The Extended Oxygen Window Concept for Programming Saturation Decompressions Using Air and Nitrox

Saturation decompression is a physiological process of transition from one steady state, full saturation with inert gas at pressure, to another one: standard conditions at surface. It is defined by the borderline condition for time spent at a particular depth (pressure) and inert gas in the breathing mixture (nitrogen, helium). It is a delicate and long lasting process during which single milliliters of inert gas are eliminated every minute, and any disturbance can lead to the creation of gas bubbles leading to decompression sickness (DCS). Most operational procedures rely on experimentally found parameters describing a continuous slow decompression rate. In Poland, the system for programming of continuous decompression after saturation with compressed air and nitrox has been developed as based on the concept of the Extended Oxygen Window (EOW). EOW mainly depends on the physiology of the metabolic oxygen window—also called inherent unsaturation or partial pressure vacancy—but also on metabolism of carbon dioxide, the existence of water vapor, as well as tissue tension. Initially, ambient pressure can be reduced at a higher rate allowing the elimination of inert gas from faster compartments using the EOW concept, and maximum outflow of nitrogen. Then, keeping a driving force for long decompression not exceeding the EOW allows optimal elimination of nitrogen from the limiting compartment with half-time of 360 min. The model has been theoretically verified through its application for estimation of risk of decompression sickness in published systems of air and nitrox saturation decompressions, where DCS cases were observed. Clear dose-reaction relation exists, and this confirms that any supersaturation over the EOW creates a risk for DCS. Using the concept of the EOW, 76 man-decompressions were conducted after air and nitrox saturations in depth range between 18 and 45 meters with no single case of DCS. In summary, the EOW concept describes physiology of decompression after saturation with nitrogen-based breathing mixtures.     

Biophysical limitations on deep diving: Some limiting performance expectations

Decompression is treated according to the conventional Haldane model, but with continuously varying gas mixture, and continuous ascent. Analytical expressions are derived for the inert gas, tissue super-saturation, during dives with optimum gas mixtures. Analog computer results are used to show the supersaturation graphically, on dives of 300 ft. with 20 minutes on the bottom, and 1,000 ft. with 4 minutes on the bottom. The decompression times are much shorter than the times expected from U. S. Navy diving tables.     

Role of oxygen in the production of human decompression sickness

In the calculation of decompression schedules, it is commonly assumed that only the inert gas needs to be considered; all inspired O2 is ignored. Animal experiments have shown that high O2 can increase risk of serious decompression sickness (DCS). A trial was performed to assess the relative risks of O2 and N2 in human no-decompression dives. Controlled dives (477) of 30- to 240-min duration were performed with subjects breathing mixtures with low (0.21-0.38 ATA) or high (1.0-1.5 ATA) Po2. Depths were chosen by a sequential dose-response format. Only 11 cases of DCS and 18 cases of marginal symptoms were recorded despite exceeding the presently accepted no-decompression limits by greater than 20%. Analysis by maximum likelihood showed a shallow dose-response curve for increasing depth. O2 was estimated to have zero influence on DCS risk, although data variability still allows a slight chance that O2 could be 40% as effective as N2 in producing a risk of DCS. Consideration of only inert gases is thus justified in calculating human decompression tables.     

Effect of inert gas switching at depth on decompression outcome in rats

The present investigation was performed to determine whether inert gas sequencing at depth would affect decompression outcome in rats via the phenomenon of counterdiffusion. Unanesthetized rats (Rattus norvegicus) were subjected to simulated dives in either air, 79% He-21% O2, or 79% Ar-21% O2; depths ranged from 125 to 175 feet of seawater (4.8-6.3 atmospheres absolute). After 1 h at depth, the dive chamber was vented (with depth held constant) over a 5-min period with the same gas as in the chamber (controls) or one of the other two inert gas-O2 mixtures. After the gas switch, a 5- to 35-min period was allowed for gas exchange between the animals and chamber atmosphere before rapid decompression to the surface. Substantial changes in the risk of decompression sickness (DCS) were observed after the gas switch because of differences in potencies (He less than N2 less than Ar) for causing DCS and gas exchange rates (He greater than Ar greater than N2) among the three gases. Based on the predicted gas exchange rates, transient increases or decreases in total inert gas pressure would be expected to occur during these experimental conditions. Because of differences in gas potencies, DCS risk may not directly follow the changes in total inert gas pressure. In fact, a decline in predicted DCS risk may occur even as total inert gas pressure in increasing.     

