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Accelerated Decompression Using Oxygen for Submarine Rescue - Summary Report and Operational Guidance
Abstract
In certain situations, a disabled submarine could become internally pressurized due to flooding, leakage of compressed gas supplies, or use of auxiliary breathing systems. This could result in the survivors being saturated with nitrogen at elevated pressures. Efficient submarine rescue requires that pressurized crew members be decompressed more rapidly than current procedures on air allow. NEDU has investigated the ability of oxygen to accelerate decompression following saturation with nitrogen-oxygen. Initial attempts resulted in an unexpectedly high incidence of severe decompression sickness. Subsequent decompression schedules including a period of isobaric oxygen breathing (pre-breathing) with a shorter total ascent time were significantly better than staged decompression of comparable length. Pre- breathing oxygen, or nitrogen-oxygen mixtures, is an effective decompression strategy. This report summarizes the experiments and presents decompression procedures for emergency use in submarine rescue.
... 44 While the conclusions from such collected observations usually hold reference to current theories, they should not form the basis for absolute rules of conduct, as they have not been tested in a scientific cognitive process and validated. 45 [9] For this reason, the uncritical use of GDPs in conditions 46 different from those in which they are proven to work, 47 can degenerate into irrational or even harmful behaviour [12]. Hence, GDPs are rather unlikely to be described in the form of recommendations, 48 even though they do provide an important rationale for conducting an analysis of residual risk R dla procesu dekompresji. ...
... The most advanced rescue method is the use of deep submergence rescue vehicles DSRV 105 . The rescued submariners can go through the accelerated decompression on board such a vehicle [10,45,46]. Regardless of whether victims can be transported under pressure TUP to decompression chambers, the implementation of accelerated decompression on board a DSRV during its ascent intensifies the rescue process. ...
... As mentioned earlier, in the part discussing the accelerated decompression, in a rescue situation special procedures are used. They involve implementing the decompression processes with an increased hazard of decompression sickness symptoms ' ƒ"… , of central oxygen toxicity ' "-…žŸ , etc. [40,45]. ...
This article is a further one in an unintended series concerning the design of diving technology [1,2,3]. It contains answers to questions raised by readers upon reading previous articles and by users of the systems described therein by way of example. The articles also refer to the discussion held at the annual NATO Working Group meeting on the various types of decompression presented by the Polish side [4,5,6,7]. The previous articles were linked to the acceptance of the results of the project No. DOB-BIO8/О9/О1/2016 carried out under the contract with the NCBiR National Centre for Research and Development entitled “Decompression schedules for MCM/EOD II diving” carried out in 2016-2021. The current article is linked to the new project No. DOBBIO-12-03-001-2022 implemented under the contract with the NCBiR entitled: “The effects of combat effort and air transport on the safety of combat divers in the execution of underwater combat operations,” scheduled for 2023-2025.
... Past attempts to eliminate gas micronuclei used short compression to very high pressures that are not applicable to humans (Vann et al. 1980;Daniels et al. 1984;McDonough and Hemmingsen 1984). Denitrogenation required a very long exposure time, lasting several hours (Webb and Pilmanis 1999;Latson et al. 2000;Pilmanis et al. 2003). If a short pretreatment could be found which took only minutes rather than hours and was effective in the mammal, it might be possible to establish a protective protocol for human use. ...
... It also has immense potential as a preparatory measure before escape from a disabled submarine or high altitude flight. In previous studies on large mammals and man, an extended period of hyperoxia (about 10 h) was required to reduce the risk of decompression sickness (Webb and Pilmanis 1999;Latson et al. 2000). This may be related to the different treatment methods we employed. ...
... All previous studies investigating the protective role of oxygen in DCS undertook to reverse the process of inert gas loading by denitrogenation, a procedure designed to wash out the inert gas from the tissues just before the start of decompression (Webb and Pilmanis 1999;Latson et al. 2000;Pilmanis et al. 2003;Mahon et al. 2006). This is in contrast to the method presented here, in which oxygen is used to flush the tissues even before loading of the inert gas. ...
