Category: LA FISIOLOGIA


INTRODUCTION

The breathing of compressed gas while immersed and exposed to increased ambient pressure

imposes significant homeostatic challenges on the body. This chapter discusses the important

mechanisms of these challenges, with particular reference to the respiratory system.

RESPIRATORY SYSTEM

Aspects of compressed gas breathing equipment and its function.

SCUBA diving equipment is the most commonly used compressed gas system in civilian diving

and illustrates the important features and function relevant to diving physiology. Basic SCUBA

equipment consists of a cylinder of air at high pressure, a demand valve regulator, and a device

for holding this equipment on the diver’s back. In the modern context the latter is usually an

inflatable jacket called a buoyancy control device (BCD) whose dual function it is to allow

buoyancy adjustment in-water and carriage of the tank and regulator. Together with the wetsuit

necessary for temperate water diving and weightbelt, this apparatus may constitute a

significantly restrictive force over the diver’s chest and abdomen.

The regulator reduces the cylinder high pressure air to ambient pressure and supplies air on

demand. Thus, at a depth of 30m where the absolute pressure is 4 bars, the regulator supplies air

at 4 bars and the air is 4 times as dense as air at sea level (1 bar). The ambient pressure is

“measured” by the regulator second stage (attached to the mouthpiece) which, in the upright

diver, is approximately 20cm above the centre of the chest. The water pressure acting on the

chest will therefore be approximately 20cm H2O higher than that of the inspired gas, creating a

negative transmural pressure which is greatest at the lung bases.

Regulator breathing resistance relates inversely to quality of manufacture and standard of

maintenance. Further, breathing resistance tends to increase with depth as denser air flows

through the regulator mechanism.

Finally, it should be noted that the internal volume of a portion of the regulator second stage is

effectively an extension of anatomical respiratory dead space.

Mechanics of breathing.

Changes in compliance. Changes in compliance are seen in the lung and chest wall. The

negative transmural pressure across the chest wall of the upright scuba diver causes some

pulmonary

capillary engorgement. This effect is enhanced by the relative centralisation of blood volume

that occurs with immersion, especially in cold water (see Cardiovascular system). This

engorgement of the pulmonary capillary vasculature causes a reduction of compliance in the

lung tissue. This reduces the vital capacity of the lung by 10-15%.

SCUBA equipment, wetsuits, and weightbelts exert a restrictive force on the chest wall and

abdomen. This effect is potentially marked if equipment is excessively tight fitting. The

compliance of the chest wall is reduced and diaphragmatic breathing is impeded.

Changes in airways resistance. Airways resistance is affected by changes in gas density.

Resistance is defined as ΔP/V, where ΔP = the pressure decrease across a tube and V = flow. In

laminar flow, flow is largely independent of the density of the gas. In turbulent flow however,

flow is inversely related to the square root of gas density. Therefore, in turbulent flow, for a

given ΔP, V will be decreased if gas density is increased, and by definition resistance to flow

will be greater.

According to Reynold’s number predictions, flow within the lungs and airways is largely laminar

although this assumption is likely to be invalid because of the vortices which occur in inspired

air at each division of the bronchial tree. Indeed, it is likely that turbulent flow occurs widely in

the large airways, particularly during rapid breathing when flow rates are much higher.

Changes in the work of breathing. Work of breathing in diving is consequently increased.

Work is performed by the respiratory muscles in stretching the elastic tissues of the lungs and

chest wall, moving inelastic tissues, and moving air through the respiratory passages. The

preceding discussion demonstrates that in the immersed scuba diver there is an increase in

elastic work (viz; decreased compliance in lung and chest wall), the work of moving inelastic

tissues (viz; constrictive equipment), and the work of moving air through airways (viz; increased

air density). Further, the airways resistance component of this increase in work of breathing is

depth dependent.

Ventilation/perfusion matching in diving.

The single most important determinant of efficient gas exchange is the matching of alveolar

ventilation (VA) to perfusion of alveolar capillaries (Q). The optimum ratio of VA to Q is unity.

Under-ventilated and over-perfused lung units (VA/Q<1) represent a “right to left” shunt. The

admixture of hypoxic blood from low VA/Q units into systemic arterial blood is an important

cause of a significant alveolar-arterial oxygen gradient.

The lungs of the SCUBA diver are subjected to changes in both perfusion and ventilation.

There is an increase in perfusion of lung units due to capillary engorgement (particularly at the

bases) and the relative centralisation of blood volume. There is a decrease in ventilation due to

reduced lung and chest wall compliance, abdominal constriction, and increased airways

resistance. The net effect is toward an increase in low VA/Q units and thus the shunting of

blood from “right to left”.

Changes in gas transport.

Oxygen. Oxygen is transported in the blood either bound to haemoglobin (Hb) or dissolved in

plasma. The solubility of O2 in plasma is low (0.003/mmHg/100mL) and in normobaric

conditions by far the greatest proportion of O2 is transported bound to Hb.

The volume of O2 bound to Hb can be calculated from:

Hb bound O2 = Hb concentration x HbO2 capacity x Hb saturation

(mL %) (g%) (1.34 mL/g) (%)

Assuming a Hb concentration of 15% and saturations of 97% and 75% for arterial (PO2 =

100mmHg) and venous (PO2 = 40mmHg) blood respectively, values for arterial (CaO2) and

venous (CvO2) oxygen contents are;

CaO2 = 19.5mL% (Hb bound) + 0.3mL (dissolved) = 19.8mL%.

CvO2 = 15.0mL% + 0.12mL% = 15.1mL%.

The relative quantitative importance of O2 transported by Hb is demonstrated. It is also apparent

that under these typical circumstances, that 5mL% of O2 is extracted from arterial blood to meet

the body’s needs.

Since Hb is normally 97% saturated breathing air at 1 bar, there is little potential for increasing

O2 transport on Hb by increasing the PO2. In contrast, dissolved O2 increases linearly with PO2

although it is only in hyperbaric conditions with a high FIO2 that the dissolved fraction becomes

significant. For example, breathing air at 3 bars gives a dissolved O2 of 1.3mL%, and breathing

100% O2 at 3 bars results in 6.7mL% of dissolved O2 (0.003ml/dl/mmHg PO2). At 3 bars

breathing air, there is still only a relatively small amount of dissolved O2. However, breathing

100% O2 at 3 bars results in a dissolved fraction sufficient to meet the body’s needs at rest in the

absence of Hb. Hence the value of hyperbaric O2 in conditions where O2 delivery is

compromised (viz; anaemia, carbon monoxide poisoning).

Carbon dioxide. Unlike O2 which is supplied at increasing partial pressures at depth, the

number of molecules of CO2 that are produced remains constant for a given workload

irrespective of depth. However, transport of the CO2 load from tissues to lungs may be less

efficient in the hyperbaric environment where an increased PO2 causes a fall in reduced Hb in

venous blood. Reduced Hb forms carbamino compounds with CO2, and buffers the H+

resulting from hydration of CO2 in red blood cells. However, these are two of the quantitatively

less important mechanisms of CO2 transport and the significance of this disturbance is

questionable.

Changes in control of respiration.

The precise anatomy and physiology of the control of breathing are still unknown but there is

little doubt that CO2 and O2 levels in CSF and arterial blood, monitored by central and

peripheral chemoreceptors are important determinants of the rate and depth (minute volume) of

respiration. A rise in the PCO2 or a fall in the PO2 of arterial blood increases the level of brain

stem respiratory centre activity, and changes in the opposite direction have an inhibitory effect.

In the hyperbaric environment, the increased PO2 is thought to produce a slight depression of

respiratory drive. Further, many divers, especially older career divers, show a reduced response

to raised CO2 levels. The mechanism of this reduced response is unknown but it has been

suggested, without good supportive data, that it is a learned response in some divers.

At a cortical level, some divers deliberately override their insensible control mechanisms in an

attempt to extend their underwater duration by conserving air supply. This unsafe practice in

which ventilation is intentionally slowed or punctuated with short periods of apnoea is called

“skip breathing”.

Net effects of respiratory alterations.

Sustained work output by tissues is largely limited by their O2 supply. In normal exercise, tissue

O2 supply is limited by cardiac output rather than ventilation or gas exchange. In the healthy

person ventilation can be dramatically increased to 200L/min or more, and a rapid transit of

blood through alveolar capillaries (normally about 0.35sec) in high output situations does not

prevent equilibration of gases across the respiratory barrier. In addition, the VA/Q profile of the

lung usually improves during exercise.

Underwater, even at the relatively modest depth of 30M (4 bars) commonly attained by sport

divers, air density/airway resistance factors mediate a reduction in maximum voluntary

ventilation to approximately half the surface value. This reduction in ventilatory capacity, the

concomitant increase in the work and O2 cost of breathing, the increase in low VA/Q units, and

dead space effects, determine that underwater work may be ventilation rather than perfusion

limited. It can be readily appreciated that a diver at modest depth, swimming into a 1 knot

current (VO2 for fin swimming at 1 knot = 2L/min), wearing ill fitting equipment, using a poorly

maintained regulator, and being subject to the above physiologic compromise, might fail to

sustain the required work to make progress.

Another important consequence of these respiratory alterations is the diver’s predisposition to

retain CO2. Factors contributing to this include: increase of work of breathing which increases

CO2 production and limits ventilation; decreased respiratory drive; decreased CO2 sensitivity in

divers; skip breathing; and dead space effects. The consequences of hypercapnia in divers

include: unpleasant and dangerous symptoms such as dyspnoea, headache, nausea, and

unconsciousness; and potentiation of nitrogen narcosis, oxygen toxicity, and decompression

illness.

CARDIOVASCULAR SYSTEM

Changes in blood volume distribution.

When the diver is immersed, the haemodynamic effect of gravity is abolished and there is a

consequent redistribution of peripheral blood into the central circulation. This effect is enhanced

in cold water when peripheral vasoconstriction further enhances the central redistribution.

The relative central hypervolaemia increases the activity of stretch receptors in the walls of the

great veins and right atrium, with receptors in the carotid sinus and aortic arch also involved if

the blood shift is sufficient to increase mean arterial pressure. The increased stretch receptor

activity mediates a decrease in ADH production from the hypothalamus/posterior pituitary. This

results in an increased permeability to water in renal distal tubule cells and therefore increased

urinary loss of water. The net result is an undesirable tendency toward dehydration which may

be exacerbated by lack of adequate drinking water and/or seasickness.

Cardiac effects.

Immersion has been demonstrated to increase cardiac output by up to 32% in thermoneutral

water. The mechanism is an increase in venous return due to the centralisation of blood volume.

The increased preload, manifest as increased stretching of the heart muscle fibres during

diastole, invokes the Starling mechanism in which the force of contraction is raised to cope with

the extra volume. Stroke volume is therefore increased. In colder water the increase in cardiac

output is less, due to a concomitant bradycardia.

There is a bradycardia associated with immersion. The so-called “mammalian dive reflex”

invoked by cold water contacting the face includes a bradycardia. In predisposed individuals the

vagal outflow can be intense enough to produce asystole or arrhythmias (viz; unexplained

drowning after leaping into cold water). However, a bradycardia is produced even in a dry

chamber at elevated ambient pressure and other explanations for the immersion bradycardia in

divers has been sought.

It has been demonstrated that an increase in PaO2 and the narcotic effect of inert gasses can

produce a fall in heart rate averaging 10 beats/min in divers, independent of the “dive reflex”.

The degree of bradycardia is increased in colder water and concomitantly, so is the risk of

arrhythmias in predisposed individuals. However, the role of these factors is diving fatalities is

largely unknown.

Another mechanism of bradycardia of questionable significance in divers, but that is often

mentioned in the diver training literature is the carotid sinus reflex. There is the theoretical

possibility that if a wetsuit hood fits too tightly around the neck, it may stimulate a carotid sinus

reflex (viz; carotid sinus massage) and therefore a bradycardia.

Views differ on the net effect of these mechanisms on mean arterial blood pressure. It is likely

that blood pressure remains largely unchanged in health in the hyperbaric environment.

 

Simon Mitchell

(When we learned of Rob Parker’s death, Fred Winstanley – the Cave Diving Group’s Technical Officer wrote the following:)

It was with great sadness that I learned of Rob’s Parker’s untimely demise. Although I only met him a couple of times I gained the impression of a modest, pleasant, genuine person full of the thrill of exploration.

Over a period of time more facts have come to light regarding the details of his dive profile and this may give some clues as to the cause of death. As I understand it Rob was completing a trimix dive and was on his way up when his accident occurred. He became distressed after a switch to air at 60m depth. The symptoms displayed were classical symptoms of those of someone suffering what is incorrectly known as a vestibular bend. In the early to mid sixties commercial diving in the North Sea depended upon a lot of heliox bounce diving as opposed to saturation. The tables devised for this procedure called for a switch from heliox to air at eighty feet. At this switch some divers would show signs of loss of balance and extreme vertigo and vomiting. The symptoms where identical to those of someone suffering from an infection in the inner ear, specifically the semi‑circular canals which are involved in control of balance. For many years it was thought that the bubbles causing the damage occurred in the vestibule part of the ear, hence the name given to that specific type of decompression sickness. It is now thought that the bubbles do not form in this region but in the cerebellum of the brain. This part of the brain controls muscles and receives the impulses from the semi‑circular canals of the ear, hence the symptoms displayed. Wherever the bubbles occur the result is the same, severe disability which can leave survivors quadriplegic. It is also thought that the symptoms shown are only the most noticeable and in fact the brain is suffering massive trauma with huge bubble formation. The divers in the North Sea where decompressing in a chamber and so did survive, anyone suffering such an occurrence in the water, especially on SCUBA, would stand little chance of survival. So what causes these bubbles to form? The answer seems to lie in an occurrence known as Isobaric Counter Gas Transport. To understand the mechanics of this phenomenon it is essential to understand gas solubility in the body’s tissues. In fatty tissues helium is twice as soluble as oxygen but nitrogen is twice as soluble as helium. This means that the body’s tissues become saturated to different levels dependent upon the inert gas breathed. Henry’s law states that the solubility of a gas in a liquid is directly proportional to the pressure exerted on that liquid. In other words the deeper you are the more inert gas you have in your body, but remember that gases are soluble at different rates. So where does this leave us in Rob’s case? As you ascend, gas comes out of saturation and is removed from the blood by the lungs. If, however, you switch to a different gas, specifically a nitrogen rich gas like air, the nitrogen dissolves into the tissues quicker than the helium can come out, creating a super saturation situation – hence bubbles of helium are formed in the blood. This bubble formation can occur with no change in depth, hence the name Isobaric, meaning “same pressure”. How do we prevent this situation arising? The answer is quite simple, during decompression never let your partial pressure of nitrogen rise. Come as shallow as is safely possible on your bottom-mix, and avoid switching to air at any stage of the decompression, using nitrox or pure oxygen instead. This procedure will result in a slightly longer decompression profile but, remember, ‑ you’re an awful long time dead.

(In reply, Rupert Skorupka, a Qualified Diver with the Cave Diving Group (Northern Section) wrote:)

Fred Winstanley’s article (copied above) on the subject of Isobaric Counter Gas Transport, whilst being generally correct and informative, was rather brief to deal with such a complex subject. I have therefore attempted to produce a more in depth explanation of the principles involved in this phenomenon. (Those divers not interested in the details of diving physiology should move on to prevent an attack of acute boredom.) My main contention with Fred’s article is that we are discussing a phenomenon governed by the principles of diffusion rather than solubility, and that the biological site at which this occurs is the cell membrane, rather than fatty tissues in general. Let us specifically follow the course of events after a gas switch from a high percentage helium mix to a high percentage nitrogen mix during ascent (partial pressures being irrelevant as we are observing at isobaric conditions), from the point of view of an interneuron (i.e. nerve cell), from which a large proportion of the cerebellum is composed. A high concentration of nitrogen is carried in solution, by bulk flow in the bloodstream. Rapid diffusion occurs via the aqueous medium into the extra cellular fluid surrounding the interneuron. A situation then exists whereby two aqueous compartments are separated by the cell membrane, one containing a high nitrogen concentration (extracellular), and one containing a high helium concentration  (intracellular). The mechanism by which equilibrium is reached is by passive diffusion through the membrane. (i.e. generated only by the concentration gradient) until the concentrations in both compartments equalise. The rate at which any molecule can pass through the cell membrane is given by its permeability constant. This will depend on factors such as the size of the molecule, its diffusion coefficient and its partition coefficient between the lipid and aqueous phases of the cell. So even though the helium atom moves three times as fast as the nitrogen molecule in terms of its diffusion rate, the nitrogen molecule can cross the cell membrane more rapidly as it has a higher permeability constant. The flux of molecules across the cell membrane therefore results in more nitrogen molecules entering the cell cytoplasm than helium atoms leaving. Since the partial pressure of any component in a mixture of gases above a solution is directly proportional to the number of molecules of that gas dissolved in the solution, it follows that as the number of molecules of nitrogen in the cytoplasm increases, then the partial pressure required to prevent them coming out of solution also increases. Consider the simplified situation of a diver decompressing at 20 metres i.e. 3atms. Supposing he arrived at the stop with tissue partial pressures of 2.5atm helium, 0.5atm nitrogen. 10 minutes after switching to air, these have changed due to isobaric counter diffusion, to 2.3atm helium, 1.0atrn nitrogen. Thus he is still not supersaturated for either gas (i.e. neither exceeds 3atm). But, the crucial principle is that these partial pressures are additive with respect to the tendency to form a gas phase. Thus bubble formation will now occur, whether for helium, nitrogen or a mixture (a difficult question). The site of bubble formation will be the cellular cytoplasm, not the bloodstream as Fred states. This simply means that damage to our interneuron is not indirectly caused by it being starved of oxygen and nutrients due to bubble occlusion of the capillaries but by physical disruption of the cellular mechanisms from within. If the damage was to effect the cerebellum alone, the diver would display very distinctive symptoms of DCS. The cerebellum does not initiate movement, but acts by influencing other regions of the brain responsible for motor activity. Destruction of the cerebellum does not cause the loss of any specific movement, rather it is associated with general inadequacy of that movement. Damage to the cerebellum would cause our diver symptoms as follows:

1 . He cannot perform movements smoothly. These are accompanied by oscillating tremors.

2. His walk is awkward and drunken, with difficulty maintaining balance.

3. He cannot start or stop movements quickly or easily.

4. He may not be able to combine the movement of several Joints into a smoothly co-ordinated motion.

The most important factor from the point of view of the cave diver decompressing in water is the rapid time scale over which these events occur. The symptoms are likely to be so severe that they result in death by drowning within minutes of the gas switch having taken place.