A model of extravascular bubble evolution: effect of changes in breathing gas composition.

Observations of bubble evolution in rats after decompression from air dives (O. Hyldegaard and J. Madsen. Undersea Biomed. Res. 16: 185-193, 1989; O. Hyldegaard and J. Madsen. Undersea Hyperbaric Med. 21: 413-424, 1994; O. Hyldegaard, M. Moller, and J. Madsen. Undersea Biomed. Res. 18: 361-371, 1991) suggest that bubbles may resolve more safely when the breathing gas is a heliox mixture than when it is pure O(2). This is due to a transient period of bubble growth seen during switches to O(2) breathing. In an attempt to understand these experimental results, we have developed a multigas-multipressure mathematical model of bubble evolution, which consists of a bubble in a well-stirred liquid. The liquid exchanges gas with the bubble via diffusion, and the exchange between liquid and blood is described by a single-exponential time constant for each inert gas. The model indicates that bubbles resolve most rapidly in spinal tissue, in adipose tissue, and in aqueous tissues when the breathing gas is switched to O(2) after surfacing. In addition, the model suggests that switching to heliox breathing may prolong the existence of the bubble relative to breathing air for bubbles in spinal and adipose tissues. Some possible explanations for the discrepancy between model and experiment are discussed.     

Decompression outcome following saturation dives with multiple inert gases in rats

This investigation examined the question of whether gas mixtures containing multiple inert gases provide a decompression advantage over mixtures containing a single inert gas. Unanesthetized male albino rats, Rattus norvegicus, were subjected to 2-h simulated dives at depths ranging from 145 to 220 fsw. At pressure, the rats breathed various He-N2-Ar-O2 mixtures (79.1% inert gas-20.9% O2); they were then decompressed rapidly (within 10 s) to surface pressures. The probability of decompression sickness (DCS), measured either as severe bends symptoms or death, was related to the experimental variables in a Hill equation model incorporating parameters that account for differences in the potencies of the three gases and the weight of the animal. The relative potencies of the three gases, which affect the total dose of decompression stress, were determined as significantly different in the following ascending order of potency: He less than N2 less than Ar; some of these differences were small in magnitude. With mixtures, the degree of decompression stress diminished as either N2 or Ar was replaced by He. No obvious advantage or disadvantage of mixtures over the least potent pure inert gas (He) was evident, although limits to the expectation of possible advantage or disadvantage of mixtures were defined. Also, model analysis did not support the hypothesis that the outcome of decompression with multiple inert gases in rats under these experimental conditions can be explained totally by the volume of gas accumulated in the body during a dive.     

Predicting the time of occurrence of decompression sickness.

Probabilistic models and maximum likelihood estimation have been used to predict the occurrence of decompression sickness (DCS). We indicate a means of extending the maximum likelihood parameter estimation procedure to make use of knowledge of the time at which DCS occurs. Two models were compared in fitting a data set of nearly 1,000 exposures, in which greater than 50 cases of DCS have known times of symptom onset. The additional information provided by the time at which DCS occurred gave us better estimates of model parameters. It was also possible to discriminate between good models, which predict both the occurrence of DCS and the time at which symptoms occur, and poorer models, which may predict only the overall occurrence. The refined models may be useful in new applications for customizing decompression strategies during complex dives involving various times at several different depths. Conditional probabilities of DCS for such dives may be reckoned as the dive is taking place and the decompression strategy adjusted to circumstance. Some of the mechanistic implications and the assumptions needed for safe application of decompression strategies on the basis of conditional probabilities are discussed.     

Predicting risk of decompression sickness in humans from outcomes in sheep.

In animals, the response to decompression scales as a power of species body mass. Consequently, decompression sickness (DCS) risk in humans should be well predicted from an animal model with a body mass comparable to humans. No-stop decompression outcomes in compressed air and nitrogen-oxygen dives with sheep (n = 394 dives, 14.5% DCS) and humans (n = 463 dives, 4.5% DCS) were used with linear-exponential, probabilistic modeling to test this hypothesis. Scaling the response parameters of this model between species (without accounting for body mass), while estimating tissue-compartment kinetic parameters from combined human and sheep data, predicts combined risk better, based on log likelihood, than do separate sheep and human models, a combined model without scaling, and a kinetic-scaled model. These findings provide a practical tool for estimating DCS risk in humans from outcomes in sheep, especially in decompression profiles too risky to test with humans. This model supports the hypothesis that species of similar body mass have similar DCS risk.     

