Open Collections

UBC Theses and Dissertations

UBC Theses Logo

UBC Theses and Dissertations

The contribution of elevated peripheral tissue temperature to venous gas emboli (VGE) formation 1988

You don't seem to have a PDF reader installed, try download the pdf

Item Metadata

Download

Media
UBC_1988_A7_5 P64.pdf [ 4.66MB ]
Metadata
JSON: 1.0077397.json
JSON-LD: 1.0077397+ld.json
RDF/XML (Pretty): 1.0077397.xml
RDF/JSON: 1.0077397+rdf.json
Turtle: 1.0077397+rdf-turtle.txt
N-Triples: 1.0077397+rdf-ntriples.txt
Citation
1.0077397.ris

Full Text

THE CONTRIBUTION OF ELEVATED PERIPHERAL TISSUE TEMPERATURE TO VENOUS GAS EMBOLI (VGE) FORMATION By NEAL WILLIAM POLLOCK B.Sc, The University of Alberta, 1983 A THESIS SUBMITTED IN PARTIAL FULFILMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF PHYSICAL EDUCATION in THE FACULTY OF GRADUATE STUDIES School of Physical Education and Recreation, Exercise Physiology We accept t h i s thesis as conforming to the required standard \ THE UNIVERSITY OF BRITISH COLUMBIA October 1988 ® Neal William Pollock, 1988 In presenting this thesis in partial fulfilment of the requirements for an advanced degree at the University of British Columbia, I agree that the Library shall make it freely available for reference and study. I further agree that permission for extensive copying of this thesis for scholarly purposes may be granted by the head of my department or by his or her representatives. It is understood that copying or publication of this thesis for financial gain shall not be allowed without my written permission. ~ ^ , P h y s i c a l E d u c Department of The University of British Columbia 1956 Main Mall Vancouver, Canada V6T 1Y3 Date 1 9 8 8 O c t o b e r 14 DE-6G/81) i i The Contribution of Elevated Peripheral Tissue Temperature To Venous Gas Emboli (VGE) Formation Abstract This purpose of t h i s study was to evaluate the contribution of post-dive peripheral t i s s u e warming to the production of venous gas emboli (VGE) i n divers. Inert gas elimination from the tissues i s l i m i t e d by both perfusion and d i f f u s i o n . I f changes i n d i f f u s i o n are matched by corresponding perfusion (vasoactive) changes, decompression should be asymptomatic (within allowable exposure l i m i t s ) . Under conditions when the d i f f u s i o n of in e r t gas from the t i s s u e s i s not matched by blood perfusion, VGE w i l l ensue. Increasing t i s s u e temperature w i l l decrease i n e r t gas s o l u b i l i t y and thus d i f f u s i o n into the blood. I t has been demonstrated that problems may a r i s e during rapid changes i n peripheral temperature, as often occurs post-dive, when divers previously exposed to cold water a c t i v e l y rewarm themselves i n showers or baths. The e f f e c t of moderate rewarming, however, may be to increase the rate of i n e r t gas elimination without the formation of VGE since increased perfusion i s encouraged. The e f f e c t of mild post-dive warming was investigated. Ten male subjects, between the ages of 21 and 29 years i i i completed two dry chamber dives to 70 feet f o r 35 minutes (no decompression l i m i t of the Canadian Forces A i r Diving t a b l e s ) . Each dive was followed by a 30 minute head-out immersion i n eith e r a thermoneutral (28°C) or warm (38°C) bath. Non-invasive Doppler ul t r a s o n i c monitoring was then carried out at 30 minute i n t e r v a l s for the next 150 minutes to assess measurable VGE. Subjects did not display VGE formation i n either the control or experimental conditions. Our findings suggest that: 1) the Canadian Forces table l i m i t s (for the p r o f i l e employed) provide safe no-decompression l i m i t s not compromised by mild post-dive warming, and 2) mild peripheral warming, since not bubble generating, may be a useful adjunctive therapy i n the management of decompression sickness by increasing the rate of i n e r t gas elimination. The Contribution Of Elevated Peripheral Tissue Temperature To Venous Gas Emboli (VGE) Formation i v Table of Contents Abstract i i Table of Contents i v L i s t of Tables v i Acknowledgements v i i I. Review of Literature v i i i Decompression Sickness.... 1 Introduction 1 H i s t o r i c a l Perspectives 1 Etiology 3 Manifestation 4 Factors A f f e c t i n g S u s c e p t i b i l i t y 8 Decompression Sickness Therapy 16 Recompression 16 Adjunctive Therapies. 17 Conclusions 20 References i 21 Doppler Ultrasound 3 0 Introduction .30 Risks Associated with Doppler Ultrasound 32 Doppler Protocol Development 33 Signal Interpretation 36 Experimental Results Using Doppler Technigues...38 Alternative Methodologies. 43 Conclusions 47 References 48 I I . Laboratory Study 52 Statement of the Problem 53 Introduction. 53 The Problem 55 Hypotheses 55 Significance of the Study 56 Delimitations 58 Limitations 58 Methodology 61 Introduction 61 V Subjects 61 Testing Procedures 62 Testing Protocols 63 Apparatus 64 Data Analysis 65 Results 66 Discussion 68 Conclusions 75 Recommendations 76 References 77 Appendices 80 A. Subject Forms/Information Materials 80 I. Policy of the School of Kinesiology on the Medical Clearance and Supervision of Human Research Subjects 81 I I . Medical Questionnaire (SFU) .84 I I I . Subject Information Package (1) 86 Project Objectives 86 Test Procedures 8 6 Risks and Discomforts 86 Hyperbaric Exposure 86 Water Immersion 87 Safety Precautions 87 Inquiries 87 Freedom of Consent 87 C o n f i d e n t i a l i t y 87 IV. Subject Information Package (2) 88 Risks During Exposure to Hypo/Hyperbaric Conditions 88 Otic Barotrauma 88 Decompression Sickness 88 A r t e r i a l Gas Embolism 91 Hypoxia or Anoxia 92 Drowning 93 Oxygen T o x i c i t y 93 Hypothermia. . . . 94 F i r e Hazards . 94 V. Informed Consent 96 VI. Subject P r e - T r i a l Preparation Information .98 VII. Dive Questionnaire 99 B. Glossary 100 v i L i s t of Tables Table I Anthropometric Charac t e r i s t i c s .67 v i i Acknowledgements I would l i k e to express my sincere appreciation to those who so generously assisted me i n the completion of t h i s t h e s i s . A p a r t i a l l i s t includes my committee members: Drs. Igor Mekjavic, Ted Rhodes and Robert Sparks (chairman) for a l l t h e i r time and e f f o r t , Ron Nishi and h i s co-workers at the Defense and C i v i l I n s t i t u t e of Environmental Medicine for t h e i r analysis of the Doppler tapes, Vic Stobbs and G a v r i l Morariu for t h e i r expert operation of the Simon Fraser University compression chamber, Don Hedges for h i s medical supervision of the experimental dives, Dusan Benicky at the Buchanan Laboratory for h i s patience with my scheduling demands, and, of course, the subjects for t h e i r p a r t i c i p a t i o n . F i n a l l y , my spe c i a l thanks w i l l always go to Lesley Green f o r her boundless support. This study was supported by the Natural Sciences and Engineering Research Council of Canada. Review of Literature 1 Decompression Sickness The e f f e c t of hyperbaric exposure i s complex. A d e b i l i t a t i n g condition that can a r i s e from the decompression following exposure i s decompression sickness (DCS). In fact, i t i s not a single condition, but a diverse syndrome, the expression of which i s variable and capricious. To understand the action of DCS, physical properties of aquatic and hyperbaric environments and human physiology and biophysical parameters must be understood as they int e r a c t with each other. The amount of attention given to t h i s i s great, our understanding somewhat less so. A number of excellent reviews have been completed on the physiology of diving (Lin, 1988), decompression theory (Vann, 1982; Hempleman, 1984), decompression procedures (Hempleman, 1982), pathogenesis and manifestation of decompression disorders ( H i l l s , 1977; Hallenbeck and Andersen, 1982; E l l i o t t and Kindwall, 1982), and the treatment of DCS (Davis and E l l i o t t , 1982; Farmer et a l . , 1984). The goal of the present introduction i s not to supersede these works but to provide background pertinent to the thesis project undertaken. H i s t o r i c a l Perspectives The f i r s t c l i n i c a l observation of decompression induced gas bubbles i s attributed to Robert Boyle (1670) and the f i r s t experimental evidence implicating gas bubbles i n the etiology of DCS to Paul Bert (1878). 2 Generally a t t r i b u t e d to the e f f o r t s of J . S. Haldane, Boycott et a l . (1908) suggested that tissues may be supersaturated to a l i m i t e d degree before symptomatic DCS would develop. Experimenting with goats, they observed that i f the ambient pressure was reduced to no l e s s than one h a l f the saturation pressure, symptoms would not a r i s e . They i d e n t i f i e d a " c r i t i c a l supersaturation r a t i o " of 1.58 to 1. Ostensibly, the body f l u i d s and tissues could t o l e r a t e 1.58 times the nitrogen pressure within them than the absolute pressure on them without complication. This finding formed the foundation upon which Haldane's decompression schedules (tables) were constructed. Haldane's decompression schedules (Boycott et a l . , 1908) portray a somewhat a r b i t r a r y attempt to produce an nitrogen uptake- elimination model representative of the f u l l range of bodily ti s s u e s . Each of f i v e 'compartments' - representing d i f f e r e n t t i s s u e types - has a corresponding 'half-time'. The half-times indicate the period of time reguired for a t i s s u e to gain or lose 50% of the available gas pressure. The compartments are thus i d e n t i f i e d as 5, 10, 20, 40 and 75 minute ti s s u e s . Experience has shown, however, that safe supersaturation r a t i o s can not be so e a s i l y calculated. Success of Haldane's model has proven to be l i m i t e d . In fact, s i g n i f i c a n t l y less pressure reduction than allowed by these decompression schedules have been shown to r e s u l t 3 i n DCS (Rivera, 1964; McLeod, 1986). Another l i m i t a t i o n of early decompression theory involves the rel a t i o n s h i p of developing bubbles to symptoms of DCS. The presumption that the onset of DCS correlates with the development of bubbles has not been born out. Behnke (1942) f i r s t suggested that asymptomatic, or ' s i l e n t bubbles 7, could r e s u l t from decompression events. Although present, they would not necessarily p r e c i p i t a t e symptomatic DCS. This was confirmed with the application of Doppler u l t r a s o n i c technology to diving ( G i l l i s et a l . , 1968; Spencer and Campbell, 1968). C i r c u l a t i n g bubbles were regularly detected p r i o r to the onset and even i n the absence of DCS. Etiology It has been generally accepted that physical bubbling i s responsible for the development of symptomatic DCS. The physiological e f f e c t s of a mechanical obstruction i n the vascular and/or lymphatic systems lead to t i s s u e ischemia. Long term ischemia can r e s u l t i n permanent injury. This i s a reasonable assumption i n view of the circumstantial evidence. Nitrogen i s f i v e times more soluble i n f a t than other tissues (Vernon, 1907; Buhlraann, 1984). This r e s u l t s i n l o c a l i z e d high concentrations of nitrogen i n f a t t y tissues that can present extensive bubble 4 formation upon decompression. An example of such a s i t e i s bone marrow, which becomes progressively more f a t t y with maturity (Ganong, 1985). Regions of high marrow concentration (such as the long bones) commonly display symptomatic problems. Recent work has improved the appreciation of biophysical and b i o l o g i c a l e f f e c t s associated with bubble formation and DCS. E t h i c a l considerations, however, w i l l continue to r e s t r i c t the experimental data c o l l e c t e d . Manifestation A number of c l a s s i f i c a t i o n schemes for the signs and symptoms of DCS can be found i n the l i t e r a t u r e . A b i p a r t i t e system has been used most extensively (Erde, 1975; Edmonds et a l . , 1981; Arthur and Margulies, 1987). Signs and symptoms are divided into Type I ('pain only', mild) and Type II ('serious'). Providing more d e t a i l , signs and symptoms can be grouped into f i v e categories - four primarily acute and one recognized as chronic: 1) Cutaneous Manifestations. Cutaneous manifestations (or 'skin bends') represent the least severe form of DCS. Included are p r u r i t i s (intense i t c h i n g ) , l i v i d i t y (abnormal co l o r a t i o n ) , mottling, blotching, a var i e t y of rashes, l o c a l i z e d swelling, and subcutaneous emphysema (Rivera, 1964). These are considered Type 5 I manifestations under the b i p a r t i t e system, although some of the signs (for example, p r u r i t i s ) are not considered to represent true DCS ( E l l i o t t and Hallenbeck, 1975) . 2) Pain Only. Pain only manifestations are generally referred to as Type I DCS under a l l c l a s s i f i c a t i o n schemes. These usually involve pain located i n t r a - and p e r i - a r t i c u l a r (in and around joints) (Kizer, 1984) . The pain i s t y p i c a l l y described as a deep, d u l l ache, and i s often associated with vague numbness (this i s not to be confused with neurological paresthesia). Movement usually aggravates the discomfort, and recompression causes rapid resolution. Shoulders, elbows and knees are the j o i n t s most commonly affected although the discomfort can be more d i f f u s e . 3) Neurological Disorders. Neurological manifestations are more serious examples of DCS. They are usually referred to as Type II problems, but as such are grouped with other d i s t i n c t manifestations under the b i p a r t i t e system. A vast array of signs and symptoms are possible, ranging from the very minor to completely d e b i l i t a t i n g . The lower thoracic, lumbar, or sacral spinal cord can be affected, producing some degree of p a r a l y s i s and/or paresthesia (Dick and Massey, 1985). A common complication i s urinary retention, i n fact, t h i s i s a strong diagnostic sign (Kizer, 1983). Although the pathophysiology remains unclear (Douglas and Robinson, 1988), the spinal cord i s recognized as remarkably susceptible to acute DCS (Hughes and Eckenhoff, 198 6). 6 Problems are often seen following dives within the conventional exposure l i m i t s (Dick and Massey, 1985). The spinal cord may also be predisposed to chronic damage a r i s i n g from repeated, asymptomatic exposure (Palmer et a l . , 1987). Any of the sensory systems also may be affected (Dick and Massey, 1985; Arthur and Margulies, 1987). Signs and symptoms involving the v i s u a l system may include blurred v i s i o n or nystagmus (uncontrollable, jerky eye movement) . Vestibulocochlear compromise can r e s u l t i n dizziness and/or vertigo (extreme dizziness and di s o r i e n t a t i o n ) , t i n n i t u s (ringing i n the ears), or deafness. Some neurological symptoms may be recognized as global. The best example i s extreme fatigue (Strauss and Prockop, 1973). I t may or may not be associated with other signs and symptoms of DCS. 4) Pulmonary Manifestations. Pulmonary manifestations (commonly c a l l e d the 'chokes') r e s u l t from f a i l i n g e f f o r t s by the pulmonary system to f i l t e r c i r c u l a t i n g bubbles out of the bloodstream. While t h i s f i l t e r i n g i s e f f i c i e n t under normal conditions (Emerson et a l . , 1967; Spencer and Oyama, 1971; H i l l s and Butler, 1981) edema ( f l u i d accumulation) may develop when more than 10% of the pulmonary vascular bed becomes obstructed by bubbles (Kizer, 1983). Responses includes tachypnea (accelerated heart rate), chest pain, non-productive cough, dyspnea ( d i f f i c u l t y breathing), and ultimately signs of c i r c u l a t o r y compromise (eg. 7 d i s t e n t i o n of neck veins) (Greenstein et a l . , 1981). Pulmonary signs and symptoms have been considered Type II manifestations under the b i p a r t i t e system (Arthur and Margulies, 1987) . They have also been l a b e l l e d independently as Type III signs and symptoms (Strauss and Samson, 1986). 5) Dysbaric Osteonecrosis. Dysbaric osteonecrosis represents a chronic DCS disorder, occasionally referred to as a Type IV manifestation (Strauss and Samson, 1986). F i r s t i d e n t i f i e d i n caisson workers i n 1911 (Bassoe, 1911), i t was f i n a l l y reported i n divers i n 1941 (Calder, 1982) . The problem i s one of bone lesions, eith e r on the shaft (medullary, Type B), or associated with j o i n t s ( j u x t a - a r t i c u l a r , Type A) developing some time a f t e r decompression i n s u l t . While shaft lesions can remain r e l a t i v e l y benign, juxta- a r t i c u l a r lesions w i l l progress to a d e b i l i t a t i n g state. A f f l i c t i o n rates, primarily estimated for the commercial diving population, display a remarkable range, from 1.7% (Sphar et a l . , 1977) to 76.6% (Ohta and Matsunaga, 1974), with reports c i t i n g v i r t u a l l y every point i n between (Kawashima, 1976 - 59.5%; Biersner and Hunter, 1983 - 33%; Asahi et a l . , 1968 - 19%; McCallum et a l . , 1976 - 2.7%). Detailed reviews can be found elsewhere (McCallum and Harrison, 1982; Walder, 1984). 