Now to the question of how we prevent the situation arising in the first place. Obviously, using trimix will have an advantage over heliox as the cells will have an inherent partial pressure of nitrogen, thereby decreasing the concentration gradient over the cell membrane after the gas switch. Fred advocates never allowing the partial pressure of nitrogen to rise during the decompression. If breathing heliox, this would entail carrying out all decompression on pure oxygen, no nitrogen would be permitted whatsoever. Consider the case of a diver using a 50% helium trimix (i.e. 40% nitrogen 10% oxygen). In order to maintain an equal nitrogen partial pressure during decompression he would have to switch to a 60% oxygen nitrox. In order to avoid acute oxygen toxicity for any significant period of decompression, it is necessary to keep the PP02 below 1.6atm. Thus for an f02 of 0.6, it would be inadvisable to switch to this mix below 17 metres. Our diver therefore would not be able to switch from his bottom mix until this depth was reached, resulting in a massive (if not unsustainable) time increase to the deeper stops. The present consensus of opinion recommends a switch to nitrox at or around 30 metres. This depth lies at an optimal point where the f02 that can be safely tolerated is sufficiently high to reduce the fN2 in our mix to a level that more closely approximates to the fN2 in our trimix (i.e. an fN2 of 0.4 as opposed to approximately 0.8 for air). Also, by maximising the f02, we take advantage of the phenomenon known as the oxygen window. Simply put, this is the mechanism whereby oxygen dissolved in the blood is absorbed and metabolised by our cells in preference to that combined with haemoglobin, which does not contribute to the PP02. At high partial pressures this is the predominant fraction of the inspired oxygen. As this oxygen is metabolised, it leaves a partial pressure “window” in the tissues, which enables the other inert gases to increase their partial pressures without bubble formation. Reading accounts of past deep diving exploits it becomes apparent that some frightening practices were used during decompression, seemingly accepting vestibular bends as a necessary occupational hazard. The problem was, predictably, evaluated by Jochen Hasenmayer during his Fontaine de Vaucluse dives. Unfortunately, the details of his decompression procedures were kept a secret. It is probable that the vestibular bend strikes with the same random pattern of distribution as DCS in general, being more common in extreme exposures but by no means limited to these cases, and not an inevitable consequence of deep gas switches. What is probable is that in the past due to an overall ignorance of the facts concerning isobaric gas diffusion, and even its existence at all, several deaths have been wrongly attributed to other factors such as severe nitrogen narcosis during decompression. For example refer to the American publication “Mixed Gas Diving” by Mount and Gilliam. I could not find one reference to vestibular bends or isobaric counter diffusion in the entire book. Hopefully, we can continue to avoid accidents in the future by learning from the mistakes of our predecessors. We owe it to them to improve our techniques and thereby prevent the pointless repetition of past tragedies.

Cave Diving Group

Dilemmas
Biophysical models of inert gas transport and bubble formation all try to prevent decompression sickness. Developed over years of diving application, they differ on a number of basic issues, still mostly unresolved today:

1. the rate limiting process for inert gas exchange, blood flow rate (perfusion) or gas transfer rate across tissue (diffusion);

2. composition and location of critical tissues (bends sites);

3. the mechanistics of phase inception and separation (bubble formation and growth);

4. the critical trigger point best delimiting the onset of symptoms (dissolved gas buildup in tissues, volume of separated gas, number of bubbles per unit tissue volume, bubble growth rate to name a few);

5. the nature of the critical insult causing bends (nerve deformation, arterial blockage or occlusion, blood chemistry or density changes).

Such issues confront every modeler and table designer, quite perplexing in their ambiguous correlations with experiment and nagging in their persistence. For every answer to these questions, others can be proposed, refuting the first. It is also very difficult to do the necessary experiments in living tissue to resolve issues. And here discussion is confined just to bubbles and Type I and II bends, to say nothing of other factors and types. The substance of these questions ultimately links to bubbles, that is, how they are formed, where they grow, when they move, and how they are eliminated. The dilemmas are formidable.

Bubble Sites
We do not really know where bubbles form nor lodge, their migration patterns, their birth and dissolution mechanisms, nor the exact chain of physico-chemical insults resulting in decompression sickness. Many possibilities exist, differing in the nature of the insult, the location, and the manifestation of symptoms. Bubbles might form directly (de~novo) in supersaturated sites upon decompression, or possibly grow from preformed, existing seed nuclei excited by compression-decompression. Leaving their birth sites, bubbles may move to critical sites elsewhere. Or stuck at their birth sites, bubbles may grow locally to pain-provoking size. They might dissolve locally by gaseous diffusion to surrounding tissue or blood, or passing through screening filters, such as the lung complex, they might be broken down into smaller aggregates, or eliminated completely. Whatever the bubble history, it presently escapes complete elucidation. Bubbles may hypothetically form in the blood (intravascular) or outside the blood (extravascular). Once formed, intravascularly or extravascularly, a number of critical insults are possible. Intravascular bubbles may stop in closed circulatory vessels and induce blood sludging and chemistry degradations (ischemia), or mechanical nerve deformation. Circulating gas emboli may occlude the arterial flow, clog the pulmonary filters, or leave the circulation to lodge in tissue sites as extravasular bubbles. Extravascular bubbles may remain locally in tissue sites, assimilating gas by diffusion from adjacent supersaturated tissue and growing until a nerve ending is deformed beyond its pain threshold. Or, extravascular bubbles might enter the arterial or venous flows, at which point they become intravascular bubbles. Spontaneous bubble formation in fluids usually requires large decompressions, like hundreds of atmospheres, somewhere near fluid tensile limits. Many feel that such circumstance precludes direct bubble formation in blood following decompression. Explosive, or very rapid decompression, of course is a different case. But, while many doubt that bubbles form in the blood directly, intravascular bubbles have been seen in both the arterial and venous circulation, with vastly greater numbers detected in venous flows (venous gas emboli). Ischemia resulting from bubbles caught in the arterial network has long been implied as a cause of decompression sickness. Since the lungs are effective filters of venous bubbles, arterial bubbles would then most likely originate in the arteries or adjacent tissue beds. The more numerous venous bubbles, however, are suspected to first form in lipid tissues draining the veins. Lipid tissue sites also possess very few nerve endings, possibly masking critical insults. Veins, thinner than arteries, appear more susceptible to extravascular gas penetration. Extravascular bubbles may form in aqueous (watery) or lipid (fatty) tissues in principle. For all but extreme or explosive decompression, bubbles are seldom observed in heart, liver, and skeletal muscle. Most gas is seen in fatty tissue, not unusual considering the five-fold higher solubility of nitrogen in lipid tissue versus aqueous tissue. Since fatty tissue has few nerve endings, tissue deformation by bubbles is unlikely to cause pain locally. On the other hand, formations or large volumes of extravascular gas could induce vascular hemorrhage, depositing both fat and bubbles into the circulation as noted in animal experiments. If mechanical pressure on nerves is a prime candidate for critical insult, then tissues with high concentrations of nerve endings are candidate structures, whether tendon or spinal cord. While such tissues are usually aqueous, they are invested with lipid cells whose propensity reflects total body fat. High nerve density and some lipid content supporting bubble formation and growth would appear a conducive environment for a mechanical insult. On the question of preformed nuclei, their presence in human tissue and blood has not been demonstrated. The existence of preformed nuclei in serum and egg albumin has been reported by Yount and Strauss. Since performed nuclei are found virtually in every aqueous substance known, their preclusion from the body would come as a surprise to many. Hence, while most regard nucleation as a random process, its occurrence in tissue seems highly probable, seen for instance in the studies of Evans, Walder, Strauss, Yount, Kunkle, and co-workers. Model correlations with incidence statistics of decompression sickness in salmon, rats, and humans speak favorably for the nucleation concept. The ultimate computational algorithm, coupling nucleation, dissolved gas uptake and elimination, bubble growth and collisional coalescence, and critical sites, would be very, very complicated, requiring supercomputers (like CRAYs, CYBERs, VPs, CONVEXs, and ESSEXs, or their massively parallel cousins, CMs, NCUBESs, IWARPs, and DAPs) for three dimensional modeling. Stochastic Monte Carlo methods and sampling techniques exist which could generate and stabilize nuclei from thermodynamic functions, such as the Gibbs or Helmholtz free energy, transport dissolved gas in flowing blood to appropriate sites, inflate, deflate, move, and collide bubbles and nuclei, and then tally statistics on tensions, bubble size and number, inflation and coalescence rate, free phase volume, and any other meaningful parameter, all in necessary geometries. Such type simulations of similarly complicated problems last for 16-32 hours at the Los Alamos and Livermore National Laboratories, on lightning fast supercomputers with near gigaflop speed (10 sup 9 floating point operations per second). While decompression meters have revolutionized diving and decompression calculations, it will be some time before the ultimate computational algorithm fits into a wrist computer.

Venous Gas Emboli
Sound reflected off a moving boundary undergoes a shift in acoustical frequency, the so-called Doppler shift. The shift is directly proportional to the speed of the moving surface (component in the direction of sound propagation) and the acoustical frequency of the wave, and inversely proportional to the sound speed. Acoustical signals in the megahertz range (10 sup 6 vibrations per second), termed ultrasound, have been directed at moving blood in the pulmonary arteries, where blood flow rates are the highest (near 20 cm/sec) due to confluence of the systemic circulation, with resulting Doppler shifts, in the form of audible chirps, snaps, whistles, and pops, noted and recorded. Sounds heard in divers have been ascribed to venous gas emboli (VGE), and in~vitro studies (gels) and have established minimum bubble detection size as a function of blood velocity. Coalesced lipids, platelet aggregates, and agglutinated red blood cells formed during decompression also pass through the pulmonary circulation, but are less reflective than bubbles, and usually smaller. Bubbles with radii in the tens of micron (10 sup -4 cm) range represent a cutoff for Doppler detection for signals of a few megahertz. Ultrasonic techniques for monitoring moving gas emboli in the pulmonary circulation are popular today. Silent bubbles, as applied to the venous gas emboli detected in sheep undergoing bends-free USN table decompression by Spencer and Campbell, were a first indication that asymptomatic free phases were present in blood, even under bounce loadings. Similar results were reported by Walder and Evans. After observing and contrasting venous gas emboli counts for various nonstop exposures at depth, Spencer suggested that nonstop limits be reduced below the USN table limits. Enforcing a 20% drop in venous gas emboli counts compared to the USN limits, corresponding nonstop limits, t sub s , at depth, d, satisfy a reduced Hempleman relationship, that is, d t sub s sup 1/2 = 465 fsw min sup 1/2. Plugging those nonstop limits into the Haldane tissue equations for all depths and across all compartments, followed by extraction of the maximum of ensuing computed tissue tensions, permits construction of a reduced set of limiting tensions for table or meter implementation. Such exercises are quite popular today, and certainly prudent. While the numbers of venous gas emboli detected with ultrasound Doppler techniques can be correlated with nonstop limits, and the limits then used to fine tune the critical tension matrix for select exposure ranges, fundamental issues are not necessarily resolved by venous gas emboli measurements. First of all, venous gas emboli are probably not the direct cause of bends per se, unless they block the pulmonary circulation, or pass through the pulmonary traps and enter the arterial system to lodge in critical sites. Intravascular bubbles might first form at extravascular sites. According to Hills, electron micrographs have highlighted bubbles breaking into capillary walls from adjacent lipid tissue beds in mice. Fatty tissue, draining the veins and possessing few nerve endings, is thought to be an extravascular site of venous gas emboli. Similarly, since blood constitutes no more than 8% of the total body capacity for dissolved gas, the bulk of circulating blood does not account for the amount of gas detected as venous gas emboli. Secondly, what has not been established is the link between venous gas emboli, possible micronuclei, and bubbles in critical tissues. Any such correlations of venous gas emboli with tissue micronuclei would unquestionably require considerable first-hand knowledge of nuclei size distributions, sites, and tissue thermodynamic properties. While some believe that venous gas emboli correlate with bubbles in extravascular sites, such as tendons and ligaments, and that venous gas emboli measurements can be reliably applied to bounce diving, the correlations with repetitive and saturation diving have not been made to work, nor important correlations with more severe forms of decompression sickness, such as chokes and central nervous system (CNS) hits. Still, whatever the origin of venous gas emboli, procedures and protocols which reduce gas phases in the venous circulation deserve attention, for that matter, anywhere else in the body. The moving Doppler bubble may not be the bends bubble, but perhaps the difference may only be the present site. The propensity of venous gas emboli may reflect the state of critical tissues where decompression sickness does occur. Studies and tests based on Doppler detection of venous gas emboli are still the only viable means of monitoring free phases in the body.

B.R. Wienke

INTRODUCTION

Modeling of decompression pheneomena in the human body is, at times, more of an art form than a science. Some take the view that deterministic modeling can only be fortuitous. technological advance, elucidation of competing mechanisms, and resolution of model issues over the past 80 years has not been rapid. Model applications tend to be ad hoc, tied to data fits, and difficult to quantify on first principles. Almost any description of decompression processes in tissue and blood can be disputed, and turned around on itself. The fact the decompression takes place in metabolic and perfused matter makes it difficult to design and analyze experiments outside living matter. Yet, for application to safe diving, we need models to build tables and meters. And deterministic models, not discounting shortcomings, are the subject of this discourse.

MODERN DIVING
A concensus of opinions, and for a variety of reasons, suggests that modern diving began in the early 1960s. Technological achievements, laboratory programs, military priorities, safety concerns, commercial diving requirements, and international business spurred diving activity and scope of operation. Diving bells, hot water heating, mixed gases, saturation, deep diving, expanded wet testing, computers, and efficient decompression algorithms signaled the modern diving era. Equipment advances in open and closed circuit breathing devices, wet and dry suits, gear weight, mask and fin design, high pressure compressors, flotation and buoyancy control vests, communications links, gauges and meters, lights, underwater tools (cutting, welding, drilling, explosives), surface supplied air, and photographic systems paced technological advances. Training and certification requirements for divers, in military, commercial, sport, and scientific sectors, took definition with growing concern for underwater safety and well being. In the conquest and exploration of the oceans, saturation diving gained prominence in the 1960s, permitting exploitation of the continental shelf impossible with the short exposure times allowed by conventional diving. Spurred by both industrial and military interests in the ability of men to work underwater for long periods of time, notable habitat experiments, such as Sealab, Conshelf, Man In Sea, Gulf Task, Tektite, and Diogene, demonstrated the feasibility of living and working underwater for long periods of time. These efforts followed proof of principle validation, by Bond and coworkers (USN) in 1958, of saturation diving. Saturation exposure programs and tests have been conducted from 35 fsw to 2,000 fsw.
The development and use of underwater support platforms, such as habitats, bell diving systems, lockout and free flooded submersibles, and diver propulsion units also accelerated in the 1960s and 1970s, for reasons of science and economics. Support platforms extended both diver usefulness and bottom time, by permitting him to live underwater, reducing descent and ascent time, expanding mobility, and lessing physical activity. Today, themselves operating from underwater platforms, remotely operated vehicles (ROVs) scan the ocean depths at 6,000 fsw for minerals and oil.
Around 1972, strategies for diving in excess of 1,000 fsw received serious scrutiny, driven by a commercial quest for oil and petroleum products, and the needs of the commercial diving industry to service that quest. Questions concerning pharmacological additives, absolute pressure limits, thermal exchange, therapy, compression-decompression procedures, effective combinations of mixed breathing gases, and equipment functionality addressed many fundamental issues, unknown or only partially understood. By the early 1980s, it became clear that open sea water work in the 1,000 to 2,000 fsw range was entirely practical, and many of the problems, at least from an operational point of view, could be solved. Today, the need for continued deep diving remains, with demands that cannot be answered with remote, or 1 atm, diver systems. Heliox and trimix have become standards for deep excursion breathing gases, with heliox the choice for shallower exposures, and trimix the choice for deeper exposures in the field.
Yet, despite tremendous advances in deep diving technology, most of the ocean floor is outside human reach. Breathing mixtures that are compressible are limiting. Breathing mixtures that are not compressible offer interesting alternatives. In the 1960s, serious attention was given to liquid breathing mixtures, physiological saline solutions. Acting as inert respiratory gas diluents, oxygenated fluids have been used as breathing mixtures, thereby eliminating decompression requirements. Some synthetic fluids, such as

Models
Most believe that the pathophysiology of decompression sickness syndrome follows formation of a gas phase after decompression. Yet, the physiological evolution of the gas phase is poorly understood. Bubble detection technology has established that moving and stationary bubbles do occur following decompression, that the risk of decompression sickness increases with the magnitude of detected bubbles, that symptomless, or silent, bubbles are also common following decompression, and that the variability in gas phase formation is likely less than the variability in symptom generation. Taken together, gas phase formation is not only important to the understanding of decompression sickness, but is also a crucial model element in theory and computation.
Bubbles can form in tissue and blood when ambient pressure drops below tissue tensions, according to dissolved-free phase mechanics. Trying to track free and dissolved gas buildup and elimination in tissue and blood, especially their interplay, is extremely complex, beyond the capabilities of even supercomputers. But safe computational prescriptions are necessary in the formulation of dive tables and digital meter algorithms. The simplest way to stage decompression, following extended exposures to high pressure with commensurate dissolved gas buildup, is to limit tissue tensions. Historically, Haldane first employed the approach, and it persists today in modified form.