Specifics of Gas Bubble Formation and Growth in Tissues during Decompression after Saturation Dives

It is shown that the decompression schedules after saturation diving to the depth of 30 m designed to hold the nitrogen supersaturation for the most “slow” tissues at the acceptable levels is significantly shorter than the decompression schedules with zero supersaturation of these tissues with nitrogen and all dissolved gases. Equality of the risk for decompression sickness (DCS) onset during this decompression schedule to the risk of DCS onset under non-stop ascent to the surface after saturation diving to the depth of 6.1 m indicates that the effect of the high ambient pressure decreases the density of gas bubble seeds in tissues and the growth rate of their total volume. The DCS symptoms in the experienced divers under dangerous decompression profiles not appear due to the lower density of gas bubble seeds in their tissues relatively to the average level inherent to the many of humans.     

REPETITIVE SHALLOW DIVES POSE DECOMPRESSION RISK IN DEEP-DIVING BEAKED WHALES

The impact of naval sonar on beaked whales is of increasing concern. In recent years the presence of gas and fat embolism consistent with decompression sickness (DCS) has been reported through postmortem analyses on beaked whales that stranded in connection with naval sonar exercises. In the present study, we use basic principles of diving physiology to model nitrogen tension and bubble growth in several tissue compartments during normal diving behavior and for several hypothetical dive profiles to assess the risk of DCS. Assuming that normal diving does not cause nitrogen tensions in excess of those shown to be safe for odontocetes, the modeling indicates that repetitive shallow dives, perhaps as a consequence of an extended avoidance reaction to sonar sound, can indeed pose a risk for DCS and that this risk should increase with the duration of the response. If the model is correct, then limiting the duration of sonar exposure to minimize the duration of any avoidance reaction therefore has the potential to reduce the risk of DCS.     

Conditions for the development of isobaric counterdiffusion of inert gases and the criteria of its evaluation]

Investigation of superficial counterdiffusion of nitrogen against helium has been carried out to evaluate a possibility of its progress in divers (107 tests) under pressures equivalent to 32-450 m of sea water when breathing trimix being saturated in heliox at a constant ambient pressure without changing chamber environment. Breathing gas mixture contained 248-800 kPa of nitrogen, while chamber heliox media contained some additions of nitrogen (6-108 kPa). Clinical manifestations of breathing trimix (itching and gas bubble formation) were studied in divers. The development of counterdiffusion depends on the partial pressure of nitrogen not only in the breathing gas mixture but also in the chamber media. The breathing nitrogen level being increased and (or) decreased in the chamber media, the counterdiffusion symptoms grow relative to the number (%) of cases. Minimal critical values of nitrogen partial pressure gradients in the mixture which induce counterdiffusion skin lesions are 260-320 kPa on the average for the nitrogen concentration in the chamber mixture to 30 kPa. Isobaric supersaturation due to inert gases countertransport in body tissues as a result of gas-switching from heliox to trimix is responsible for the syndrome development.     

Theoretical evaluation of safety of dives completed by non-stop ascent to surface

Our model of decompression sickness determines the cumulative probability of developing symptoms of this illness by the exponential equation whose index is the integral cumulative risk function of all body tissue lesions by bubbles, F _cum(t) = ΣF _n(t). The underwater dives may be considered as practically safe in the context of this model when the function F _cum(t) during its growth will not exceed some small value F _cum-max = ΣF _n-max. Using hypothetical values of parameters of tissues and functions F _n(t), we calculated the curves depth-duration for practically safe non-stop dives with air and with mixtures of oxygen with helium, neon and argon. Doing so, we obtained the distributions of values F _n-max in regard to the values of inert gas washout half-times from tissues which show that the tissues experienced the largest risks of bubble lesions are different for dives with different duration. The comparison of the indicated curves shows that the short-term dives with air are less dangerous and the long-term dives are more dangerous than the dives with helium-oxygen mixture. At the same time, the least risk of bubble lesions of tissues arises at dives with neon-oxygen mixture and the greatest risk arises at dives with argon-oxygen mixture.     

Decompression sickness in the rat following a dive on trimix: recompression therapy with oxygen vs. heliox and oxygen.