8 Factors A f f e c t i n g S u s c e p t i b i l i t y Undoubtedly, the greatest l i m i t a t i o n of any set of decompression tables i s the i n a b i l i t y to assess i n d i v i d u a l v a r i a b i l i t y i n s u s c e p t i b i l i t y to DCS. This i s exemplified by the number of cases where only one diver i n a p a i r becomes symptomatic when both were together for the entire dive, or when an i n d i v i d u a l becomes symptomatic following a p r o f i l e that he or she had completed any number of times previously without complications. An extensive range of factors, both ph y s i o l o g i c a l and environmental, have been found to a f f e c t i n d i v i d u a l s on a day to day and a long term basis. Included are: adiposity, age, dehydration, smoking, r e s t r i c t e d l o c a l c i r c u l a t i o n (possibly caused by previous t i s s u e i n j u r i e s or limb p o s i t i o n i n g ) , exceptional exertion, and exceptional thermal exposures. Many other factors have also been proposed as contributing to increased s u s c e p t i b i l i t y . These include gender and the use of b i r t h control p i l l s . Conversely, some factors have been reported to increase resistance to DCS, such as acclimatization, prophylactic use of a s p i r i n , race, and the use of non-standard decompression schedules. Increased adiposity, usually assessed i n terms of percent body f a t has been correlated to an increased r i s k of developing DCS (Gray, 1951; Dembert et a l . , 1984). Since f a t t y tissues have a greater capacity to absorb nitrogen and are generally more poorly perfused than other tissues, they are susceptible to the formation 9 of bubbles and ultimately decompression ' h i t s ' , due to t h e i r greater loading and r e l a t i v e i n a b i l i t y to o f f load gas during and following decompression. Obesity, defined as being more than 20% above recommended weight, has been suggested as a guideline for r e s t r i c t i n g p a r t i c i p a t i o n i n commercial div i n g a c t i v i t y (Linaweaver, 1984; McCallum and Petrie, 1984). The majority of subjects involved i n experiments to determine safe decompression l i m i t s usually have optimal health and physiologic function. From a researchers point of view, t h i s reduces the number of p o t e n t i a l l y confounding variables to be considered. I t i s often reported that the U.S. Navy decompression schedules are based on the responses of 'young, healthy, male subjects'. Perhaps the c r i t i c a l component of t h i s 'optimality' involves c i r c u l a t o r y performance. As indivi d u a l s move further a f i e l d from t h i s optimum the uptake and elimination of gases can be impaired. Increasing age i s correlated with impaired c i r c u l a t o r y patterns. This may be due to progressive a r t e r i o s c l e r o s i s . Regardless of the mechanism, advancing age does increase i n d i v i d u a l p r e disposition to DCS (Szasz, 1982; Becker and P a r e l l , 1983). Gray (1951) demonstrated a roughly l i n e a r increase between age and s u s c e p t i b i l i t y . Few experimental data are avai l a b l e to confirm t h i s r e l a t i o n s h i p , but i t i s generally recommended that with increasing age, decompression safety w i l l be improved i f additional 10 safety factors are calculated into a l l dive planning, and that t h i s should contraindicate involvement i n commercial types of exposure (Linaweaver, 1984). A recommendation often promoted within the recreational diving community i s that an additional 10 minutes be cut o f f the no-decompression l i m i t s f o r every decade of l i f e beyond 20 years of age. Age i s only one of several conditions a f f e c t i n g c i r c u l a t i o n . Over the short term, dehydration r e s u l t s i n hemoconcentration which e f f e c t s the q u a l i t y of c i r c u l a t i o n . I n s u f f i c i e n t f l u i d intake can r e s u l t from inadequate t h i r s t perception (Manjarrez and B i r r e r , 198 3) or from the concern over discomfort a r i s i n g from increased urination associated with immersion i n water (Epstein, 1978; Shiraki, 1987). Alcohol ingestion w i l l also aggravate body f l u i d l o s s . Any degree of hemoconcentration w i l l aggravate and be aggravated by the bubble development concomitant with DCS (Hallenbeck et a l . , 1973; Bove, 1982), thus aggressive replacement of f l u i d s should be an important concern of a l l divers. Limb positioning can also have important c i r c u l a t o r y a f f e c t s . While not well documented, disruptions i n l o c a l c i r c u l a t i o n may p r e c i p i t a t e DCS. Divers wearing wet or dry s u i t s during decompressed i n a b e l l often display p r u r i t i s at areas where excessive pressure has been applied by the s u i t (Igor Mekjavic, personal communication). Similar problems may be expected i n ind i v i d u a l s s u f f e r i n g l o c a l c i r c u l a t o r y i n s u f f i c i e n c i e s caused by scar t i s s u e from previous i n j u r i e s . I t i s a common pra c t i c e during chamber exposures to encourage divers to move around at regular i n t e r v a l s and to avoid positions that may compromise c i r c u l a t i o n (eg. cross-legged) (Don Hedges, personal communication). Extreme dives, i n terms of excessive exertion or cold can also increase the r i s k of developing DCS. Exertion w i l l increase c i r c u l a t i o n , thus enhancing the uptake of i n e r t gas during the compression or bottom phases of a dive. The greater the uptake, the greater the l i k e l i h o o d that decompression w i l l r e s u l t i n supersaturation r a t i o s high enough to cause bubble formation. Moderate exercise during decompression may a c t u a l l y protect against the development of DCS since increased perfusion w i l l enhance i n e r t gas elimination (Vann, unpublished). However, aggressive exertion during decompression or post-decompression exercise may f a c i l i t a t e the onset of symptomatic DCS through c a v i t a t i o n e f f e c t s of stretching tendons/muscles or simple a g i t a t i o n encouraging bubble evolution (Brown, 1979). A f i n a l concern associated with exertion involves the ro l e of increased C02 l e v e l s . Exercise w i l l enhance the C02 retention already associated with hyperbaric exposure (Anthonisen et a l . , 1976; Dwyer et a l . , 1977; Van Liew and Sponholtz, 1981). Although the rol e , and c e r t a i n l y the mechanism, remain unclear (Hickey et a l . , 1983), C02 retention would appear to encourage DCS (Bell et a l . , 1986). Extremely cold diving exposures complicate pressure e f f e c t s 12 as well. Dunford and Hayward (1981) suggest that cold exposures r e s u l t i n a rapid decrease i n peripheral c i r c u l a t i o n which w i l l lead to decreased i n e r t gas uptake. They compared subjects wearing well i n s u l a t i n g dry-suits with those wearing poorly i n s u l a t i n g 1/8 inch wet s u i t s i n 10°C water. Results from t h e i r study confirmed t h i s e f f e c t under the conditions they created. However, i t i s expected i n r e a l i t y that most divers w i l l wear reasonably appropriate exposure equipment for the s i t u a t i o n s they expect to encounter and w i l l therefore s t a r t t h e i r dives warm and i n a near optimal c i r c u l a t o r y state. This ensures a f a i r l y rapid uptake of i n e r t gas through at least the early compressive phase, which i s t r a d i t i o n a l l y the deepest part of the dive. As the cold s t a r t s to take a f f e c t , however, peripheral c i r c u l a t i o n i s decreased, which subsequently reduces the peripheral tissue's a b i l i t y to eliminate gas during and following compression u n t i l rewarming i s complete. I f t h i s post-dive rewarming i s c a r r i e d out too rapidly, the r e s u l t can be the manifestation of signs and symptoms of DCS i n the peripheral t i s s u e s . This i s demonstrated by post-dive, cold exposed subjects that suffered skin bends following hot showers taken at the end of t h e i r experimental t r i a l s (Mekjavic and Kakitsuba, unpublished). Unfortunately, despite general recommendation to avoid hot post-dive showers (Mebane and Dick, 1985), experimental evidence has not appeared to refute or confirm these postulations. Smoking i s implicated i n predisposing, and perhaps most importantly, i n complicating the e f f e c t s of DCS. I t has been suggested to increase p l a t e l e t adhesiveness and w i l l increase the l i k e l i h o o d of developing gas trapping diseases l i k e emphysema and bronchitis ( S h i l l i n g , 1984). This may r e s u l t i n increased c l o t t i n g a c t i v i t y i n response to a given decompression i n s u l t . While the standard treatment of recompression w i l l mitigate the e f f e c t s of physical bubbles, i t w i l l not e f f e c t e x i s t i n g blood c l o t s . Subsequently, possibly complicated adjunctive treatment becomes necessary. P r i o r incidence with DCS i s another consideration i n determining predisposition. Many of the i n d i v i d u a l s having suffered from DCS figure i n repeat cases (Golding et a l . , 1960). This would appear to indicate a pattern for personal s u s c e p t i b i l i t y . Many authors have reported gender as a predisposing factor, with females the more susceptible (Bassett, 1973; Bangasser, 1979). A preliminary report based on female involvement i n m i l i t a r y diving has recently challenged t h i s p o s i t i o n (Zwingelberg et a l . , 1987). S t a t i s t i c a l review of t h i s report, however, has indicated that the data accumulated to date are inadequate to allow v a l i d comparison between male and female counterparts (Robinson, 1988). Use of b i r t h control p i l l s has also been suggested to predispose to or aggravate DCS. They have been shown to increase 14 p l a t e l e t adhesiveness and potentiate blood c l o t development (Kizer, 1981a). As with smoking, t h i s could complicate any case of DCS. However, because of the number of women employing them with apparent impunity and the lack of c l i n i c a l evidence, t h e i r use i s not contraindicated at t h i s time ( F i f e , 1984). Countering the predisposing factors are those suggested to confer an increased resistance against DCS. Acclimatization i s one reported to have a dramatic e f f e c t . Golding et a l . (1960) found that the rate of DCS could f a l l to 0.1% of the f i r s t day incidence a f t e r two to three weeks of d a i l y exposure i n caisson workers. This benefit was rapi d l y l o s t when d a i l y exposure ceased. They estimated that only half of the f u l l protection was present a f t e r seven days. The differences i n exposures between caisson workers and divers may make t h i s e f f e c t inapplicable to the diver. In fact, recent analysis of the Divers A l e r t Network (DAN) accident f i l e s for North America found that multi-day and r e p e t i t i v e diving i s involved i n 55% and 64%, respectively of the reported cases of DCS (DAN, unpublished). A s p i r i n has been proposed to provide a prophylactic benefit (when administered i n combination with other a n t i p l a t e l e t drugs) by decreasing p l a t e l e t a c t i v i t y and blood v i s c o s i t y (Catron and Flynn, 1982). No c l i n i c a l or experimental t r i a l s have confirmed the benefits of a s p i r i n alone. Reliance on t h i s type of proposed safeguard has obviously not been encouraged. 15 Racial trends have been observed i n r e l a t i o n to DCS s u s c e p t i b i l i t y (Kawashima, 1976; Wade et a l . , 1978). While unconfirmed at present, these l i k e l y represent acclimatization I ( H i l l s , 1977), rather than a race e f f e c t . ! The use of a l t e r n a t i v e decompression schedules (as compared to the standard U.S. Navy tables) may increase safety. S i g n i f i c a n t controversy e x i s t s as to optimal decompression stop depths. B r i t i s h procedures employ s i g n i f i c a n t l y deeper stop depths than the U.S. (Edmonds et a l . , 1981). Supporting the B r i t i s h approach i t has been demonstrated that adding deeper stops to those outlined i n the U.S. tables w i l l decrease bubble formation i n divers (Neuman et a l . , 1976). The Canadian Forces A i r Diving Tables and Procedures (1986), developed at the Defense and C i v i l I n s t i t u t e of Environmental Medicine (DCIEM) r e l y on the same decompression stop depths as the U.S. Navy, but are s i g n i f i c a n t l y more conservative i n terms of allowable exposure time. Either approach i s expected to confer a greater degree of protection on the divers. The factors discussed above, predisposing or protective, can not be e a s i l y controlled. Therefore, i t i s c l e a r that a single set of tables w i l l not be s a t i s f a c t o r y for a l l i n d i v i d u a l s . For t h i s reason, procedures focus on minimizing apparent r i s k , and managing the r e s u l t when problems develop. 16 Decompression Sickness Therapy Recompression D e f i n i t i v e management of DCS r e l i e s on recompression therapy. Although open water recompression has been proposed to meet t h i s end i n the absence of recompression f a c i l i t i e s (Edmonds et a l . , 1981; Canadian Forces A i r Diving Tables, 1986), chamber treatments are generally considered to be the only s a t i s f a c t o r y a l t e r n a t i v e due to the treatment time required and the p o t e n t i a l for complications that can be i l l handled under less c o n t r o l l e d underwater conditions (Boettger, 1983; Mebane and Dick, 1985). S p e c i f i c treatment w i l l vary based on the f a c i l i t y , equipment and personnel available. Recompression can be approached i n one of three ways: 1) to a pressure (depth) dependent upon the depth and duration of the o r i g i n a l dive, or 2) to a predetermined fixed depth ( i e . according to standard tables of recompression therapy), or 3) to a depth which produces a c l i n i c a l l y acceptable r e s u l t . While the t h i r d option i s often employed i n A u s t r a l i a (Edmonds et a l . , 1981) the c l a s s i c a l approach i n North America i s to follow (and often modify) the established U.S. Navy derived procedures that r e l y on the second option (U.S. Navy Handbook, 1979). U.S. Navy Table 6 (employing oxygen) c a l l s for an i n i t i a l treatment depth of 2.8 ATA (60 fsw), After a given period of time at t h i s 17 depth, the subject i s decompressed to 1.4 ATA (30 fsw) and spends a s i m i l a r period of time p r i o r to returning to surface ambient pressure. A review of treatments has demonstrated that while rare cases displaying dramatic deterioration at the maximum depth of t h i s protocol may p r o f i t from exposure to 6.0 ATA (165 fsw), the majority of cases would not benefit (Leitch and Green, 1985). There are three benefits of recompression. F i r s t , e x i s t i n g bubbles are p h y s i c a l l y decreased i n s i z e . Further, bubble reabsorption i s promoted. F i n a l l y , further bubble evolution i s prevented (Kunkle and Beckman, 1983). Even i f recompression must be delayed, benefit from treatment i s gained (Rivera, 1964; Kizer, 1982) . Adjunctive Therapies While recompression w i l l remain the mainstay treatment for DCS, adjunctive therapies can be c r u c i a l . Secondary bubble e f f e c t s , with a general theme of inflammatory responses, can complicate cases by aggravating the already s i g n i f i c a n t hematologic e f f e c t s r e s u l t i n g from hyperbaric exposure (Philp et a l . , 1975; Diercks and Eisman, 1977; Andersen et a l . , 1981; Neuman et a l . , 1981) . These w i l l most l i k e l y to be seen when recompression i s delayed more than 8 to 10 minutes (Bove, 1982). 18 A number of adjunctive therapies have been proposed to accompany recompression. Oxygen therapy i s the most accepted of these. I t i s used as an interim measure to mitigate or completely r e l i e v e signs and symptoms during transport and p r i o r to recompression. In t h i s capacity i t i s proving to have long range benefits. While data are limited, i t i s suggested that aggressive oxygen therapy p r i o r to recompression can lead to fa s t e r and more complete resolution of the condition with le s s permanent damage (DAN, unpublished). Use of oxygen breathing i n conjunction with recompression therapy i s also b e n e f i c i a l . In fact, i t i s the norm of present treatments (Berghage and McCracken, 1979; Myers and Schnitzer, 1984). The U.S. Navy Table 6 recompression protocol previously outlined r e l i e s on oxygen breathing. The following four benefits are gained from oxygen breathing: 1) the gradient for nitrogen elimination at the a l v e o l a r - c a p i l l a r y interface i s maximized; 2) the pote n t i a l for adequate oxygen d i f f u s i o n i n lungs with reduced function r e s u l t i n g from edema i s increased; 3) the dissolved oxygen content i n the plasma i s increased r e s u l t i n g i n increased t i s s u e oxygenation (Boerema et a l . (1960) demonstrated that with a l l t h e i r hemoglobin removed, swine s t i l l received adequate oxygenation through dissolved transport to survive when breathing 100% oxygen at three atmospheres pressure); and 4) high p a r t i a l pressures of oxygen w i l l cause a r e f l e x i v e vasoconstriction (Bird and T e f l e r , 1965), t h i s r e s u l t i n g i n reduced swelling and edema i n insulted tissues. While a t o x i c response to oxygen breathing i s possible (Butler and Thalmann, 1986), t h i s can usually 19 be co n t r o l l e d with periodic ' a i r breaks'. Table 6 c a l l s for f i v e minutes of a i r breathing following every 20 minutes of oxygen breathing. Confirming expectations, recent i n v e s t i g a t i o n has demonstrated that oxygen should not create a r i s k i n encouraging DCS through i t s application (Weathersby et a l . , 1987). Different breathing media are presently being assessed for t h e i r effectiveness i n t r e a t i n g DCS. A preliminary animal study has shown that the addition of perfluorocarbon emulsions (to enhance the s o l u b i l i t i e s of both oxygen and nitrogen) to a 100% oxygen medium w i l l increase both hemodynamic and neurologic protection from DCS (Spiess et a l . , 1988). Further data must be c o l l e c t e d regarding t h i s technique. Exemplifying the complicated nature of treatment, reports reviewing helium-oxygen combinations i n t r e a t i n g DCS have ranged from very p o s i t i v e (Douglas and Robinson, 1988) to very negative (Catron et a l . , 1987; L i l l o et a l . , 1988) . Other adjunctive aids recommended include: blood volume expanders and f l u i d administration (Cockett and Nakamura, 1964; Wells et a l . , 1978; Merton et a l . , 1983), a n t i p l a t e l e t drugs (Whitcraft and Karas, 1976; Philp et a l . , 1979), antiedematous drugs such as c o r t i c o s t e r o i d s (Pauley and Cockett, 1970; Kizer, 1981b; J a f f e , 1986), hypothermia (Erde, 1963; Simmons et a l . , 1982), anticonvulsants (Cox, 1980), antiarrhythmics (Kizer, 1980), and anticoagulants (Cockett et a l . , 1970; Reeves and Workman, 20 1971). The l i m i t e d data available provide generally inconclusive or c o n f l i c t i n g r e s u l t s (Catron and Flynn, 1982). Although warranting further investigation, the general approach to adjunctive therapies other than oxygen (U.S. Navy Handbook, 1979; Mebane and Dick, 1985) and f l u i d administration (Cockett et a l . , 1965; Heimbecker et a l . , 1968; Strauss and Samson, 1986) i s very cautious (Bayne, 1978; Greene and Lambertsen, 1980). Conclusions Exposure to the stress of decompression i s not benign. The i n t e r a c t i o n of a number of factors may r e s u l t i n development of DCS. Predisposing factors e x i s t which a l t e r i n d i v i d u a l r i s k , and the l i m i t a t i o n s of present understanding demands that a cautious approach be taken at a l l l e v e l s of involvement. Further invest i g a t i o n i s required to overcome these l i m i t a t i o n s . References: Decompression Sickness 21 Andersen JC, Vann RD, Dick AP. Correlation of hematologic a l t e r a t i o n s with Doppler bubble score and c l i n i c a l bends following shallow c l o s e d - c i r c u i t nitrogen-oxygen dives (abstr). Undersea Biomed Res 1981; 8(1): 43. Anthonisen NR, Utz G, Kryger MH, Urbanetti JS. Exercise tolerance at 4 and 6 ATA. Undersea Biomed Res 1976; 3(2): 95-102. Arthur DC, Margulies RA. A short course i n diving medicine. Ann Emerq Med 1987; 16(6): 689-701. Asahi S, Ohiwa H, Nashimoto I. Avascular bone necrosis i n Japanese diving fishermen. B u l l Toyko Med Dent Univ 1968; 15(3): 247-257. Bangasser SA. Incidence of decompression sickness i n women scuba divers. In: Proceedings of the Annual S c i e n t i f i c Meeting of the Undersea Medical Society. Bethesda : Undersea Medical Society, 1979. Bassett BE. Decompression sickness i n female students exposed to a l t i t u d e during physiological t r a i n i n g . Paper presented at the 44th Annual S c i e n t i f i c Meeting of the Aerospace medical Association, 1973. Bassoe P. Compressed a i r disease. J Nerv Ment Pis 1911; 38: 368- 369. Bayne CG. Acute decompression sickness: 50 cases. J Amer C o l l Emerg Physic 1978; 7(10): 351-354. Becker GD, P a r e l l GJ. Medical examination of the sport scuba diver. Otolaryngol Head Neck Surg 1983; 91: 246-250. Behnke AR. E f f e c t s of high pressures; prevention and treatment of compressed a i r i l l n e s s . Med C l i n North Amer 1942; July: 1213-1236. B e l l PY, Harrison JR, Page K, Summerfield M. An e f f e c t of C02 on the maximum safe d i r e c t decompression to 1 bar from oxygen-nitrogen saturation. Undersea Biomed Res 1986; 13(4): 443-455. Berghage TE, McCracken TM. Use of oxygen f o r optimizing decompression. Undersea Biomed Res 1979; 6(3): 231-239. Bert P. La Pression Barometrigue; Recherche de Physiologic Experimental. Paris: G. Mason, 1878. Barometric Pressure. Translated by MA Hitchcock and FA Hitchcock, Columbus, Ohio; College Book Company, 1943. 22 Biersner RJ, Hunter WL. Comparison of diving experience factors between divers c l a s s i f i e d as p o s i t i v e and negative f o r bone cysts. Undersea Biomed Res 1983; 10(1): 63-68. Bird AD, T e f l e r AMB. E f f e c t of hyperbaric oxygen on limb c i r c u l a t i o n . Lancet 1965; 1:355-356. Boerema I, Meyne NG, Brummelkamp WK, Bouma S, Mensch MH, Kamermans F, Stern Hanf M, Van Aalderen W. L i f e without blood. J Cardiovasc Sura 1960; 1: 133-146. Boettger ML. Scuba diving emergencies: pulmonary overpressure accidents and decompression sickness. Ann Emerg Med 1983 12(9): 563-567. Bove AA. The basis for drug therapy i n decompression sickness. Undersea Biomed Res 1982; 9(2): 91-111. Boycott AE, Damant GCC, Haldane JS. The prevention of compressed- a i r i l l n e s s . J Hyg (Lond) 1908; 8: 342-444. Boyle R. New pueumatical experiments about r e s p i r a t i o n . Philos Transact 1670; 5(62): 2011-2031. Brown CV. The physiology of decompression sickness. In: Graver D, ed. Decompression i n Depth: The Proceeding of the Seminar. Santa Ana : Professional Association of Diving Instructors; 1979: 29-37. Buhlmann AA. Decompression - Decompression Sickness. New York : Springer-Verlag; 1984. 