History
Tables and schedules for diving at sea level can be traced to a model proposed in 1908 by the eminent English physiologist, John Scott Haldane. He observed that goats, saturated to depths of 165 feet of sea water (fsw), did not develop decompression sickness (DCS) if subsequent decompression was limited limited to half the ambient pressure. Extrapolating to humans, researchers reckoned that tissues tolerate elevated dissolved gas pressures (tensions), greater than ambient by factors of two, before the onset of symptoms. Haldane then constructed schedules which limited the critical supersaturation ratio to two in hypothetical tissue compartments. Tissue compartments were characterized by their halftime, tau . Halftime is also termed halflife when linked to exponential processes, such as radioactive decay. Five compartments (5, 10, 20, 40, 75 minutes) were employed in decompression calculations and staged procedures for fifty years. Some years following, in performing deep diving and expanding existing table ranges in the 1930s, US Navy investigators assigned separate limiting tensions (M-values) to each tissue compartment. Later in the 1950s and early 1960s, other US Navy investigators, in addressing repetitive exposures for the first time, advocated the use of six tissues (5, 10, 20, 40, 80, 120 minutes) in constructing decompression schedules, with each tissue compartment again possessing its own limiting tension. Temporal uptake and elimination of inert gas was based on mechanics addressing only the macroscopic aspects of gas exchange between blood and tissue. Exact bubble production mechanisms, interplay of free and dissolved gas phases, and related transport phenomena were not quantified, since they were neither known nor understood. Today, we know much more about dissolved and free phase dynamics, bubbles, and transport mechanisms, but still rely heavily on the Haldane model. Inertia and simplicity tend to sustain its popularity and use, and it has been a workhorse.
To maximize the rate of uptake or elimination of dissolved gases, the gradient, simply the difference between arterial and tissue tension, is maximized by pulling the diver as close to the surface as possible. Exposures are limited by requiring that the tissue tensions, never exceed limits (called M-values), for instance, written for each compartment in the US Navy approach (5, 10, 20, 40, 80, and 120 minute tissue halftimes, tau , as M = M sub 0 + DELTA M d, with, M sub 0 = 152.7 tau sup -1/4 , and, DELTA M = 3.25 tau sup -1/4 , as a function of depth, d, for DELTA M the change per unit depth. Obviously, M, is largest for fast tissue compartments ( tau small), and smallest for slow tissue compartments ( tau large). Fast compartments control short deep excursions, while slow compartments control long shallow excursions. Surfacing values, M sub 0 , are principal concerns in nonstop diving, while values at depth, DELTA M d , concern decompression diving. In both cases, the staging regimen tries to pull the diver as close to the surface as possible, in as short a time as possible. By contrast, free phase (bubble) elimination gradients, as seen, increase with depth, directly opposite to dissolved gas elimination gradients which decrease with depth. In actuality, decompression is a playoff between dissolved gas buildup and free phase growth, tempered by body ability to eliminate both. But dissolved gas models cannot handle both, so there are problems when extrapolating outside tested ranges.
In absolute pressure units, the corresponding critical gradient, G = Q – P, is related to ambient pressure, P, and critical nitrogen pressure, M, with, Q = 1.27 M. In bubble theories, supersaturation is limited by the critical gradient, G. In decompressed gel experiments, Strauss suggested that G approx 20 fsw at ambient pressures less than a few atmospheres. Other studies suggest, 14 <= G <=”30″ fsw, as a range of critical gradients (G-values). In diffusion-dominated approaches, the tissue tension can be limited by a single, pressure criterion, such as, M=”709″ P / P + 404 .
Blood rich, well-perfused, aqueous tissues are usually thought to be fast (small tau ), while blood poor, scarcely-perfused, lipid tissues are thought to be slow (large tau ), though the spectrum of halftimes is not correlated with actual perfusion rates in critical tissues. As reflected in relationship above, critical parameters are obviously larger for faster tissues. The range of variation with compartment and depth is not insignificant. Fast compartments control short deep exposures, while slow compartments control long shallow, decompression, and saturation exposures.

Bulk Diffusion Model
Diffusion limited gas exchange is modeled in time by a sum of exponential response functions, bounded by arterial and initial tissue tensions. However, instead of many tissue compartments, a single bulk tissue is assumed for calculations, characterized by a gas diffusion constant, D. Tissue is separated into intravascular (blood) and extravascular (cells) regions. Blood containing dissolved inert and metabolic gases passes through the intravascular zone, providing initial and boundary conditions for subsequent gas diffusion into the extravascular zone. Diffusion is driven by the difference between arterial and tissue tensions, according to the strength of a single diffusion coefficient, D, appropriate to the media. Diffusion solutions, averaged over the tissue domain, resemble a weighted sum over effective tissue compartments with time constants, alpha sub 2n-1 sup 2 D, determined by diffusivity and boundary conditions, with alpha sub 2n-1 = (2n – 1) pi / l for tissue thickness, l.
Applications fit the time constant, K = pi sup 2 D / l sup 2 , to exposure data, with a typical value employed by the Royal Navy given by, K = 0.007928 min sup -1 , approximating the US Navy 120 minute compartment used to control saturation, decompression, and repetitive diving. Corresponding critical tensions in the bulk model, M = 709 P / P + 404 , fall somewhere between fixed gradient and multitissue values. At the surface, M = 53 fsw, while at 200 fsw, M = 259 fsw. A critical gradient, G = P ( 493 – P ) / ( P + 404 ), also derives from the above. Originally, a critical gradient, G, near 30 fsw was used to limit exposures. Such value is too conservative for deep and bounce exposures, and not conservative enough for shallow exposures. Hempleman introduced the above relationship, providing the means to parameterize bounce and saturation diving.
Bulk models are attractive because they permit the whole dive profile to be modeled with one equation, and because they predict a t sup 1/2 behavior of gas uptake and elimination. Nonstop time limits, t sub n , are related to depth, d, by the bulk diffusion relationship, d t sub n sup 1/2 = C, with approximate range, 400 <= C <=”500″ fsw min sup 1/2 , linking nonstop time and depth simply through the value of C. For the US Navy nonstop limits, C approx 500 fsw min sup 1/2 , while for the Spencer reduced limits, C approx 465 fsw min sup 1/2 . In the Wienke-Yount model, C approx 400 fsw min sup 1/2 .

Multitissue Model
Multitissue models, variations of the original Haldane model, assume that dissolved gas exchange, controlled by blood flow across regions of varying concentration, is driven by the local gradient, that is, the difference between the arterial blood tension and the instantaneous tissue tension. Tissue response is modeled by exponential functions, bounded by arterial and initial tensions, and perfusion constants, lambda , linked to the tissue halftimes, tau , for instance, 1, 2, 5, 10, 20, 40, 80, 120, 180, 240, 360, 480, and 720 minute compartments assumed to be independent of pressure.
In a series of dives or multiple stages, initial and arterial tensions represent extremes for each stage, or more precisely, the initial tension and the arterial tension at the beginning of the next stage. Stages are treated sequentially, with finishing tensions at one step representing initial tensions for the next step, and so on. To maximize the rate of uptake or elimination of dissolved gases the gradient, simply the difference between arterial and tissue tensions is maximized by pulling the diver as close to the surface as possible. Exposures are limited by requiring that the tissue tensions never exceed M = M sub 0 + DELTA M d, as a function of depth, d, for DELTA M the change per unit depth. A set of M sub 0 and DELTA M are listed in Table 1.
At altitude, some critical tensions have been correlated with actual testing, in which case, an effective depth, d = P – 33, is referenced to the absolute pressure, P, with surface pressure, P sub h = 33 exp ( -0.0381 h ), at elevation, h, and h in multiples of 1,000 ft. However, in those cases where critical tensions have not been tested, nor extended, to altitude, an exponentially decreasing extrapolation scheme, called similarity, has been employed. Extrapolations of critical tensions, below P = 33 fsw, then fall off more rapidly then in the linear case. A similarity extrapolation holds the ratio, R = M/P, constant at altitude. Estimating minimum surface tension pressure of bubbles near 10 fsw, as a limit point, the similarity extrapolation might be limited to 10,000 ft in elevation, and neither for decompression nor heavy repetitive diving.
Models of dissolved gas transport and coupled bubble formation are not complete, and all need correlation with experiment and wet testing. Extensions of basic (perfusion and diffusion) models can redress some of the difficulties and deficiencies, both in theory and application. Concerns about microbubbles in the blood impacting gas elimination, geometry of the tissue region with respect to gas exchange, penetration depths for gas diffusion, nerve deformation trigger points for pain, gas uptake and elimination asymmetry, effective gas exchange with flowing blood, and perfusion versus diffusion limited gas exchange, to name but a few, motivate a number of extensions of dissolved gas models.
The multitissue model addresses dissolved gas transport with saturation gradients driving the elimination. In the presence of free phases, free-dissolved and free-blood elimination gradients can compete with dissolved-blood gradients. One suggestion is that the gradient be split into two weighted parts, the free- blood and dissolved-blood gradients, with the weighting fraction proportional to the amount of separated gas per unit tissue volume. Use of a split gradient is consistent with multiphase flow partitioning, and implies that only a portion of tissue gas has separated, with the remainder dissolved. Such a split representation can replace any of the gradient terms in tissue response functions.
If gas nuclei are entrained in the circulatory system, blood perfusion rates are effectively lowered, an impairment with impact on all gas exchange processes. This suggests a possible lengthening of tissue halftimes for elimination over those for uptake, for instance, a 10 minute compartment for uptake becomes a 12 minute compartment on elimination. Such lengthening procedure and the split elimination gradient obviously render gas uptake and elimination processes asymmetric. Instead of both exponential uptake and elimination, exponential uptake and linear elimination response functions can be used. Such modifications can again be employed in any perfusion model easily, and tuned to the data.

Thermodynamic Model
The thermodynamic approach suggested by Hills, and extended by others, is more comprehensive than earlier models, addressing a number of issues simultaneously, such as tissue gas exchange, phase separation, and phase volume trigger points. This model is based on phase equilibration of dissolved and separated gas phases, with temporal uptake and elimination of inert gas controlled by perfusion and diffusion. From a boundary (vascular) zone of thickness, a, gases diffuse into the cellular region. Radial, one dimensional, cylindrical geometry is assumed as a starting point, though the extension to higher dimensionality is straightforward. As with all dissolved gas transfer, diffusion is controlled by the difference between the instantaneous tissue tension and the venous tension, and perfusion is controlled by the difference beween the arterial and venous tension. A mass balance for gas flow at the vascular cellular interface, a, enforces the perfusion limit when appropriate, linking the diffusion and perfusion equations directly. Blood and tissue tensions are joined in a complex feedback loop. The trigger point in the thermodynamic model is the separated phase volume, related to a set of mechanical pain thresholds for fluid injected into connective tissue.
The full thermodynamic model is complex, though Hills has performed massive computations correlating with the data, underscoring basic model validity. One of its more significant features can be seen in Figure 3. Considerations of free phase dynamics (phase volume trigger point) require deeper decompression staging formats, compared to considerations of critical tensions, and are characteristic of phase models. Full blown bubble models require the same, simply to minimize bubble excitation and growth.

Reduced Gradient Bubble Model
The reduced gradient bubble model (RGBM), developed by Wienke, treats both dissolved and free phase transfer mechanisms, postulating the existence of gas seeds (micronuclei) with permeable skins of surface active molecules, small enough to remain in solution and strong enough to resist collapse. The model is based upon laboratory studies of bubble growth and nucleation, and grew from a similar model, the varying permeability model (VPM), treating bubble seeds as gas micropockets contained by pressure permeable elastic skins
Inert gas exchange is driven by the local gradient, the difference between the arterial blood tension and the instantaneous tissue tension. Compartments with 1, 2, 5, 10, 20, 40, 80, 120, 240, 480, and 720 halftimes, tau , are again employed. While, classical (Haldane) models limit exposures by requiring that the tissue tensions never exceed the critical tensions, fitted to the US Navy nonstop limits, for example. The reduced gradient bubble model, however, limits the supersaturation gradient, through the phase volume constraint. An exponential distribution of bubble seeds, falling off with increasing bubble size is assumed to be excited into growth by compression-decompression. A critical radius, r sub c , separates growing from contracting micronuclei for given ambient pressure, P sub c . At sea level, P sub c = 33 fsw , r sub c = .8 microns, and DELTA P = d. Deeper decompressions excite smaller, more stable, nuclei.
Within a phase volume constraint for exposures, a set of nonstop limits, t sub n , at depth, d, satisfy a modified law, d t sub n sup 1/2 = 400 fsw min sup 1/2 , with gradient, G, extracted for each compartment, tau , using the nonstop limits and excitation radius, at generalized depth, d = P – 33 fsw. Tables 2 and 3 summarize t sub n , G sub 0 , DELTA G , and delta , the depth at which the compartment begins to control exposures.

Table 2.
Critical Phase Volume Time Limits.
______________________________________________
depth nonstop limit depth nonstop limit
d(fsw) t sub n (min) d (fsw) t sub n (min)
30  250 130 9.
40  130. 140 8.
50    73. 150 7.
60    52. 1606 5
70    39. 1705 8
80    27. 1805 3
90    22. 1904 6
100  18. 2004 1
110   15. 2103 7
120  12. 2203 1

Gas filled crevices can also facilitate nucleation by cavitation. The mechanism is responsible for bubble formation occuring on solid surfaces and container walls. In gel experiments, though, solid particles and ragged surfaces were seldom seen, suggesting other nucleation mechanisms. The existence of stable gas nuclei is paradoxical. Gas bubbles larger than 1 micron should float to the surafce of a standing liquid or gel, while smaller ones should dissolve in a few seconds. In a liquid supersaturated with gas, only bubbles at the critical radius, r sub c , would be in equilibrium (and very unstable equilibrium at best). Bubbles larger than the critical radius should grow larger, and bubbles smaller than the critical radius should collapse. Yet, the Yount gel experiments confirm the existence of stable gas phases, so no matter what the mechanism, effective surface tension must be zero.

Table 3.
Critical Phase Volume Gradients.
__________________________________________________________________________
halftime threshold depth surface gradient gradient change
tau (min) delta (fsw) G sub 0 (fsw) DELTA G
________________________ ____________ ____________
2 190 151.0 .518
5 135 95.0 .515
10 95 67.0 .511
20 65 49.0 .506
40 40 36.0 .468
80 30 27.0 .417
120 28 24.0 .379

Although the actual size distribution of gas nuclei in humans is unknown, these experiments in gels have been correlated with a decaying exponential (radial) distribution function. For a stabilized distribution accommodated by the body at fixed pressure, P sub c , the excess number of nuclei excited by compression-decompression must be removed from the body. The rate at which gas inflates in tissue depends upon both the excess bubble number, and the supersaturation gradient, G. The critical volume hypothesis requires that the integral of the product of the two must always remain less than some volume limit point, alpha V , with alpha a proportionality constant. A conservative set of bounce gradients, G bar , can be also be extracted for multiday and repetitive diving, provided they are multiplicatively reduced by a set of bubble factors, eta sup rep, eta sup reg , eta sup exc , all less than one, such that G bar = eta sup rep eta sup reg eta sup exc G.
These three bubble factors reduce the driving gradients to maintain the phases volume constraint. The first bubble factor reduces G to account for creation of new stabilized micronuclei over time scales of days. The second factor accounts for additional micronuclei excitation on deeper-than-previous dives. The third bubble factor accounts for bubble growth over repetitive exposures on time scales of hours. Clearly, the repetitive factors, eta sup rep , relax to one after about 2 hours, while the multiday factors, eta sup reg , continue to decrease with increasing repetitive activity, though at very slow rate. Increases in bubble elimination halftime and nuclei regeneration halftime will tend to decrease eta sup rep and increase eta sup reg . The repetitive fractions, eta sup rep , restrict back to back repetitive activity considerably for short surface intervals. The multiday fractions get small as multiday activities increase continuously beyond 2 weeks. Deeper-than-previous excursions incur the greatest reductions in permissible gradients (smallest eta sup exc ) as the depth of the exposure exceeds previous maximum depth.

Tissue Bubble Diffusion Model
The tissue bubble diffusion model (TBDM), according to Gernhardt and Vann, considers the diffusive growth of an extravascular bubble under arbitrary hyperbaric and hypobaric loadings. The approach incorporates inert gas diffusion across the tissue-bubble interface, tissue elasticity, gas solubility and diffusivity, bubble surface tension, and perfusion limited transport to the tissues. Tracking bubble growth over a range of exposures, the model can be extended to oxygen breathing and inert gas switching. As a starting point, the TBDM assumes that, through some process, stable gas nuclei form in the tissues during decompression, and subsequently tracks bubble growth with dynamical equations. Diffusion limited exchange is invoked at the tissue-bubble interface, and perfusion limited exchange is assumed between tissue and blood, very similar to the thermodynamic model, but with free phase mechanics. Across the extravascular region, gas exchange is driven by the pressure difference between dissolved gas in tissue and free gas in the bubble, treating the free gas as ideal. Initial nuclei in the TBDM have assumed radii near 3 microns at sea level, to be compared with .8 microns in the RGBM.
As in any free phase model, bubble volume changes become more significant at lower ambient pressure, suggesting a mechanism for enhancement of hypobaric bends, where constricting surface tension pressures are smaller than those encountered in hyperbaric cases. For instance, a theoretical bubble dose of 5 ml correlates with a 20% risk of decompression sickness, while a 35 ml dose correlates with a 90% risk, with the bubble dose representing an unnormalized measure of the separated phase volume. Coupling bubble volume to risk represents yet another extension of the phase volume hypothesis, a viable trigger point mechanism for bends incidence.

SATURATION CURVE
The saturation curve, relating permissible gas tension, Q, as a function of ambient pressure, P, for air, sets a lower bound, so to speak, on decompression staging. All staging models and algorithms must collapse to the saturation curve as exposure times increase in duration. In short, the saturation curve represents one extreme for any staging model. Bounce curves represent the other extreme. Joining them together for diving activities in between is a model task, as well as joining the same sets of curves over varying ambient pressure ranges. In the latter case, extending bounce and saturation curves to altitude is just such an endeavor.
Models for controlling hypobaric and hyperbaric exposures have long differed over range of applicability. Recent analyses of very high altitude washout data question linear extrapolations of the hyperbaric saturation curve, to hypobaric exposures, pointing instead to correlation of data with constant decompression ratios in animals and humans. Correlations of hypobaric and hyperbaric data, however, can be effected with a more general form of the saturation curve, one exhibiting the proper behavior in both limits. Closure of hypobaric and hyperbaric diving data can be managed with one curve, exhibiting linear behavior in the hyperbaric regime, and bending through the origin in the hypobaric regime. Using the RGBM and a basic experimental fact that the number of bubble seeds in tissue increase exponentially with decreasing bubble radius, just such a single expression can be obtained. The limiting forms are exponential decrease with decreasing ambient pressure (actually through zero pressure), and linear behavior with increasing ambient pressure. Asymptotic forms are quite evident. Such general forms derive from the RGBM, depending on a coupled treatment of both dissolved and free gas phases. Coupled to the phase volume constraint, these models suggest a consistent means to closure of hypobaric and hyperbaric data.