We have previously hypothesised that the number of bubbles evolving during decompression from a dive, and therefore the incidence of decompression sickness (DCS), might be reduced by pretreatment with hyperbaric oxygen (HBO). The inert gas in the gas micronuclei would be replaced by oxygen, which would subsequently be consumed by the mitochondria. This has been demonstrated in the transparent prawn. To investigate whether our hypothesis holds for mammals, we pretreated rats with HBO at 304, 405, or 507 kPa for 20 min, after which they were exposed to air at 1,013 kPa for 33 min and decompressed at 202 kPa/min. Twenty control rats were exposed to air at 1,013 kPa for 32 min, without HBO pretreatment. On reaching the surface, the rat was immediately placed in a rotating cage for 30 min. The animal's behaviour enabled us to make an early diagnosis of DCS according to accepted symptoms. Rats were examined again after 2 and 24 h. After 2 h, 65% of the control rats had suffered DCS (45% were dead), whereas 35% had no DCS. HBO pretreatment at 304, 405 and 507 kPa significantly reduced the incidence of DCS at 2 h to 40, 40 and 35%, respectively. Compared with the 45% mortality rate in the control group after 24 h, in all of the pretreated groups this was 15%. HBO pretreatment is equally effective at 304, 405 or 507 kPa, bringing about a significant reduction in the incidence of DCS in rats decompressed from 1,013 kPa.
... The effectiveness of oxygen pre-breathing (OPB) at saturation, intermittent high inspired oxygen during staged decompression and combined approaches for reducing decompression time from saturation exposures have been demonstrated experimentally, with manifest oxygen toxicity considered within acceptable limits for emergency use. [101][102][103][104][105][106] Minimum safe accelerated oxygen decompression schedules have consequently been developed 102 and incorporated into US Navy SRS decompression plans. 59 Their implementation is however subject to oxygen delivery capability and the condition of survivors, both of which present ongoing issues. ...
... The effectiveness of oxygen pre-breathing (OPB) at saturation, intermittent high inspired oxygen during staged decompression and combined approaches for reducing decompression time from saturation exposures have been demonstrated experimentally, with manifest oxygen toxicity considered within acceptable limits for emergency use. [101][102][103][104][105][106] Minimum safe accelerated oxygen decompression schedules have consequently been developed 102 and incorporated into US Navy SRS decompression plans. 59 Their implementation is however subject to oxygen delivery capability and the condition of survivors, both of which present ongoing issues. ...
... In circumstances where there are extreme constraints on decompression time it may be necessary to utilise schedules with multiple periods of oxygen breathing. Since inhalation of O 2 for a long period can cause pulmonary oxygen toxicity (POT), these schedules are of considerably shorter durations but carry risks of higher incidence of DCS than in the case of the long air schedules [6]. Moreover, for deeper exposures, when pressure is more than 2.8 bar, the risk of severe POT prohibits the use of oxygen breathing to accelerate decompression. ...
... Greater depths of air saturation have been tested on a limited number of subjects [28,29]. In a large experimental study, the US Navy Experimental Diving Unit evaluated accelerated decompression procedures using pure oxygen in a significant number of subjects i.e. 175 man-dives [6]. The incidence of DCS (17 incidents were observed) and circulating bubbles was monitored after ten alternative decompression schedules from Nitrox saturations between 40 and 60 feet (12– 18 msw equivalent air depth). ...
Recent advances in submarine rescue systems have allowed a transfer under pressure of crew members being rescued from a disabled submarine. The choice of a safe decompression procedure for pressurised rescuees has been previously discussed, but no schedule has been validated when the internal submarine pressure is significantly increased i.e. exceeding 2.8 bar absolute pressure. This study tested a saturation decompression procedure from hyperbaric exposures up to 6 bar, the maximum operating pressure of the NATO submarine rescue system. The objective was to investigate the incidence of decompression sickness (DCS) and clinical and spirometric indices of pulmonary oxygen toxicity. Two groups were exposed to a Nitrogen-Oxygen atmosphere (pO2 = 0.5 bar) at either 5 bar (N = 14) or 6 bar (N = 12) for 12 h followed by 56 h 40 min resp. 60 h of decompression. When chamber pressure reached 2.5 bar, the subjects breathed oxygen intermittently, otherwise compressed air. Repeated clinical examinations, ultrasound monitoring of venous gas embolism and spirometry were performed during decompression. During exposures to 5 bar, 3 subjects had minor subjective symptoms i.e. sensation of joint discomfort, regressing spontaneously, and after surfacing 2 subjects also experienced joint discomfort disappearing without treatment. Only 3 subjects had detectable intravascular bubbles during decompression (low grades). No bubbles were detected after surfacing. About 40% of subjects felt chest tightness when inspiring deeply during the initial phase of decompression. Precordial burning sensations were reported during oxygen periods. During decompression, vital capacity decreased by about 8% and forced expiratory flow rates decreased significantly. After surfacing, changes in the peripheral airways were still noticed; Lung Diffusion for carbon monoxide was slightly reduced by 1% while vital capacity was normalized. The procedure did not result in serious symptoms of DCS or pulmonary oxygen toxicity and may be considered for use when the internal submarine pressure is significantly increased.