87 pp. Butler FK J r , Thalmann ED. Central nervous system oxygen t o x i c i t y i n closed c i r c u i t scuba diver I I . Undersea Biomed Res 1986; 13(2): 193-223. Calder IM. Bone and j o i n t diseases i n workers exposed to hyperbaric conditions. In: Berry CL, Grundmann E, Kirsten WH, eds. Current Topics i n Pathology: Bone and J o i n t Diseases 1982; 71: 105- 122. Canadian Forces A i r Diving Tables and Procedures. Downsview, Ontario : Department of National Defence, Defense and C i v i l I n s t i t u t e of Environmental Medicine, 1986. 57 pp. Catron PW, Flynn ET J r . Adjuvant drug therapy for decompression sickness: a review. Undersea Biomed Res 1982; 9: 161-173. Catron PW, Thomas LB, Flynn ET J r , McDermott J J , Holt MA. E f f e c t s of He-02 breathing during experimental decompression sickness following a i r dives. Undersea Biomed Res 1987; 14(2): 101-111. 23 Cockett ATK, Nakamura RM. Newer concepts i n the pathophysiology of experimental dysbarism decompression sickness. Am Surg 1964; 30(7): 447-451. Cockett ATK, Nakamura RM, Franks J J . Recent findings i n the pathogenesis of decompression sickness (dysbarism). Surgery 1965; 58 (2): 384-389. Cockett ATK, Pauley SM, Roberts AP. Advances i n treatment of decompression sickness: an evaluation of heparin. In: Third International Conference on Hyperbaric and Underwater Physiology. June 08-11. J970. Paris : DOIN, 1972: 156-159. Cox RAF. The use of drugs under pressure. In: Walsh JM, ed. Interaction of Drugs i n the Hyperbaric Environment. Bethesda, MD : Undersea Medical Society, 1980: 37-48. Davis JC, E l l i o t t DH. In: Bennett PB, E l l i o t t DH, eds. The Physiology and Medicine of Diving, 3 r d ed. London : B a i l l i e r e T i n d a l l , 1982: 473-487. Dembert ML, Jekel JF, Mooney LW. Health r i s k factors f o r the development of decompression sickness among US Navy divers. Undersea Biomed Res 1984; 11(4): 395-406. Dick APK, Massey EW. Neurologic presentation of decompression sickness and a i r embolism i n sport divers. Neurology 1985; 35(5): 667-671. Diercks KJ, Eisman PT. Hematologic changes a f t e r d a i l y asymptomatic dives. Undersea Biomed Res 1977; 4(4): 325-331. Douglas J DM, Robinson C. Heliox treatment for spinal decompression sickness following a i r dives. Undersea Biomed Res 1988; 15(4): 315-319. Dunford R, Hayward J . Venous gas bubble production following cold stress during a no-decompression dive. Undersea Biomed Res 1981; 8(1): 41-49. Dwyer J, Saltzman HA, O'Bryan R. Maximal physical-work capacity of man at 43.4 ATA. Undersea Biomed Res 1977; 4(4): 359-372. Edmonds C, Lowry C, Pennefather J . Diving and Subaquatic Medicine, 2 n d ed. Mosman, NSW : Diving Medical Center, 1981. E l l i o t t DH, Hallenbeck JM. The pathophysiology of decompression sickness. In: Bennett PB, E l l i o t t DH, eds. The Physiology and Medicine of Diving and Compressed a i r Work. Baltimore : williams & Wilkins, 1975: 76-92. ' 24 E l l i o t t DH, Kindwall EP. Manifestations of the decompression disorders. In: Bennett PB, E l l i o t t DH, eds. The Physiology and Medicine of Diving. 3 r d ed. London : B a i l l i e r e Tirtdall, 1982: 461- 472. Emerson LV, Hempleman HV, Lentle RG. The passage of gaseous emboli through the pulmonary c i r c u l a t i o n . Respir Physiol 1967; 3: 213- 219. Epstein M. Renal e f f e c t s of head-out immersion i n man: implications f o r an understanding of volume homeostasis. Physiol Rev 1978; 58: 529-581. Erde A. Experience with moderate hypothermia i n the treatment of nervous system symptoms of decompression sickness. In: Lambertsen CJ, Greenbaum LJ, eds. Proceedings of the Second Symposium on Underwater Physiology. National Research Publications 1963; 1181: 66-81. Erde A, Edmonds C. Decompression sickness: a c l i n i c a l s e r i e s . J Occup Med 1975; 17(5): 324-328. Farmer JC, Goad RF, Leitch DR, Hallenbeck JM, Hamilton RW. Diagnosis and treatment of decompression sickness. In: S h i l l i n g CW, Carlston CB, Mathias RA, eds. The Physician's Guide to Diving Medicine. New York : Plenum Press, 1984: 283-331. F i f e WP. Women and diving. In: S h i l l i n g CW, Carlston CB, Mathias RA, eds. The Physician's Guide to Diving Medicine. New York : Plenum Press, 1984: 136-144. Ganong WF. Review of Medical Physiology. 12 t h ed. Los Altos : Lange Medical Publications, 1985. 654 pp. G i l l i s MF, Karagianes MT, Peterson PL. Bends: detection of c i r c u l a t i n g gas emboli with external sensor. Nature 1968; 161(3841): 579-580. Gplding FC, G r i f f i t h s P, Hempleman HV, Paton WDM, Walder DN. Decompression sickness during construction of the Dartford Tunnel. B r i t J Indust Med 1960; 17: 167-180. Gray JS. Constitutional factors a f f e c t i n g s u s c e p t i b i l i t y to decompression sickness. In: Fulton JF, ed. Decompression Sickness. Philadelphia : Saunders; 1951: 182-191. Greene KM, Lambertsen CJ. Nature and treatment of decompression sickness occurring a f t e r deep excursion dives. Undersea Biomed Res 1980; 7(2): 127-139. 25 Greenstein A, Sherman D, Melamed Y. Chokes - favourable response to delayed recompression therapy: a case report. Aviat Space Environ Med 1981; 52(9): 559-560. Hallenbeck JM, Andersen JC. In: Bennett PB, E l l i o t t DH, eds. The Physiology and Medicine of Diving. 3 r d ed. London : B a i l l i e r e T i n d a l l , 1982: 435-460. Hallenbeck JM, Bove AA, Moquin RB, E l l i o t t DH. Accelerated coagulation of whole blood and c e l l - f r e e plasma by bubbling i n v i t r o . Aerosp Med 1973; 44(7): 712-714. Heimbecker RO, Lemire G, Chen CH, Koven I, Leask D, Drucker WR. Role of gas embolism i n decompression sickness - a new look at "the bends". Surgery 1968; 64(1): 264-272. Hempleman HV. History of evolution of decompression procedures. In: Bennett PB, E l l i o t t DH, eds. The Physiology and Medicine of Diving. 3 r d ed. London : B a i l l i e r e T i n d a l l , 1982: 319-351. Hempleman HV. Decompression theory. In: S h i l l i n g CW, Carlston CB, Mathias RA, eds. The Physician's Guide to Diving Medicine. New York : Plenum Press, 1984: 223-272. Hickey DD, Lundgren CEG, Pasche AJ. Influence of exercise on maximal voluntary v e n t i l a t i o n and forced expiratory flow at depth. Undersea Biomed Res 1983; 10(3): 241-254. H i l l s BA. Decompression Sickness. Volume 1: The Biophysical Basis of Prevention and Treatment. New York : John Wiley and Sons; 1977. 322 pp. H i l l s BA, Butler BD. Size d i s t r i b u t i o n of intravascular a i r emboli produced by decompression. Undersea Biomed Res 1981; 8(3): 163- 170. Hughes JS, Eckenhoff RG. Spinal cord decompression sickness a f t e r standard US Navy a i r decompression. M i l i t Med 1986; 151 (3): 166- 168. J a f f e R. Sports medicine emergencies. Prim Care 1986; 13(1): 207- 215. Kawashima M. Aseptic bone necrosis i n Japanese divers. B u l l Tokyo Med Dent Univ 1976; 23(2): 71-92. Kizer KW. Vent r i c u l a r dysrhythmia associated with serious decompression sickness. Ann Emerg Med 1980; 9: 580-584. Kizer KW. Women and diving. Physic Sportsmed 1981a; 9(2): 84-92. 26 Kizer KW. Corticosteroids i n treatment of serious decompression sickness. Ann Emerq Med 1981b; 10(9): 485-488. Kizer KW. Delayed treatment of dysbarism: a retrospective review of 50 cases. JAMA 1982; 247(18): 2555-2558. Kizer KW. Management of dysbaric diving c a s u a l t i e s . Emerq Med C l i n North Amer 1983; 1(3): 659-670. Kizer KW. Diving Medicine. Emerq Med C l i n North Amer 1984; 2(3): 513-530. Kunkle TD, Beckman EL. Bubble d i s s o l u t i o n physics and the treatment of decompression sickness. Med Phys 1983; 10(2): 184- 190. Leitch DR, Green RD. Additional pressurization f o r t r e a t i n g nonresponding cases of serious a i r decompression sickness. Aviat Space Environ Med 1985:.56(12): 1139-1143. L i l l o RS, MacCallum ME, P i t k i n RB. A i r vs. He-0? recompression treatment of decompression sickness i n guinea pigs. Undersea Biomed Res 1988; 15(4): 283-300. Lin YC. Applied physiology of diving. Sports Med 1988; 5(1): 41- 56. Linaweaver PG. Physical and psychological examination f o r diving. In: S h i l l i n g CW, Carlston CB, Mathias RA. The Physician's Guide to Diving Medicine. New York : Plenum Press, 1984: 489-507. Manjarrez C, B i r r e r R. N u t r i t i o n and a t h l e t i c performance. Amer Fam Physic 1983; 28(5): 105-115. McCallum RI, Harrison JAB. Dysbaric osteonecrosis: aseptic necrosis of bone. In: Bennett PB, E l l i o t t DH, eds. The Physiology and Medicine of Diving. 3 r d ed. London : B a l l i e r e - T i n d a l l , 1982; 488-506. McCallum RI, Petrie A. Optimum weights for commercial divers. B r i t J Indust Med 1984; 41: 275-278. McCallum RI, Walder DN, Thickett VB. Bone necrosis i n commercial divers (abstr). Undersea Biomed Res 1976; 3(1): A41. McLeod JG. The hazards of underwater diving. Med J Aust 1986; 14(8): 394-395. Mebane GY, Dick AP. DAN: Underwater Diving Accident Manual. Durham : Duke University (Divers A l e r t Network); 1985. 35 pp. Merton DA, F i f e WP, Gross DR. An evaluation of plasma volume expanders i n the treatment of decompression sickness. Aviat Space Environ Med 1983; 54: 218-222. Myers RAM, Schnitzer BM. Hyperbaric oxygen use: update 1984. Postgrad Med 1984; 76(5): 83-86, 89-91, 94-95. Neuman TS, H a l l DA, Linaweaver PG J r . Gas phase separation during decompression i n man: ultrasound monitoring. Undersea Biomed Res 1976; 3(2): 121-130. Neuman TS, Spragg RG, Wohl H. P l a t e l e t aggregates following decompression (abstr). Undersea Biomed Res 1981; 8(1): 42. Ohta Y, Matsunaga H. Bone lesions i n divers. J Bone J o i n t Surg 1974; 56B(1): 3-16. Palmer AC, Calder IM, Hughes JT. Spinal cord degeneration i n divers. Lancet 1987; 2(8572): 1365-1366. Pauley SM, Cockett ATK. Role of l i p i d s i n decompression sickness. Aerosp Med 1970; 47(1): 56-60. Philp RB, Bennett PB, Anderson JC, et a l . E f f e c t s of a s p i r i n and dypridamole on p l a t e l e t function, hematology, and blood chemistry of saturation divers. Undersea Biomed Res 1979; 6: 127-146. Philp RB, Freeman D, Francey I, Bishop B. Hematology and blood chemistry i n saturation diving: I A n t i p l a t e l e t drugs, a s p i r i n , and VK744. Undersea Biomed Res 1975; 2(4): 233-249. Reeves E, Workman RD. Use of heparin for the therapeutic / prophylactic treatment of decompression sickness. Aerosp Med 1971; 42: 20-23. Rivera JC. Decompression sickness among divers: an analysis of 935 cases. M i l i t Med 1964; 129(4): 314-334. Robinson TJ ( l e t t e r ) . Decompression sickness i n women divers. Undersea Biomed Res 1988; 15(1): 65-66. S h i l l i n g CW. Safety considerations. In: S h i l l i n g CW, Carlston CB, Mathias RA. The Physician's Guide to Diving Medicine. New York : Plenum Press, 1984: 567-597. Shir a k i K. Diuresis i n hyperbaria. In: Shiraki K, Yousef MK, eds. Man i n S t r e s s f u l Environments: Diving. Hyper- and Hypobaric Physiology. S p r i n g f i e l d , I l l i n o i s : Charles C Thomas, 1987: 93- 114. 28 Simmons EH, O'Driscoll SW, Gamarra JA. C l i n i c a l and experimental evidence f o r the use of hypothermia i n decompression sickness. Aviat Space Environ Med 1982; 53(3): 266-268. Spencer MP, Campbell SD. Development of bubbles i n venous and a r t e r i a l blood during hyperbaric decompression. B u l l Mason C l i n i c 1968; 22(1): 26-32. Spencer MP, Oyama Y. Pulmonary capacity for d i s s i p a t i o n of venous gas emboli. Aerosp Med 1971; 42(8): 822-827. Sphar RI, Hunter WI, Biersner RJ, Harvey CA. Aseptic bone necrosis i n US Navy divers: prevalence and associated factors. Med Aero Spat Med Subaa HVP 1977; 64: 402-404. Spiess BD, McCarthy RJ, Tuman KJ, Woronowicz AW, Tool KA, Ivankovich AD. Treatment of decompression sickness with a perfluorocarbon emulsion (FC-43). Undersea Biomed Res 1988; 15(1): 31-37. Strauss RH, Prockop LD, Decompression sickness among scuba divers. JAMA 1973; 223(6): 637-640. Strauss MB, Samson RL. Decompression sickness: An update. Physic Sportsmed 1986 14(3): 196-205. Szasz MS. Evaluating the sport scuba diver. Amer Fam Physic 1982; 25(5): 131-134. US Navy A i r Decompression Table Handbook and Decompression Chamber Operator's Handbook. Carson, CA : Best Bookbinders, 1979. 172 pp. Van Liew HD, Sponholtz DK. Effectiveness of a breath during exercise i n a hyperbaric environment. Undersea Biomed Res 1981; 8(3): 147-161. Vann RD. Decompression theory and applica t i o n . In: Bennett PB, E l l i o t t DH, eds. The Physiology and Medicine of Diving. 3 r d ed. London : B a i l l i e r e T i n d a l l , 1982: 352-382. Vernon HM. The s o l u b i l i t y of a i r i n fats and i t s r e l a t i o n to caisson disease. Lancet 1907; 691-693. Wade CE, Hayashi EM, Cashman TM J r , Beckman EL. Incidence of dysbaric osteonecrosis i n Hawaii's diving fishermen. Undersea Biomed Res 1978; 5(2): 137-147. Walder DN. Osteonecrosis. In: S h i l l i n g CW, Carlston CB, Mathias RA, eds. The Physician's Guide to Diving Medicine. New York : Plenum Press, 1984; 397-405. 29 Weathersby PK, Hart BL, Flynn ET, Walker WF. Role of oxygen i n the production of human decompression sickness. J Appl Physiol 1987; 63(6): 2380-2387. Wells CH, H i l t o n JG, H a l l CB. Microcirculatory e f f e c t s of intravenous f l u i d r e s u s c i t a t i o n i n dysbarism. Undersea Biomed Res 1978; 5(suppl 1): 18. Whitcraft DD, Karas S. A i r embolism and decompression sickness i n scuba divers. J Amer C o l l Emerq Physic 1976; 5(5): 355-361. Zwingelberg KM, Knight MA, B i l e s JB. Decompression sickness i n women divers. Undersea Biomed Res 1987; 14(4): 311-317. 30 Doppler Ultrasound Doppler u l t r a s o n i c assessment has become a common component of diving research. This i s not to imply that the methodology i s u n i v e r s a l l y accepted. Controversy remains regarding the techniques. This review w i l l present background on the development of u l t r a s o n i c technology and techniques pertinent to the diving researcher. Technical reviews of u l t r a s o n i c theory and equipment are not included i n t h i s paper. They have been completed by Kalmus (1954), Wells (1969, 1977{a & b}), Rubissow and MacKay (1971), Nishi (1972), Spencer and Clarke (1972), Spencer and Johanson (1974), Kisman (1977), and Eatock et a l . (1985). Referring to the diving l i t e r a t u r e related to u l t r a s o n i c evaluation one sees a v a r i e t y of nomenclature. 'Bubbles' are equivalent to 'vascular gas emboli^ or VGE, and bubble formation to 'gas phase separation'. The terminology used i n t h i s review w i l l be standardized, unless the introduction of secondary descriptors benefits the discussion. The Doppler u l t r a s o n i c flowmeter was f i r s t reviewed by Kalmus (1954) . Baldes et a l . (1957) used t h i s technology to measure blood flow v e l o c i t y . Subsequently, Franklin et a l . (1961) observed that c i r c u l a t i n g bubbles could be detected during the evaluation of blood flow. In fact, bubbles w i l l produce a much stronger r e f l e c t e d s i g n a l than s i m i l a r sized blood c e l l s . The f i r s t report that ultrasound could be used to i d e n t i f y bubbles caused by decompression sickness was made by Mackay (1963). He detected bubbles i n a rat that had been ra p i d l y decompressed following a severe hyperbaric exposure. G i l l i s et a l . (1968a) demonstrated that s u r g i c a l l y implanted Doppler u l t r a s o n i c blood flowmeters could detect c i r c u l a t i n g bubbles i n decompressing swine before they reached the f i r s t decompression stop recommended by the U.S. Navy exposure tables. Spencer and Campbell (1968) reported s i m i l a r r e s u l t s with sheep. Both G i l l i s et a l . (1968a) and Spencer and Campbell (1968) suggested that further e f f o r t s with u l t r a s o n i c technology would allow i t to be used successfully with human subjects. This was encouraged by the development of transcutaneous transducers that allowed for uncomplicated and non-invasive monitoring of subjects ( G i l l i s et a l . , 1968b). As a r e s u l t of the early success and enthusiasm apparent i n the l i t e r a t u r e and the new a b i l i t y to apply i t non-invasively, Doppler u l t r a s o n i c analysis received extensive use and review. A more dramatic range of re s u l t s were found through the subsequent investigations. 32 Risks Associated With Doppler Ultrasound The r i s k factors of human exposure to ultrasound have long been recognized. The energy l e v e l s employed by some ul t r a s o n i c systems have been shown to cause c a v i t a t i o n and production of physical bubbles. In fact, the i n t e n s i t i e s used i n physiotherapy are reportedly above c a v i t a t i o n l e v e l s (Smith and Spencer, 1970). Most of the early investigators applying u l t r a s o n i c technology to the evaluation of decompression derived bubbles expressed t h e i r awareness of t h i s concern ( G i l l i s et a l . , 1969; Spencer et a l . , 1969; Smith and Spencer, 1970; Spencer and Clarke, 1972; Rubissow and Mackay, 1974; H i l l s and Grulke, 1975; Spencer, 1976; Daniels et a l . , 1979). G i l l i s et a l . (1969), recognizing the hazards of ul t r a s o n i c c a v i t a t i o n , recommended that investigators l i m i t the power of the units to be employed. Smith and Spencer (1970) then reported that i n t e n s i t y l e v e l s required to produce c a v i t a t i o n were 100 W-cm"2 i n blood and v a r i a b l e i n tissu e with the minimum i n t e n s i t y being 1.3 to 1.6 W-cm"2 i n brain t i s s u e . Their ultrasound system applied power l e v e l s of approximately 0.01 W-cm"2, as they express i t , "two magnitudes below reported c a v i t a t i o n thresholds for t i s s u e and four magnitudes below water or blood". Supported by the lack of complications, they concluded that the working equipment and techniques did not present a s i g n i f i c a n t r i s k to subjects. Spencer et a l . (1969) experimentally tested the impact during the f i r s t t r i a l s using human subjects. They a l t e r n a t e l y started and stopped an upstream detector to evaluate any changes noted at a downstream detector. They found no changes r e s u l t i n g from t h i s action. Subsequent investigators have generally accepted that n e g l i g i b l e r i s k i s associated with the power l e v e l s required by these u l t r a s o n i c techniques (Rubissow and Mackay, 1974; Spencer, 1976; Daniels et a l . , 1979). Doppler Protocol Development Early investigations did not lend themselves to cross- c o r r e l a t i o n or replication." Researchers generally used subjective and often undescribable bubble evaluation schemes. G i l l i s et a l . (1968b) reported that c h a r a c t e r i s t i c bubble sounds could be best described as "chirps". Evans and Walder (1970) categorized them as "plops" - these being "not so high pitched as the chirps". Powell's (1974) scoring procedure was described as follows: 0 = normal heart sounds free of bubbles; 1 = "running water" sounds; 2 = "popping" sounds; 3 = "roaring" sounds. H i l l s and Grulke (1975) c l a s s i f i e d bubbles as those sounds best described as "blups" or "chirps". To t h i s point, the evaluation of recorded signals was not highly s a t i s f a c t o r y . Dramatic improvements i n standardization of signal i n t e r p r e t a t i o n were r e a l i z e d when Spencer and Johanson (1974) developed a simple but more quantifiable grading system. They c l a s s i f i e d bubble sounds as follows: Grade 0 = NO bubble signals. Grade I = An occasional bubble s i g n a l . The great majority of cardiac cycles are free of bubble signals. Grade II = Many but less than h a l f of the cardiac cycles contain bubble signals. Grade 111= A l l of the cardiac cycles contain bubble signals, but not obscuring signals of cardiac motion. Grade IV = Bubble signals sounding continuously throughout systole and di a s t o l e and obscuring normal cardiac signals. Spencer and Johanson's (1974) system was then adopted as the standard for many subsequent investigations (Spencer, 1976; Neuman et a l . , 1976; Spencer, 1978; Powell et a l . , 1983; Daniels, 1984; Huggins, 1984; Bayne et a l . , 1985; Eckenhoff et a l . , 1986). While the r e l i a b i l i t y of Spencer and Johanson's (1974) grading system was applauded, further factors had to be considered. Manley (1969) f i r s t observed that muscular movement resulted i n a marked increase i n sensible bubbles. Spencer and Clarke (1972) noted that bodily movements considerably augmented the signals measured, at both precordial and b a s i l i c vein measuring s i t e s . These movements included arm r a i s i n g , f i s t clenching and passive compression of the forearm. There was then no doubt that bubble grades during movement were always higher than bubble grades while at rest (Gardette, 1979; Eckenhoff et a l . , 1986). Refinements to the evaluation procedures included comparison of 'at r e s t ' and 'movement' (ie. limb flexing) conditions (Kisman et a l . , 1978). This was f e l t to enhance the detection of early bubble development. Further experience with the Kisman-Masurel scale led to the adapted procedures presented i n d e t a i l by Eatock and Nishi (1986). They maintained the Grade O-IV scale, evaluated during r e s t and movement cases, and quantified bubbles based on three parameters: 1) frequency - number of bubbles per cardiac period, 2) percentage/duration - percentage of cardiac periods with s p e c i f i e d bubble frequency, and 3) amplitude - bubble sounds i n comparison to normal cardiac sounds. This methodology provides the most current approach available i n the l i t e r a t u r e . 