Abyss incorporates RGBM
Dr. Bruce Wienke, Director of the Computation Testbed for Industry, Advanced Computing Laboratory at Los Alamos National Laboratory, and the creator of the RGBM (Reduced Gradient Bubble Model) has joined the Abysmal Diving team. Dr. Wienke will be assisting us in the implementation of his latest decompression model into Abyss.
This means that Abyss will be the first and only product in the world with a fully operational Bubble Mechanics model.
1. This will allow Abyss to more effectively handle Technical Repetitive decompression diving!!!(not a small issue in itself!!)
2. Dives in which the following dive is deeper than the first. (a real potential problem area).
3. This will also allow Abyss to run active tracking, in real time, of actual bubble growth based upon his published and proprietary unpublished research.

RGBM/ABYSS Implementation
The Reduced Gradient Bubble Model (RGBM) is a dual phase (dissolved and free gas) algorithm for diving calculations. Incorporating and coupling historical Haldaniean dissolved gas transport with bubble excitation and growth, the RGBM extends the range of computational applicability of traditional methods. The RGBM is correlated with diving and exposure data on more complete physical principles. Much is new in the RGBM algorithm, and troublesome multidiving profiles with higher incidence of DCS are a target here. Some highlighted extensions for the ABYSS implementation of the Buhlmann basic algorithm include:
1. Standard Buhlmainiann nonstop time limits;
2. Restricted repetitive exposures, particularly beyond 100 ft, based on reduction in permissible bubble diffusion gradients within 2 hr time spans;
3. Restricted yo-yo and spike (multiple ascents and descents) dives based on excitation of new bubble seeds;
4. Restricted deeper-than-previous divers based on excitation of very small bubble seeds over 2 hr time spans:
5. Restricted multiday diving based on adaptation and regrowth of new bubble seeds;
6. Smooth coalescence of bounce and saturation limit points using 32 tissue compartments;
7. Consistent treatment of altitude diving, with proper zero point extrapolation of limiting tensions and permissible bubble gradients (through zero as pressure approaches zero);
8. Algorithm linked to diving data (tests), Doppler bubble, and laboratory micronuclei experiments;
9. Overall, parameters in RGBM/ABYSS are conservative, but flexible and easy to change or fit to new data.

What’s in store for the future?
Quoting from Dr. Bruce Wienke…”The ultimate computational algorithm, coupling nucleation, dissolved gas uptake and elimination, bubble growth and collisional coalescence, and critical sites, would be very, very complicated, requiring supercomputers such as CRAYS or their massively parallel cousins CMs for three dimensional modeling. Stochastic Monte Carlo methods and sampling techniques exist which could generate and stabilize nuclei from the thermodynamic functions, such as Gibbs or Helmholtz free energy, transport dissolved gas in flowing blood to appropriate sites, inflate, deflate, move, and collide bubbles and nuclei, and then tally statistics on tensions, bubble size and number, inflation and coalescence rate, free phase volume, and any other meaningful parameter, all in necessary geometrics.”
Such types of simulations of similarly complicated problems last for 16-32 hours at the Los Alimos Laboratories, on lightning fast supercomputers with near Gigaflop speed (1billion floating point operations per second)

B.R. Wienke

Fino a non molti anni fa era prassi normale che gli allievi dei corsi subacquei, per essere giudicati idonei

all’immersione, venissero sottoposti a una visita medico-sportiva d’idoneità all’attività agonistica. La visita

comportava tutta una serie di esami clinici stabiliti dal Ministero della Sanità e permetteva un buon

accertamento delle condizioni di salute del paziente.

Vi erano però degli inconvenienti: liste d’attesa a volte troppo lunghe, costi da aggiungere ai già elevati

prezzi dei corsi e perdite di tempo notevoli negli affollati centri di medicina dello sport. Inoltre, molti si

chiedevano come mai dovessero sottoporsi a una visita d’idoneità all’attività agonistica anche se di

agonismo non ne facevano proprio. Per spiegare questo piccolo mistero bisogna ricorrere alla lettura delle

circolari ministeriali, che in linguaggio burocratico ci spiegano le ragioni di tanta stranezza.

Ecco quello che dice in proposito la circolare del 28 febbraio 1983: «La maggior parte delle difficoltà

interpretative pervenute, hanno avuto per oggetto soprattutto l’identificazione dei limiti e delle caratteristiche

dell’attività sportiva agonistica». Di seguito gli esperti del Ministero specificano che: «L’aspetto competitivo,

da solo non è sufficiente a configurare nella forma agonistica un’attività sportiva. L’attività sportiva agonistica

non è quindi sintomo di competizione». La Commissione Tecnica consultiva voluta dal Ministero per

decidere quali fossero gli sport agonistici ritenne di non essere in grado d’identificarli; per cui decise di

delegare alle Federazioni Sportive e agli Enti di Promozione Sportiva riconosciuti dal Coni il compito di

decidere quali attività sportive richiedessero una certificazione di tipo agonistico.

In campo subacqueo la Federazione riconosciuta dal Coni era la Fips, che affermò: «Svolge attività

agonistica chi pratica sport subacqueo, il nuoto pinnato e l’orientamento»; per cui tutte le organizzazioni

subacquee in quegli anni si adeguarono a queste direttive richiedendo la certificazione di tipo medicosportivo

per i propri corsisti. Poi arrivarono in Italia i corsi gestiti dalle organizzazioni commerciali e il

problema si risolse, in quanto la maggior parte di esse non richiede un certificato di idoneità all’attività

agonistica, ma solo un certificato di idoneità all’attività sportiva generica, il quale può essere rilasciato dal

medico di famiglia. Questo è dovuto al fatto che negli Usa non esiste una disciplina legislativa per la

medicina dello sport e tutto viene lasciato al libero arbitrio degli individui, senza che si verifichino grossi

problemi.

La semplificazione delle procedure che si realizza con la certificazione del medico di base apre però alcune

problematiche. Mentre una volta gli allievi sofferenti di asma o diabete al momento della visita di idoneità

medico- sportiva erano giudicati non idonei “ope legis”, adesso potrebbe verificarsi il caso in cui il medico

che certifica non sia a conoscenza dell’esistenza della malattia, o non sappia che esistono delle

incompatibilità fra certi sport e alcune malattie. Non bisogna dimenticare, infine, che la scienza fa progressi e

mentre una volta si pensava che alcune malattie costituissero una controindicazione assoluta e definitiva

all’attività subacquea, oggi molti studiosi sono meno categorici e preferiscono analizzare i singoli casi.

Diabete

Il diabete è una malattia per cui si verifica un inadeguato controllo del livello del glucosio circolante nel

sangue. Siccome tutte le nostre cellule si nutrono per mezzo del glucosio, che per il corpo umano è un po’

quello che è la benzina per i motori, quando ne arriva troppo poco queste cellule vanno prima in riserva, e se

il carburante manca del tutto, si fermano, come tutte le macchine.

Questo fenomeno, che in termini medici si chiama ipoglicemìa, può avere delle conseguenze catastrofiche

per il cervello, perché può dare origine a debolezza muscolare, convulsioni e perdita di coscienza. Gli

episodi ipoglicemici sono estremamente imprevedibili e i loro segni premonitori, che sono la sudorazione, il

senso di fame e il nervosismo, sono molto difficili da rilevare sott’acqua. Le altre conseguenze del diabete si

sviluppano di solito in pazienti che hanno sofferto di questa malattia per molti anni e sono soprattutto a

carico delle arterie, che nei diabetici invecchiano molto più rapidamente, con una serie di conseguenze

anche gravi per il cuore, gli occhi, il rene e il cervello.

Ovviamente, di fronte a tanti rischi i medici sportivi non potevano astenersi dal vietare le immersioni a questi

malati; però negli ultimi anni si comincia a vedere un cambiamento nel modo di considerare la malattia.

Il Bsac (British Sub Aqua Club), dopo un attento esame degli incidenti registrati nel passato e sulla base

dell’esperienza accumulata da diabetici che si immergevano senza autorizzazione medica, dal 1992 ha

cominciato ad accettare all’interno della propria associazione quelli per i quali risultavano soddisfatti certi

precisi requisiti medici.

Prendendo il via da tali considerazioni e constatando che negli Usa esiste un significativo numero di diabetici

che fa immersioni, l’American Diabetes Association ha pubblicato delle linee guida da seguire da parte dei

diabetici che vogliono immergersi.

Pertanto, i diabetici possono immergersi se:

1) c’è un buon controllo dei livelli glicemici, che non devono avere grossi sbalzi;

2) non ci deve essere nessuna delle gravi complicazioni dovute al diabete;

3) il paziente deve avere una perfetta comprensione delle relazioni che esistono fra esercizio fisico e

glicemia (l’esercizio fisico provoca un consumo di zuccheri, per cui il paziente deve provvedere a sostituire

quello che ha consumato).

L’immersione è invece da vietare ai diabetici che:

1) hanno avuto un grave episodio ipoglicemico negli ultimi dodici mesi;

2) hanno qualche grave complicazione secondaria alla malattia;

3) hanno un cattivo controllo della glicemia e non riescono a rendersi conto dei segni premonitori

dell’ipoglicemia;

4) non si rendono conto delle relazioni che intercorrono fra esercizio fisico e glicemia.

Il Bsac, inoltre, ha redatto uno schema che specifica anche quello che i diabetici dovrebbero portare

sott’acqua e quello che devono fare prima e dopo l’immersione.

In conclusione, bisogna essere consci che dalle immersioni possono derivare dei rischi per i diabetici, ma

quanto più aumentano i dati a disposizione della comunità scientifica, tanto più i medici scoprono che non è

indispensabile imporre a questi pazienti un divieto assoluto all’attività sportiva e che ogni caso può e deve

essere analizzato individualmente. Questo è certamente un passo avanti rispetto a quando i diabetici, per

potersi immergere, dovevano nascondere la propria malattia.

Asma

Anche gli asmatici soffrono di una segregazione simile a quella dei diabetici, per cui per lungo tempo sono

stati giudicati non idonei all’immersione a causa dei rischi connessi a questa malattia. Il problema

dell’asmatico è causato dal restringimento del diametro dei bronchioli più piccoli, che si può verificare a

contatto con sostanze in grado di scatenare reazioni allergiche.

Il verificarsi di una crisi asmatica sott’acqua potrebbe provocare due differenti condizioni patologiche,

entrambe catastrofiche.

Nella prima, se si dovesse verificare una crisi asmatica con un restringimento generalizzato delle vie aeree

mentre il paziente è sott’acqua, si potrebbe verificare una grave difficoltà respiratoria in grado di portare

all’annegamento; nel secondo caso si potrebbe verificare un intrappolamento d’aria localizzato ad alcuni

alveoli, per cui durante la risalita, non riuscendo a scaricare l’aria racchiusa al loro interno, potrebbero

andare incontro a sovradistensione e infine a rottura, per cui si potrebbe verificare un’embolia gassosa

traumatica.

Anche in questo caso, il Bsac ha fatto un lavoro molto utile accertando che in Gran Bretagna il 4% dei

subacquei può essere definito “asmatico”, ma che in questi pazienti non si è verificata una più alta quantità

di incidenti rispetto agli altri.

In questo caso non sono ancora stati stabiliti dei criteri rigidi per cui l’immersione può essere concessa o, al

contrario, debba essere vietata. Mentre ci sono alcuni medici che considerano gli asmatici come dei soggetti

a potenziali rischi, la maggior parte dei medici iperbarici negli Stati Uniti pensa che dopo adeguate indagini

possano immergersi senza rischi aggiuntivi. Ogni asmatico deve essere esaminato individualmente ed è

essenziale che il medico sappia quali sono i fattori che possono scatenare un attacco acuto di asma nel suo

caso specifico.

In conclusione, per poter immergersi in sicurezza è indispensabile che questi pazienti informino il proprio

compagno e il leader dell’immersione della propria situazione; inoltre, ogni anno devono essere controllati e

visitati da medici adeguatamente preparati su questi argomenti. Le suddette considerazioni non sono

comunque valide per i militari e per i subacquei professionisti, i quali possono andare incontro a fattori

ambientali sfavorevoli che potrebbero scatenare un attacco asmatico. Il diabete Il diabete è una malattia in

cui si verifica la diminuzione di un ormone chiamato insulina da parte di alcune cellule del pancreas.

L’insulina è la sostanza che permette all’uomo di utilizzare lo zucchero che entra nel corpo con la dieta, e

permette all’organismo di utilizzare il glucosio per produrre energia. Si distinguono due forme di questa

malattia: il diabete di tipo I, cosiddetto insulino-dipendente e il diabete di tipo II non insulino-dipendente. Il

diabete di tipo I interessa soprattutto i giovani ed è caratterizzato dalla mancanza delle cellule che

producono l’insulina, per cui questi pazienti devono introdurne nel loro corpo in dose adeguata per il resto

della loro vita mediante delle iniezioni. I segni precoci di questa malattia sono: perdita di peso, sete costante

e frequente bisogno di urinare. In questi pazienti l’esercizio fisico è utile soprattutto per motivi psicologici. Il

diabete di tipo II è una malattia tipica delle persone di mezza età, obese e spesso si verifica grazie ad una

forte componente ereditaria. Queste persone hanno dei livelli di insulina inadeguati e di solito riescono a

controllare la loro malattia con la dieta, l’esercizio fisico ed una terapia ipoglicemizzante orale con

compresse. Normalmente questi pazienti non hanno bisogno di insulina. Per quanto li riguarda, i segni tipici

della malattia sono dati dall’obesità, dalla fame costante e dal frequente bisogno di urinare. L’esercizio fisico

può aiutarli a migliorare il controllo della malattia. L’asma Gli alveoli polmonari sono dotati di un minuscolo

anello muscolare situato al termine del bronchiolo che porta loro l’aria. Esiste una lunga serie di sostanze in

grado di provocare reazioni allergiche a livello del polmone e il suddetto anello muscolare risponde a questa

stimolazione allergica con una contrazione che restringe il diametro del bronchiolo. Di conseguenza, l’aria

che viene fatta entrare all’interno dei polmoni dalla robusta muscolatura inspiratoria non riesce più ad uscire,

perché i muscoli espiratori sono deboli; inoltre l’espirazione, che dovrebbe verificarsi passivamente grazie

alla retrazione spontanea del polmone, non riesce a verificarsi in tempi normali. La contrazione dei muscoli a

livello bronchiolare impedisce lo svuotamento spontaneo del polmone, per cui la successiva inspirazione è

molto più difficoltosa in quanto il polmone è già pieno d’aria. Esistono molti farmaci in grado di controllare

questa situazione: i principali sono i cortisonici che diminuiscono la risposta allergica e l’infiammazione ed i

farmaci attivi sulla muscolatura dei bronchi,come la teofillina.

Giuseppe Ridulfo

DEEP STOPS

The Basics

Deep stops – what are they?

Actually, just what the name suggests. Deep stops are decompression stops made at deeper depths than those traditionally dictated by classical (Haldane) dive tables or algorithms. They are fairly recent (last 15 years) protocols, suggested by modern decompression theory, but backed up by extensive diver practicum with success in the mixed gas and decompression arenas – so called technical diving. Tech diving encompasses scientific, military, commercial, and exploration underwater activities. The impact of deep stops has been a revolution in diving circles. So have slower ascent rates across recreational and technical diving. In quantifiable terms, slower ascent rates are very much akin to deep stops, though not as pronounced as decompression stops. Deep stops plus slow ascent rates work together. And they work together safely and efficiently.

Many regard deep stops as the most significant development in modern diving. Here’s why.

Deep stops usually reduce overall decompression time (hang time) too. And when coupled to the use of heliumin the breathing mixture (trimix) to reduce narcotic effects of nitrogen, technical divers report feeling much better physically today when they leave the water. The reduction in hang time ranges from 10% to as high as 50%, depending on diver, mix, depth, and exposure time. Feeling better while decompressing for shorter periods of time is certainly a win-win situation that would have been thought an impossibility not too long ago. The basic tenets of Haldane decompression theory (and neo-classical dissolved gas theory) postulate that deeper exposures (deep stop plus bottom time) incur greater offgassing penalties in the shallow zone. Just look at those deco tables based upon Haldane methodolgy. You know, the ones you used before you bought a dive computer. Even the bulk of dive computers still stage divers using Haldane approaches. But that is changing too. New computers invoking the dual science of dissolved gases and bubbles are emerging. And deep stops are a natural result of their operation.

The depth at which the first deep stops are made can be dramatically deeper than those required by conventional tables. For instance, a dive to 300 ft on trimix for 30 minutes, with switches to progressively higher enrichments of nitrox at 120, 70, and 20 ft, calls for the first deep stops in the 250 ft range. Conventional tables require the first stops in the 100 ft range.

For most early technical divers, obtaining deep and mixed gas decompression tables constituted one of many road-blocks to safe deep and exploration diving. Existing tables ranged from ultra-conservative as an insulation against harm to a hodgepodge of protocols based on total misunderstanding. From this background, and driven by a need to optimize decompression schedules, deep stops steadily advanced as a safe and efficient change to diver staging. And this even though formal tests were usually not conducted in controlled environments, like hyperbaric chambers.

The History

Though deep stops are regarded as a major development in diving, the first experiments were more trial-and-error than scientific in nature. Just like so many other important developments in the real world. Underlying science with mechanistics would follow in the late 80s and 90s, albeit with considerable flack from the expert s of the time. And so with helium breathing mixtures, the voodoo gas that “does not decompress”.

Maybe experiments is too strict a description. Individuals, particularly in the cave diving community, toyed with decompression regimens in hopes of mimimizing their decompression time. The cave exploration Woodville Karst Plain Project (WKPP), mapping subsurface topographies in Florida, pioneered deep stop technology, establishing many rule-of-thumb protocols to be imposed on conventional tables. Irvine and Jablonski stand at the forefront here, success-fully conducting 6 hour dives at 280 ft in the Wakulla cave complex with deep stop decompression times of 12 hours versus traditional Haldane hang times of 20 hours. Also, the horizontal penetrations of 19,000 ft are world records (Guinness). Figure 1 sketches comparison profiles, along with mixtures, times, switches, and depths. Spectacular is a gross understatement. Certainly such contributions to diving science and spinoff model validation parallel Haldane a hundred years ago.

WKPP initially found that common decompression assumptions subjected divers to extremely long decompression obligations, and ones that, regardless of their length, were inefficient. Divers also felt badly upon surfacing from extended deco dives. Operationally (many dives over many years), WKPP divers found that the insertion of deep stops permitted shortening of shallower stops with an overall reduction in total decompression time. The decompression schedule was more effective, with effectiveness represented by subjective diver health and sense of well being.