Trimix (a mixture of helium, nitrogen, and oxygen) has been used in deep diving to reduce the risk of high-pressure nervous syndrome during compression and the time required for decompression at the end of the dive. There is no specific recompression treatment for decompression sickness (DCS) resulting from trimix diving. Our purpose was to validate a rat model of DCS on decompression from a trimix dive and to compare recompression treatment with oxygen and heliox (helium-oxygen). Rats were exposed to trimix in a hyperbaric chamber and tested for DCS while walking in a rotating wheel. We first established the experimental model, and then studied the effect of hyperbaric treatment on DCS: either hyperbaric oxygen (HBO) (1 h, 280 kPa oxygen) or heliox-HBO (0.5 h, 405 kPa heliox 50%-50% followed by 0.5 h, 280 kPa oxygen). Exposure to trimix was conducted at 1,110 kPa for 30 min, with a decompression rate of 100 kPa/min. Death and most DCS symptoms occurred during the 30-min period of walking. In contrast to humans, no permanent disability was found in the rats. Rats with a body mass of 100-150 g suffered no DCS. The risk of DCS in rats weighing 200-350 g increased linearly with body mass. Twenty-four hours after decompression, death rate was 40% in the control animals and zero in those treated immediately with HBO. When treatment was delayed by 5 min, death rate was 25 and 20% with HBO and heliox, respectively.     

Factors determining temporal pattern of isobaric supersaturation

It is possible to produce a transient supersaturation or undersaturation in tissues and blood by sequentially breathing gases with different equilibration rates. If the ambient gas pressure is sufficiently high, the induced supersaturation can produce vascular bubbles. By means of the classical perfusion-dependent model of inert gas elimination, which assumes that the effects of diffusion are minimal, the magnitude of the total inert gas pressure can be predicted. If, however, the effects of diffusion cannot be ignored, the supersaturation could be substantially larger. This paper estimates the effects of diffusion in a Krogh cylinder on the supersaturation produced by suddenly changing the inert gas partial pressure in the blood. The results of these estimates indicate that diffusion plays a role in this transient supersaturation only in long Krogh cylinders with high blood flows. The effects of diffusion are further reduced by the finite time necessary to switch the inert gases in arterial blood. The conclusions are supported by experiments that measure vascular bubble production after a switch of the inert portion of the inspired gas. These experiments further show that the formation of vascular bubbles after such a switch cannot be entirely explained by the different diffusion constants of the gases used.     

Short oxygen prebreathing and intravenous perfluorocarbon emulsion reduces morbidity and mortality in a swine saturation model of decompression sickness.

Disabled submarine (DISSUB) survivors will achieve inert gas tissue saturation within 24 h. Direct ascent to the surface when saturated carries a high risk of decompression sickness (DCS) and death, yet may be necessary during rescue or escape. O(2) has demonstrated benefits in decreasing morbidity and mortality resulting from DCS by enhancing inert gas elimination. Perfluorocarbons (PFCs) also mitigate the effects of DCS by decreasing bubble formation and increasing O(2) delivery. Our hypothesis is that combining O(2) prebreathing (OPB) and PFC administration will reduce the incidence of DCS and death following saturation in an established 20-kg swine model. Yorkshire swine (20 +/- 6.5 kg) were compressed to 5 atmospheres (ATA) in a dry chamber for 22 h before randomization into one of four groups: 1) air and saline, 2) OPB and saline, 3) OPB with PFC given at depth, 4) OPB with PFC given after surfacing. OPB animals received >90% O(2) for 9 min at depth. All animals were returned to the surface (1 ATA) without decompression stops. The incidence of severe DCS < 2 h after surfacing was 96%, 63%, 82%, and 29% for groups 1, 2, 3, and 4, respectively. The incidence of death was 88%, 41%, 54%, and 5% for groups 1, 2, 3, and 4, respectively. OPB combined with PFC administration after surfacing provided the greatest reduction in DCS morbidity and mortality in a saturation swine model. O(2)-related seizure activity before reaching surface did not negatively affect outcome, but further safety studies are warranted.     

Oxygen or carbogen breathing before simulated submarine escape.