36 Signal Interpretation The Spencer and Johanson (1974) scale discussed previously provides the common reference point f o r Doppler signal i n t e r p r e t a t i o n . The most straightforward aspect of the inte r p r e t a t i o n involves bubble grades. I t i s generally accepted that the bubble grades of III and IV are more strongly correlated with the development of c l i n i c a l signs and symptoms of decompression sickness (DCS) than the lower grades (Gardette, 1979; Daniels, 1984; Strauss and Samson, 1986; Webb et a l . , 1988). VGE development i s affected by i n t e r - and i n t r a - i n d i v i d u a l v a r i a b i l i t y . Both aspects demand further i n v e s t i g a t i o n . Inter- i n d i v i d u a l s u s c e p t i b i l i t y has been considered by Spencer (1976). He concluded that individuals who were "bubble prone" would be "bends prone". I f so, Doppler assessments could be used to pre- screen divers p r i o r to regular p a r t i c i p a t i o n . This was subsequently attempted by Spencer and Aggenbach (1978). They completed 31 chamber exposures to 165 feet for 10 minutes followed by d i r e c t ascent to the surface (ascent rate standard 60 feet per minute). Six subjects then completed equivalent dives i n open water. VGE scores were notably higher following the open water exposures, and most importantly, trends towards i n d i v i d u a l s u s c e p t i b i l i t y following open water dives could be estimated from chamber scores, t h i s supporting the findings of Spencer and Johanson (1974). The r e l i a b i l i t y of c o r r e l a t i n g i n d i v i d u a l scores to s u s c e p t i b i l i t y has not been v e r i f i e d by other investigators. Powell et a l . (1983) reviewed 150 man-dives with exposures ranging from 100-220 meters i n depth and between 15-60 minutes i n bottom time. They contradict Spencer's (1976) conclusion regarding proneness and report extreme i n t e r - i n d i v i d u a l v a r i a t i o n with some "bubble prone" indivi d u a l s being "not bends prone" and some "bends prone" in d i v i d u a l s being "not bubble prone". This seems a doubtful challenge since measurable bubble presence appears to be a prerequisite of decompression sickness (Daniels, 1984) and that increasing bubble grades, as reported e a r l i e r , c o r r e l a t e most strongly. I n t r a - i n d i v i d u a l v a r i a b i l i t y has been considered by Eckenhoff et a l . (1986). They used Doppler ultrasound to quantify bubbles i n 34 subjects completing a i r saturation dives for 48 hours at 1.77 atmospheres absolute (ATA) (25.5 fsw, n = 19), and at 1.89 ATA (29.5 fsw, n = 15). Decompression back to 1 ATA following these exposures was completed i n approximately two minutes. They found four cases of DCS (27%) and three "possible DCS" (20%) following 29.5 fsw exposure, and f i v e "possible" (26%) at 25.5 fsw. Their data support the findings of Spencer (197 6), that there i s s i g n i f i c a n t i n t e r - i n d i v i d u a l v a r i a b i l i t y i n s u s c e p t i b i l i t y to decompression sickness. They suggest that the length of time venous bubbles are present may be more representative of decompression stress than the peak score. Once more, no 38 corroborating reports have been found i n the l i t e r a t u r e . Experimental Results Using Doppler Techniques The use of u l t r a s o n i c bubble detection to evaluate human subjects a f t e r diving was f i r s t reported by G i l l i s et a l . (1969) and Spencer et a l . (1969). Neither of these studies reported major success with the techniques. G i l l i s et a l . (1969) dived one i n d i v i d u a l to 175 feet for 60 minutes (decompression according to U.S. Navy t a b l e s ) . No bubbles were i d e n t i f i e d despite the fact that t h i s subject became symptomatic. This was f e l t to be a r e s u l t of inadequate t r a i n i n g of the subject/technician i n p o s i t i o n i n g the transducer and a subsequent poor qu a l i t y s i g n a l . They dived two other subjects to 60 feet for 45 minutes. Again, no bubbles were i d e n t i f i e d . The mildness of t h i s exposure made the lack of i d e n t i f i a b l e bubble signals understandable. Spencer et a l . (1969) reported on seven exposures ranging from 100 feet for 80 minutes to 200 feet for 60 minutes ( a l l decompressions according to U.S. Navy ta b l e s ) . Although three of t h e i r subjects became symptomatic, they observed only "possible" bubble signals i n two of them (none of the other displayed measurable bubbles). This was suggested to r e s u l t from some unsuccessful experimentation with evaluation s i t e s . Lack of experience i n i n t e r p r e t i n g the signals was also reported to be a 39 factor (Spencer and Clarke, 1972). Human experiments that were more successful i n terms of assessment were completed by Spencer and Clarke (1972). A single male subject was dived to 200 fsw for 30 minutes (decompression according to the U.S. Navy Tables). The resultant bubble signals were c l e a r and extensive. Counting i n d i v i d u a l bubbles was often impossible. Despite the bubble severity, however, i n t h i s case the subject did not become symptomatic. Spencer (1976) exposed human subjects to a wide range of dry chamber schedules (from 233 fsw for 7 minutes to 25 fsw f o r 720 minutes) and open water dives to 165 fsw f o r 10 minutes. Although h i s statements remain conjectural about s p e c i f i c exposures, he generalized that: 1) there was notable i n t e r - and i n t r a - i n d i v i d u a l v a r i a t i o n i n the formation of VGE, c o r r e l a t i n g with s u s c e p t i b i l i t y to developing DCS; 2) DCS did not develop without the p r i o r detection of precordial VGE; and 3) open ocean exposures increased the percentage of VGE and DCS when compared to chamber exposures. Neuman et a l . (1976) completed two series of dives. The f i r s t , to 210 fsw for a 50 minute bottom time. This involved 18 man-dives. The second series involved 16 subjects exposed to 132 fsw f o r a 30 minute t o t a l bottom time (TBT). Again, they achieved encouraging u l t r a s o n i c r e s u l t s . They observed: 1) a s i g n i f i c a n t l i n e a r increase i n bubble scores during the decompression stages of the dives; 2) a s t a t i s t i c a l l y s i g n i f i c a n t bubble score reduction for those divers being exposed to an additional deep decompression stop (not c a l l e d for i n the U.S. Navy exposure tables) that was not s o l e l y r e l a t e d to the additional decompression time involved; 3) that there was a s t a t i s t i c a l l y s i g n i f i c a n t r e l a t i o n s h i p between bubble scores and decompression sickness. A l l seven of the divers who experienced decompression sickness had Grade IV bubble scores during t h e i r l a s t three recordings, whereas only 12 of the other 27 divers had s i m i l a r bubble scores; and 4) there were no s i g n i f i c a n t c o rrelations between age, weight, or body composition and the occurrence of eith e r decompression sickness or mean bubble score. The investigations reported above r e f l e c t an early trend of increasing confidence i n Doppler u l t r a s o n i c r e s u l t s . Unfortunately, the exposures employed i n each of the successful examples are the more severe ones. Less conclusive but s t i l l supportive r e s u l t s can be seen from the more moderate studies. They confirm the e f f i c a c y of Doppler u l t r a s o n i c procedures with some q u a l i f i c a t i o n . These involve a wide v a r i e t y of exposures; Gardette (1979) reviewed Doppler assessments completed during 67 helium-oxygen chamber dives, evaluating 232 subjects with over 2000 observations. These included bounce, excursion and saturation dives. Depths ranged from 35 to 480 meters, with bottom times from 30 minutes to eight days. Gardette found that bubbles i d e n t i f i e d during movement generally indicated less r i s k than bubbles found while at re s t . He reported a 1% incidence of DCS i n subjects with no detectable bubbles at rest f o r bounce and excursion dives. Saturation dives yielded d i f f e r e n t r e s u l t s , though. Absence of bubbles at res t was associated with a 14% incidence of pain, and no bubbles during movement corresponded to a pain incidence of 10%. Gardette concluded that a higher incidence of DCS related problems would be found with higher bubble grades i n general and that 'movement' case bubbles would be less i n d i c a t i v e of decompression sickness r i s k . However, i t would not be possible to predict pain. Further, i t appeared that while Doppler evaluation could be acceptable for bounce and excursion diving, i t was not suit a b l e for saturation exposures. Gardette's findings are supported by other investigators. DCS incidence, s i m i l a r to hi s 1%, have been reported for a i r dives by Spencer and Johanson (1974) at 1.3% and Nashimoto and Gotoh (1978) at 0%. Likewise, h i s 14% becoming symptomatic i n the absence of bubbles at rest i s s i m i l a r to Powell et a l . ' s (1983) finding of 16%. Brubakk et a l . (1986) confirmed the d i f f i c u l t y i n assessing saturation dives. They followed s i x saturation divers executing ascending excursions from 300 to 250 msw. They found no co r r e l a t i o n between c i r c u l a t i n g bubbles and the development of decompression sickness. Bayne et a l . (1985) used Doppler to follow 83 subjects during chamber dives to 285 fsw for bottom times ranging from 6 to 11 minutes (decompression according to standard U.S. Navy t a b l e s ) . Based on Doppler scores alone, 36 of the subjects had decompression sickness. Only f i v e of these indiv i d u a l s had c l i n i c a l l y demonstrable signs or symptoms. False p o s i t i v e scoring was acceptable i n that Doppler assessments are supposed to be more se n s i t i v e than subjective reporting. Their concern was with three cases that required treatment without Doppler signs. This represented a 38% f a l s e negative rate. Using a Chi-square t e s t of independence they report a p r o b a b i l i t y between 25% and 50% that the c l i n i c a l and Doppler diagnoses r e f e r to independent processes. They concluded that bubble scores may be weakly rel a t e d to c l i n i c a l symptoms, but f a r too weakly to be of diagnostic value i n i n d i v i d u a l cases. Bayne et a l . ' s concerns present few d i f f i c u l t i e s to those interested i n u l t r a s o n i c assessment. Doppler u l t r a s o n i c detection has generally been promoted as an early warning system to encourage closer observation of i n d i v i d u a l s following the recognition of bubbles. I t has not been promoted as a replacement f o r c l i n i c a l diagnosis. The majority of investigators use Doppler derived information i n a more r e s t r i c t e d manner. For instance, Masurel et a l . (1978) followed s i x divers over a s i x day saturation dive to 430 msw with d a i l y excursions (fiv e to 460 msw and one to 501 msw for durations between 2.5 and f i v e hours). They reported that while bubble scores did not necessarily indicate immediate danger for divers, they were useful i n adjusting decompression schedules to minimize the flow of bubbles. This dynamic implementation of Doppler r e s u l t s i s probably the most s i g n i f i c a n t benefit to be derived from the technology. In fact, Bayne et a l . ' s (1985) concerns simply act to reinforce t h i s d i s t i n c t i o n and the importance of developing a l t e r n a t i v e methodologies as discussed below. Alter n a t i v e Methodologies Doppler u l t r a s o n i c systems are l i m i t e d i n that they are only s e n s i t i v e to bubbles moving within the narrow fo c a l range of the transducer. Individual bubble si z e and progression can not be monitored and t i s s u e bubbles or stationary vascular bubbles can not be i d e n t i f i e d . Problematically, i t has been reported that t i s s u e bubbles appear p r i o r to c i r c u l a t i n g bubbles. To meet t h i s concern, a l t e r n a t i v e methodologies that are s e n s i t i v e to both moving and stationary bubbles have been proposed and employed (Christman et a l . , 1986). Pulsed-echo ultrasound i s the most commonly reported (Walder et a l . , 1968; Manley, 1969; Rubissow and MacKay, 1974; Horton and Wells, 1976; Daniels et a l . , 1979; H i l l s et a l . , 1983; Daniels, 1984; Brubakk et a l . , 1986). Aco u s t i c a l - o p t i c a l imaging techniques have also been proposed (Buckles and Knox, 1969). Rubissow and MacKay (1974) employed a non-invasive pulsed-echo (scanning) u l t r a s o n i c system. Using a frequency of 7.5 MHz, bubbles with diameters within the range of 2-5 microns were "routinely" imaged, with some as small as 0.5-1.0 microns i n diameter were detected under optimal conditions. A v a r i e t y of subject species were used i n t h e i r work. Guinea pigs to v e r i f y the d i r e c t e f f e c t of pressure (Boyle's Law) on bubble s i z e during recompression. Goldfish for t h e i r a b i l i t y to repeatedly survive severe bubble formation, and Transparent Glass Fish (Ambassis l a l a ) for simultaneous u l t r a s o n i c and o p t i c a l bubble growth studies. Human subjects were used (12 man-dives, 400 fsw saturation dive using helium as the breathing medium) to compare u l t r a s o n i c imaging with a commercially available Doppler system. The pulsed-echo imaging picked up bubbles at the s i t e of bends pain (the knees) i n two diver and " p r e - c l i n i c a l " bubbles i n the knee of another. The Doppler system picked up no bubble signals during the t r i a l s . Since saturation dives seem to y i e l d the worst Doppler r e s u l t s , i t i s possible that t h i s exposure was not optimal for comparing the two systems. Horton and Wells (1976) introduced t h e i r own "pulsed, ul t r a s o n i c echo-ranging system". Backed up by a l i m i t e d number of t r i a l s with dogs, they primarily based t h e i r work on simulated 'bubble' assessment. They were able to locate bubbles to a minimum si z e of 26 microns. Daniels et a l (1979) presented a pulse-echo u l t r a s o n i c imaging system operating on a frequency of 8 MHz. Using guinea pigs they were able to detect bubbles down to 10 microns. As they expected, they could e s t a b l i s h no uniform r e l a t i o n s h i p between bubble radius and image s i z e . Semi-quantitative assessment of re l a t i o n s h i p was possible. Precise measurements of rates of growth of bubbles less than 300 microns i n diameter could not be made. H i l l s et a l (1983) reported on a pulsed-echoing system that overcame i n s t a b i l i t i e s of the e a r l i e s t models. The problem, however, i s that the apparatus i s too complex and not robust enough for routine use outside of the laboratory. They used a lower frequency system than employed by previous investigators (1.5 MHz) to evaluate p o t e n t i a l change i n the v e l o c i t y of sound with change in bubble s i z e . They found that the s e n s i t i v i t y of the v e l o c i t y of sound to bubble content was great enough that they f e l t they could detect a 2:1 reduction i n the v e l o c i t y of sound with a much simpler and less-expensive apparatus than they employed. They f e l t that monitoring the v e l o c i t y of sound would allow for the detection of a l l t i s s u e gas, whether stationary or moving, and could form the basis for an inexpensive device s u f f i c i e n t l y acceptable f o r routine use offshore. Daniels (1984) expressed concern over the d i f f i c u l t i e s of previous investigators i n achieving strong co r r e l a t i o n s between the presence of c i r c u l a t i n g bubbles and the development of symptomatic decompression sickness. He completed a serie s of studies employing both animal and human subjects using pulse- echoing imaging that allowed the evaluation of c i r c u l a t i n g as well as stationary bubbles. He was able to conclude that: 1) i n i t i a l bubbles are intravascular; 2) both the number of bubbles and the number of s i t e s of formation are dependent on the magnitude of the decompression; and 3) before symptoms of DCS occur, an accumulation of stationary bubbles w i l l be observed. Daniels' (1984) finding that stationary bubbles accumulate p r i o r to the onset of symptoms of DCS emphasizes the benefits of the pulse-echo analysis. However, the fac t that intravascular bubbles w i l l be detected f i r s t promotes the idea that more sen s i t i v e Doppler systems may hold the ultimate appeal. Buckles and Knox (1969) proposed a second a l t e r n a t i v e to Doppler systems with acoustic-optical imaging. They attained d i r e c t o p t i c a l images from acoustic wave forms. They exposed hamsters to 13.6 ATA for 30 minutes followed by explosive decompression completed within f i v e seconds. They were then able to i d e n t i f y bubbles to less than 700 microns i n diameter. Buckles and Knox concluded that these findings warranted further inv e s t i g a t i o n . Possibly because of the increased complexity of t h e i r system over other el u c i d a t i v e equipment, no follow-up has been found i n the l i t e r a t u r e . 47 Conclusions Despite inherent weaknesses i n the techniques and numerous proposals f o r a l t e r n a t i v e approaches, the basic Doppler techniques continue to be used. While more comprehensive or co n t r o l l e d analysis might be preferable, Doppler techniques remain s i g n i f i c a n t l y easier and less expensive to employ. I t must be emphasized, however, that the s e n s i t i v i t y of Doppler techniques i s l i m i t e d . At best, they permit only gross analysis of subjects and rough cr o s s - c o r r e l a t i o n of bubble "grades" with the r i s k of developing decompression sickness. Nevertheless, they represent techniques that are worthwhile within the scope of t h e i r design. 