But even before these deep stop protocols emerged, utilitarian diving practices among diving fisherman and pearl gatherers suggested traditional staging was in need of rethinking. And early deco models, such as the so called thermo-dynamic model of Hills, suggested why and how. Deep stops likely evolved from cognizance of both by tech divers.

Pearling fleets, operating in the deep tidal waters off northern Australia, employed Okinawan divers who regularly journeyed to depths of 300 ft for as long as one hour, two times a day, six days per week, and ten months out of the year. Driven by economics, and not science, these divers developed optimized decompression schedules empirically. As reported by Le Messurier and Hills, deeper decompression stops, but shorter decompression times than required by Haldane theory, were characteristics of their profiles. Such protocols are entirely consistent with minimizing bubble growth and the excitation of nuclei through the application of increased pressure, as are shallow safety stops and slow ascent rates. With higher incidence of surface decompression sickness, as expected, the Australians devised a simple, but very effective, in-water recompression procedure. The stricken diver is taken back down to 30 ft on oxygen for roughly 30 minutes in mild cases, or 60 minutes in severe cases. Increased pressures help to constrict bubbles, while breathing pure oxygen maximizes inert gas washout (elimination). Recompression time scales are consistent with bubble dissolution experiments.

Similar schedules and procedures have evolved in Hawaii, among diving fishermen, according to Farm and Hayashi. Harvesting the oceans for food and profit, Hawaiian divers make beween 8 and 12 dives a day to depths beyond 350 ft. Profit incentives induce divers to take risks relative to bottom time in conventional tables. Repetitive dives are usually necessary to net a school of fish. Deep stops and shorter decompression times are characteristics of their profiles. In step with bubble and nucleation theory, these divers make their deep dive first, followed by shallower excursions. A typical series might start with a dive to 220 ft, followed by 2 dives to 120 ft, and culminate in 3 or 4 more excursions to less than 60 ft. Often, little or no surface intervals are clocked between dives. Such types of profiles literally clobber conventional tables, but, with proper reckoning of bubble and phase mechanics, acquire some credibility. With ascending profiles and suitable application of pressure, gas seed excitation and bubble growth are likely constrained within the body’s capacity to eliminate free and dissolved gas phases. In a broad sense, the final shallow dives have been tagged as prolonged safety stops, and the effectiveness of these procedures has been substantiated in vivo (dogs) by Kunkle and Beckman. In-water recompression procedures, similar to the Australian regimens, complement Hawaiian diving practices for all the same reasons.

So deep stops work and are established. But why?

The Science

The science is fairly simply. It’s just a matter of how dissolved gases and bubbles behave under pressure changes. We use to think that controlling dissolved gas buildup and elimination in tissue and blood was the basis for staging divers and astronauts. And that bubbles didn’t form unless dissolved gas trigger points were exceeded. At least that was the presumption that went into conventional (Haldane) tables. Chemists, physicists, and engineers never bought off on that. When silent bubbles were tracked in divers not experiencing any decompression problems, of course, this changed. And since bubbles need be controlled in divers, focus changed and switched from just-dissolved-gases to both-bubbles-and-dissolved-gases. Within such framework, deep stops emerge as a natural consequence. So do dual phase (bubbles plus dissolved gas) models.

Here’s how.

To eliminate dissolved gases, the driving outgassing gradient is maximized by reducing ambient pressure as much as possible. That means bringing the diver as close to the surface as possible. But, to eliminate bubbles (the gases inside them), the outgassing gradient is maximized by increasing ambient pressure as much as possible. That means holding the diver at depth when bubbles form. Deep stops accomplish the latter.

But the staging paradigm has a few more wrinkles.

Clearly, from all of the above, dominant modes for staging diver ascents depend upon the preponderance of free (bubbles) or dissolved phases in the tissues and blood, their coupling, and their relative time scales for elimination. This is now (will always be) a central consideration in staging hyperbaric or hypobaric excursions to lower ambient pressure environments. The dynamics of elimination are directly opposite, as stated and depicted in Figure 2. To eliminate dissolved gases (central tenet of Haldane decompression theory), the diver is brought as close as possible to the surface. To eliminate free phases (coupled tenet of bubble decompression theory), the diver is maintained at depth to both crush bubbles and squeeze gas out by diffusion across the bubble film surface. Since both phases must be eliminated, the problem is a playoff in staging. In mathematical terms, staging is a minimax problem, and one that requires full blown dual phase models, exposure data, and some concensus of what is an acceptable level of DCI incidence.

Enter dual phase models which generate deep stops consistently within free and dissolved gas phase constraints.

The Models And Diving Algorithms

The earliest prescriptions for deep stops were imbedded in conventional tables. Something like this was employed, trial and error, and this one is attributed to Pyle, an underwater fish collector in Hawaii:

1. calculate your decompression schedule from tables, meters, or software;

2. half the distance to the first deco stop and stay there a minute or two;

3. recompute your decompression schedule with time at the deep stop included as way time (software), or bottom time (tables);

4. repeat procdeure until within some 10 -30 ft of the first deco stop;

5. and then go for it.

Within conventional tables, such procedure was somewhat arbitrary, and usually always ended up with a lot of hang time in the shallow zone. Such is to be expected within dissolved gas deco frameworks. So, deep stop pioneers started shaving shallow deco time off their schedules. And jumped back into the water, picking up the trial and error testing where it left off.

Seasoned tech divers all had their own recipes for this process. And sure, what works works in the diving world. What doesn’t is usually trashed.

Concurrently, full up dual phase models, spawned by the inadequacies and shortcomings of conventional tables, emerged on the diving scene. Not only did deep stops evolve self consistently in these models, but dive and personal computers put deco scheduling with these new models in the hands of real divers. And real on the scene analysis and feedback tuned arbitrary, trial and error, and theoretical schedules to each other.

One thing about these bubble models, as they are collectively referenced, that is common to all of them is deeper stops, shorter decompression times in the shallow zone, and shorter overall deco times. And they all couple dissolved gases to bubbles, not focusing just on bubbles or dissolved gas.

Without going into gory details, a few of the more important ones can be summarized. The thermodynamic model of Hills really got the ball rolling so to speak:

1. thermodynamic model (Hills, 1976) – assumes free phase (bubbles) separates in tissue under supersaturation gas loadings. Advocates dropout from deco schedule somewhere in the 20 ft zone.

2. varying permeability model (Yount, 1986) – assumes preformed nuclei permeate blood and tissue, and are excited into growth by compression-decompression. Model patterned after gel bubbles studied in the laboratory.

3. reduced gradient bubble model (Wienke, 1990) – abandons gel parametrization of varying parmeability model, and extends bubble model to repetitive, altitude, and reverse profile diving. Employed in recreational and techni-cal diving meters, and basis for new NAUI tables;

4. tissue bubble diffusion model (Gernhardt and Vann, 1990) – assumes gas transfer across bubble interface, and correlates growth with DCI statistics. Probably employed in the commercial diving sector.

Not all these models have seen extensive field testing, but since they are all similar, the following, addressing testing and validation of the reduced gradient bubble model (RGBM), holds in broad terms. The 1000s of tech dives on deep stops, of course, already validate deep stop technology and models to most, but the testing and validation described next spans deep stops to recreational diving in single model framework. And that is a very desired feature of any decompression theory and/or model.

The Testing And Validation

Models need validation and testing. Often, strict chamber tests are not possible, economically nor otherwise, and bubble models employ a number of benchmarks and regimens to underscore viability. The following are some support-ing the RGBM phase model and NAUI released nitrox, heliox, and trimix diving tables:

1. counterterror and countermeasures (LANL) exercises have used the RGBM (full up iterative deep stop version) for a number of years, logging some 456 dives on mixed gases (trimix, heliox, nitrox) without incidence of DCI – 35% were deco dives, and 25% were repets (no deco) with at least 2 hr SIs, and in the forward direction (deepest dives first);

2. NAUI Technical Diving has been diving the deep stop version for the past 3 yrs, some estimated 500 dives, on mixed gases down to 250 f sw, without a single DCI hit. Some 15 divers, late 1999, in France used the RGBM to make 2 mixed gas dives a day, without mishap, in cold water and rough seas. Same in the warm waters of Roatan in 2000 and 2001.

3. modified RGBM recreational algorithms (Haldane imbedded with bubble reduction factors limiting reverse pro-file, repetitive, and multiday diving), as coded into ABYSS software and Suunto, Plexus, and Hydrospace de-cometers, lower an already low DCI incidence rate of approximately 1/10,000 or less. More RGBM decompres-sion meters, including mixed gases, are in the works;

4. a cadre of divers and instructors in mountainous New Mexico, Utah, and Colorado have been diving the modified (Haldane imbedded again) RGBM at altitude, an estimated 450 dives, without peril. Again, not surprising since the altitude RGBM is slightly more conservative than the usual Cross correction used routinely up to about 8,000ft elevation, and with estimated DCI incidence less than 1/10,000;

5. within decometer implementations of the RGBM, only two DCI hits have been reported in nonstop and multidiv-ing categories, beyond 40,000 dives or more, up to now;

6. extreme chamber tests for mixed gas RGBM are in the works, and less stressful exposures will be addressed shortly – extreme here means 300 f swand beyond;

7. probabilistic decompression analysis of some selected RGBM profiles, calibrated against similar calculations of the same profiles by Duke, help validate the RGBM on computational bases, suggesting the RGBM has no more theoretical risk than other bubble or dissolved gas models (Weathersby, Vann, Gerth methodology at USN and Duke).

8. all divers and instructors using RGBMdecometers, tables, or NET software have been advised to report individual profiles to DAN Project Dive Exploration (Vann, Gerth, Denoble and many others at Duke).

9. ABYSS is a NET sotware package that offers the modified RGBM (folded over the Buhlmann ZHL) and the full up, deep stop version for any gas mixture, has a fairly large contingent of tech divers already using the RGBM and has not received any reports of DCI,

10. NAUI Worldwide is releasing a set of tested no-group, no-calc, no-fuss RGBM tables for recreational sea level and altitude air and nitrox diving, with simple rules linking surface intervals, repets, and flying-after-diving.

It almost goes without saying that models such as these have reshaped our decompression horizons – and will continue doing so.

One last item concerning deep stops remains. What about controlled laboratory testing?

The Experiments

Doppler and utrasound imaging are techniques for detecting moving bubbles in humans and animals following compression-decompression. While bubble scores from these devices do not always correlate with the incidence of DCI, the presence or non-presence of bubbles is an important metric in evaluating dive profiles.

So let’s consider some recent tests, and see how they relate to deep stops.

Analysis of more than 16,000 actual dives by Diver’s Alert Network (DAN), prompted Bennett to suggest that decompression injuries are likely due to ascending too quickly. He found that the introduction of deep stops, without changing the ascent rate, reduced high bubble grades to near zero, from 30.5% without deep stops. He concluded that a deep stop at half the dive depth should reduce the critical fast gas tensions and lower the DCI incidence rate.

Marroni concluded studies with DAN’s European sample with much the same thought. Although he found that ascent speed itself did not reduce bubble formation, he suggested that a slowing down in the deeper phases of the dive (deep stops) should reduce bubble formation. He will be conducting further tests along those lines.

Brubakk and Wienke found that longer decompression times are not always better when it comes to bubble formation in pigs. They found more bubbling in chamber tests when pigs were exposed to longer but shallower decompression profiles, where staged shallow decompression stops produced more bubbles than slower (deeper) linear ascents. Model correlations and calculations using the reduced gradient bubble model suggest the same.

Cope studied 12 volunteer divers performing conventional (Haldane tables) dives with and without deep stops. His

results are not available yet – but should be very interesting.

The Bottom Line

To most of us in the technical and recreational diving worlds, the bottom line is simple.

Deep stop technology has developed successfully over the past 15 years or so. Tried and tested in the field, now some in the laboratory, deep stops are backed up by diver success, confidence, theoretical and experimental model underpinnings, and general acceptance by seasoned professionals.

Amen.
And dive on.

B.R. Wienke

 

“Introduction”
Biophysical models of inert gas transport and bubble formation all try to prevent decompression sickness. Developed over years of diving application, they differ on a number of basic issues, still mostly unresolved today:

1. the rate limiting process for inert gas exchange, blood flow rate (perfusion) or gas transfer rate across tissue (diffusion);
2. composition and location of critical tissues (bends sites);
3. the mechanistics of phase inception and separation (bubble formation and growth);
4. the critical trigger point best delimiting the onset of symptoms (dissolved gas buildup in tissues, volume of separated gas, number of bubbles per unit tissue volume, bubble growth rate to name a few);
5. the nature of the critical insult causing bends (nerve deformation, arterial blockage or occlusion, blood chemistry or density changes).
Such issues confront every modeler and table designer, perplexing and ambiguous in their correlations with experiment and nagging in their persistence. And here comments are confined just to Type I (limb) and II (central nervous system) bends, to say nothing of other types and factors. These concerns translate into a number of what decompression modelers call dilemmas that limit or qualify their best efforts to describe decompression phenomena. Ultimately, such concerns work their way into table and meter algorithms, with the same caveats. A closer look at these issues is illuminating. .uh “Perfusion And Diffusion” Perfusion and diffusion are two mechanisms by which inert and metabolic gases exchange between tissue and blood. Perfusion denotes the blood flow rate in simplest terms, while diffusion refers to the gas penetration rate in tissue, or across tissue-blood boundaries. Each mechanism has a characteristic rate constant for the process. The smallest rate constant limits the gas exchange process. When diffusion rate constants are smaller than perfusion rate constants, diffusion dominates the tissue-blood gas exchange process, and vice-versa. In the body, both processes play a role in real exchange process, especially considering the diversity of tissues and their geometries. The usual Haldane tissue half-lives are the inverses of perfusion rates, while the diffusivity of water, thought to make up the bulk of tissue, is a measure of the diffusion rate.

Clearly in the past, model distinctions were made on the basis of perfusion or diffusion limited gas exchange. The distinction is somewhat artificial, especially in light of recent analyses of coupled perfusion-diffusion gas transport by Hills and Hennessy, recovering limiting features of the exchange process in appropriate limits. The distinction is still of interest today, however, since perfusion and diffusion limited algorithms are used in mutually exclusive fashion in diving. The obvious mathematical rigors of a full blown perfusion-diffusion treatment of gas exchange mitigate against table and meter implementation, where model simplicity is a necessity. So one or another limiting models is adopted, with inertia and track record sustaining use. Certainly Haldane models fall into that categorization. Still, within the context of just perfusion or diffusion limited gas exchange, a number of interesting anomalies arise, discussed by Kety and Schmidt, Hills, Tepper and Lightfoot, Roughton, and Hempleman.

In multitissue (Haldane) models, a nagging question of interpretation of a spectrum of half-lives and critical tensions arises. If the hypothetical compartments represent local differences in circulation within the same anatomical tissue, they should have the same critical tension, as originally proposed by Haldane. But, if they represent different anatomical identities, then the same insult to to different tissues should produce different clinical signs and manifestations, yet, the same set of symptoms occurs independent of the compartment affected. Some would argue that it is better to introduce critical tensions as variables depending on depth, time, temperature, and so on, while holding them independent of half-life. In single tissue models, of course, this happens de facto.

While the spectrum of half-lives in perfusion models is reasonable from the perspective of inert gas washout times, diffusion coefficients assigned to model calculations, or extracted from data fits, are more ambiguous. In calculational models, gas diffusivities in tissue are five orders of magnitude smaller than in water, comprising the bulk of tissue matter. Typical water diffusivities are on the order of 10 sup -5 ~cm sup 2 ~sec sup -1 , while model tissue values are near 10 sup -10 cm sup 2 ~ sec sup -1 . In critical sites, anomalously reduced diffusion might be ascribed to geometry of the site, or composition of the tissue. Hills suggested cellular effects, while Hempleman was concerned about avascularity, both implying longer diffusion time scales.

Such questions, of course, suffer from the same problem common to other vital issues, namely identification of the critical tissue and site. Another way to look at the question of perfusion-versus-diffusion might be through the bounce data for different breathing mixtures. In bounce diving, selection of helium or nitrogen as the inert gas is a trade between the lower solubility of helium, less than nitrogen by a factor of 3-5, and the greater diffusivity, about 2.7 times greater than nitrogen by Graham’s law. For long exposure times, solubility factors dominate and helium is a better breathing gas than nitrogen. The solubility advantage should also hold up for short exposures if gas exchange is perfusion limited, while if diffusion is rate limiting, the 2.7 diffusion advantage of helium might be expected to outdistance its 3-5 solubility advantage over nitrogen, and so air (nitrogen) would be better for bounce diving. Goat experiments clearly show that nitrogen is better for bounce exposures of less than 20 minutes duration, that is, longer nonstop time limits compared to helium. The implication is then simple, namely that some gas uptake in critical tissues is diffusion limited.

But the controversy does not end there. An obvious way to differentiate between blood perfusion and diffusion is to measure the time it takes for inert gas to diffuse into tissue. Kety and Roughton measured this transit time, and found that the mean extravascular tension attained 95-99% of the blood tension in 1-5 seconds. This is so very rapid that diffusion cannot play a rate limiting role, that is, values smaller than water diffusivities are precluded.

Bubble Sites
We do not really know where bubbles form nor lodge, their migration patterns, their birth and dissolution mechanisms, nor the exact chain of physico-chemical insults resulting in decompression sickness. Many possibilities exist, differing in the nature of the insult, the location, and the manifestation of symptoms. Bubbles might form directly (de novo) in supersaturated sites upon decompression, or possibly grow from preformed, existing seed nuclei excited by compression-decompression. Leaving their birth sites, bubbles may move to critical sites elsewhere. Or stuck at their birth sites, bubbles may grow locally to pain-provoking size. They might dissolve locally by gaseous diffusion to surrounding tissue or blood, or passing through screening filters, such as the lung complex, they might be broken down into smaller aggregates, or eliminated completely. Whatever the bubble history, it presently escapes complete elucidation.

Bubbles may hypothetically form in the blood (intravascular) or outside the blood (extravascular). Once formed, intravascularly or extravascularly, a number of critical insults are possible. Intravascular bubbles may stop in closed circulatory vessels and induce ischemia, blood sludging, chemistry degradations, or mechanical nerve deformation. Circulating gas emboli may occlude the arterial flow, clog the pulmonary filters, or leave the circulation to lodge in tissue sites as extravasular bubbles. Extravascular bubbles may remain locally in tissue sites, assimilating gas by diffusion from adjacent supersaturated tissue and growing until a nerve ending is deformed beyond its pain threshold. Or, extravascular bubbles might enter the arterial or venous flows, at which point they become intravascular bubbles.