Raised internal pressure in a distressed submarine increases the risk of bubble formation and decompression illness after submarine escape. The hypothesis that short periods of oxygen breathing before submarine escape would reduce decompression stress was tested, using Doppler-detectable venous gas emboli as a measure. Twelve goats breathed oxygen for 15 min at 0.1 MPa before exposure to a simulated submarine escape profile to and from 2.5 MPa (240 m/seawater), whereas 28 control animals underwent the same dive without oxygen prebreathe. No decompression sickness (DCS) occurred in either of these two groups. Time with high bubble scores (Kisman-Masurel >or=3) was significantly (P < 0.001) shorter in the prebreathe group. In a second series, 30 goats breathed air at 0.2 MPa for 6 h. Fifteen minutes before escape from 2.5 MPa, animals were provided with either air (n = 10), oxygen (n = 12), or carbogen (97.5% O(2) and 2.5% CO(2)) gas (n = 8) as breathing gas. Animals breathed a hyperoxic gas (60% O(2)-40% N(2)) during the escape. Two animals (carbogen group) suffered oxygen convulsions during the escape but recovered on surfacing. Only one case of DCS occurred (carbogen group). The initial bubble score was reduced in the oxygen group (P < 0.001). The period with bubble score of Kisman-Masurel >or=3 was also significantly reduced in the oxygen group (P < 0.001). Oxygen breathing before submarine escape reduces initial bubble scores, although its significance in reducing central nervous system DCS needs to be investigated further.     

Gas transport and blood acid-base balance in diving sea snakes.

The values of hemoglobin concentration, Hb-O2 affinity and buffering capacity of the blood of six sea snake species considerably overlap values from terrestrial squamates. Decreased blood pH had little effect on the P50 but increased the n-value of Hb-O2 equilibrium curves. The O2 saturation of blood in the dorsal aorta varied between about 30 and 70% during voluntary diving in Acalyptophis peronii and Lapemis hardwickii. Voluntary dives ended when the lung PP02 was about 50 mm Hg and the arterial PO2 about 30 mm Hg indicating that roughly half of the O2 reserves had been used. In conjunction with relatively stable blood lactate concentration and pH, this indicates that voluntary dives occurred largely aerobically. In contrast, forced dives resulted in depletion of O2 reserves and large changes in blood acid-base balance. Long recovery periods following forced dives are inconsistent with field observations and thus suggest that extensive anaerobic metabolism does not normally occur in sea snakes. Bradycardia was not evident during forced dives. Large differences in PO2 between the lung and dorsal aorta indicated considerable right to left shunting either in the heart or in the lung. Venous blood represented over 50% of the systemic flow when there was considerable O2 in the lung. Therefore blood PO2 may remain relatively low despite elevated lung PO2 resulting from diving. In view of substantial capability for extra-pulmonary gas exchange, high shunting reduces the possibility of losing O2 through the skin and also may help prevent decompression sickness following deep dives.     

Cerebral gas embolism absorption during hyperbaric therapy: theory.

Cerebral gas embolism is a serious consequence of diving. It is associated with decompression sickness and is assumed to cause severe neurological dysfunction. A mathematical model previously developed to calculate embolism absorption time based on in vivo bubble geometry is used in which various conditions of hyperbaric therapy are considered. Effects of varying external pressure and inert gas concentrations in the breathing mixtures, according to US Navy and Royal Navy diving treatment tables, are predicted. Recompression alone is calculated to reduce absorption times of a 50-nl bubble by up to 98% over the untreated case. Lowering the inhaled inert gas concentration from 67.5% to 50% reduces absorption time by 37% at a given pressure. Bubbles formed after diving and decompression with He are calculated to absorb up to 73% faster than bubbles created after diving and decompression with air, regardless of the recompression gas breathed. This model is a useful alternative to impractical clinical trials in assessing which initial step in hyperbaric therapy is most effective in eliminating cerebral gas embolisms should they occur.     

Further considerations in a theoretical description of gas transport in lung airways

A discrete one-dimensional model of convection-diffusion in branching alveolar ducts is described and it is shown that, for a suitable choice of effective axial dispersion, the solution closely approximates that for an axially symmetric representation, at least for Peclet numbers Pe<1. Following earlier work a composite model of a uniform lung is formed by matching such a respiratory pathway (now having the more convenient one-dimensional form) onto a trumpet representation of the conducting airways. Enhanced mixing due to heart action, and isotropic volume changes of trumpet (in addition to the pathway) during breathing are additional factors included. Calculations are made of O₂ concentrations during steady-state breathing and of the concentration of inert gas during single breath wash-out of a gas mixture containing it. Predicted alveolar levels in each case agree extremely well with published data, although no alveolar slope is obtained for the inert gas.