48 References: Doppler Ultrasound Baldes EJ, F a r r a l l WR, Haugen MC, Herrick JF. A forum on an ul t r a s o n i c method f o r measuring the v e l o c i t y of blood. In: K e l l y E, ed. Ultrasound i n Biology and Medicine. American I n s t i t u t e of B i o l o g i c a l Sciences : Washington, 1957; 3: 165-176. Bayne CG, Hunt WS, Johanson DC, Flynn ET, Weathersby PK. Doppler bubble detection and decompression sickness: a prospective c l i n i c a l t r i a l . Undersea Biomed Res 1985; 12(3): 327-332. Brubakk AO, Peterson R, Grip A, Holand B, Onarheim J, Segadal K, Kunkle TD, Tonjum S. Gas bubbles i n the c i r c u l a t i o n of divers a f t e r ascending excursions from 300 to 250 msw. J Appl Physiol 1986; 60(1): 45-51. Buckles RG, Knox C. In vivo bubble detection by a c o u s t i c - o p t i c a l imaging techniques. Nature 1969; 222(5195): 771-772. Christman CL, Catron PW, Flynn ET, Weathersby PK. In vivo microbubble detection i n decompression sickness using a second harmonic resonant bubble detector. Undersea Biomed Res 1986 13(1): 1-18. Daniels S. Ultrasonic monitoring of decompression procedures. P h i l Trans R Soc Lond (B) 1984; 304(1118): 153-175. Daniels S, Paton WDM, Smith EB. Ultrasonic imaging system for the study of decompression-induced gas bubbles. Undersea Biomed Res 1979; 6(2): 197-207. Eatock BC, Nis h i RY. Procedures for Doppler u l t r a s o n i c monitoring of divers f o r intravascular bubbles. Department of National Defense : Defense and C i v i l I n s t i t u t e of Environmental Medicine (DCIEM) Report No. 86-C-25, 1986, 28 pp. Eatock BC, Nis h i RY, Johnston GW. Numerical studies of the spectrum of low-intensity ultrasound scattered by bubbles. J Acoust Soc Am 1985; 77(5): 1692-1701. Eckenhoff RG, Osborne SF, Parker JW, Bondi KR. Direct ascent from shallow a i r saturation exposures. Undersea Biomed Res 1986; 13(3): 305-316. Evans A, Walder DN. Detection of c i r c u l a t i n g bubbles i n the i n t a c t mammal. Ultrasonics 1970; 8(4): 216-217. Franklin DL, Schlegel W, Rushmer RF. Blood flow measured by Doppler frequency s h i f t of back-scattered ultrasound. Science 1961; 134(3478): 564-565. 49 Gardette B. Correlation between decompression sickness and c i r c u l a t i n g bubbles i n 232 divers. Undersea Biomed Res 1979; 6(1): 99-107. G i l l i s MF, Karagianes MT, Peterson PL. In vivo detection of c i r c u l a t i n g gas emboli associated with decompression sickness using the Doppler flowmeter. Nature (London) 1968a; 217: 965. G i l l i s MF, Karagianes MT, Peterson PL. Bends: detection of c i r c u l a t i n g gas emboli with external sensor. Nature (London) 1968b; 161(3841): 579-580. G i l l i s MF, Karagianes MT, Peterson PL. Detection of gas emboli associated with decompression using the Doppler flowmeter. J Occup Med 1969; 11(5): 245-247. H i l l s BA, Grulke DC. Evaluation of u l t r a s o n i c bubble detectors i n v i t r o using c a l i b r a t e d microbubbles at selected v e l o c i t i e s . Ultrasonics 1975; 13(4): 181-184. H i l l s BA, Kanani B, James PB. V e l o c i t y of ultrasound as an indicator of bubble content. Undersea Biomed Res 1983; 10(1): 17- 22. Horton JW, Wells CH. Resonance u l t r a s o n i c measurements of microscopic gas bubbles. Aviat Space Environ Med 1976; 47(7) : 777- 781. Huggins KE. Doppler evaluation of m u l t i - l e v e l dive p r o f i l e s . Michigan Sea Grant Publication MICHU-SG-84-300. Reprinted from : Proceedings of the Fourteenth International Conference on Underwater Education, November 3-6, 1984: 125-130. Kalmus HP. E l e c t r o n i c flowmeter system. Rev S c i Instrum 1954; 25(3): 201-206. Kisman K. Spectral analysis of Doppler u l t r a s o n i c decompression data. Ultrasonics 1977; 5: 105-110. Kisman KE, Masurel G, Guillerm R. Bubble evaluation code for Doppler u l t r a s o n i c decompression data (abstr). Undersea Biomed Res 1978; 5(suppl 1): 28. Mackay RS. Proceedings of the second symposium on underwater physiology. Washington, DC : Nat Acad Sci/Nat Res Council, 1963: 1181: 41. Manley DMJP. Ultrasonic detection of gas bubbles i n blood. Ultrasonics 1969; 7(2): 102-105. 50 Masurel G, Gardette B, Comet M, Kisman K, Guillerm R. Ultrasonic detection of c i r c u l a t i n g bubbles during Janus IV excursion dives at sea to 460 and 501 msw (abstr). Undersea Biomed Res 1978; 5(suppl 1): 29. Nashimoto I, Gotoh Y. Relationships between precordial Doppler ultrasound records and decompression sickness. In: S h i l l i n g CW, Beckett MW, eds. Underwater Physiology VI. Proceedings of the Sixth Symposium on Underwater Physiology. Bethesda : Federation of American Societies for Experimental Biology, 1978: 497-501. Neuman TS, H a l l DA, Linaweaver PG J r . Gas phase separation during decompression i n man: ultrasound monitoring. Undersea Biomed Res 1976; 3(2): 121-130. Nishi RY. Ultrasonic detection of bubbles with Doppler flow transducers. Ultrasonics 1972; 10: 173-179. Powell MR. Doppler ultrasound monitoring of venous gas bubbles i n pigs following decompression with a i r , helium, or neon. Aerosp Med 1974; 45(5): 505-508. Powell MR, Thoma w, Fust HD, Cabarrou P. Gas phase formation and Doppler monitoring during decompression with elevated oxygen. Undersea Biomed Res 1983; 10(3): 217-224. Rubissow GJ, MacKay RS. Ultrasonic imaging of i n vivo bubbles i n decompression sickness. Ultrasonics 1971; 9(4): 225-234. Rubissow GJ, MacKay RS. Decompression study and control using u l t r a s o n i c s . Aerosp Med 1974; 45(5): 476-478. Smith KH, Spencer MP. Doppler indices of decompression sickness: t h e i r evaluation and use. Aerosp Med 1970; 41(12): 1396-1400. Spencer MP. Decompression l i m i t s for compressed a i r determined by u l t r a s o n i c a l l y detected blood bubbles. J Appl Physiol 1976; 40(2): 229-235. Spencer MP. A method for development of safe decompression schedules using Doppler u l t r a s o n i c bubble detection (abstr). Undersea Biomed Res 1978; 5(suppl 1): 28. Spencer MP, Aggenbach WJ. A laboratory method to screen divers for s u s c e p t i b i l i t y to bends, oxygen t o x i c i t y and nitrogen narcosis (abstr). Undersea Biomed Res 1978; 5(suppl 1): 29. Spencer MP, Campbell SD. Development of bubbles i n venous and a r t e r i a l blood during hyperbaric decompression. B u l l Mason C l i n i c 1968; 22(1): 26-32. Spencer MP, Campbell SD, Sealey JL, Henry FC, Lindbergh J . Experiments on decompression bubbles i n the c i r c u l a t i o n using u l t r a s o n i c and electromagnetic flowmeters. J Occup Med 1969; 11(5): 238-244. Spencer MP, Clarke HF. Precordial monitoring of pulmonary gas embolism and decompression bubbles. Aerosp Med 1972; 43(7): 762- 767. Spencer MP, Johanson DC. Investigation of new p r i n c i p l e s for human decompression schedules using the Doppler blood bubble detector. O f f i c e of Naval Research Tech Rep ONR Contract N00014-73-C-0094, 1974. Strauss MB, Samson RL. Decompression sickness: An update. Physic Sportsmed 1986 14(3): 196-205. Walder DN, Evans A, Hempleman HV. Ultrasonic monitoring of decompression. Lancet 1968; A p r i l 27: 897-898. Webb JT, Smead KW, Jauchem JR, Barnicott PT. Blood factors and venous gas emboli: surface to 429 mmHg (8.3 p s i ) . Undersea Biomed Res 1988; 15(2): 107-121. Wells PNT. Physical P r i n c i p l e s of Ultrasonic Diagnosis. Academic Press : New York, 1969. 281 pp. Wells PNT. Biomedical Ultrasonics. Academic Press : New York, 1977a. 635 pp. Wells PNT. Basic P r i n c i p l e s . In: Wells PNT (ed), Ultrasonics i n C l i n i c a l Diagnosis. 2nd ed. C h u r c h i l l Livingstone : New York, 1977b. 3-17. Laboratory Study 53 Statement of the Problem Lit e r a t u r e concerned with the e f f e c t of thermal v a r i a t i o n on compression/decompression i s sparse. In related work, nitrogen washout studies employing human subjects have demonstrated that s i g n i f i c a n t l y greater i n e r t gas elimination i s seen when ambient temperatures are warm as opposed to thermoneutral (Bal l d i n and Lundgren, 1972; B a l l d i n , 1973). This increase, c o r r e l a t i n g with temperature r i s e , can be seen to r e s u l t from va s o d i l a t i o n increasing c i r c u l a t i o n to the periphery thereby encouraging nitrogen outflow. This response to hyperthermia has been supported by the work of Bove et a l . (1978) with rabbits. Measuring 1 3 3Xenon washout, they found elimination rates to be higher during heat stress. Dunford and Hayward (1981) demonstrated that divers cooled during compression displayed post-decompression venous gas emboli (VGE or bubble) scores one-third as high as those seen i n subjects kept warm during the compression phase. They postulated that cooling the body would decrease both the uptake and the elimination of i n e r t gas. Thermoregulatory vasoconstriction would cause a decrease i n blood flow to the peripheral t i s s u e s , thereby decreasing the rate of nitrogen exchange. Conversely, elevating the ambient temperature should r e s u l t i n vasodilation, increased perfusion and subsequently an increase i n the rate of uptake or elimination of i n e r t gas (depending on the phase being considered). 54 Indeed, Dunford and Hayward (1981) reported that subjects demonstrate a more rapid decline i n post-dive bubble scores following active warming compared to passive warming. Unfortunately, they were inconsistent i n that active rewarming employed water immersion while passive rewarming took place i n sleeping bags. Without providing a control, Dunford and Hayward indicated that the increased hydrostatic pressure r e s u l t i n g from the water immersion of t h e i r rewarming procedure was responsible for the accelerated decline i n bubble scores. This could be i n d i r e c t l y supported by B a l l d i n and Lundgren (1972), who found that immersion i n water to the neck increased nitrogen elimination during oxygen breathing. Studies comparing thermally d i f f e r e n t post-dive immersion responses have not been found. The complex, often paradoxical, nature of temperature e f f e c t s on gas uptake and elimination and the p r a c t i c a l implications should make thermal factors an important point of research concern. Reduced thresholds for bubble formation have been reported to accompany both hypo- and hyperthermic exposure (Shida et a l . , 1982; Li n et a l . , 1984) . In fact, opposing mechanisms may be responsible fo r the s i m i l a r response to either form of thermal stress. The paucity of l i t e r a t u r e makes i t d i f f i c u l t to prescribe optimal dive and post-dive thermal practices or treatment protocols. Further investigation seemed warranted. In t h i s study, the e f f e c t of post-dive peripheral warming on i n e r t gas elimination 55 i s investigated. The Problem This study evaluates the e f f e c t of post-dive thermal status on i n e r t gas elimination. Hypotheses Three major hypotheses are evaluated: 1) Id e n t i c a l dive p r o f i l e s w i l l r e s u l t i n s i m i l a r VGE scores immediately post-dive i n subjects with s i m i l a r physical c h a r a c t e r i s t i c s . 2) Post-dive warming w i l l r e s u l t i n higher immediate post- immersion VGE scores than thermoneutral post-dive exposure. 3) Post-dive warming w i l l r e s u l t i n f a s t e r elimination of nitrogen, hence VGE scores w i l l f a l l more rapidl y following warm post-dive conditions compared to thermoneutral post-dive conditions. 56 Significance of the Study To date, most concern regarding thermal conditions and diving has been l i m i t e d to cold instead of heat stress. While t h i s may not be completely inappropriate, a balance must be struck i n l i g h t of modern divi n g equipment and operating procedures. The prevalent use of drysuits by divers (recreation, s c i e n t i f i c and commercial) makes cold stress less of a problem that i t has been i n the past. Further, given the present emphasis on diver comfort, i t i s not uncommon to f i n d hot showers, saunas, and even whirlpools r e a d i l y available for post-dive comfort- This suggests a need fo r a c l e a r understanding of the e f f e c t s of heat stress on divers. I t i s generally recognized that increasing the rate of nitrogen elimination can be b e n e f i c i a l . Shorter obligatory surface i n t e r v a l s would be required i f off-gassing rates could be increased. Such benefits w i l l not e x i s t , however, i f l o c a l i z e d gas phase separation exceeds perfusion rates. Perfusion rates act as the l i m i t e r for bodily elimination of i n e r t gas. The gas must reach the a l v e o l a r - c a p i l l a r y interface i n manageable volumes and sizes to pass into the a l v e o l i without coalescing into large bubbles capable of disrupting any aspect of transport, c i r c u l a t i o n and/or a l v e o l a r - c a p i l l a r y membrane exchange. A postulation on the possible e f f e c t s of thermal factors may provide a good example of the poten t i a l complications. An 57 i n d i v i d u a l who i s warm on i n i t i a l exposure to hyperbaric conditions may demonstrate rapid uptake of i n e r t gas throughout the body since perfusion rates w i l l be r e l a t i v e l y high throughout the core and periphery. Subsequent cooling over the course of the exposure may r e s u l t i n decreased perfusion rates i n some of the now nitrogen loaded t i s s u e s . Active rewarming following decompression may r e s u l t i n the peripheral t i s s u e being supersaturated with nitrogen since gas s o l u b i l i t y decreases with increasing temperature (Mack and- Lin, 1986) . This may r e s u l t i n the formation of bubbles i n peripheral tissues before perfusion rates can be restored or increased to the point that the gas can be eliminated i n a controlled manner. As suggested by the preliminary work of Mekjavic and Kakitsuba (unpublished) , t h i s could r e s u l t i n an increased incidence of cutaneous bends and therefore i s contraindicated. This study was conceived as a step towards quantifying the e f f e c t s of post-dive thermal factors on nitrogen elimination i n divers. I t i s anticipated that the findings w i l l contribute to the c l a r i f i c a t i o n of optimal post-dive behaviour for divers and possibly of management procedures for diving accidents that have been complicated by thermal factors. 58 Delimitations Dry chamber dives were employed to enhance the r e l i a b i l i t y of t h i s experimentation. I t i s understood that t h i s approach may a f f e c t the v a l i d i t y of the r e s u l t s . Caution i s advised i n applying these findings to les s controlled s i t u a t i o n s . In the i n t e r e s t of minimizing p o t e n t i a l l y confounding factors, intersubject v a r i a t i o n was r e s t r i c t e d . P a r t i c i p a t i o n was li m i t e d to males to remove possible gender e f f e c t s . An age range of 18 to 35 years was established to minimize e f f e c t s of rela t e d physical changes, such as changes i n c i r c u l a t o r y performance. In addition, the minimum age of 18 years s i m p l i f i e d consent procedures. Limitations While the c l i n i c a l patterns of decompression sickness are well recognized, controversy exists regarding the dominant mechanisms involved and t h e i r etiology. This study considers peripheral areas without dwelling on these issues. The appropriateness of Doppler u l t r a s o n i c techniques has been questioned by some investigators and are therefore not u n i v e r s a l l y accepted. Reservations notwithstanding, they continue to be used. While a l t e r n a t i v e procedures might e x i s t , they are generally 59 s i g n i f i c a n t l y more d i f f i c u l t and expensive to employ. I t must be emphasized, though, that the s e n s i t i v i t y of Doppler ultrasound i s lim i t e d . At best, only gross analysis of c i r c u l a t i n g VGE within subjects and rough cross-correlation of bubble "grades" with the r i s k of developing decompression sickness i s permitted (Gardette, 1979; Powell et a l . , 1983; Dunford, 1988). A further l i m i t a t i o n of t h i s study i s the hyperbaric exposure selected. The protocol employed a dive p r o f i l e (70 feet f o r 35 minutes) t y p i c a l l y more conservative than many regularly experienced by recreational, s c i e n t i f i c or commercial divers. I t was markedly le s s severe than those selected by previous investigators that demonstrated good Doppler r e s u l t s (Spencer and Clarke, 1972; Dunford and Hayward, 1981). Spencer and Clarke completed a chamber dive to 200 feet for 30 minutes (decompression according to U.S. Navy ta b l e s ) . Dunford and Hayward (1981) exposed t h e i r subjects to open water (10°C) dives to 78 feet for 38 minutes. A recent s h i f t i n appreciation of the po t e n t i a l hazards of hyperbaric exposure has necessitated a more conservative approach. Like many Canadian i n s t i t u t i o n s / organizations involved i n diving experimentation, Simon Fraser University has adopted a more conservative set of exposure tables than have been employed i n the past. These were developed at the Defense and C i v i l I n s t i t u t e of Environmental Medicine (DCIEM) i n Ontario with the intent of l i m i t i n g dives to minimal grade or bubble free exposures (Lauckner et a l . , 1984(a&b), 1985). Further concerns of the University regarding the ethics of exposing humans to situ a t i o n s expected to produce VGE made obtaining clearance for the experimentation d i f f i c u l t . To a l l a y these concerns, the very moderate exposure was used. I t was recognized, therefore, that the combination of a mild hyperbaric exposure and the r e l a t i v e i n s e n s i t i v i t y of the Doppler technique might r e s u l t i n indistinguishable differences between the conditions. Despite t h i s , the lower r i s k to the subjects dictated that a preliminary inve s t i g a t i o n use t h i s protocol. F i n a l l y , l i m i t a t i o n s of time, money and equipment necessarily r e s t r i c t the focus of t h i s study to the post-dive status of divers following warm dives. Other possible protocols would include post- dive status following cold exposures as well as warm exposures, however, these w i l l have to await future work. 61 Methodology A l l dives were completed i n the Environmental Physiology Unit hyperbaric chamber at Simon Fraser University. Anthropometric assessments were completed i n the Buchanan Fitness Laboratory at the University of B r i t i s h Columbia. This project was conducted i n accordance with guidelines reviewed i n the x P o l i c y of the School of Kinesiology on the Medical Clearance and Supervision of Human Research Subjects' (Appendix I) . Subj ects Ten male subjects p a r t i c i p a t e d i n the study. A l l were c e r t i f i e d divers between the ages of 18 and 35 years. Advertisement was c a r r i e d out among divers registered with the University of B r i t i s h Columbia Diving Operations O f f i c e , divers associated with the Simon Fraser University School of Kinesiology and through p r i v a t e l y owned scuba stores i n the greater Vancouver area. Selection was based upon voluntary a v a i l a b i l i t y and medical assurance of f i t n e s s for diving (Appendix I I ) . 62 Testing Procedures No subject was allowed to p a r t i c i p a t e i n the study without f i r s t being made aware of the purpose of the study, the t e s t i n g procedures and protocols and any known or suspected problems which might r e s u l t from the experimental procedure (Appendix I I I ) , or general hyperbaric exposure (Appendix IV) . Written consent was provided by each subject at t h i s point (Appendix V). Subjects were requested to avoid diving a c t i v i t y seven days p r i o r to a l l experimental t r i a l s to avoid possible confounding caused by residual nitrogen. They were further asked to standardize t h e i r dietary and behaviourial patterns p r i o r to a l l t r i a l s (Appendix VI). Subjects completed two t r i a l s . One with warm, and the other with thermoneutral post-dive exposure. The order of warm and thermoneutral exposures was randomized within the study group. T r i a l s were held on separate days at lea s t four days apart to ensure complete offgassing from p r i o r exposure and t r i a l s f or ind i v i d u a l subjects were scheduled at the same time of day to avoid i n t r a i n d i v i d u a l v a r i a t i o n due to circadian rhythms. A questionnaire was administered to a l l subjects p r i o r to both t r i a l s to i d e n t i f y factors p o t e n t i a l l y a f f e c t i n g the outcome of the t r i a l s (Appendix VII). 