Spontaneous bubble formation in fluids usually requires large decompressions, like hundreds of atmospheres, somewhere near fluid tensile limits. Many feel that such circumstance precludes direct bubble formation in blood following decompression. Explosive, or very rapid decompression, of course is a different case. But, while many doubt that bubbles form in the blood directly, intravascular bubbles have been seen in both the arterial and venous circulation, with vastly greater numbers detected in venous flows (venous gas emboli). Ischemia resulting from bubbles caught in the arterial network has long been implied as a cause of decompression sickness. Since the lungs are effective filters of venous bubbles, arterial bubbles would then most likely originate in the arteries or adjacent tissue beds. The more numerous venous bubbles, however, are suspected to first form in lipid tissues draining the veins. Lipid tissue sites also possess very few nerve endings, possibly masking critical insults. Veins, thinner than arteries, appear more susceptible to extravascular gas penetration.

Extravascular bubbles may form in aqueous (watery) or lipid (fatty) tissues in principle. For all but extreme or explosive decompression, bubbles are seldom observed in heart, liver, and skeletal muscle. Most gas is seen in fatty tissue, not unusual considering the five-fold higher solubility of nitrogen in lipid tissue versus aqueous tissue. Since fatty tissue has few nerve endings, tissue deformation by bubbles is unlikely to cause pain locally. On the other hand, formations or large volumes of extravascular gas could induce vascular hemorrhage, depositing both fat and bubbles into the circulation as noted in animal experiments. If mechanical pressure on nerves is a prime candidate for critical insult, then tissues with high concentrations of nerve endings are candidate structures, whether tendon or spinal cord. While such tissues are usually aqueous, they are invested with lipid cells whose propensity reflects total body fat. High nerve density and some lipid content supporting bubble formation and growth would appear a conducive environment for a mechanical insult.

On the question of preformed nuclei, their presence in human tissue and blood has not been demonstrated. The existence of preformed nuclei in serum and egg albumin has been reported by Yount and Strauss. Since performed nuclei are found virtually in every aqueous substance known, their preclusion from the body would come as a surprise to many. Hence, while most regard nucleation as a random process, its occurrence in tissue seems highly probable, seen for instance in the studies of Evans, Walder, Strauss, Yount, Kunkle, and co-workers. Model correlations with incidence statistics of decompression sickness in salmon, rats, and humans speak favorably for the nucleation concept. .uh “Computational Algorithms And Complexity” The establishment and evolution of gas phases, and possible bubble trouble, involves a number of distinct, yet overlapping, steps:

1. nucleation and stabilization (free phase inception);
2. supersaturation (dissolved gas buildup);
3. excitation and growth (free-dissolved phase interaction);
4. coalescence (bubble aggregation);
5. deformation and occlusion (tissue damage and ischemia).

Over the years, much attention has focused on supersaturation. Recent studies have shed much light on nucleation, excitation and bubble growth, even though in vitro. bubble aggregation, tissue damage, ischemia, and the whole question of decompression sickness trigger points are difficult to quantify in any model, and remain obscure. Complete elucidation of the interplay is presently asking too much. Yet, the development and implementation of better computational models is necessary to address problems raised in workshops, reports, publications, disclaimers, and as a means to safer diving.

The computational issues of bubble dynamics (formation, growth, and elimination) are mostly outside the traditional framework, but get folded into half-life specifications in a nontractable mode. The very slow tissue compartments (half-lives large, or diffusivities small) might be tracking both free and dissolved gas exchange in poorly perfused regions. Free and dissolved phases, however, do not behave the same way under decompression. Care must be exercised in applying model equations to each component. In the presence of increasing proportions of free phases, dissolved gas equations cannot track either species accurately.

Computational algorithms tracking both dissolved and free phases offer broader perspectives and expeditious alternatives, but with some changes from classical schemes. Free and dissolved gas dynamics differ. The driving force (gradient) for free phase elimination increases with depth, directly opposite to the dissolved phase elimination gradient which decreases with depth. Then, changes in operational procedures become necessary for optimality. Considerations of growth and growth invariably require deeper staging procedures than supersaturation methods. Though not as dramatic, similar constraints remain operative in multiexposures, that is, multilevel, repetitive, and multiday diving.

Other issues concerning time sequencing of symptoms impact computational algorithms. That bubble formation is a predisposing condition for decompression sickness is universally accepted. However, formation mechanisms and their ultimate physiological effect are two related, yet distinct, issues. On this point, most hypotheses makes little distinction between bubble formation and the onset of bends symptoms. Yet we know that silent bubbles have been detected in subjects not suffering from decompression sickness. So it would thus appear that bubble formation, per se, and bends symptoms do not map onto each other in a one-to-one manner. Other factors are truly operative, such as the amount of gas dumped from solution, the size of nucleation sites receiving the gas, permissible bubble growth rates, deformation of surrounding tissue medium, and coalescence mechanisms for small bubbles into large aggregates, to name a few. These issues are the pervue of bubble theories, but the complexity of mechanisms addressed does not lend itself easily to table, nor even meter, implementation.

The ultimate computational algorithm, coupling nucleation, dissolved gas uptake and elimination, bubble growth and collisional coalescence, and critical sites, would be very, very complicated, requiring supercomputers (like CRAYs, CYBERs, VPs, CONVEXs, and ESSEXs, or their massively parallel cousins, CMs, NCUBESs, IWARPs, and DAPs) for three dimensional modeling. Stochastic Monte Carlo methods and sampling techniques exist which could generate and stabilize nuclei from thermodynamic functions, such as the Gibbs or Helmholtz free energy, transport dissolved gas in flowing blood to appropriate sites, inflate, deflate, move, and collide bubbles and nuclei, and then tally statistics on tensions, bubble size and number, inflation and coalescence rate, free phase volume, and any other meaningful parameter, all in necessary geometries. Such type simulations of similarly complicated problems last for 16-32 hours at the Los Alamos and Livermore National Laboratories, on lightning fast supercomputers with near gigaflop speed (10 sup 9 floating point operations per second). While decompression meters have revolutionized diving and decompression calculations, it will be some time before the ultimate computational algorithm fits into a wrist computer. .uh “Slow Tissue Compartments” Based on concerns in multiday and heavy repetitive diving, with the hope of controlling staircasing gas buildup in exposures through critical tensions, slow tissue compartments (half-lives greater than 80 minutes) have been incorporated into some algorithms. Calculations, however, show that virtually impossible exposures are required of the diver before critical tensions are even approached, literally tens of hours of near continuous activity. As noted in many calculations, slow compartment cannot really control multidiving through critical tensions, unless critical tensions are reduced to absurd levels, inconsistent with nonstop time limits for shallow exposures. That is a model limitation, not necessarily a physical reality. The physical reality is that bubbles in slow tissues are eliminated over time scales of days, and the model limitation is that the arbitrary parameter space does not accommodate such phenomena.

And that is no surprise either, when one considers that dissolved gas models are not suppose to track bubbles and free phases. Repetitive exposures do provide fresh dissolved gas for excited nuclei and growing free phases, but it is not the dissolved gas which is the problem just by itself. When bubble growth is considered, the slow compartments appear very important, because, therein, growing free phases are mostly left undisturbed insofar as surrounding tissue tensions are concerned. Bubbles grow more gradually in slow compartments because the gradient there is typically small, yet grow over longer time scales. When coupled to free phase dynamics, slow compartments are necessary in multidiving calculations.

For additional perspective, it should be noted that slow compartments have always been important in decompression and saturation diving, and flying-after-diving protocols. It is not clear now to what extent slow compartments are important to multidiving. As testing continues, that should become clearer in the near future. But, based on inert gas washout experiments, some physiologists suggest that tissue compartments with half-lives near 720 minutes are to be found in bone, and possibly other sites. And bubbles have been found in subjects as long as three days after diving exposures. So, caution is the signal and models insensitive to slow compartments are limited at best.

In using tables and meters without slow compartments, care must be exercised to dive only within their recommended ranges. For sport diving activities, this usually implies nominal bounce and a few shallow repetitive exposures separated by an hour or more surface interval. Multi-day activities cannot be controlled through fixed critical tensions in compartments as slow as 6 hours anyway, and a suggestion is to take a day off after 3 days of light repetitive diving. Even more study and testing are necessary in cases of heavy multidiving.

Venous Gas Emboli
Sound reflected off a moving boundary undergoes a shift in acoustical frequency, the so-called Doppler shift. The shift is directly proportional to the speed of the moving surface (component in the direction of sound propagation) and the acoustical frequency of the wave, and inversely proportional to the sound speed. Acoustical signals in the megahertz range (10 sup 6 cycles per second), termed ultrasound, have been directed at moving blood in the pulmonary arteries, where blood flow rates are the highest (near 20 cm/sec) due to confluence of the systemic circulation, with resulting Doppler shifts, in the form of audible chirps, snaps, whistles, and pops, noted and recorded. Sounds heard in divers have been ascribed to venous gas emboli (VGE), and in vitro (gels) simulations and evaluations have established minimum bubble detection size as a function of blood velocity. Coalesced lipids, platelet aggregates, and agglutinated red blood cells formed during decompression also pass through the pulmonary circulation, but are less reflective than bubbles, and usually smaller. Bubbles with radii in the 20 micron (10 sup -6 m) range represent a cutoff for Doppler detection for signals of a few megahertz.

Ultrasonic techniques for monitoring moving gas emboli in the pulmonary circulation are popular today. Silent bubbles, as applied to the venous gas emboli detected in sheep undergoing bends-free USN table decompression by Spencer and Campbell, were a first indication that asymptomatic free phases were present in blood, even under bounce loadings. Similar results were reported by Walder and Evans. After observing and contrasting venous gas emboli counts for various nonstop exposures at depth, Spencer suggested that nonstop limits be reduced below the USN table limits. Enforcing a 20% drop in venous gas emboli counts compared to the USN limits, corresponding nonstop limits are roughly 15% shorter.

While the numbers of venous gas emboli detected with ultrasound Doppler techniques can be correlated with nonstop limits, and the limits then used to fine tune the critical tension matrix for select exposure ranges, fundamental issues are not necessarily resolved by venous gas emboli measurements. First of all, venous gas emboli are probably not the direct cause of bends per se, unless they block the pulmonary circulation, or pass through the pulmonary traps and enter the arterial system to lodge in critical sites. Intravascular bubbles might first form at extravascular sites. According to Hills, electron micrographs have highlighted bubbles breaking into capillary walls from adjacent lipid tissue beds in mice. Fatty tissue, draining the veins and possessing few nerve endings, is thought to be an extravascular site of venous gas emboli. Similarly, since blood constitutes no more than 8% of the total body capacity for dissolved gas, the bulk of circulating blood does not account for the amount of gas detected as venous gas emboli. Secondly, what has not been established is the link between venous gas emboli, possible micronuclei, and bubbles in critical tissues. Any such correlations of venous gas emboli with tissue micronuclei would unquestionably require considerable first-hand knowledge of nuclei size distributions, sites, and tissue thermodynamic properties. While some believe that venous gas emboli correlate with bubbles in extravascular sites, such as tendons and ligaments, and that venous gas emboli measurements can be reliably applied to bounce diving, the correlations with repetitive and saturation diving have not been made to work, nor important correlations with more severe forms of decompression sickness, such as chokes and central nervous system (CNS) hits.

Still, whatever the origin of venous gas emboli, procedures and protocols which reduce gas phases in the venous circulation deserve attention, for that matter, anywhere else in the body. The moving Doppler bubble may not be the bends bubble, but perhaps the difference may only be the present site. The propensity of venous gas emboli may reflect the state of critical tissues where decompression sickness does occur. Studies and tests based on Doppler detection of venous gas emboli are still the only viable means of monitoring free phases in the body.

Phase Constraints And Multi-Diving
Concerns with multidiving can be addressed through variable critical gradients, or equivalently tissue tensions, in bubble models. While variable gradients or tensions are difficult to codify in table frameworks, they are easy to implement in digital meters. Reductions in critical parameters result from what is called the phase volume constraint, a constraint employing the separated volume of gas in tissue as trigger point for the bends, not dissolved gas buildup alone in tissue compartments. The phase volume is proportional to the product of the dissolved-free gas gradient times a bubble number representing the number of gas nuclei excited into growth by the compression-decompression. And it replaces just slow tissue compartments in controlling multidiving.

In considering bubbles and free-dissolved gradients within critical phase hypotheses, repetitive criteria develop which require reductions in Haldane critical tensions or dissolved-free gas gradients. This reduction simply arises from lessened degree of bubble elimination over repetitive intervals, compared to long bounce intervals, and need to reduce bubble inflation rate through smaller driving gradients. Deep repetitive and spike exposures feel the greatest effects of gradient reduction, but shallower multiday activities are impacted. Bounce diving enjoys long surface intervals to eliminate bubbles while repetitive diving must contend with shorter intervals, and hypothetically reduced time for bubble elimination. Theoretically, a reduction in the bubble inflation driving term, namely, the tissue gradient or tension, holds the inflation rate down. Overall, concern is bubble excess driven by dissolved gas. And then both bubbles and dissolved gas are important. In such an approach, multidiving exposures experience reduced permissible tensions through lessened free phase elimination over time spans of two days. Parameters are consistent with bubble experiments, and both slow and fast tissue compartments must be considered.

Adaptation
Divers and caisson workers have long contended that tolerance to decompression sickness increases with daily diving, and decreases after a few weeks layoff. Paton and Walder, Golding and Griffiths have confirmed such suggestions, pointing out that in large groups of compressed air workers, new workers were at higher risk than those who were exposed to high pressure regularly. This acclimatization might result from either increased body tolerance to bubbles (physiological adaptation), or decreased number and volume of bubbles (physical adaptation). Walder advocated physical adaptation, resulting from systematic destruction or reduction in gas micronuclei, from which bubbles grow. Kunkle and Beckman monitored venous gas emboli in the pulmonary arteries of dogs, noting that the number of total emboli counted decreased as the repetitive frequency increased, but that the same bubble number precipitated decompression sickness in all cases. Repetitve spacings were on the order of a day or two in the experiments, and results are clearly consistent with physical adaptation.

Acclimatization And Repetitive Exposures
Yet, there is slight inconsistency here. Statistics point to slightly higher bends incidence in repetitive and multiday diving. Some hyperbaric specialists confirm the same, based on experience. The situation is not clear, but the resolution plausibly links to the kinds of first dives made and repetitive frequency in the sequence. If the first in a series of repetitive dives are kept short, deep, and conservative with respect to nonstop time limits, initial excitation and growth are minimized. Subsequent dives would witness minimal levels of initial phases. If surface intervals are also long enough to optimize both free and dissolved gas elimination, any nuclei excited into growth could be efficiently eliminated outside repetitive exposures, with adapatation occurring over day intervals as noted in experiments. But higher frequency, repetitive and multiday loading may not afford sufficient surface intervals to eliminate free phases excited by earlier exposures, with additional nuclei then possibly excited on top of existing phases. Physical adaptation seems less likely, and decompression sickness more likely, in the latter case. Daily regimens of a single bounce dive with slightly increasing exposure times are consistent with physical adaptation, and conservative practices. The regimens also require deepest dives first. In short, acclimatization is as much a question of eliminating any free phases formed as it it a question of crushing or reducing nuclei as potential bubbles in repetitive exposures. And then time scales on the order of a day might limit the adapatation process.

Conservative Protocols
Conclusions of adaptation experiments underscore reductions in physical disposition to bubble formation, seen in venous gas emboli counts, and not increases in physiological tolerance to bubbles. Acclimatization is principally a physical process, relating to free phases in the body. If bubbles grow from preformed, stable miconuclei that are destroyed when gross bubbles are excited, then controlled and conservative repetitive diving could reduce, by attrition, numbers of such bubble micronuclei. But, as discussed above, the important adjectives here are controlled and conservative.

Conservative repetitive protocols, recently proposed are consistent with such reasoning, as are bubble models employing growth and elimination time constants on the same time scale. Previous tables for humans were based upon unsupported assumptions because many of the underlying processes by which dissolved gas is liberated from blood and tissues were poorly understood. Some of those assumptions, as enumerated by Hills, Yount, and Wienke are known to be wrong. Recent developments in bubble nucleation models, linked to experiments, have made it possible to calculate diving tables from established principles. Both flexibilty and range of applicability are impressive, and they recover dissolved gas models in the proper limits. Bubble models more naturally incorporate protocols suggested for repetitive diving, speaking well for the models. These protocols include:

1. safety stops in the l0-20 foot zone for a few minutes;

2. ascent rates limited by 60 ft/min;

3. restricted repetitive and multiday exposures for deeper dives;

4. reduced nonstop time limits;

5. deeper-to-shallower repetitive schedules.

In terms of the above protocols, acclimatization becomes qualified within a regimen of reduced nonstop limits, slow ascent rates, safety stops, and most importantly, shallower-than-previous and low frequency repetitive activity. Outside of such framework, adaptation appears less favorably disposed. Certainly, more controlled study of multidiving diving and associated statistics is necessary to answer these questions conclusively. There is a paucity of repetitive and multiday data now, but that will probably change in time.

B.R. Wienke

 

Un nuovo approccio per la prevenzione della malattia da decompressione?

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L’azoto si scioglie nel sangue durante le immersioni, ma esce di soluzione in presenza di sub tornare alla normale pressione troppo rapidamente. Bolle di azoto causare una serie di effetti da eruzioni cutanee a convulsioni, coma e morte. Si ritiene che queste bolle da formare nuclei precursori bolla (gas). Recentemente abbiamo dimostrato che una singola seduta di esercizio 20 h, ma non 48 ore, prima di un tuffo simulato evita la formazione di bolle e protegge i topi da una grave malattia da decompressione (DCS) e la morte. Inoltre, abbiamo dimostrato che la somministrazione di N ω -nitro- L -arginina estere metilico, un non-selettivo inibitore della NO sintetasi (NOS), si trasforma un tuffo dal sicuro non sicuro nei ratti sedentari ma non esercitate. Pertanto in base a dati precedenti un’ipotesi attraente è che può essere possibile utilizzare sia esercitare o libera NO agenti prima di una immersione di inibire la formazione di bolle e quindi proteggere DCS. Di conseguenza, gli obiettivi del presente studio sono stati di determinare se la protezione contro la formazione di bolle in “immersione” ratti sono state fornite dal (1) somministrazione cronica e acuta di un NO-agente di rilascio e (2) l’esercizio inferiore a 20 h prima dell’immersione . NO dato per 5 giorni e poi 20h prima di un’immersione di formazione di bolle 700 kPa durata 45 min aria respirabile significativamente ridotto e impedito la morte. Lo stesso effetto è stato osservato se NO è stato dato solo 30 minuti prima dell’immersione. Esercizio 20h prima di una formazione di bolle surpressed immersione e ha impedito la morte, senza alcun effetto in qualsiasi altro momento (48, 10, 5 e 0.5h prima dell’immersione). Pre-immersione attività non sono state considerate per influenzare la crescita delle bolle e quindi il rischio di gravi DCS. Le nuove scoperte attuali di un effetto protettivo contro la formazione di bolle e la morte con l’esercizio opportunamente a tempo e un NO-agente di rilascio possono costituire la base di un nuovo approccio per prevenire grave malattia da decompressione.