... brain oxygen partial pressure; cerebral blood flow; central nervous system oxygen toxicity TWO APPROACHES are favored for prevention of decompression sickness (DCS) or arterial gas embolism due to rapid decompression or for use as adjuncts to primary therapies for treatment or mitigation of these conditions. One method, breathing pure O 2 prior to decompression (O 2 prebreathing), was initially developed to reduce the risk of DCS in military aviation (12,13) and has been adopted for use by underwater divers (15), as well as for preparation of astronauts for extravehicular excursions in the hypobaric microenvironment of a spacesuit (22). The benefit of O 2 breathing prior to decompression has been demonstrated in humans (15) and animals (1,25) and is attributed to the accelerated elimination of inert gas from blood and tissue. ...
... One method, breathing pure O 2 prior to decompression (O 2 prebreathing), was initially developed to reduce the risk of DCS in military aviation (12,13) and has been adopted for use by underwater divers (15), as well as for preparation of astronauts for extravehicular excursions in the hypobaric microenvironment of a spacesuit (22). The benefit of O 2 breathing prior to decompression has been demonstrated in humans (15) and animals (1,25) and is attributed to the accelerated elimination of inert gas from blood and tissue. ...
Intravenous perfluorocarbon (PFC) emulsions, administered with supplemental inspired O(2), are being evaluated for their ability to eliminate N(2) from blood and tissue prior to submarine escape, but these agents can increase the incidence of central nervous system (CNS) O(2) toxicity, perhaps by enhancing O(2) delivery to the brain. To assess this, we infused a PFC emulsion (Oxycyte, 6 ml/kg iv) into anesthetized rats and measured cerebral Po(2) and regional cerebral blood flow (rCBF) in cortex, hippocampus, hypothalamus, and striatum with 100% O(2) at 1, 3, or 5 atmospheres absolute (ATA). At 1 ATA, brain Po(2) stabilized at >20 mmHg higher in animals infused with PFC emulsion than in control animals infused with saline, and rCBF fell by ~10%. At 3 ATA, PFC emulsion raised brain Po(2) >70 mmHg above control levels, and rCBF decreased by as much as 25%. At 5 ATA, brain Po(2) was ≥159 mmHg above levels in control animals for the first 40 min but then rose sharply; rCBF showed a similar profile, reflecting vasoconstriction followed by hyperemia. Conscious rats were also pretreated with PFC emulsion at 3 or 6 ml/kg iv and exposed to 100% O(2) at 5 ATA. At the lower dose, 80% of the animals experienced seizures by 33 min compared with 50% of the control animals. At the higher dose, seizures occurred in all rats within 25 min. At these doses, administration of PFC emulsion poses a clear risk of CNS O(2) toxicity in conscious rats exposed to hyperbaric O(2) at 5 ATA.
... (11). In humans, OPB at 18 msw (2.52 ATA) saturation significantly reduced DCS, allowing for a safe 8--10-h decompression schedule (9). Unfortunately, it is unlikely that a DISSUB would have a pre-existing OPB capability; transport of oxygen to the DISSUB will be difficult and application of OPB at 40 msw depth might result in severe toxicities. ...