63 Testing Protocols Physical c h a r a c t e r i s t i c s were determined f o r a l l subjects. These included height, weight and percentage body f a t . Skinfold values were measured at s i x s i t e s to provide information requested by the agency a s s i s t i n g i n analyzing the study r e s u l t s (Defense and C i v i l I n s t i t u t e of Environmental Medicine - DCIEM). The percentage of body weight made up of f a t was estimated by a hydrostatic weighing technique outlined by Katch et a l . (1967). Upon a r r i v a l at the hyperbaric laboratory, subjects were given r e c t a l temperature probes to be inserted 15 cm. Core temperature was then evaluated for each subject. Following t h i s and p r i o r to diving, a reference signal was recorded for each subject using a Doppler Ultrasonic Bubble Detector interfaced with a cassette recorder. This according to the protocol described by Eatock and Nish i (1986). The baseline allowed comparison with post-dive signals to estimate c i r c u l a t i n g bubble a c t i v i t y r e s u l t i n g from the dive and post-dive exposures. The x d i v e s ' were dry hyperbaric chamber exposures to an equivalent ocean depth of 70 feet for an actual bottom time of 35 minutes (no staged decompression required). Subjects were instructed to remain at re s t throughout. Immediately following the dive, subjects walked to four feet deep "hot tubs" set up i n the laboratory. Just p r i o r to entering the water, core temperature was evaluated. Subjects were then immersed to the neck while i n a s i t t i n g p o s i t i o n (at rest) i n either 64 thermoneutral (28°C) or warm (38°C) water for 30 minutes. Following the water immersion, subjects moved out of the tubs and were evaluated u l t r a s o n i c a l l y i n a manner s i m i l a r to the baseline evaluation. Simultaneously, core temperature was assessed to determine any changes r e s u l t i n g from the immersion exposure. Subjects were then encouraged to remain at rest for the next 2.5 hours within the laboratory area. At 30 minute i n t e r v a l s u l t r a s o n i c evaluations were made. The r e c t a l probes were removed when and i f subjects demonstrated core temperature s t a b i l i t y over the period of two evaluations. Apparatus The hyperbaric chamber employed i n t h i s study was a multi- person/multi-lock hypo/hyperbaric chamber constructed by Perry Oceanographies, F l o r i d a . The Doppler Ultrasonic Bubble Detector (Model 1032 G) was produced by the I n s t i t u t e of Applied Physiology, Seattle. This was used i n conjunction with a precordial lead and headphones. Sound transmission was increased with Aquasonic 100 ultrasound transmission g e l . Ultrasound recordings were made using a Sony Stereo Cassette Deck (Model TC-188SD) and high qu a l i t y Maxell 90 minute tapes. 65 Data Analysis Ultrasound recordings were evaluated i n terms of bubble *grade' (VGE score) according to a protocol described by Eatock and Nishi (1986). This was completed at DCIEM, Downsview, Ontario. This protocol i s a refinement based on the o r i g i n a l Kisman-Masurel coding procedure (Kisman et a l . , 1978). Evaluations were completed i n a b l i n d manner, with no reference to experimental conditions. Resultant bubble grades were to be compared using a two-way analysis of variance (ANOVA) and trend analysis to determine differences between the two exposure conditions. Only complete subject r e s u l t s were to be analyzed s t a t i s t i c a l l y . Incomplete r e s u l t s were to be included i n the discussion. 66 Results Physical c h a r a c t e r i s t i c s of the subjects are presented i n Table I. Mean age was 24.9 +/- 2.8 years (range 21-29 years). Mean height was 182.3 +/- 4.6 cm (range 173.4-190.1 cm). Mean weight was 76.7 +/" 5.6 kg (range 71.7-88.8 kg) . Mean percent body fat was 13.4 +/" 4.6% (range 6.6-21.7%). Core temperature was evaluated r e c t a l l y f o r most of the subjects through both experimental t r i a l s . Subjects 01, 07, and 09 declined evaluation during t h e i r second t r i a l s f o r personal reasons. No changes i n core temperature were observed i n those monitored throughout eith e r condition. A l l u l t r a s o n i c evaluations were completed according to the planned schedule. At the time of recording, no bubbles could be i d e n t i f i e d a u r a l l y by the recording technician. Interpretation of the tape records by two independent evaluators at the Defense and C i v i l I n s t i t u t e of Environmental Medicine confirmed that measurable bubbles were not present i n any subject under e i t h e r condition. Subsequently, no s t a t i s t i c a l i n t e r p r e t a t i o n was conducted. Table I Anthropometric Charact e r i s t i c s Subj ect Age (yrs) Height (cm) Weight (kg) Body Fat (%) 01 22 178.2 74.5 8.2 02 23 185.7 73.2 12.0 03 29 184.9 73.4 16.0 04 25 190.1 78.8 13.0 05 21 185.0 77.1 6.6 06 23 181.3 73.1 12.2 07 27 182.9 71.7 10.6 08 25 173 .4 72.2 14.7 09 29 179.9 88.8 21.7 10 25 181.9 83.7 18.6 X 24.9 182.3 76.7 13.4 SD 2.8 4.6 5.6 4.6 68 Discussion The human system has not s p e c i f i c a l l y evolved f o r ra p i d l y changing pressure, but within a narrow optimal operating range i t has a remarkable capacity for protecting i t s e l f . The body can withstand repeated compression and decompression r e s p i r i n g gases of varying densities, and i n some instances, compositions. Present appreciation of the impact of hyperbaric exposure high l i g h t s the marvel of the human system's adap t a b i l i t y under adverse conditions. Decompression sickness (DCS) arises when the a b i l i t y of the body to adequately manage a given decompression stress i s surpassed. Assessing safe parameters i s a complicated task. Actual response can diverge dramatically from phy s i o l o g i c a l baselines as a r e s u l t of i n t e r - and i n t r a - i n d i v i d u a l v a r i a b i l i t y . The best general protection i s probably to ensure that a l l phys i o l o g i c a l systems are operating within t h e i r optimal range. E s s e n t i a l l y , safe decompression w i l l occur i f the uptake and elimination of i n e r t gas can be regulated so that excessive gas phase separation (bubble formation) does not occur. The extent of VGE ( c i r c u l a t i n g bubbles) presence i s normally used as a rough measure of r e l a t i v e r i s k . The primary impact of thermal stress (warm or cold) i s the 69 a l t e r a t i o n of c i r c u l a t i o n / p e r f u s i o n rates. Both d i f f u s i o n ( H i l l s , 1967; 1977) and perfusion (Ohta et a l . , 1978) are important i n the uptake and elimination of i n e r t gas. Perfusion rates are more variable and are therefore considered the prime governor of gas exchange under optimal conditions (Ohta et a l . , 1978), but the key consideration i s that perfusion must balance d i f f u s i o n . Unmatched d i f f u s i o n w i l l r e s u l t i n excessive gas phase separation - p o t e n t i a l l y leading to DCS. Therefore, factors which a f f e c t perfusion can s i g n i f i c a n t l y a l t e r the p e r f u s i o n / d i f f u s i o n balance and p o t e n t i a l l y challenge the norms established i n the e x i s t i n g decompression tables (Bove et a l . , 1978). This would act as a c r i t i c a l element i n a l t e r i n g the r i s k of developing DCS. Exposure to cold w i l l cause vasoconstriction, subsequently reducing peripheral perfusion. I f experienced during compression, reduced gas uptake w i l l r e s u l t . Dunford and Hayward (1981) found that t h i s could confer added protection against DCS since lesser quantities of gas w i l l have been absorbed during compression, thereby decreasing the r i s k of excessive gas phase separation upon decompression. I f the cold stress i s introduced during the bottom time, or during or a f t e r the decompression phase, more insidious r e s u l t s may be expected. Peripheral tissues w i l l be at l e a s t p a r t i a l l y loaded with i n e r t gas before the vasoconstriction occurs. Excess gas (compared to surface p a r t i a l pressures) would be trapped i n the periphery and therefore increase the p r o b a b i l i t y of bubble formation during decompression i f supersaturation i s not matched by perfusion rates. Gas phase separation could then r e s u l t i n p o t e n t i a l l y disruptive bubble growth and coalescence before the bubbles could be removed. Exposure to heat w i l l cause vasodilatation and perfusion rate increases. Occurring immediately before or during compression or during bottom time, gas uptake w i l l be increased. During non- saturation dives, t h i s can be seen to increase the r i s k of developing DCS during or following decompression since an increased gas load w i l l be borne by the body. Mild heat applied during decompression may counter t h i s e f f e c t . Enhanced perfusion during decompression could be seen to confer protection against DCS by increasing the rate of elimination. Vann (1982) and Dick et a l . (1984) demonstrated that mild exercise during a dive w i l l increase the rate of post-dive nitrogen elimination due to increased perfusion and reduced hypothermic vasoconstriction. The important point to observe i s that hypothermic vasoconstriction was reduced, not reversed. The energy expenditure kept the divers adequately perfused throughout the exposure and enhanced the decompression gas elimination. Applying external sources of heat to an already cold diver w i l l not provide the same response. Gas s o l u b i l i t y i s strongly affected by temperature. Most gases decrease i n s o l u b i l i t y by one to s i x percent for every 1°C r i s e i n temperature (Weathersby and Homer, 1980). Warming peripheral t i s s u e may then r e s u l t i n problematic gas phase separation before the perfusion rates increase s u f f i c i e n t l y to remove the gas. Indeed, t h i s was seen by Mekjavic and Kakitsuba (unpublished). They observed that while s i x hours post-decompression were uneventful, hot showers then p r e c i p i t a t e d symptoms of cutaneous DCS i n three out of four subjects who had come from a three hour post-decompression cold exposure. Symptoms were not observed i n subjects coming from a s i m i l a r post-decompression hot a i r exposure. They concluded that should post-dive warming be c a r r i e d out, i t should not be applied r a p i d l y at the r i s k of p r e c i p i t a t i n g DCS. I n d i r e c t l y supporting t h i s recommendation, Simmons et a l . (1982) observed a higher incidence of DCS associated with summer caisson work compared to winter operations. Since the pressurized area had r e l a t i v e l y uniform temperatures throughout the year they suggested that the higher incidence may be a r e s u l t of the rapid post-decompression heating. A series of studies have been completed evaluating the impact of various aspects of thermal stress. B a l l d i n (1973) demonstrated that increased ambient temperatures cause s i g n i f i c a n t increases i n the rate of nitrogen elimination during oxygen breathing. B a l l d i n and Liner (1978) demonstrated that chemically induced vasodilatation enhanced elimination and provided dramatic protection against DCS i n rabbits. Shida et a l . (1982) found that rats exposed to hyperthermic conditions throughout compression and decompression phases of a dive to 10 ATA were able to withstand s i g n i f i c a n t l y greater pressure reductions before detectable bubble formation ensued. Unfortunately, work has not been reported to consider vexternal post-dive warming and the p o t e n t i a l l y complicated interactions between s o l u b i l i t y , gas phase separation and perfusion. Since post-dive external warming i s commonly experienced by divers through showers or hot tubs, t h i s area demands further attention. The present investigation was designed to evaluate the impact of post-decompression warming on divers. Employing a protocol that had subjects warm throughout the compression and decompression phases i t was expected that post-dive warming would accelerate i n e r t gas elimination rates due to the increased perfusion. Using measurable bubble formation as a guide to elimination rates, i t was expected that higher bubble grades would be seen immediately following warm as compared to thermoneutral immersions. More rapid degradation of the bubble grades i n the warmed group would confirm the accelerated elimination. Demonstrating t h i s phenomenon, the next step would be to contrast these r e s u l t s with s i m i l a r immersion protocols following dives where: 1) the subjects were warm through the compression and bottom phases of the dive and cold through the decompression phase, and 2) the subject was cold throughout a l l phases of the dive. Cold throughout, divers should demonstrate lower bubble grades following rewarming. Warm during compression and cold during decompression, the divers would demonstrate the greatest s u s c e p t i b i l i t y to DCS with post-dive warming since peripheral tissues would have s i g n i f i c a n t i n e r t gas loads that would be trapped due to vasoconstriction through the decompression phase. These subjects would display the highest and sustained bubble grades r e f l e c t i n g the greater volume of dissolved gas and the delay i n elimination u n t i l VGE were allowed to form. These subjects would have the greatest r i s k of developing cutaneous DCS. The present study did not produce measurable VGE following e i t h e r thermoneutral and warm post-dive immersion exposures. This r e f l e c t e d the moderateness of the dive protocol employed. The majority of research r e l y i n g on Doppler assessments have used the more stringent exposure l i m i t s allowed by the U.S. Navy tables. The 50 minute no-decompression l i m i t of these tables i s contrasted to the 35 minute l i m i t established of the Canadian Forces A i r Diving Tables (1986). While previous work has confirmed that caution must be exercised when following the U.S. Navy tables, i t i s concluded from the present investigation that within the l i m i t s of the Canadian tables, mild post-dive warming does not appear to pose a s i g n i f i c a n t r i s k to the diver. I t must be stressed that only mild post-dive heating should be considered by divers. Large d i f f e r e n t i a l s between skin temperature and heating temperature may s t i l l p r e c i p i t a t e VGE formation and DCS following moderate dive exposures f o r the reasons of s o l u b i l i t y and perfusion/diffusion i n e q u i t i e s . The best recommendation i s that a temperate approach be maintained i n a l l a c t i v i t i e s r elated to diving. The present investigation supports the use of mild peripheral warming as an adjunctive therapy for decompression sickness. There are two separate l i n e s of l o g i c for t h i s recommendation. Using the endogenous heat production of exercise to maintain subject warmth (Dunford and Hayward, 1981) has resulted i n s i g n i f i c a n t l y greater VGE scores than the presently employed passive peripheral warming. This suggests that some combination of the mechanical i r r i t a t i o n and c a v i t a t i o n associated with muscular contraction, the decreased s o l u b i l i t y of muscle tissu e r e s u l t i n g from l o c a l i z e d warming, and the increased p a r t i a l pressure of C02 associated with exertion may be responsible for the development of VGE. Passive peripheral warming may provide the safest means of increasing i n e r t gas elimination without encouraging VGE development. The second benefit of peripheral warming r e l a t e s to one of the most accepted adjunctive therapies i n the present management of DCS - oxygen therapy. The benefits of oxygen i n maximizing the gradient for nitrogen elimination, improving oxygen transport i n the lung, and increasing dissolved oxygen transport are well established. However, high p a r t i a l pressures of oxygen have also been demonstrated to s i g n i f i c a n t l y reduce peripheral c i r c u l a t i o n (Bird and T e f l e r , 1965) . While t h i s has been reported to have only minimal e f f e c t on nitrogen elimination (Plewes and Farhi, 1983) , i t may exacerbate perfusion/diffusion imbalances i n peripheral t i s s u e s . Passive peripheral warming would a s s i s t i n reversing t h i s development. 75 Conclusions The e x i s t i n g l i t e r a t u r e o f f e r s scant consideration of the impact of thermal factors on decompression safety. Experimental invest i g a t i o n i s required to elucidate the mechanisms and responses r e s u l t i n g from thermal stress. The present investigation has confirmed that the Canadian Forces A i r Diving Tables provide a safe l i m i t of hyperbaric exposure f o r the p r o f i l e tested, regardless of moderate post-dive thermal s t r e s s . For p r a c t i c a l application, i t i s emphasized that only moderate heating should be considered. Increased i n e r t gas elimination i n the absence of VGE formation caused by mild post-dive peripheral warming suggests that t h i s could be an appropriate adjunctive therapy f o r decompression sickness. 76 Recommendations Further investigation should consider: 1) the ro l e of skin temperature, perfusion and peripheral warming i n i n e r t gas elimination and VGE formation - to provide recommendations for diving practices and possibly DCS therapy; 2) the importance of p a r t i a l pressures of C02 and mechanical i r r i t a t i o n i n the generation of VGE - to provide recommendations for post-dive a c t i v i t y l e v e l s . 77 References: Laboratory Study B a l l d i n UI. E f f e c t s of ambient temperature and body p o s i t i o n on ti s s u e nitrogen elimination i n man. Aerospace Med 1973; 44(4): 365-370. B a l l d i n UI, Liner M. Preventive e f f e c t of a vasodilator on the occurrence of decompression sickness i n rabbits. Aviat Space Environ Med 1978; 49(6): 759-762. B a l l d i n UI, Lundgren CEG. E f f e c t s of immersion with the head above water on t i s s u e nitrogen elimination i n man. Aerospace Med 1972; 43(10): 1101-1108. Bird AD, T e f l e r AMB. E f f e c t of hyperbaric oxygen on limb c i r c u l a t i o n . Lancet 1965; 1: 355-356. Bove AA, Hardenbergh E. Miles JA J r . E f f e c t of heat and cold stress on i n e r t gas ( 1 3 Xenon) exchange i n the rabbit. Undersea Biomed Res 1978; 5(2): 149-158. Canadian Forces A i r Diving Tables and Procedures. Downsview, Ontario : Department of National Defence, Defense and C i v i l I n s t i t u t e of Environmental Medicine, 1986. 57 pp. Dick APK, Vann RD, Mebane GY, Freezor MD. Decompression induced nitrogen elimination. Undersea Biomed Res 1984; 11(4): 369-380. Dunford R. Better tables? ( l e t t e r ) . Diver 1988; 14(4): 8. Dunford R, Hayward J . Venous gas bubble production following cold stress during a no-decompression dive. Undersea Biomed Res 1981; 8(1): 41-49. Eatock BC, Nis h i RY. Procedures for Doppler u l t r a s o n i c monitoring of divers for intravascular bubbles. Department of National Defense : Defense and C i v i l I n s t i t u t e of Environmental Medicine (DCIEM) Report No. 86-C-25, 1986. 28 pp. Gardette B. Correlation between decompression sickness and c i r c u l a t i n g bubbles i n 232 divers. Undersea Biomed Res 1979; 6(1): 99-107. H i l l s BA. Diffus i o n versus blood perfusion i n l i m i t i n g the rate of uptake of i n e r t non-polar gases by s k e l e t a l rabbit muscle. C l i n S c i 1967; 33: 67-87. H i l l s BA. Decompression Sickness Volume I: The Biophysical Basis of Prevention and Treatment. New York : John Wiley and Sons, 1977. 