Milioni di persone in tutto il mondo partecipare subacquea ricreativa e professionale. Malattia da decompressione (DCS) dopo un’immersione o ritorno da elevata pressione si crede essere iniziato dalla formazione di bolle di gas in tessuto e sangue. L’azoto si scioglie nel sangue durante le immersioni, ma esce di soluzione in presenza di sub tornare alla normale pressione troppo rapidamente. Bolle di azoto causare una serie di effetti da eruzioni cutanee a convulsioni, coma e morte ( Francesco & Gorman, 1993 ). La teoria predominante è che bolle crescono da nuclei preformato composto piccoli (circa 1 pm) bolle di gas stabili ( Yount e Strauss, 1982 ).

Recentemente abbiamo dimostrato che una singola seduta di esercizio 20h, ma non 48 ore, prima di un tuffo simulato evita la formazione di bolle e protegge topi da DCS gravi e morte ( Wisløff & Brubakk, 2001 ). Inoltre, abbiamo dimostrato che la somministrazione di N ω -nitro- L -arginina metil estere ( L -NAME), un non-selettivo inibitore della NO sintetasi (NOS), si trasforma un tuffo dal sicuro non sicuro nei ratti sedentari ma non esercitate ( Wisløff et al. 2003 ). Pertanto, sia l’esercizio acuto e NOS influenzare la formazione di bolle, ma non possono essere collegate. Noi ipotizziamo che sia esercizio e NOS ostacolano la formazione di bolle tramite alterazione delle proprietà endoteliali vascolari da preesistenti nuclei di gas sono probabilmente attaccata all’endotelio, dove crescono in bolle che vengono sloggiati nel flusso sanguigno ( Harvey et al. 1944 ; Harvey, 1951 ).

Pertanto in base a dati precedenti ( Wisløff & Brubakk, 2001 ; Wisløff . et al 2003 ), un’ipotesi attraente è che può essere possibile utilizzare sia esercitare o libera NO agenti prima di una immersione di inibire la formazione di bolle e quindi proteggere DCS.

Tuttavia, il tempo corretto di questo tipo di intervento non è chiaro, in quanto il beneficio di esercizio è pronunciato a 20 ma non 48 ore dopo l’allenamento ( Wisløff & Brubakk, 2001 ; Wisløff . et al 2003 ). Come crediamo esercizio può esaurire (lavare via) i precursori bolla, dovrebbe prendere 10-100h per rigenerare una popolazione nuclei impoverito ( Yount & Strauss, 1982 ). Così, a meno di esercitare 20h prima dell’immersione deve anche proteggere contro la formazione di bolle. Di conseguenza, gli obiettivi del presente studio sono stati di determinare se la protezione contro la formazione di bolle nei ratti immersioni sono state fornite dal (1) somministrazione cronica e acuta di un NO-agente di rilascio e (2) l’esercizio meno di 20h prima della immersione.

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Metodi

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  6. Riferimenti
  7. Appendice

Studio della popolazione e l’amministrazione NO

Un totale di adulto femmina 84 310 ± 7 g Sprague-Dawley (Møllegaards, Danimarca) sono stati mantenuti sei in ogni gabbia con luce controllati su 12h-12h scuro ciclo di luce. Temperatura era 21 ± 2 ° C e umidità del 50 ± 4%. Gli animali sono stati alimentati con una dieta a pellet roditore ad libitum e aveva libero accesso all’acqua. I ratti sono stati assegnati in sette gruppi, come descritto in Tabella 1 . Ratti in gruppi I-V stati usati in esperimenti per determinare la durata dell’esercizio indotta beneficio contro la formazione di bolle e la morte. Esercizio è stata eseguita 48h, 20h, 10h, 5h e 30 min prima dell’immersione simulata in gruppi I-V, rispettivamente. Nei gruppi VI-VII abbiamo determinato l’effetto della somministrazione di un NO-agente di rilascio (mononitrato isosorbid, Roche, Svizzera, 65 mg kg -1 ) per 5 giorni (l’ultima volta 20 ore prima dell’immersione) e subito (30 min) prima per l’immersione sulla formazione di bolle e la sopravvivenza. L’isosorbide isosorbid è stato disciolto in acqua e somministrata a ratti mediante intubazione gastrica. Ratti di controllo ricevuto acqua da intubazione gastrica.

Protocollo      Numero di    ratti

Tabella 1.  Assegnazione    gruppo e il numero di topi in ciascun protocollo

Gruppo

  1.   Numero totale di ratti viene presentato. C’erano sei   ratti di controllo esercitati e sei dei gruppi I-V. Sei ratti di entrambi i   gruppi VI e VII ricevuto acqua invece di un donatore di NO.
Io Esercizio o sedentari, 48 ore   prima dell’immersione

12

II Esercizio o sedentario, 20h prima   dell’immersione

12

III Esercizio o sedentario, 10h prima   dell’immersione

12

IV Esercizio o sedentario, 5h prima   dell’immersione

12

V Esercizio o sedentari, 30 minuti   prima dell’immersione

12

VI NO-agente di rilascio o di acqua,   5 giorni, 20 ore l’ultima volta prima di immersioni

12

VII NO-agente di rilascio o di acqua,   una volta, 30 minuti prima dell’immersione

12

Massimo consumo di ossigeno                         e protocollo di esercizio

Nove giorni prima assegnazione di gruppo, consumo di ossigeno e il rapporto di scambio respiratorio sono stati misurati durante il tapis roulant come precedentemente descritto in dettaglio ( Wisløff & Brubakk, 2001 ). In breve, il funzionamento intervallo (1.5h durata complessiva) alternando 8 min a 85-90% di e 2 min a 50-60%. Dopo la sessione di allenamento, ogni ratto è stato premiato con 0,5 g di cioccolato (Crispo, Nidar Bergene, Norvegia). Ratti sedentari hanno avuto la stessa ricompensa.

Dive protocollo e l’analisi bolla

Coppie di ratti (sperimentale e di controllo) sono stati compressi ad una velocità di 200 kPa min -1 ad una pressione di 700kPa, mantenuta per 45 min aria respirazione e decompresso alla superficie (100kPa) ad una velocità di 50kPa min -1 . Subito dopo l’affioramento gli animali sono stati anestetizzati con Midazolam (Dormicum ‘Roche’)-fentanil-fluanison (Hypnorm) (0,1 ml (100 g) -1 sc ), e il ventricolo destro è stata insonated con un GE Vingmed Vivid 5 scanner ad ultrasuoni, con un trasduttore 10 MHz come precedentemente descritto in dettaglio ( Wisløff & Brubakk, 2001 ; Wisløff . et al 2003 ). Immagini sono stati classificati secondo un metodo descritto in precedenza ( Eftedal & Brubakk, 1997 ) con l’osservatore ignaro del gruppo allocazione del ratto. Uno studio pilota ha mostrato che i topi sopravvissuti 60 min erano apparentemente influenzati dal protocollo e vissuto normalmente successivamente; quindi i tempi di sopravvivenza fino a 60 minuti sono stati registrati sono stati. Ratti sopravvissuti sono stati uccisi per decapitazione.

Le procedure sperimentali adeguati alle Convenzione europea per la protezione degli animali vertebrati utilizzati a fini sperimentali o ad altri , e il protocollo è stato approvato dal Consiglio norvegese per la ricerca degli animali.

Statistica

I dati sono espressi come media ± DS o come mediana e range. Test non parametrici sono stati impiegati a causa del numero limitato di ratti di ciascun gruppo. A Mann-Whitney U test è stato utilizzato per valutare le differenze di formazione di bolle, mentre il test di Wilcoxon generalizzato Gehan stato utilizzato per valutare le differenze di tempo di sopravvivenza tra i gruppi. P <0.05 è stato considerato statisticamente significativo. Dimensione del gruppo e la potenza statistica sono stati stimati utilizzando nQuery Advisor software (versione 3.0, statistica Solutions Ltd, Cork, Irlanda). Sulla base di stime prudenti di uno studio precedente ( Wisløff & Brubakk, 2001 ) sei ratti di ciascun gruppo avrebbe permesso di rilevare una differenza del 15% tra i gruppi nel grado bolla e il tempo di sopravvivenza ( p = 0,01, power = 0,80) .

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Risultati

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Mononitrato Isosorbid amministrato per 5 giorni e poi 20h prima dell’immersione formazione di bolle notevolmente ridotto rispetto ai ratti amministrato acqua, e la maggior parte dei topi sopravvissuti per 60 min. Lo stesso effetto è stato osservato se NO è stata data solo 30 minuti prima dell’immersione ( Tabella 2 ).

Donatore    di NO, 5 giorni (Gruppo VI)      Donatore    di NO, acuta (gruppo VII)

Acqua      Ismo      Acqua

Tabella 2.  Effetti di un    NO-donatore di formazione di bolle e la sopravvivenza

 

Ismo

  1.   § p <0,001, significativamente   diverso dal suo gruppo di controllo corrispondente. Pesi del corpo sono   presentati come media ± DS , il resto dei dati sono   riportati come mediana (range). Tempo di decompressione era 12 min per tutti   i gruppi. Ismo, mononitrato isosorbid.
Peso corporeo (g) 310 ± 7 309 ± 10 308 ± 6 307 ± 6
Scansione di qualità 0 (0-5) § 5 (3-5) 0 (0-5) § 5.0 (3-5)
Sopravvivenza (min) 60 (15-60) § 27 (2-39) 60 (23-60) § 19 (8-60)

Esercizio 20h prima di un tuffo per la formazione di bolle 700kPa durata di 45 min ad aria ‘soppressa’ e la maggior parte dei topi sopravvissuti per 60 min. Non c’era alcun effetto di esercizio in qualsiasi altro momento punto ( Tabella 3 ).

Assegnazione      Peso    corporeo (g)      Scansione    di qualità      Sopravvivenza    (min)

Tabella 3.  Effetti    dell’esercizio fisico sulla formazione di bolle e la sopravvivenza

Gruppo

  1.   § p <0,001, significativamente   diverso dal suo gruppo di controllo corrispondente. * P <0,001, molto diversa da tutte   le altre preparazione muscolare. Si noti che i ratti registrati come morti   dopo 60 minuti erano in realtà ancora in vita, a quel punto, ma sono stati   uccisi dopo 60 min. Pesi del corpo sono presentati come media ± DS , il   resto dei dati sono riportati come mediana (range). Tempo di decompressione   era 12 min per tutti i gruppi.
Io Esercizio (48h prima   dell’immersione) 315 ± 6 4 (3-5) 35 (26-60) §
Sedentario 310 ± 9 5 (-) 12 (4-20)
II Esercizio (20 ore prima   dell’immersione) 316 ± 9 0,5 (0-2) § * > 60 (-) § *
Sedentario 313 ± 8 5.0 (4-5) 13 (2-47)
III Esercizio (10h prima   dell’immersione) 314 ± 9 5 (-) 11 (3-15)
Sedentario 318 ± 12 5 (-) 14 (2-31)
IV Esercizio (5h prima   dell’immersione) 309 ± 8 4 (2-5) 20 (10-60)
Sedentario 312 ± 6 5 (3-5) 23 (17-60)
V Esercizio (30 minuti prima   dell’immersione) 315 ± 8 5 (-) 11 (3-23)
Sedentario 317 ± 9 5 (-) 8 (2-17)

Vai a …

Discussione

  1. Inizio pagina
  2. Astratto
  3. Metodi
  4. Risultati
  5. Discussione
  6. Riferimenti
  7. Appendice

L’ipotesi di lavoro di questo e dei precedenti studi ( Wisløff & Brubakk, 2001 ; Wisløff . et al 2003 ) era che i precursori di bolle (nuclei) che aderiscono all’endotelio sono a disposizione per crescere in bolle con decompressione. In un precedente studio abbiamo dimostrato che la sintesi di NO basale è necessaria per evitare la formazione di bolle in ratti che normalmente non producono bolle ( Wisløff et al. 2003 ). Oltre effetti sul tono vascolare, NO ha proprietà fisiologiche che possono essere antiatherogenic, compresa l’inibizione della proliferazione delle cellule muscolari lisce, l’aggregazione piastrinica e l’adesione, e l’attivazione dei leucociti e adesione ( Bath, 1993 ). Precedentemente abbiamo suggerito che indotta dall’esercizio protezione contro la formazione di bolle è mediata attraverso la via NO; cambiando le proprietà dell’endotelio vascolare riduce la possibilità di precursori bolla si attacca alla parete del vaso. Questo è stato sostenuto dalla osservazione che la somministrazione di un donatore di NO prima di un tuffo protegge contro la formazione di bolle e la morte ( Tabella 2 ). E ‘ragionevole supporre che l’esercizio difficile può portare ad un aumento della formazione di precursori bolla o che possono aumentare la loro dimensione ( Dervay et al. 2002 ). La nostra ipotesi è, tuttavia, che tali bolle non aderisce all’endotelio se NO è presente e quindi non sarà disponibile per la crescita quando sovrasaturazione è presente. L’esercizio fisico, che è noto per aumentare acutamente la produzione di NO ( Roberts et al. 1999 ) vicino l’immersione, non ha la protezione contro la formazione di bolle, mentre la somministrazione di un donatore di NO immediatamente prima dell’immersione fatto di protezione offerta. Inoltre, in uno studio precedente, abbiamo scoperto che nessun blocco aumentato la formazione di bolle nel sedentario, ma non nei ratti esercitate ( Wisløff et al. 2003 ). Questo indica che l’effetto di esercizio possono essere mediati da fattori diversi ossido nitrico. Si può speculare se aumento del flusso sanguigno durante l’esercizio fisico può essere semplicemente ‘lavare via’ nuclei. Tuttavia, questo è improbabile, come l’esercizio fisico più vicino alla 20h di immersione offerto alcuna protezione. Diversi studi hanno dimostrato che il movimento passivo o attivo durante la decompressione aumenta acutamente la formazione di bolle ( Harvey et al. 1944 ; McDonough & Hemmingsen, 1985 a , b ). Uno studio recente ha dimostrato che la durata di bolle formate da esercizio è dell’ordine di minuti ad alcune ore ( Dervay et al. 2002 ). Pertanto, potrebbe essere che l’esercizio fisico vicino agli offset immersione l’effetto positivo di esercizio indotta aumento NO, e può spiegare i dipendenti dal tempo effetti dell’esercizio visto in questo studio ( Tabella 3 ). Attività fisica può innescare una specie molecolare che si esprime nel endotelio circa 20h tardi, conseguente esercizio indotta protezione contro la formazione di bolle. Questi nuovi dati rivelano che NON possono essere coinvolti in questo processo ( Tabella 2 ) ed è quindi ragionevole ipotizzare che l’esercizio 20 ore prima dell’immersione attiva la trascrizione del gene di eNOS / iNOS che porta ad un aumento NO generazione.

Per chiarire meglio il ruolo di NO in esercizio indotta protezione contro la formazione di bolle, ulteriori studi dovrebbero includere ratti che normalmente producono un sacco di bolle di azoto e di (1) determinare l’effetto di allenamento 20h prima di un’immersione in L -NAME-trattati ratti, e (2) determinano l’effetto dell’esercizio fisico vicino alla immersione in ratti trattati con un donatore di NO prima l’incontro esercizio.

I dati attuali mostrano chiaramente che il meccanismo di protezione indotta da esercizio fisico richiede un lasso di tempo di 10-20h per essere pienamente attivato, mentre un ritardo di 20-48 h nega l’effetto protettivo. È noto che a breve termine ad alta intensità di esercizio (circa il 90% dei ) possono indurre ipervolemia ( Gillen et al. 1991 ; Richardson . et al 1996 ), e le risposte di aldosterone, renina angiotensina-e peptide natriuretico atriale (tra gli altri ) tutti avere conseguenze significative che durano 24-48h ( Richardson et al. 1996 ). Un aumento del volume plasmatico potrebbe aumentare la funzionalmente attiva letto capillare e il tasso di scambio del plasma attraverso il letto muscolo, suscettibile di aumentare la velocità di eliminazione dell’azoto. È interessante notare, è noto che l’espansione di volume diminuisce la gravità della DCS ( Merton et al. 1983 ). Così, il noto espansione di volume sviluppato un giorno dopo l’esercizio intenso può indurre l’osservato esercizio legate protezione contro la formazione di bolle.

Conclusione

Sforzi per impedire di DCS sono tradizionalmente focalizzati sulla riduzione di sovrasaturazione dell’azoto nei tessuti. È, tuttavia, ben documentato che la presenza di nuclei è probabilmente necessaria per formare bolle a livello di sovrasaturazione incontrato in immersione umana ( Vann, 1989 ). L’idea che la rimozione dei nuclei può impedire DCS non è nuova. Vann et al. (1980) hanno dimostrato che l’esposizione a pressioni significativamente più elevati prima di un tuffo, che presumibilmente schiacciato i nuclei, ha ridotto significativamente l’incidenza di MDD. Tuttavia fino ad ora, non sono riuscite a rimuovere nuclei è stato suggerito.

Pre-immersione attività non sono state considerate per influenzare la crescita delle bolle e quindi il rischio di gravi DCS. Le nuove scoperte attuali di esercizio a tempo e in modo appropriato l’uso di un NO-agente di rilascio possono costituire la base per un nuovo approccio alla prevenzione della malattia da decompressione grave.

  • Getting a dive accident      victim with decompression sickness or arterial gas

embolism to the hospital as quickly as possible is essential.

  • Begin first-aid      oxygen as soon as possible on the dive boat.
  • Transport to shore on      the diver’s own boat should be initiated as soon as

possible.

  • Notify the Coast      Guard of the accident on ship-to-shore radio Channel 16.
  • Request that the Coast      Guard notify Escambia       County (FL) 911 of      the dive

accident.