... A previous study showed OPB for as little as 1 h prior to dropout from 18 msw saturation completely prevented death in 70-kg swine (15). Latson was unable to show that OB at decompression stops < 18 msw decreased OCS in humans decompressing from 18 msw saturation until OPB at 18 msw was added to the decompression schedule (9). We reproduced this effect in Profile 3 with OPB at 40 msw, on the hypothesis that initiating oxygen at the deepest portion of the profile would accelerate the initial ascent phase. ...
Submarine disaster survivors can be transferred from a disabled submarine at a pressure of 40 meters of seawater (msw) to a new rescue vehicle; however, they face an inherently risky surface interval before recompression and an enormous decompression obligation due to a high likelihood of saturation. The goal was to design a safe decompression protocol using oxygen breathing and a trial-and-error methodology. We hypothesized that depth, timing, and duration of oxygen breathing during decompression from saturation play a role to mitigate decompression outcomes.
Yorkshire swine (67-75 kg), compressed to 40 msw for 22 h, underwent one of three accelerated decompression profiles: (1) 13.3 h staged air decompression to 18 msw, followed by 1 h oxygen breathing, then dropout; (2) direct decompression to 18 msw followed by 1 h oxygen breathing then dropout; and (3) 1 h oxygen prebreathe at 40 msw followed by 1 h mixed gas breathing at 26 msw, 1 h oxygen breathing at 18 msw, and 1 h ascent breathing oxygen. Animals underwent 2-h observation for signs of DCS.
Profile 1 (14.3 h total) resulted in no deaths, no Type II DCS, and 20% Type I DCS. Profile 2 (2.1 h total) resulted in 13% death, 50% Type II DCS, and 75% Type I DCS. Profile 3 (4.5 h total) resulted in 14% death, 21% Type II DCS, and 57% Type I DCS. No oxygen associated seizures occurred.
Profile 1 performed best, shortening decompression with no death or severe DCS, yet it may still exceed emergency operational utility in an actual submarine rescue.
... Oxygen prebreathing (OPB) is currently used by aviators [3], during spacewalks [4], and during emergency submarine rescue [5] to denitrogenate tissues and thereby minimize the risk of DCS. During OPB nitrogen is expired from venous blood, creating a gradient for tissue nitrogen to move into venous blood and be expired. ...
Background
Breathing pure oxygen causes nitrogen washout from tissues, a method commonly deployed to prevent decompression sickness from hypobaric exposure. Theoretically prebreathing oxygen increases the capacity for nitrogen uptake and potentially limits supersaturation during dives of short duration. We aimed to use 13N2, a radioactive nitrogen isotope, to quantify tissue nitrogen following normobaric and hyperbaric exposures.
Methods
Twenty Sprague Dawley rats were divided in 4 conditions; normobaric prebreathe, normobaric control, hyperbaric prebreathe, hyperbaric control. Prebreathed rats breathed oxygen for 1 h prior to the experiment whilst controls breathed air. Normobaric rats breathed air containing 13N2 at 100 kPa for 30 min, whereas hyperbaric rats breathed 13N2 at 700 kPa before being decompressed and sedated using air-isoflurane (without 13N2 for a few minutes). After euthanization, blood, brain, liver, femur and thigh muscle were analyzed by gamma counting.
Results
At normobaria prebreathing oxygen resulted in higher absolute nitrogen counts in blood (p = .034), as well as higher normalized counts in both the liver and muscle (p = .034). However, following hyperbaric exposure no differences were observed between conditions for any organ (p>.344). Both bone and muscle showed higher normalized counts after hyperbaria compared to normobaria.
Conclusions
Oxygen prebreathing caused nitrogen elimination in normobaria that led to a larger “sink” and uptake of 13N2. The lack of difference between conditions in hyperbaria could be due to the duration and depth of the dive mitigating the effect of prebreathing. In the hyperbaric conditions the lower counts were likely due to off-gassing of nitrogen during the sedation procedure, suggest a few minutes was enough to off-gas in rodents. The higher normalized counts under hyperbaria in bone and muscle likely relate to these tissues being slower to on and off-gas nitrogen. Future experiments could include shorter dives and euthanization while breathing 13N2 to prevent off-gassing.