322 pp. 78 Katch FI, et a l . Estimation of body volume by underwater weighing : description of a simple method. J Appl Physiol 1967; 23(5): 811- 813. Kisman KE, Masurel G, Guillerm R. Bubble evaluation code for Doppler u l t r a s o n i c decompression data (abstr). Undersea Biomed Res 1978; 5(suppl 1): 28. Lauckner GR, Nis h i RY, Eatock BC. Evaluation of the DCIEM 1983 decompression model for compressed a i r diving (series A-F). Department of National Defence, Defense and C i v i l I n s t i t u t e of Environmental Medicine Report No. 84-R-72, 1984(a). 30 pp. Lauckner GR, Nis h i RY, Eatock BC. Evaluation of the DCIEM 1983 decompression model for compressed a i r diving (series G-K). Department of National Defence, Defense and C i v i l I n s t i t u t e of Environmental Medicine Report No. 84-R-73, 1984(b). 29 pp. Lauckner GR, Nis h i RY, Eatock BC. Evaluation of the DCIEM 1983 decompression model for compressed a i r diving (series L-Q). Department of National Defence, Defense and C i v i l I n s t i t u t e of Environmental Medicine Report No. 85-R-18, 1985. 31 pp. Lin YC, Mack GW, Watanabe DK, Shida KK. Experimental attempts to influence the bubble threshold from saturation dives i n animals. In: Bachrach AJ, Matzen MM, eds. Underwater Physiology VIII. Proceedings of the eighth symposium on underwater physiology. Bethesda : Undersea Medical Society, 1984: 259-268. Mack GW, L i n YC. Hypothermia impairs but hyperthermia does not promote i n e r t gas elimination i n the r a t . Undersea Biomed Res 1986; 13(2): 133-145. Ohta Y, Song SH, Groom AC, Farhi LE. Is i n e r t gas washout from the t i ssues l i m i t e d by diffusion? J Appl Physiol Respirat Environ Exercise Physiol 1978; 45(6): 903-907. Plewes JL, Farhi LE. Peripheral c i r c u l a t o r y responses to acute hyperoxia. Undersea Biomed Res 1983; 10(2): 123-129. Powell MR, Thoma W, Fust HD, Caborrou P. Gas phase formation and Doppler monitoring during decompression with elevated oxygen. Undersea Biomed Res 1983; 10(3): 217-224. Shida KK, Watanabe DK, L i n YC. E f f e c t of ambient temperature on decompression threshold from a saturation dive i n r a t s . Undersea Biomed Res 1982; 9(suppl 1): 28. Simmons EH, O'Driscoll SW, Gamarra JA. C l i n i c a l and experimental evidence f o r the use of hypothermia i n decompression sickness. Aviat Space Environ Med 1982; 53(3): 266-268. Spencer MP, Clarke HF. Precordial monitoring of pulmonary gas embolism and decompression bubbles. Aerosp Med 1972; 43(7): 762- 767. Vann RD. The e f f e c t of exercise during decompression (abstr). Undersea Biomed Res 1982; 9(suppl 1): 26. Weathersby PK, Homer LD. S o l u b i l i t y of i n e r t gases i n b i o l o g i c a l f l u i d s and ti s s u e s : a review. Undersea Biomed Res 1980; 7(4): 277- 296. Appendices Subject Forms/Information Materials 81 Appendix I Pol i c y Of The School Of Kinesiology On The Medical Clearance And Supervision Of Human Research Subjects Informed Consent Informed consent must include evidence that the subject has agreed to p a r t i c i p a t e i n the experiment on the basis of a cl e a r description of the r i s k s and p o t e n t i a l benefits involved as well as the understanding that withdrawal from p a r t i c i p a t i o n i s the subject's r i g h t at any time without prejudice. Informed consent must be secured by the experimenter before the subject can p a r t i c i p a t e i n the research. Medical Clearance Medical clearance must be obtained i n advance fo r a l l subjects i n research which involves s i g n i f i c a n t r i s k of injury or disease, and i n p a r t i c u l a r when research involves exposure to hypoxia, hyperbaric oxygen or other hyperbaric a p p l i c a t i o n of b i o l o g i c a l , chemical or physical toxins. The examining physician must be informed of the nature of the hazards the subject w i l l face. In hyperbaric research, the standard medical clearance form authorized by the Simon Fraser University Diving Control Board must be used. Medical Supervision a. The following areas of research require the presence of a physician on campus who i s informed of the nature of the research and available to render assistance i n an emergency: i . hypothermia i i . hyperthermia i i i . hyperbaric oxygenation i v . hyperbaric exposure b. The following stressors require the presence of a physician i n the lab during experimental sessions: i . hypothermia with the subject's core temperature f a l l i n g below 35°C during the a p p l i c a t i o n of cold stres s ; 82 i i . hyperthermia with core temperature r i s i n g above 408C; i i i . hyperbaric oxygenation with Pj0 2 greater than 2 ATA; i v . hypoxia with Pj0 2 l e s s than 90 mm Hg, or with ambient temperature less than 19°C or greater than 24°C and Pj0 2 l e s s than 105 mm Hg; v. exercise stress t e s t s when: (a) the subject i s exercised to exhaustion and has a predicted V0 2 max less than 40 ml/kg/min, or (b) the subject has an underlying disease or condition which i s a s i g n i f i c a n t predisposition to cardiac arrest during exercise c. During exercise stress t e s t s other than as described i n section 3.b.v., above, a physician must be available within approximately three minutes access of the s i t e of the t e s t s , and must be informed i n advance that such t e s t i n g w i l l be taking place. d. During hyperbaric research, i n the event that the supervising physician must enter the chamber to assess or t r e a t a subject, a back-up physician must be avail a b l e to provide medical supervision from outside the chamber. e. During a l l research described i n t h i s section (3) , at le a s t one person i n the lab must hold v a l i d c e r t i f i c a t i o n i n basic cardiopulmonary r e s u s c i t a t i o n . Resuscitation Supplies The "crash c a r t " containing equipment and supplies f o r use i n re s u s c i t a t i o n of victims of cardiac arrest, decompression accidents and hypo/hyperthermic accidents s h a l l be available on s i t e whenever research i s undertaken i n which there i s a s i g n i f i c a n t r i s k of such accidents. Normally, the cart w i l l remain i n the Environmental Physiology Unit and w i l l not be moved nor disturbed unless so ordered by a physician involved i n medical supervision. The physicians on fa c u l t y i n Kinesiology s h a l l p e r i o d i c a l l y check such equipment and supplies and arrange for necessary replacements or repairs, the costs being borne by the School of Kinesiology. Compensation For Physician's Services Medical clearance and medical supervision i n research i n Kinesiology s h a l l normally be among the r e s p o n s i b i l i t i e s of the physicians on faculty, with f u l l respect given to these physicians' teaching, professional and i n d i v i d u a l research r e s p o n s i b i l i t i e s i n scheduling such clearance and supervision. Research funded by external agencies and requiring medical 83 clearance of subjects should have, as a budget item, compensation to the School of Kinesiology i f physicians on facu l t y are asked to provide t h i s service. Contract work which requires the medical clearance and/or supervision of subjects by physicians should include budget items f o r d i r e c t f i n a n c i a l compensation of such physicians, be they on fa c u l t y or not. Provision of such medical services i n contract work i s not one of the r e s p o n s i b i l i t i e s of the physicians on faculty. 6. University Ethics Committee Kinesiology ethics p o l i c y for human experimentation w i l l n a t u r a l l y be subordinate to University p o l i c y i n case of c o n f l i c t between the two. Submissions of research proposals from Kinesiology to the University Ethics committee s h a l l include s u f f i c i e n t l y d e t ailed information concerning r i s k s and safeguards to permit that committee to judge the adequacy of such safeguards i n t h e i r deliberations. 7. Application Of This Policy Copies of t h i s p o l i c y s h a l l be d i s t r i b u t e d to a l l faculty, students, and s t a f f involved i n research on human subjects involving a s i g n i f i c a n t r i s k of injury or disease, whenever such research i s done under the aegis of the School of Kinesiology. Adherence to t h i s p o l i c y i s mandatory unless exemption i s granted i n advance by the School of Kinesiology and the University Ethics Committee. R a t i f i e d 09 October 1985 84 Appendix II Medical Questionnaire (Confidential) Surname Given Name Address Phone • Date of B i r t h Weight . Family Physician Address Phone Medical History Please answer the following questions accurately since they are designed to i d e n t i f y subjects who should not p a r t i c i p a t e within the proposed study. Please place a check-mark by any condition which applies to you. Responses w i l l be viewed only by the p r i n c i p a l investigator and departmental physician. Have you suffered, or dp you now suff e r from any of the following? 1. asthma [ ] 2. b r o n c h i t i s [ ] 3. tuberculosis, emphysema, f i b r o s i s , p l e u r i s y [ ] 4. other respiratory abnormality or scarring [ ] 5. pneumothorax or collapsed lung [ ] 6. nasal obstruction [ ] 7. frequent or severe nose bleeds [ J 8. frequent cold or sore throats [ ] 9. chest pain and persistent cough [ ] 85 10. coughing up blood (hemoptysis) 11. heart disease 12. high or low blood pressure 13. abnormal EKG 14. claustrophobia 15. alcohol or drug abuse 16. a l l e r g i e s 17. communicable diseases or contact with patients with same 18. diabetes 19. dizziness, f a i n t i n g s p e l l s or f i t s 20. do you smoke or have you smoked i n the past? 21. are you under medical care now or taking medication? Please c l a r i f y affirmative answers. I declare the above answers are, to the best of my knowledge, a true and accurate statement of my medical his t o r y . Signed Date Witness 86 Appendix III Subject Information Package (1) The E f f e c t s Of Post-Dive Warming On Vascular Gas Emboli Production Item 1 Project Objectives: The primary objective of t h i s study i s to investigate the ef f e c t s of post-dive thermal exposure on the production of vascular gas emboli. Item 2 Test Procedures: Volunteers who p a r t i c i p a t e i n t h i s study must f i r s t meet minimal standards of good health as c e r t i f i e d by them i n the subject Medical Questionnaire and a f t e r examination by a diving physician. I f the physician i s other than Don Hedges, MD (diving medical o f f i c e r of the SFU School of Kinesiology) the completed medical records must be made ava i l a b l e for h i s review. A l l subjects w i l l undergo two hyperbaric chamber dives (dry) completed seven days apart (note: a l l subjects s h a l l r e f r a i n from any other hyperbaric exposure seven days p r i o r to both t e s t sessions). A l l exposures w i l l be to an equivalent ocean depth of 70 feet (fsw) for 35 minutes. Subjects s h a l l remain at r e s t throughout the exposure. Following the dive subjects w i l l be immersed to the neck i n thermoneutral (30°C) or warm (37°C) water for 30 minutes. Monitoring of subjects for vascular gas bubbles w i l l be done non-invasively employing a Doppler Ultrasonic Bubble Detector. Observations w i l l be made immediately a f t e r the dive and at 30 minute i n t e r v a l s for the next four hours. Throughout t h i s period subjects w i l l remain at rest i n the Environmental Physiology Laboratory. Item 3 Risks and Discomforts: a(i) Hyperbaric Exposure Exposure to hyperbaric a i r at 70 fsw i s considered to be a f a i r l y conservative diving exposure commonly experienced by sport divers. Subjects should be aware, however, of the serious r i s k s of hyperbaric chamber diving. These are outlined i n the separate section 87 e n t i t l e d "Risks During Exposure to Hypo/Hyperbaric Conditions" (Subject Information Package {2}). I t i s important that subjects READ THIS INFORMATION CAREFULLY. a ( i i ) Water Immersion The immersion of subjects to the neck i n t h i s study should o f f e r l i t t l e discomfort and no r i s k . Sensation of temperature w i l l be mild and not uncomfortable. a ( i i i ) Safety Precautions During each dive f u l l y trained technical s t a f f , including two chamber operators and a physician trained i n diving medicine w i l l be on hand. In addition, a tender trained i n CPR w i l l accompany subjects during the chamber dives. Instruments and materials needed for r e s u s c i t a t i o n and for the treatment of decompression sickness and related condition w i l l be available i n the laboratory at a l l times. Sessions i n the chamber w i l l be undertaken during hours when the Health Services i s open and physicians there w i l l be informed i n advance of the nature of the sessions i n the remote chance that t h e i r assistance would be required (eg. should the physician on s i t e need to enter the chamber to a s s i s t a subject). Item 4 Inquiries: Questions regarding the procedures are welcome. I f you have any doubts please ask for further explanations. Item 5 Freedom of Consent: P a r t i c i p a t i o n i s on a voluntary basis. You are free to deny consent at any time during or between t r i a l s . Item 6 C o n f i d e n t i a l i t y : A l l questions, answers, and r e s u l t s from t h i s study w i l l be i d e n t i f i e d i n the resultant manuscript and/or publications by use of subject codes only. 88 Appendix IV Subject Information Package (2) Risks During Exposure To Hypo/Hyperbaric Conditions Environmental Physiology Unit School of Kinesiology Simon Fraser University February, 1986 Risks during open-water or hypo/hyperbaric chamber diving include the following: 1. Otic Barotrauma Known as an "ear squeeze", t h i s injury i s caused by f a i l u r e to equalize a i r pressure between the external environment and the middle ear, generally during pressurization. I t involves ear discomfort, pain and sometimes ringing i n the ears or bleeding i n the ear drum; occasionally the drum i s perforated. I t generally resolves rapidly (days) but i f severe may require medication and/or a s p e c i a l i s t ' s attention. I t s prevention requires gentle ear-clearing manoeuvres every second or two during changes i n surrounding pressure. I f such manoeuvres f a i l , reducing the pressure difference (eg. by p a r t i a l ascent during a dive) should be t r i e d , with r e p e t i t i o n of the c l e a r i n g manoeuvres. i f t h i s f a i l s , the exposure should be terminated i n an orderly manner. Correction i s easiest i f undertaken at the f i r s t sign of i n a b i l i t y to equalize. DO NOT WAIT UNTIL YOU FEEL PAIN! Equalization w i l l be harder i f you have a cold or " f l u " ; under these circumstances hypo/hyperbaric exposure must be postponed. Seasonal a l l e r g i e s may also require postponement of an exposure, unless advised otherwise by the physician responsible for medical aspects of the dive. DO NOT TAKE over-the-counter remedies unless so advised by the physician. 2. Decompression Sickness Generally known as "the bends", t h i s condition develops when nitrogen bubbles form i n body tissues during depressurization. Some nitrogen i s dissolved i n tissues even at the surface, but much more i s "loaded" into the tissues during compressed a i r breathing, i n d i r e c t proportion to the depth or pressure and to the time spent at hyperbaric pressure. On depressurization, the nitrogen i s "supersaturated" i n the tissues and i f t h i s depressurization occurs too r a p i d l y to allow the offloading of the nitrogen from the blood into the 89 a l v e o l i of the lungs, the nitrogen i n the blood and tissues can form bubbles large enough to do damage and to cause symptoms as described below. a. Limb Bends I f the bubbles form i n tissues i n and around j o i n t s , the r e s u l t w i l l be a s t e a d i l y increasing deep aching pain i n the involved j o i n t ( s ) . This pain increases with time and can become excruciating i f not treated. Predispositions include previous injury or surgery i n a j o i n t or, during exposure, a cramped posture l i m i t i n g c i r c u l a t i o n i n the j o i n t area. Treatment i s immediate repressurization i n a hyperbaric chamber using a well established protocol alternating air/oxygen breathing (U.S. Navy treatment tables are used at Simon Fraser U n i v e r s i t y ) ; t h i s i s v i r t u a l l y 100% e f f e c t i v e i n uncomplicated cases treated rapi d l y . I t i s thus mandatory for a l l divers, subjects and tenders exposed to hyperbaric conditions to maintain a one hour (or more) "bends watch", i e . to stay under supervision for that time i n the chamber laboratory; to report any and a l l symptoms which a r i s e immediately to the chamber operator or physician responsible, to wear a diver's medical a l e r t bracelet for the next 24 hours during which s/he must not be l e f t alone; to report any and a l l symptoms during that or the subsequent period (to the operator, physician, or nearest treatment f a c i l i t y - eg. Vancouver General Hospital); and during that 24 hours to abstain from f l y i n g or diving except as approved by the operator and physician, since a l t i t u d e depressurization (flying) increases the rate of bubble formation and r e p e t i t i v e dives increases the onloading of nitrogen at a time when nitrogen from the f i r s t exposure may not have been f u l l y off-loaded. b. Nervous System Bends Bubble formation during decompression can occur i n the c i r c u l a t i o n of the central nervous system, producing deleterious e f f e c t s by d i r e c t mechanical obstruction of blood flow or i n d i r e c t l y by complex interactions with blood components. Commonly these e f f e c t s occur at the spinal cord l e v e l , due to the sluggish blood flow i n the extra-vertebral venous system. Spinal involvement can produce a v a r i e t y of symptoms including numbness, weakness or p a r a l y s i s of one or more limbs, loss of coordination, and changes i n bowel or bladder control. Other manifestations of nervous system bends include dizziness with or without "ringing" i n the ears and hearing loss (vestibular and/or auditory system involvement) as well as decreased alertness, l e v e l of consciousness and a b i l i t y to think c l e a r l y . THESE 90 EFFECTS INDICATE AN EMERGENCY! They must be reported immediately since any delay i n treatment reduces the l i k e l i h o o d of f u l l recovery. Treatment i s immediate recompression, as for limb bends, but with a d i f f e r e n t treatment table plus or minus the addition of c e r t a i n drugs (eg. steroids) and resuscitatory manoeuvres as needed. Although symptoms of nervous system involvement t y p i c a l l y develop within the f i r s t few minutes a f t e r decompression, they may be subtle and/or a r i s e l a t e r ; the same bends watch and 24 hour surveillance i s required as described for limb bends. c. "The Chokes" This condition develops when large numbers of bubbles come out of solution into the venous c i r c u l a t i o n and overwhelm the capacity of the lungs to f i l t e r them out ( a l l venous blood passes from the r i g h t side of the heart into the pulmonary c i r c u l a t i o n , the vessels of which subdivide many times into smaller and smaller vessels where bubbles are trapped). Symptoms include a burning sort of chest pain, shortness of breath and a cough with or without hemoptysis (blood). Treatment i s immediate recompression as described for limb and neurologic bends. d. "Skin Bends" Skin bends usually develops a f t e r short, deep dry chamber dives and involves bubble formation i n the skin during depressurization. i t i s generally not serious although i t may produce s i g n i f i c a n t discomfort, including itchiness and tenderness with a reddening of the skin and/or a splotchy red rash. Although recompression i s r a r e l y required, skin bends may be associated with a higher p r o b a b i l i t y of co-existent more serious forms of