  • Transport the injured      diver back to the Coast Guard Station Pensacola pier.
  • GPS Numbers for Coast      Guard pier are:

N 30-20-67

W 087-17-40

  • Baptist Life Flight      and Escambia EMS      ambulance will both meet the dive boat at the Coast Guard pier.
  • The injured diver will      then be transported to Baptist       Hospital by the most      expeditious method (typically Baptist Life Flight) for evaluation and      treatment.

 

Pre-Dive and Planning Considerations

 

Recommended Diver Equipment

Should include a signal sausage, a strobe light, a whistle, and a signal mirror in case the diver is separated from the boat upon surfacing and needs to signal it. A compressed-air activated signaling device may also be useful.

 

Recommended Dive Boat Equipment/Training; (in addition to other standard equipment)

  • Emergency Oxygen – should have two-hour delivery capacity (120 cubic      ft)

-  Diver’s Alert Network Dual Rescue Pak Extended care with MTV-100

(approximately $825) which has two Jumbo-D cylinders (advertised 120 minute oxygen duration)

or

-  Steel/aluminum scuba bottles filled with oxygen (and clearly marked

as oxygen bottles) with oxygen-clean demand valve and regulator

  • Cell phone as backup to ship-to-shore radio
  • CPR training for dive boat Captain (and crew if possible)

 

Communications

  • Ship-to-shore VHF-FM radio – Channel 16
  • All Coast Guard stations in the area monitor this channel (Panama City, Pensacola, Destin, Mobile)
  • Cell phones do not work from the Oriskany site

 

Dive Planning/Briefing

  • Conduct a radio check to ensure ship-to-shore VHF radio is      working.
  • Coast Guard requests that boats not do radio checks with Coast      Guard stations.
  • Plan dives so that all divers reach the surface at approximately      the same time insofar as possible.
  • No excursions below the flight deck of the Oriskany for non-technical      divers.
  • If there is an accident, the dive boat will WAIT for all divers from that boat to be on board before transporting the injured diver back to shore.
  • If the Dive Boat Captain is diving, there should be a crew member      who understands the Oriskany Dive Accident Management Plan and is licensed      to operate the dive boat present on the surface at all times while the dive      is being conducted.

 

Dive Accident Management

 

Who Has the Lead?

  • The Dive Boat Captain initially.
  • The Coast Guard acts as the Search and Rescue (SAR) mission      coordinator and activates the Escambia       County Emergency      Medical System (EMS) when notified of a      maritime emergency.
  • The Dive Boat Captain’s responsibility for his or her injured      diver does not end when the Coast Guard vessel arrives on scene.
  • The Baptist Hospital Emergency Department physician has control      once the injured diver has been transferred to an air or ground ambulance      for transport to Baptist       Hospital.

First-Aid for the Injured Diver

  • If a diver surfaces with signs or symptoms of decompression      sickness or arterial gas embolism, perform the steps listed below.
  • Remove the diver’s gear and have him or her lie down.
  • Ensure that the airway is open.
  • Start oxygen via demand valve or reservoir mask.
  • Patient Assessment: perform a rapid neurological exam – a detailed      neurological exam is not required at this point.

- If there are obvious signs/symptoms – not needed.

- If signs/symptoms are subtle – Baptist will repeat anyway.

  • Monitor the injured diver closely for changes in status during the      transport.
  • Secure the injured diver’s equipment for investigation. Do not      tamper with equipment; the Coast Guard will take possession of the equipment      for follow-up investigation as noted below.

 

Recover All Divers from the Boat before Leaving the Dive Site

  • No immediate departure with      another boat then picking up the rest of the divers from the injured      diver’s boat.
  • Don’t plan on the injured diver going in with another boat that      might be able to leave the site sooner:  1) all divers must be assured that their      boat will be there for them on surfacing; 2) the Dive Boat Captain needs      to maintain responsibility for his or her diver; and 3) transferring the diver      to another boat would entail an unwanted transfer of liability for the injured      diver to the receiving boat.

 

 

Begin Transport Back to the Coast Guard Station Pier on Own Dive Boat ASAP

  • Do not stay at the dive site and wait for Coast Guard vessel to      arrive.
  • Baptist Life Flight does not fly over the Gulf to do rescues at      sea.
  • There is no transfer at sea to the Coast Guard vessel in the      primary plan.

- Time-consuming

- May be hazardous to the casualty and individuals assisting.

- May not be feasible at all if there are large swells.

  • A transfer of the injured diver at sea would typically be undertaken      only if this would significantly reduce the transport time to Baptist Hospital and if the sea state      allows.
  • If the injured diver is transferred at sea, be sure to transfer      the first-aid oxygen and the person trained to administer it as well.
  • Docking at the Coast Guard pier – use the lower dock to the right      of the larger pier.
  • The Coast Guard Station Pensacola      pier has a helicopter landing pad nearby.
  • The Coast Guard will coordinate docking and movement of the      injured diver from pier side to the helicopter landing pad.
  • The Coast Guard conducts an investigation into any diving accident      that results in death or incapacitation for more than 72 hours. Do not      tamper with the diving equipment; the diver’s equipment should be turned      over to the Coast Guard at the pier and the name of the receiving person      noted.

 

Accident Notification – Emergency Medical Services Activation

  • The Coast Guard is the primary communications relay point.
  • Call Coast Guard Station Pensacola      on Channel 16 VHF-FM radio.
  • Coast Guard stations at Mobile      and Panama City      may respond to calls for

“Coast Guard.” Be sure to hail “Coast Guard Station Pensacola” when calling.

  • The Coast Guard Station Pensacola      watch will:

1) Call Escambia County (FL) 911 and notify them of a dive

accident.

2) Call the Naval Air Station Pensacola duty numbers.

Command Duty Officer Cell Phone     (850-418-5175)

Commanding Officer    (850-452-2713) (during duty hours)

3) Ensure that the Coast Guard Station access gate is open for the

ambulance.

  • Escambia County EMS will call Baptist Life Flight       Communications Center (850-434-4586) and notify      them of the dive accident.
  • The injured diver will be transported to the chamber by the most expeditious      method – typically Baptist Life Flight – with Escambia County       EMS ground ambulance      as the backup.
  • Backup telephone numbers for Coast Guard:

Coast Guard Station Emergency Search and Rescue Line

850-453-8178

Coast Guard Station Main Number

850-453-8282

  • If no communications can be established with Coast Guard Station Pensacola, call Escambia County (FL) 911 on cell phone when      feasible, tell them that you have a diving accident, and ask for them to      relay your call to the Coast Guard. Request that 911 record your vessel      name, location, cell phone number, and the nature of the emergency to      provide to the Coast Guard when transferring the call.

 

Dive Boat Captain Passes the Following Information to the Coast Guard

  • First Transmission

1.  Name and location of vessel

2.  Nature of distress – scuba diving accident

3.  Name, age and sex of casualty

4.  Dive profile

Depth/time

Gas mix used on dive

Time of surfacing

Omitted decompression?

Emergency ascent made by diver?

5.  Presenting signs and symptoms

6.  Current status

Conscious                          Yes/No

Breathing difficulty           Yes/No

Pain                                       Yes/No          Where?

Weakness/Paralysis        Yes/No          Where?

Sensory loss                      Yes/No          Where?

  • Second Transmission

Provide Coast Guard requested information outlined in Appendix A

 

Which Chamber Should the Injured Diver Be Evacuated To?

  • Baptist Hospital (Pensacola, FL) is PRIMARY

Two monoplace chambers

24-hour bends watch

Can do two treatments simultaneously

Can treat only one ventilated patient at a time

Does not recompress unconscious or critical patients

Staff trained in management of diving accidents

Has emergency room capability

  • Springhill Medical Center (Mobile, AL) – Second Option

Two-person chamber

24-hour bends watch

Staff trained in management of diving accidents

Will recompress unconscious or critical patients

60 miles from Pensacola

  • Capitol Regional Medical Center (Tallahassee,       FL) – Third Option

Multiplace chamber

24-hour bends watch

Staff trained in management of diving accidents

Will recompress unconscious or critical patients

180 miles from Pensacola

 

* Note: Baptist Life Flight may or may not be able to reach Capitol Regional Medical Center without refueling – depends on flying conditions.

 

Who Makes the Call on Where the Casualty Goes after the Injured Diver Is Transferred to EMS at the Coast Guard Station Pensacola Pier?

  • The Baptist Hospital Emergency Department physician

-  Has responsibility for supervising air/ground emergency transport.

-  This is not a Dive Boat Captain or Coast Guard call.

 


Larry D. Weiss, MD; and Keith W. Van Meter, MD

Significant shallow-water injuries can occur in scuba

divers, even in swimming pools. Two asthmatic patients

are presented who sustained cerebral air emboli during

Scuba classes in a swimming pool. Such injuries may be

more common in asthmatics. Asthma is a contraindication

to Scuba diving.

There are at least 5 million active certified selfcontained

underwater breathing apparatus (scuba)

divers in the United States, with more than

500,000 new divers trained each year (personal

communications, Professional Association of Diving

Instructors [PADI], Santa Ana, Calif; Divers Alert

Network [DAN], Durham, NC). Diving is now popular

throughout the United States, not only in coastal

communities. Opportunities exist in almost every

state for diving in lakes, caves, abandoned mines and

quarries, and behind dams.

Asthma has long been considered a strong contraindication

to diving.”3 Asthmatics may be more

susceptible to barotrauma of ascent. Prospective

asthmatic divers will often contact their internist for

“medical clearance” to dive. These cases illustrate the

risks that asthmatic Scuba divers take, even in shallow

water.

CASE REPORTS

CASE 1

A 32-year-old woman presented to the emergency department

complaining of persistent bilateral lower extremity paresthesias.

Approximately 2 h earlier she had participated in a Scuba diving

class in a swimming pool.

When ascending from a depth of 3.6m, she had an episode of

near-syncope. She developed transient vertigo, profound weakness,

and palpitations when she arrived at the surface. She then

experienced persistent lightheadedness and dizziness. There was

no depletion of air, contamination of air, or equipment malfunction.

About 10 min after surfacing, she developed total body

paresthesias and nausea while lying by the side of the pool. Her

symptoms partially resolved and she drove herself to the hospital.

On arrival, she complained only of persistent paresthesias of the

right lower extremity (entire right leg and foot) and left foot.

The patient denied any history of asthma but later admitted

that she had a history of episodic shortness of breath since childhood.

These episodes were relieved by using an inhaler. Occasionally,

she used an inhaler prophylactically before diving. Results

of the patient’s physical examination (including a detailed

*From the Department of Medicine, Section of Emergency

Medicine, Louisiana State University School of Medicine, New

Orleans.

Manuscript received July 15, 1994; revision accepted October 7,

1994.

AGE=acute gas embolism DAN=Divers Alert Network;

scuba=self-contained underwater breathing apparatus

Key words: decompression sickness; diving; embolism, air

neurologic examination) were unremarkable. Her initial diagnostic

workup was unremarkable (complete blood cell count,

electrolytes, serum urea nitrogen, creatinine, glucose, platelet

count, prothrombin time/partial thromboplastin time, sedimentation

rate, creatine kinase, ECG, chest radiograph, and arterial

blood gas).

In preparation for treatment in a hyperbaric chamber, the patient

received high-flow oxygen by mask, intravenous saline

solution, dexamethasone, 10 mg intravenously, and aspirin, 650

mg orally. She received hyperbaric oxygen therapy on a US Navy

Treatment Table 6A. This involved a “dive” to a simulated depth

of 49.5m, of sea water. Her symptoms completely resolved while

in the hyperbaric chamber.

Further evaluation included a series of somatosensory evoked

responses, brain-stem evoked auditory response, electronystagmogram,

audiogram, spectamine and magnetic resonance imaging

brain scans, and a transesophageal echocardiogram to look for

a patent foramen ovale. She refused pulmonary function testing.

The patient required several more hyperbaric oxygen treatments

because of recurrent mild and vague complaints during the following

week (lethargy, tingling sensation in feet). These symptoms

were of questionable significance but resolved. She had no

neurologic residue.

CASE 2

A 33-year-old woman developed a severe headache while ascending

from a depth of 5.4m in a swimming pool. She was participating

in a scuba diving class. After surfacing, she developed

a 30-s episode of vertigo that abruptly subsided. Her instructor

noted that she had ascended quickly. There was no depletion of

air, contamination of air, or equipment malfunction. Several

hours later, she had three episodes of vomiting, an episode of

near-syncope, and confusion. She presented to our hyperbaric

facility about 12 h after the onset of her symptoms.

The patient had a life-long history of asthma. Her pulmonologist

had refused to provide her with medical clearance to take

scuba diving lessons. She than went to another physician and

concealed her history of asthma. She had been using albuterol,

beclomethasone, cromolyn, and epinephrine inhalers at the time

of her injury.

Her physical examination was positive for bilateral hemorrhagic

middle ear effusions (middle ear barotrauma), an air conduction

deficit of the right ear, and an abnormal sharpened

Romberg test. The patient received bilateral pressure-equalization

tubes of her tympanic membranes. She received hyperbaric

oxygen therapy on a modified US Navy Treatment Table 6A. She

had multiple episodes of bronchospasm during ascent in the

chamber. She required eight albuterol breathing treatments in the

chamber, and it took more than 8 h to ascend to surface pressure.

evaluation (CT, magnetic resonance imaging, EEG, somatosensory

evoked potentials, brain-stem evoked auditory response, and

audiogram) were normal. The patient did not comply with

follow-up examinations, but she did contact us by telephone to

relate a persistence of headaches, decreased hearing, and memory

loss.

DISCUSSION

Acute gas embolism (AGE) in divers occurs during

ascent. According to Boyle’s law, there is an inverse

relationship between the pressure and volume of an

ideal gas (PV=constant). As a diver ascends, the

pressure of the gas in the diver’s lungs decreases.

Therefore, the volume of the gas increases. If divers

ascend too quickly or hold their breath while ascending,

a gas embolism may occur. The greatest relative

changes in pressure occur in shallow water. Consequently,

the risk of AGE is theoretically greatest as

divers approach the surface. Rapid uncontrolled ascents

occasionally occur due to inflation of the

buoyancy compensator, inadvertant triggering of a

CO2 cartridge, gas depletion, or other underwater

emergencies. We have interviewed many asthmatic

divers who claimed that their physicians gave them

approval to dive in “shallow water only.

” This is an apparently common recommendation.

For reasons stated above,this is an inappropriate

recommendation. Asthmatics may have a greater risk

of AGE because of possible regional air-trapping on

ascent,34 overinflation,5 and decreased compliance.

6 Asthmatics possibly have an increased risk of acute

bronchospasm when diving, as airway resistance and

work of breathing increase at depth.

7 Also, contamination of air supply and exposure

to cold air may cause bronchospasm. The sudden

expansion of gas from pressures of 2,000 psi or greater

causes great cooling of the gas according to Charles’

law. For cold-induced asthmatics, this constitutes

another theoretical hazard.

The history determined the diagnosis of AGE in

these two cases. Often, one establishes the di’agnosis

of AGE (and also decompression sickness) by clinical

evaluation. The history and physical examination is

still the “gold standard.” The paucity of positive

findings on diagnostic evaluation in these cases is

typical. In the second case, most of the symptoms

could be attributed to middle ear, inner ear, or sinus

barotrauma. However, confusion and later memory

loss warranted a presumptive diagnosis of air embolism

and a trial of therapy.

Detailed recommendations are available regarding

the medical contraindications of diving.3’8 These

recommendations are rarely based on substantial

scientific data. Most of these general guidelines

developed from historical consensus among the military,

the commercial diving industry, and physicians

with expertise in diving medicine (such as the

Undersea and Hyperbaric Medical Society).

It is difficult to determine a relative risk of injury

for asthmatic divers. The incidence of diving injuries,

ie, decompression sickness and AGE, among asthmatics

is unknown. Many asthmatic divers attempt to

hide the presence of their disease. Several surveys

have revealed many asthmatics with active disease

who dive on a regular basis.”9-“1

DAN attempts to document every significant injury

in recreational divers in the United States. DAN

recently attempted to detect whether asthmatic

divers were at increased risk for diving injuries. The

authors show a twofold increase in the risk of AGE in

asthmatic divers.’ Yet, because of a small sample size,

this difference did not reach statistical significance.

Their data came from questionnaires that were

completed by divers (70% response rate). The authors

could not verify the accuracy of the information.

In summary, based on the limited data available,

the known pathophysiology of AGE in divers, and the

general standards of practice among diving physicians

around the world, asthma is considered a strong

contraindication for diving. These cases illustrate the

risk of recommending shallow water diving for

asthmatic patients.

REFERENCES

1 Corson KS, Dovenbarger JA, Moon RE, et al. Risk assessment

of asthma for decompression illness [abstract]. Undersea Biomed

Res 1991; 18(suppl):16-7

2 Neuman TS. Pulmonary disorders in diving. In: Bove AA, Davis

JC, eds. Diving medicine. Philadelphia: WB Saunders, 1990;

233-38

3 Davis JC. Medical examination of sport SCUBA divers. San

Antonio, Tex: Medical Seminars Inc, 1986; 35-6

4 Liebow AA, Stark JE, Vogel J, et al. Intra-pulmonary air-trapping

in submarine escape training casualties. US Armed Forces

Med J 1959; 10:265-89

5 Schaefer KE, McNulty WP, Carey C, et al. Mechanisms in development

of interstitial edema and air embolism on decompression

from depth. J Appl Physiol 1958; 13:15-29

6 Colebatch HJH, Smith MM, Ng CKY. Increased elastic recoil

as a determinant of pulmonary barotrauma in divers. Respir

Physiol 1976; 26:55-64

7 US Navy diving manual, vol 1, rev 3. Washington, DC: Naval

Sea Systems Command, 1993; 3:16-7

8 Davis JC. Medical evaluation for diving. In: Bove AA, Davis JC,

eds. Diving medicine. Philadelphia: WB Saunders, 1990; 290-

301

9 Bove AA, Neuman T, Kelsen S, et al. Observations on asthma

in the recreational diving population [abstract]. Undersea

Biomed Res 1992; 19(suppl):18

10 Corson KS, Moon RE, Nealen ML, et al. A survey of diving

asthmatics [abstract]. Undersea Biomed Res 1992; 19(suppl):

18-9

11 Farrell PJS, Glanvill P. Diving practices of SCUBA divers with

asthma. BMJ 1990; 300:166

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