... Such knowledge could be of great value also for practical use of the model for planning of saturation decompressions in case of emergency, when high partial pressure of oxygen is empirically used for accelerating desaturation. Some modeling research has already been done [55], some studies on animals have been conducted [56], several procedures have been recommended [57,58], and recently, this method has been investigated in humans [11,59]. Even if "the advantages of oxygen appear far less than predicted by current decompression models" [60], using a high amount of oxygen for accelerating decompression is already recommended in case of emergency [55,61]. ...
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.
... The procedure used in the present study has proven to be a useful method of reducing the neurologic risks of DCS. It is not the same as denitrogenation, i.e., oxygen pretreatment just before decompression to flush the inert gas out of the tissues after it has already been loaded, as used in previous studies (19,21,25,31). In contrast to denitrogenation, in our procedure oxygen washes the tissues before hyperbaric air exposure and any loading of inert gas. ...
During sudden or too rapid decompression, gas is released within supersaturated tissues in the form of bubbles, the cause of decompression sickness. It is widely accepted that these bubbles originate in the tissue from preexisting gas micronuclei. Pretreatment with hyperbaric oxygen (HBO) has been hypothesized to shrink the gas micronuclei, thus reducing the number of emerging bubbles. The effectiveness of a new HBO pretreatment protocol on neurologic outcome was studied in rats. This protocol was found to carry the least danger of oxygen toxicity. Somatosensory evoked potentials (SSEPs) were chosen to serve as a measure of neurologic damage. SSEPs in rats given HBO pretreatment before a dive were compared with SSEPs from rats not given HBO pretreatment and SSEPs from non-dived rats. The incidence of abnormal SSEPs in the animals subjected to decompression without pretreatment (1,013 kPa for 32 min followed by decompression) was 78%. In the pretreatment group (HBO at 304 kPa for 20 min followed by exposure to 1,013 kPa for 33 min and decompression) this was significantly reduced to 44%. These results call for further study of the pretreatment protocol in higher animals.
... One such scenario is a disabled submarine (DISSUB). It is possible that the internal pressure of a DISSUB would increase based on partial flooding and the use of emergency air-breathing systems (25). Under such circumstances, it is likely that submariners waiting for the deployment of submarine rescue assets will achieve inert gas saturation. ...
Disabled submarine (DISSUB) survivors are expected to achieve saturation with inert gas. However, rescue procedures may not accommodate staged decompression, raising the potential for severe decompression sickness (DCS). Alternatives to standard recompression therapy are needed. It has been demonstrated in humans that isobaric oxygen "prebreathing" (OPB) can accelerate decompression in a DISSUB scenario. In-70 kg swine saturated at 2.82 atm absolute (ATA), 1 h of OPB eliminated death and reduced severe DCS. We hypothesized that even shorter periods (<1 h) of OPB before no-stop decompression from saturation at 2.82 ATA could reduce the incidence of DCS in a large animal model. Catheterized Yorkshire swine (68.8 +/- 1.7 kg) in individual Plexiglas boxes within a large animal hyperbaric chamber were compressed to 2.82 ATA for 22 h. Following saturation and while still at depth, breathing gas was switched to >95% O(2) for 45 min (OPB(45)), 15 min (OPB(15)), or 5 min (OPB(05)) of OPB, or no OPB (control). The chamber was then decompressed without stops (0.91 ATA/min). Observers then entered the chamber and recorded signs of DCS for 2 h. All OPB periods significantly reduced the risk of developing type II DCS. OPB(45) eliminated severe DCS. Controls had a 2.5 times greater risk of developing type II DCS than OPB(05) (P = 0.016). OPB(45) and OPB(15) significantly reduced type I DCS compared with controls. These results support the potential of OPB as an alternative to staged decompression and that OPB could be expected to improve outcome in a DISSUB rescue scenario.
... Submarines operate at 1 atmosphere absolute (ATA) internal pressure. Although rare, submarine accidents have occurred with loss of ability to maintain the vessel at 1 ATA [11][12][13][14]. If power to run environmental systems is lost, ambient pressure inside the submarine will slowly increase, potentially reaching ambient pressure outside the ship. ...
Decompression illness (DCI) results from sudden changes in ambient pressure leading to super-saturation and bubble formation in tissues and the blood stream. Perfluorocarbon emulsions (PFC) increase both oxygen and nitrogen solubility when infused into the blood stream. This study hypothesized that PFC would increase N(2) removal as well as O(2) delivery to tissues.
