teydemonstrated a correlation between the presence of gas anoccurrence of localized pain. Te effectiveness of local prin relieving such pain, such as by in ating a blood-pressureadds legitimacy to the hypothesis. Importantly, DCI oftecurs simultaneously in several sites and limb pain may dphysicians from more sinister neurological abnormalitiesure 2).

While bubbles within tissues are clearly a cause forcern, signi cant numbers of venous gas emboli may be rec without any clinical manifestations. In fact, precordial Do


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the lungs is large, the ltering capabilities of the lungs will beexceeded and gas will enter the arterial circulation. An increasein pulmonary artery pressure of only about 30% is consideredsuffi cient to cause arterialization of venous gas bubbles

Central nervous system alterations in DCI are believed toresult from multiple mechanisms, including intra- and extra-vascular (tissue) bubbles (Francis et al., 1990). Vascular bubblesdo not seem to be an important pathophysiological feature ofspinal cord DCI. In a group of 10 amateur and 10 professionaldivers, ve of whom had neurological DCI, no changes could beseen (Morild and Mork, 1994). However, the same authors re-ported changes in the endothelial layer of the brain ventricles ina group of divers (Morild and Mork, 1994; Mork et al., 1994).

Brubakk (1994) has entertained the possibility that thismay not so much be evidence of intravascular gas bubbles in thebrain as it may be indicative of an increase in venous pressuredue to venous gas embolism of the lung interfering with venousreturn. Another possible explanation may be gas bubbles in the

spinal uid adhering to the lining of the ventricles and caus-ing changes in the adjacent endothelium. Chryssanthou et al.(1977) has indeed shown that animals exposed to decompres-sion show changes in the integrity of the blood-brain barrierand Broman et al. (1966) has also con rmed that even shortcontact between gas bubbles and endothelium (i.e., 1-2 mins)leads to such changes. Further studies in rabbits have shownthat bubble-endothelium contact causes endothelial damageand progressive reduction of cerebral blood ow and function(Helps and Gorman, 1991).

CLINICAL MANIFESTATIONS OF DCI

Tere is ongoing controversy about the best way to clas-sify decompression disorders. Until 1990, these disorders weredivided into DCS and AGE. DCS was then divided into twobroad categories based on the severity of symptoms and the as-sociated treatment regimens. However, today we recognize thatcertain forms of DCS may be the result of paradoxical or evenfrank AGE. Terefore, in the application of the traditional clas-si cation that follows, a modi er (DCS or DCI) is added to in-dicate where such pathophysiological ambiguity exists. Certainmanifestations of decompression disorders are known never tobe associated with arterial gas embolism and therefore can con-dently be classi ed as decompression sickness. Tese includelimb bends and lymphatic DCS. ime of symptom onset in cases (all manifestations):

50% occur within 30 minutes of surfacing; 85% occur within 1 hour of surfacing; 95% occur within 3 hours of surfacing; 1% are delayed more than 12 hours; and, Some symptoms have been reported to begin as late

as 24 hours and more after surfacing and even longerif there is subsequent altitude exposure (e.g., ying ormountaineering).

1. TYPE I

P AIN O NLY - DCS

In recreational compressed-air diving the upper extremare involved three times more often than the lower limbs

is reversed for caisson workers and in commercial satudiving. Te pain can range from slight discomfort to a ddeep, boring or even unbearable pain. It is usually unaffecmovement of the joint and there may be overlying edemregional numbness.

LYMPHATIC M ANIFESTATIONS - DCS

Te lymphatic manifestations of DCS presumably refrom obstruction of lymphatics by bubbles. Te manifestatcan include pain and swelling of lymph nodes, with lyedema of the tissues drained by the obstructed lymph nNew data are suggesting that normobaric oxygen may imthe ow of lymph and may assist in resolving inert gas bucontained within the lymphatic system or even to removetiny micronuclei that can behave like proteins and thus betured by the lymphatics (Balestra et al., 2004). Oxygen prditioning is a known factor to reduce venous gas emboldiving, which may be explained by micronuclei eliminatthe lymphatic system. Some recent results show a reductpost-diving bubble grades after a known boosting of lymcaptation by whole body vibration (Figure 3); more evideneeded to asses the hypothesis