decompression sickness; hence, symptoms of skin bends must be reported immediately. e. Dysbaric Osteonecrosis This i s a delayed form of decompression sickness i n which cysts form i n bones, usually near large j o i n t s , and commonly i n people who dive frequently over several years. I t i s believed that t h i s condition r a r e l y , i f ever, develops unless the diver has missed a decompression stop (see below) during a previous dive. I t i s slowly progressive, so that continued diving may cause the cysts to enlarge, which i s p a r t i c u l a r l y problematic i f the cysts come to involve the c a r t i l a g e within a j o i n t . Periodic long bone x-rays are sometimes used i n monitoring for cyst development among very frequent divers. There i s no s p e c i f i c treatment for t h i s 91 condition. Evidence suggesting dysbaric osteonecrosis includes bone or j o i n t pain and/or a fracture of a long bone; c y s t i c bone breaks more e a s i l y than normal bone. Management includes orthopaedic consultation and sometimes surgery, as well as a discontinuation of diving. f. Miscellaneous Lymphatic congestion (bubbles) may develop on decompression, often manifested by f a c i a l swelling. Abdominal pain may sometimes a r i s e and has been attr i b u t e d to expanding gas i n the i n t e s t i n e s during decompression. Vague or unusual symptoms may also a r i s e . A l l symptoms must be reported a f t e r decompression (including hypobaric exposure) ; decisions about treatment and follow-up and management should be l e f t to the physician, not the i n d i v i d u a l exposed to pressure changes. g. Prevention of DCS Controlled depressurization i s the key to the prevention of decompression sickness. Diving tables e x i s t (eg. U.S. Navy tables) which require a s p e c i f i c rate of pressure change (eg. so many feet per minute ascent from a dive) as well as "stops" for s p e c i f i e d periods at s p e c i f i c depths (pressure levels) during ascent from a dive. Use of these tables i s mandatory and i s meant to allow a controlled off-loading of nitrogen from the tissues, into the blood and thence into the lungs, such that the r i s k of bends i s reduced to less than 3-5%. These tables were derived empirically, that i s , based on data from many dives i n which various decompression p r o f i l e s were used and the r e l a t i v e r i s k of decompression sickness was determined. A further decrease i n r i s k can be obtained by over-estimating the amount of exposure to pressurization (depth and time), and by breathing 100% oxygen during one or more decompression stops (this increases the d i f f u s i o n gradient for nitrogen both from the tissues to the blood and from the blood to the a l v e o l i of the lungs). During chamber dives, the chamber operator and diving physician s e l e c t the decompression table (ascent protocol) to be used. 3. A r t e r i a l Gas Embolism This i s a f a i r l y rare, but sometimes l e t h a l condition i n which gas bubbles form i n the a r t e r i a l c i r c u l a t i o n ; these bubbles can obstruct blood flow to the heart ("heart attack") or brain ("stroke"), producing emergency sit u a t i o n s and/or death. The usual cause i s a rapid decompression with the g l o t t i s closed (ed. breath-holding on ascent), such that the a i r trapped within the lung space, increasing as i t does i n volume on depressurization, bursts through the lung membranes and enters the a r t e r i a l c i r c u l a t i o n there. In t h i s context i t i s important to remember that the volume of a uni t amount of a i r doubles as pressure goes from twice normal to normal (atmospheric) pressure, eg., as a diver ascends from 33 feet of seawater to the surface. Evidence of gas embolism i s usually dramatic, with the commonest presentation being the unconscious diver on the surface, who has l o s t consciousness on ascent due to brain damage or a heart attack and who i s therefore also at r i s k of drowning. In the conscious diver, evidence includes impaired alertness or thinking, d e f i c i t s i n movement, speech or sensation, or a symptom complex including chest pain ( l e f t of c e n t r a l ) , shortness of breath and nausea. Treatment includes r e s u s c i t a t i o n immediately (hence the need for persons trained i n cardiopulmonary r e s u s c i t a t i o n to be on the scene during any hyperbaric exposure — including recreational dives), 100% oxygen and transport i n a head-down po s i t i o n (reduces bubble c i r c u l a t i o n to the brain) to the nearest hyperbaric treatment f a c i l i t y (hence the need for divers to know i n advance where such f a c i l i t i e s are and how transportation can be acquired). At S.F.U., we are able to i n i t i a t e r e s u s c i t a t i o n and to undertake treatment by recompression within the hyperbaric chamber. The best form of treatment i n t h i s and a l l other conditions i s prevention, by proper breathing techniques on ascent and by the exclusion from hyperbaric exposure of a l l indiv i d u a l s who are known to be predisposed to gas embolism. These people include anyone with a h i s t o r y of surgery i n which the chest wall was opened (eg. bypass grafts) as well as people with a known abnormal communication between the venous c i r c u l a t i o n by which venous gas bubbles can pass into the a r t e r i e s (eg. i n t e r v e n t r i c u l a r septal defect) or with known obstructive lung disease (chronic br o n c h i t i s , emphysema, asthma. e t c ) . People with asthma, for example, must not dive because they run a high r i s k of gas trapping i n a pulmonary segment at depth, due to airway spasm and mucous secretions, with a consequent r i s k of "burst lung" and gas embolism on decompression. Although p e r i o d i c chest x-rays with f u l l inhalation and exhalation can help determine which in d i v i d u a l s should be excluded from diving, some underlying conditions cannot be determined c l i n i c a l l y , so that r i s k s cannot be reduced to zero. Hypoxia or Anoxia Periods of inadequate or zero oxygen supply to bodily tissues can lead to permanent injury or even death. Equipment f a i l u r e or other accidents, both underwater and i n the hyperbaric/hypobaric chamber, can p o t e n t i a l l y cause hypoxia or anoxia, f o r which the treatment i s c l e a r l y the restoration 93 of adequate oxygenation. Prevention requires proper maintenance and use of equipment, with s p e c i a l attention to equipment status before use (eg., the c h e c k - l i s t the chamber operators use) and to the provision of adequate back-up equipment as well as an emergency protocol which i s rehearsed and understood beforehand. Individuals c e r t i f i e d i n cardiopulmonary r e s u s c i t a t i o n mst be present during exposure. 5. Drowning. This s p e c i a l hazard of open-water diving occurs most often as a r e s u l t of equipment f a i l u r e or misuse, or as a r e s u l t of unconsciousness due to one of the other r i s k s l i s t e d above. Inadequate equipment preparation and maintenance, sudden weather changes, solo diving, panic, fatigue and hypothermia a l l contribute to the r i s k of drowning. Cardiopulmonary r e s u s c i t a t i o n and transport to a treatment centre are the immediate needs. 6. Oxygen t o x i c i t y . Oxygen i s a d i r e c t toxin to tissues when present i n concentrations s i g n i f i c a n t l y higher than normal (about 0.21 atmospheres of pressure). Nerve t i s s u e and the lungs are p a r t i c u l a r l y s e n s i t i v e . Lung t o x i c i t y develops gradually, during exposure to hyperbaric oxygen for hours or days. T o x i c i t y v a r i e s d i r e c t l y with the oxygen p a r t i a l pressure and the duration of exposure, and manifests i n i t i a l l y as a measurable decrease i n v i t a l capacity ( r e f l e c t i n g i n part a decreased e l a s t i c i t y of the lungs). This decrease i s r e v e r s i b l e once the hyperbaric oxygenation has ceased. Oxygen t o x i c i t y to the nervous system develops much more rap i d l y (sometimes within minutes), producing i n the extreme a grand-mal type of convulsions which may or may not be preceded by warning signs such as twitching of f a c i a l muscles, nausea, numbness and t i n g l i n g sensations, dizziness, confusion or shortness of breath. The r i s k of convulsions varies d i r e c t l y with oxygen p a r t i a l pressure, though there i s great i n t e r - i n d i v i d u a l v a r i a t i o n i n s u s c e p t i b i l i t y and the r i s k i s increased with exercise and with elevated temperature. Treatment includes basic r e s u s c i t a t i o n (airway, breathing, c i r c u l a t i o n and d i s a b i l i t y ) , discontinuation of hyperbaric oxygenation (as soon as that can safe l y be done) and, occasionally, the administration of medications by a physician. The convulsions stop once hyperbaric oxygenation i s discontinued and there are apparently no long-term e f f e c t s of the convulsions, nor i s there an increased r i s k of e p i l e p t i c seizures outside the hyperbaric environment i n these i n d i v i d u a l s . Those indivi d u a l s who have a h i s t o r y of 94 epilepsy, however, must not undertake hyperbaric exposure, both because of the strong l i k e l i h o o d of severe injury or death i n the event of seizure onset "at depth" and because of a probable increased r i s k of oxygen convulsions i n these i n d i v i d u a l s , rendering hyperbaric oxygenation treatment of diving-related accidents problematic. I t should be stressed that i t i s the p a r t i a l pressure of oxygen rather than i t s percentage composition i n the gas mixture that i s c r i t i c a l i n oxygen t o x i c i t y . Thus, breathing 40% oxygen i n nitrogen at 6 atmospheres of pressure ( p a r t i a l pressure equals 2.4 atmospheres) could cause convulsions i n some ind i v i d u a l s who would not succumb breathing 100% oxygen at 2 atmospheres of pressure ( p a r t i a l pressure equals 2.0 atmospheres). 7. Hypothermia Of s p e c i a l concern i n open-water diving i n B.C., hypothermia i s defined as a lowering of the body core temperature. Mild hypothermia (core temperature i n the range of 35-36°C) i s generally well tolerated; further decreases i n core temperature are associated with impairment of cognitive function (planning, making judgments, responding to emergencies), decreased psychomotor a b i l i t y , decreasing l e v e l of consciousness progressing to loss of consciousness and ultimately death due d i r e c t l y to hypothermia (ventricular f i b r i l l a t i o n , or cardiac muscle contraction i n an asynchronous manner that f a i l s to pump blood, occurs at temperatures below 28°C) or to drowning related to loss of consciousness. Prevention i n cold waters, other than l i m i t i n g the time of exposure, requires the use of a drysuit or a wet s u i t at lea s t 3/8 of an inch thick. Treatment requires rewarming, which on the scene i n open water diving generally s t a r t s with body-to- body heat transfer (eg. the vi c t i m and companion i n skin contact i n a sleeping bag), as well as basic CPR, with urgent tr a n s f e r to a medical f a c i l i t y f or further treatment and follow-up. 8. F i r e Hazards F i r e may occur whenever combustible materials are brought into contact with oxygen, e s p e c i a l l y hyperbaric oxygen and es p e c i a l l y i n the presence of sparks. Work i n the hyperbaric chamber requires s t r i c t adherence to the regulations banning smoking and pr o h i b i t i n g the use of equipment which may produce sparks. Work i n the dry chamber requires the wearing of flame-resistant s u i t s and the elimination insofar as i s possible of the accumulation of flammable materials inside the chamber. The inside and outside operators must be f a m i l i a r 95 with the f i r e - f i g h t i n g apparatus, which must be kept i n working order. The above material describes the major r i s k s and hazards associated with hyperbaric exposure of short duration i n a chamber and with hyperbaric exposure both i n the chamber and i n open water. Before agreeing to undertake such exposure i t i s your r e s p o n s i b i l i t y to become informed of the r i s k s and hazards well enough to be able to give t r u l y informed consent to such exposure. ********************************* I have read and understood t h i s document. Name Signature Date 96 Appendix V Informed Consent Environmental Physiology Unit School of Kinesiology Simon Fraser University Note: The University and those conducting t h i s project subscribe to the e t h i c a l conduct of research and to the protection at a l l times of the i n t e r e s t s , comfort and safety of subjects. This form and the information i t contains are given to you for your own protection and f u l l understanding of the procedures, r i s k s and benefits involved. Your signature on t h i s form w i l l s i g n i f y that you have received the document described below regarding t h i s project, that you have received adequate opportunity to consider the information i n the document, and that you v o l u n t a r i l y agree to p a r t i c i p a t e i n the project. ^Having been asked by Dr. Igor Mekjavic of the School of Kinesiology of Simon Fraser University to p a r t i c i p a t e i n a research project experiment, I have read the procedures s p e c i f i e d i n the document e n t i t l e d : Subject Information Package: 1) The e f f e c t s of post-dive warming on vascular gas emboli production. 2) Risks during exposure to hypo/hyperbaric conditions. I understand the procedures to be used i n t h i s experiment and the personal r i s k s to me i n taking part. I understand that I may withdraw my p a r t i c i p a t i o n i n t h i s experiment at any time. I also understand that I may r e g i s t e r any complaint I might have about the experiment with the chief researcher named above or with Dr. J . Dickinson, Director of the School of Kinesiology, Simon Fraser University. I may obtain a copy of the r e s u l t s of t h i s study, upon i t s completion, by contacting Dr. Igor Mekjavic or Neal Pollock. I agree to p a r t i c i p a t e by completing the chamber dive, post-dive immersion period and subsequent observation period while remaining at r e s t as described i n the document referred to above, during the period of 05/87 to 06/87 at the Environmental Physiology Unit 97 (School of Kinesiology) at Simon Fraser University. Name (Please Print) Address _ _ Signature Date Signature of Witness Once signed, a copy of t h i s consent form and a subject feedback form should be provided to you. Appendix VII Dive Questionnaire Name: P r o f i l e : Date Dived: 1. In the 24 hours p r i o r to the dive did you p a r t i c i p a t e i n physical exercise? Yes No 2. I f so, what did you do? 3. Is t h i s a regular a c t i v i t y ? Yes No 4. Did you injure or stress any part of your body? Yes No 5. I f so, please describe the injury or stress. 6. What medication, i f any, did you take during the 24 hours p r i o r to diving? 7. What was your alcohol intake during the 24 hours p r i o r to diving? 8. I f you are a smoker, how many c i g a r e t t e s / c i g a r s / p i p e f u l l s did you smoke i n the 24 hours p r i o r to diving? 9. I f you dove previously i n the series, did you have any unusual f e e l i n g of fatigue or mood i n the 24 hours following your l a s t dive? Yes No 10. I f so, please describe these feelings, and give the date of the dive. 100 B. Glossary 101 Glossary Absolute Pressure - the sum of barometric and hydrostatic pressures Atmospheres Absolute (ATA) - see 'Absolute Pressure' Bounce Dive - short, non-saturation dive beginning and ending at the surface Bubble - physical formation caused by decompression r e s u l t i n g i n supersaturation of t i s s u e and /or vascular nitrogen Bubble Grade/Score - assigned r a t i n g of vascular gas emboli (bubble) severity, usually determined by some v a r i a t i o n of the Kisman-Masurel (K-M) Code Caisson - watertight pressure chamber used for underwater construction Cavitation - formation of a phase separation (bubbles) due to a l o c a l i z e d p a r t i a l vacuum i n a l i q u i d . Ultrasonic energy may cause c a v i t a t i o n i n the body by producing transient but substantial reductions i n the l o c a l f l u i d pressure. Supersaturation, pressure, and temperature can a f f e c t the growth rate of c a v i t a t i o n bubbles Decompression Sickness (DCS) - condition caused by too rapid a reduction i n pressure and having a great v a r i e t y of signs and symptoms. Synonyms: bends, caisson disease, compressed a i r i l l n e s s . Forms include: Cutaneous - skin symptoms may include i t c h i n g , rash, d i s c o l o r a t i o n and/or swelling Mild ('Pain Only', Type I) - most common symptoms may involve l o c a l i z e d pain (usually i n the joints) and extreme fatigue Neurological (serious, Type II) - common symptoms may involve central nervous system (whole or p a r t i a l p a r a l y s i s , loss of consciousness, d i s o r i e n t a t i o n ) , or sensory systems (vertigo [extreme d i z z i n e s s / d i s o r i e n t a t i o n ] , nausea, t i n n i t u s [ringing i n ears], blurred vision) Pulmonary - common symptoms include shortness of breath, non- productive cough, and rapid heart rate Dysbaric Osteonecrosis - long term complications of DCS a f f e c t i n g the s k e l e t a l system; r e s u l t s i n j u x t a - a r t i c u l a r (associated with joints) or medullary (shaft) bone lesions Decompression - i n diving, a phase when the pressure i s being reduced 102 Dif f u s i o n - process i n which p a r t i c l e s of l i q u i d s , gases, or s o l i d s intermingle as the r e s u l t of movement caused by thermal a g i t a t i o n and, i n dissolved substances, move from a region of higher to one of lower concentration Dive - exposure to hyperbaria and subsequent return to normal ambient pressure r e s u l t i n g i n phases of compression and decompression Doppler - process for evaluating moving r e f l e c t i v e objects, i n diving, gas bubbles i n the blood Dysbarism - term denoting any pathological condition caused by a change i n pressure; includes but i s not synonymous with DCS Equivalent Ocean Depth - the depth i n seawater r e s u l t i n g i n an equivalent post-dive pressure d i f f e r e n t i a l to that achieved following a dive completed at ambient pressures le s s than sea l e v e l ( i e . altitude) Excursion Dive - movement of a diver ei t h e r v e r t i c a l l y (up or down) or h o r i z o n t a l l y from the work platform, b e l l , chamber, or habitat, usually during a saturation dive FSW/fsw - depth of sea water i n feet Gas Phase Separation - formation of physical bubbles by previously dissolved gas Half-Time - the time required to reach 50 percent of the f i n a l state; i n diving, the time required for a t i s s u e to absorb or eliminate one-half the equilibrium amount of i n e r t gas Kisman-Masurel (K-M) Code - a three dimensional c l a s s i f i c a t i o n system evaluating doppler detected bubbles; considers frequency, amplitude, and percentage (or duration); combination of the three parameters y i e l d s a single bubble grade/score MSW/msw - depth of sea water i n meters Perfusion - flow of blood (or lymph) through an organ or t i s s u e Saturation Dive - dive of such a duration that no more gas can be absorbed into the tissues of the body. The tissues and the free gas i n the environment are i n equilibrium Tissue Half-Time - see Half-Time Total Bottom Time (TBT) - time of compression plus time at depth Venous Gas Emboli (VGE) - see 'Bubble'

Cite

Citation Scheme:

    

Usage Statistics

Country Views Downloads
United States 29 0
United Kingdom 3 0
France 3 0
China 2 12
Netherlands 1 0
City Views Downloads
Cupertino 23 0
Unknown 9 11
Redmond 2 0
Beijing 1 3
Amsterdam 1 0
Shenzhen 1 9
Ashburn 1 0

{[{ mDataHeader[type] }]} {[{ month[type] }]} {[{ tData[type] }]}

Share

Share to:

Comment

Related Items