Juvenile swine (20 kg) were anesthetized and highly instrumented with arterial monitoring, pulmonary artery catheterization, EDAC ultrasound bubble detection, and end tidal N(2) by mass spectrometry. Blood gases were monitored in both the mixed venous and arterial circulation. Full hemodynamics were calculated using standard equations. Four groups of animals were randomized to be either sham controls or compressed and to receive either saline or PFC at 4.5 ml/kg. Animals were dry compressed to 6.8 ATA for 30 minutes of time on the bottom and then rapidly decompressed. Animals were monitored for 120 minutes after surfacing, then euthanized.
DCI was created by the dive profile but the severity was variable. Sham animals had no significant changes except that those who received PFC developed significant pulmonary hypertension and decreased cardiac output. This held true for those that also underwent DCI. Respiratory N(2) washout was not significantly different with and without PFC. However, O(2) delivery to tissues was improved with PFC and EDAC bubble count was dramatically less with PFC.
PFC decreased bubble generation but the data was confounded by a species specific pulmonary hypertensive response. Even with this as a problem O(2) delivery to tissues was enhanced by PFC. Future work with PFC in different species will help to further understand the contribution of these two mechanisms to treatment efficacy by PFC in DCI.
The most effective method to mitigate decompression sickness in divers is hyperbaric oxygen (HBO2) pre-breathing. However, divers breathing HBO2 are at risk for developing central nervous system oxygen toxicity (CNS-OT), which can manifest as symptoms that might impair a diver's performance, or cause more serious symptoms like seizures. In this study, we have collected electrodermal activity (EDA) signals in fifteen subjects at elevated oxygen partial pressures (2.06 ATA, 35 FSW) in the "foxtrot" chamber pool at the Duke University Hyperbaric Center, while performing a cognitive stress test for up to 120 minutes. Specifically, we have computed the time-varying spectral analysis of EDA (TVSymp) as a tool for sympathetic tone assessment and evaluated its feasibility for the prediction of symptoms of CNS-OT in divers. The preliminary results show large increase in the amplitude TVSymp values derived from EDA recordings ~2 minutes prior to expert human adjudication of symptoms related to oxygen toxicity. An early detection based on TVSymp might allow the diver to take countermeasures against the dire consequences of CNS-OT which can lead to drowning.Clinical Relevance-This study provides a sensitive analysis method which indicates a significant increase in the electrodermal activity prior to human expert adjudication of symptoms related to CNS-OT.
The ever-present desire of humankind to explore new limits introduced us to the syndrome of decompression sickness (DCS). This broad overview of DCS is aimed at its pathophysiology and basics of therapeutic strategies. After a brief explanation of decompression theory, historical vignettes will serve to inform the practical application of our increasing understanding of DCS risks. The pathophysiology, current practices, role of bubble monitoring, risk factors, and potential long-term effects of DCS are also discussed. The goal is to explain the current state of DCS understanding in the context of a robust observational and empirical history. However, DCS remains a syndrome consisting of a constellation of symptoms following a change in ambient pressure. Though great strides have been made, significant knowledge gaps remain. If the coming years advance the field even a fraction of what its predecessors accomplished, the health and safety of those who endeavor in the environment of changing pressures most certainly will be improved. Published 2014 American Physiological Society. Compr Physiol 4:1157-1175, 2014.
The use of hyperbaric oxygen (HBO) to expedite decompression from saturation has not been proven and may increase risk of toxicity to the pulmonary system. To evaluate any benefit of HBO during decompression, we used a 70-kg swine model of saturation and examined lung tissue by microarray analysis for evidence of RNA regulation.
Unrestrained, non-sedated swine were compressed to 132 fsw (5 ATA) for 22 h to achieve saturation. Animals then underwent decompression on air (AirD) or HBO (HBOD) starting at 45 fsw (2.36 ATA). Animals were evaluated for Type I and Type II decompression sickness (DCS) for 24 h. Control (SHAM) animals were placed in the chamber for the same duration, but were not compressed. Animals were sacrificed 24 h after exposure and total RNA was isolated from lung samples for microarray hybridizations on the Affymetrix platform.