C UTANEOUS M ANIFESTATIONS - DCI

Itching is common following decompression fromchamber dives where the skin is in direct contact with the cber atmosphere rather than with water. Tis condition, somtimes called divers lice, is thought to be the result of gsolving directly into the skin and causing cutaneous irritand the release of histamines with subsequent itchiness decompression. Tis is not a true or systemic form of DCIdoes not require recompression. On the other hand, itchof the skin following a dive in which the skin was wet, islikely to be true cutaneous DCI. Note that some in-water are performed in drysuits. Under these conditions the skindirect contact with compressed gas and divers lice m

pear. However, this is usually accompanied by some degskin rash or visible skin change. Cutis marmorata is a form of DCI which is thought to rsult from a complex interaction between bubbles, venousgestion and the immune system. It usually manifests itsbluish-red blotches, frequently affecting the upper bacchest. Prominent linear purple markings are also frequentserved. Tese manifestations are a systemic form of DCIsuggest signi cant bubble formation that may also be affeother areas of the body. As a result, prompt recompress


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BALES RA: CLINICAL ASPEC S OF DCI 23

recommended, which usually leads to prompt resolution. Tissign frequently heralds more serious forms of DCI and there isa statistical association with PFO even if the physiopathologicallink is currently not fully understood.

2. TYPE II DCI

P ULMONARY DCI

Tis is a syndrome usually presenting with a triad of symptoms:

a) Substernal pain that usually burns and progressively in-creases. Initially, the pain may be noted only when cough-ing or with deep inspiration. Over time the pain may be-come constant;

b) Cough that is initially intermittent and provoked by ciga-rette smoking (Behnkes sign). Paroxysms of coughing maybecome intractable; and,

c) Progressive respiratory and dyspnea.

Te manifestations of pulmonary DCI are believed to re-sult from the combined effects of gas emboli in the pulmonaryartery and obstruction of the vascular supply to the bronchialmucosa. Untreated pulmonary DCI may be fatal.

NEUROLOGICAL DCI

Although the exact mechanisms of neurological DCI arenot fully understood, they are believed to include embolism, au-tochthonous (i.e., spontaneous interstitial bubble formation),venous stasis and immunological phenomena. Tese mecha-nisms have different latencies and show different responses to

recompression. Te neurological manifestations of Dtherefore unpredictable, and any focal neurological or sign may be a manifestation of its presence. Any neabnormality following a dive should always be assumcentral origin and treated accordingly.

C EREBRAL DCI

Brain involvement in DCI appears to be especiamon in high altitude aviators (i.e., ying in excess of 25in unpressurized aircraft). In this group pulmonary veembolism is also common and hypoxia and positivebreathing may facilitate the transfer of bubbles or immcal products into the systemic circulation. Not surprmigraine-like headache accompanied by visual distua common manifestation of DCI. In divers, brain invusually presents more overtly with stroke-like symptlapse with unconsciousness is a rare presentation of

common in AGE. If it does occur, it represents a very gof DCI.

S PINAL C ORD DCI

Paraplegia is a classic symptom of DCI in dclearly represents spinal cord involvement. Bladder with urinary retention and fecal incontinence frequcompany such paraplegia. Recent years have seen a both the proportion and absolute number of cases oparalysis in recreational divers (from 13.4 percent inonly 2.9 percent in 1997). Similarly, loss of conscioudropped from 7.4 percent to 3.9 percent during the saod. Te incidence of loss of bladder function has dropp2.2 percent to 0.4 percent during this period (DAN Dicident Reports). Interestingly, the reduction in severlogical symptoms has not been balanced by a proportin pain-only or skin manifestations. Rather, there hasunexpected appearance of mild, ambiguous neurologifestations, such as paresthesia or tingling, which appspond well to oxygen administration and recompressi

INNER E AR DCI

Audiovestibular DCI is a not an uncommon maniof CNS involvement. Usually both the cochlea and vapparatus are involved and the presenting symptomtinnitus, deafness, vertigo, nausea, vomiting, and atatagmus may be present on physical examination. It is whether the situation depends predominantly on bubmation in the perilymph or is due to embolization of tory vestibular Inner ear DCI is a serious medical eand must be treated immediately to avoid permanentSince the nutrient arteries of the inner ear are very smreduction in bubble diameter, with immediate 100%

FIGURE 3. Bubble score after 30 min. of whole-body vibrationpreconditioning 2 hours before the dive (25 m/25 min), n = 6.


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administration and prompt recompression is essential.

S HOCK - DCI

Shock occasionally occurs in DCI and is usually associ-ated with serious pulmonary manifestations indicating a hyper-acute form of DCI. Multiple mechanisms may contribute tothe pathogenesis of shock in DCI, including loss of vasculartone from spinal cord involvement, myocordial depression fromhypoxemia and acidosis, pulmonary embolization, and hypovo-lemia due to increased capillary permeability resulting in loss ofplasma water and hemoconcentration.

B ACK , ABDOMINAL , OR C HEST P AIN - DCI

Pain in these areas, in contrast to limb pain, should be con-sidered with great attention, as it frequently represents spinalcord involvement.

E XTREME F ATIGUE - DCI

Fatigue, out of proportion from that normally occurringafter a dive, has long been regarded as a serious manifestation ofDCI. However, the biochemical and pathophysiological mecha-nism of this symptom are unknown.

NEW DCI CLASSIFICATION

Te simple classi cation into ype I and ype II DCI im-plies that the different categories are well de ned disease entitiesand that there is reasonable agreement about the classi cation(Brubakk, 1994; Brubakk and Eftedal, 2001).

However, two separate studies (Kemper et al., 1992; Smithet al., 1992), showed considerable uncertainty between expertsusing the classical classi cation system. For instance, cerebral

DCI could not in many cases be distinguished from arteriembolism or vestibular barotrauma. Other studies have sthat solely articular symptoms are rare, as they are usuacompanied by central nervous system symptoms (Vann 1993; Freiberger et al., 2002). Extreme fatigue can be claas a minor symptom, but could also be a sign of subclipulmonary embolism (Hallenbeck et al., 1975). FrancisSmith (1991) therefore suggested the currently widely adterm DCI, to include the two previously used de nitiondecompression sickness and arterial gas embolism. Teysuggested avoidance of the classi cations of ype I and yp while adopting instead a descriptive classi cation methocording to the clinical manifestations (signs and/or sympand their evolution in time. Using this classi cation schemvery high degree of concordance between different spec was possible (Pollard et al., 1995). Francis and Smith (proposed the following Classi cation able for DecompresInjuries ( able 2), which is a useful guideline to correctly

scribe the various possible manifestations of a decomprdisorder.

DCI TREATMENT

Air was nearly always used as the breathing gas and otreatment was not really explored until Yarbrough and Beh(1939) preliminary experiments. Te early treatment the was conceptually homeopathic in trying to decide how detake the injured diver. Te original depth of the dive was uas a guide. For example, if decompression from a depthmeters caused the symptoms, recompression to the samesure should alleviate them. However, there were controvas others thought that the situation of the diver should the decision and that the depth of relief should mark thetial treatment pressure. Still others argued that bubbles mcompressed but never disappear and should always be as

ABLE 2. Classi cation of DCI symptoms.

DEFINI ION ABRUP EVOLVING S AICONSE IME IMMEDIA E FIRS DAY DAYS O YEARS PAINFUL Limb bend: Limb Bend: uctuating Osteonecrosis Periarticular pain pain after dive

PARES HE IC ingling or numbness, ingling or numbness, Recurrent or episodic afte may herald spinal DCI may be combined with pain treatment; probably be

ASYMP OMAIC Skin changes or painless Skin changes or painless Asymptomatic osteo swelling swelling CEREBRAL Loss of consciousness, Hemiparesis, delirium, Chronic neuropsych hemiplegia, air embolism brainstem signs, vertigo changes SPINAL Girdle pain, loss of leg Waxing and waning weakness, Chronic gait and bla

movement and bladder control bladder dysfunction, sensory disturbances levels CEREBRO-SPINAL Unconscious diver with Combined spinal and Combined cerebral a

spinal ndings cerebral signs, varying disability; spinal predom SYS EMIC Chokes; acute systemic Fatigue, rare visceral DCI Rare cases of ARDS respiratory collapse

proceedings haldane

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