There was no evidence of Type I DCS or severe cardiopulmonary DCS in any of the animals; abnormal gaits were noted only in the HBOD group (4/9).Three genes (nidogen 2, calcitonin-like receptor, and pentaxin-related gene) were significantly up-regulated in both the AirD and HBOD groups compared to controls. Three other genes (TN3, platelet basic protein, and cytochrome P450) were significantly down-regulated in both groups.
HBO during decompression from saturation did not reduce the incidence of DCS. Gene regulation was apparent and similar in both the AirD and HBOD groups, particularly in genes related to immune function and cell signaling.
Escuela Universitaria de Ingeniería Técnica Naval
Bubbles that grow during decompression are believed to originate from preexisting gas micronuclei. We showed that pretreatment of prawns with 203 kPa oxygen before nitrogen loading reduced the number of bubbles that evolved on decompression, presumably owing to the alteration or elimination of gas micronuclei (Arieli Y, Arieli R, and Marx A. J Appl Physiol 92: 2596-2599, 2002). The present study examines the optimal pretreatment for this assumed crushing of gas micronuclei. Transparent prawns were subjected to various exposure times (0, 5, 10, 15, and 20 min) at an oxygen pressure of 203 kPa and to 5 min at different oxygen pressures (PO2 values of 101, 151, 203, 405, 608, and 810 kPa), before nitrogen loading at 203 kPa followed by explosive decompression. After the decompression, bubble density and total gas volume were measured with a light microscope equipped with a video camera. Five minutes at a PO2 of 405 kPa yielded maximal reduction of bubble density and total gas volume by 52 and 71%, respectively. It has been reported that 2-3 h of hyperbaric oxygen at bottom pressure was required to protect saturation divers decompressed on oxygen against decompression sickness. If there is a shorter pretreatment that is applicable to humans, this will be of great advantage in diving and escape from submarines.
Gas bubbles are the primary agent in producing the pathogenic effects of decompression sickness. Bubble formation during decompression is not simply the consequence of inert gas supersaturation. Numerous experiments indicate that bubbles originate as pre-existing gas nuclei. Radii are on the order of 1 microm or less. Heterogeneous nucleation processes are involved in generating these gas entities. Musculoskeletal activity could be the main promoter of gas nuclei from stress-assisted nucleation. The half-life and faculty for nuclei to initiate bubble formation during decompression depend on many factors. Oxygen window and surface tension are involved in resolving bubbles. Two factors have been proposed to stabilize gas nuclei against dissolution: gas nuclei trapped in hydrophobic crevices and gas nuclei coated with surface-active molecules such as surfactants. Diffusion and surface tension could play an important role in the formation of gas nuclei crevices. However, while the concept of in vivo hydrophobic crevices remains a theoretical possibility, none have yet been identified in tissues and/or in microcapillaries. Moreover, while surfactants seem present in numerous tissues and could play a role in gas nuclei stabilization, they could also be involved in bubble elimination. The understanding of such mechanisms is of primary importance to neutralize nuclei and for modeling bubble growth. Here we present in a single document a summary of the original findings and views from authors in this field.
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.
With the development of the so-called "technical diving" techniques the depth capability of untethered divers took a major step downward, providing access for scientists and explorers to a depth range formerly available only to commercial and military divers with massive equipment systems. Dives to depths of 80 to 100 msw are now routine for many divers. A major aspect of this capability is the creative application of the properties of different inert gases and gas mixtures and the judicious use of oxygen to hasten decompression. The leading benefit of alien gases is the use of helium to reduce narcosis; narcosis makes diving to such depths with air both unsafe and ineffective. Diving beyond the "air range" of 40 or so msw immediately invokes the need for sophisticated decompression techniques; it was the development of procedures for managing these decompressions that opened up this category of diving. Decompression involves not only calculating or otherwise determining the profile to be followed, but also managing the necessary gas logistics, oxygen exposure, thermal protection, and other endurance factors, and having a place to do the decompression. The latter task may be assisted by a variety of semi-dry stations or "habitats" or by drifting in a controlled way in the open sea. Future developments are sure to include more efficient decompressions by the incorporation of empirical findings such as the benefit of deeper stops
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