Hyperbaric Oxygen Therapy Emergencies.

Emergent indications for HBO2 are not only for some of the most serious conditions, but also may be the only modality to directly target the patient's pathophysiology. They are to begin emergently or urgently, but may be limited by either the instability of the patient's condition or transfer logistics. Often these emergent treatments involve several treatments in the first 24 hours for best outcomes. If one considers the effects of HBO2 upon the body while breathing 100% oxygen at pressure many benefits become evident. This article will concisely review hyperbaric oxygen's emergent indications.

A novel device for air removal from vascular access line: a bench study.

Efficient air removal from a vascular access line is a key step to prevent air embolism. Existing devices, especially for rapid infusers, are far from optimum. In this study, we developed a novel device, vascular access line air removal device (VALARD), and compared its efficiency of air removal and pause time of forward bulk flow with a commonly used device, the Belmont pump. Part I experiment, saline was infused at a forward bulk flow rate of 250, 500, and 750 mL/min. Meanwhile, air was introduced into the infusion line at a rate of 5, 10, and 15 mL/min for each bulk flow rate. Air bubbles > 10 µL downstream from either the VALARD or the Belmont pump and the fraction of pause time of the forward bulk flow were determined. Part II experiment, 120 mL of air was rapidly introduced into the VALARD at a bulk flow rate of about 500 mL/min. Air bubbles > 10 µL downstream from the VALARD, fraction of pause time of the forward bulk flow, and the transit time of the 120 mL of air at the working chamber were recorded. The VALARD: no air bubbles > 10 µL were detected during any tested combination of air injection and bulk flow rates without pause of forward flow. The Belmont pump: air bubbles > 10 µL were detected in 60% of the tests with pause of the forward flow. The VALARD eliminates air efficiently without pause of the forward bulk flow. Further clinical trials are needed to compare the VALARD with other devices and to assess its efficiency, safety, and user friendliness.

Venous gas emboli are involved in post-dive macro, but not microvascular dysfunction.

PURPOSE: Previous studies have shown vascular dysfunction of main conductance arteries and microvessels after diving. We aim to evaluate the impact of bubble formation on vascular function and haemostasis. To achieve this, we used a vibration preconditioning to influence bubble levels without changing any other parameters linked to the dive. METHODS: Twentty-six divers were randomly assigned to one of three groups: (1) the "vibrations-dive" group (VD; n = 9) was exposed to a whole-body vibration session 30 min prior the dive; (2) the "diving" group (D; n = 9) served as a control for the effect of the diving protocol; (3) The "vibration" protocol (V; n = 8) allowed us to assess the effect of vibrations without diving. Macro- and microvascular function was assessed for each subject before and after the dive, subsequently. Bubble grades were monitored with Doppler according to the Spencer grading system. Blood was taken before and after the protocol to assess any change of platelets or endothelial function. RESULTS: Bubble formation was lower in the VD than the diving group. The other measured parameters remained unchanged after the "vibration" protocol alone. Diving alone induced macrovascular dysfunction, and increased PMP and thrombin generation. Those parameters were no longer changed in the VD group. Conversely, a microvascular dysfunction persists despite a significant decrease of circulating bubbles. CONCLUSIONS: Finally, the results of this study suggest that macro- but not microvascular impairment results at least partly from bubbles, possibly related to platelet activation and generation of pro-coagulant microparticles.

Should Air Bubble Detectors Be Used to Quantify Microbubble Activity during Cardiopulmonary Bypass?

Air bubble detectors (ABDs) are utilized during cardiopulmonary bypass (CPB) to protect against massive air embolism. Stockert (Munich, Germany) ABD quantify microbubbles >300 µm; however, their reliability has not been reported. The aim of this study was to assess the reliability of the microbubble data from the ABD with the SIII and S5 heart-lung machines. Microbubble counts from the ABD with the SIII (SIII ABD) and S5 (S5 ABD) were measured simultaneously with the emboli detection and classification (EDAC) quantifier in 12 CPB procedures using two EDAC detectors and two ABDs in series in the arterial line. Reliability was assessed by the Spearman correlation co-efficient (r) between measurements for each detector type, and between each ABD and EDAC detector for counts >300 µm. No correlation was found between the SIII ABD (r = .008, p = .793). A weak negative correlation was found with the S5 ABD (r = -.16, p < .001). A strong correlation was found between the EDAC detectors (SIII; r = .958, p < .001), (S5; r = .908, p < .001). With counts >300 µm, the SIII ABDs showed a correlation of small-medium effect size between EDAC detectors and ABD1 (r = .286, p < .001 [EDAC1], r = .347, p < .001 [EDAC2]). There was no correlation found between ABD2 and either EDAC detector (r = .003, p = .925 (EDAC1), r = .003, p = .929 [EDAC2]). A correlation between EDAC and the S5 ABD, was not able to be determined due to the low bubble count detected by the EDAC >300 µm. Both SIII ABD and S5 ABD were found to be unreliable for quantification of microbubble activity during CPB in comparison with the EDAC. These results highlight the importance of ensuring that data included in the CPB report is accurate and clinically relevant, and suggests that microbubble counts from devices such as the SIII ABD and S5 ABD should not be reported.

Relationships between plasma lipids, proteins, surface tension and post-dive bubbles.

Decompression sickness (DCS) in divers is caused by bubbles of inert gas. When DCS occurs, most bubbles can be found in the venous circulation: venous gas emboli (VGE). Bubbles are thought to be stabilized by low molecular weight surfactant reducing the plasma-air surface tension (γ). Proteins may play a role as well. We studied the interrelations between these substances, γ and VGE, measured before and after a dry dive simulation. VGE of 63 dive simulations (21-msw/40-minute profile) of 52 divers was examined 40, 80, 120 and 160 minutes after surfacing (precordial Doppler method) and albumin, total protein, triglycerides, total cholesterol and free fatty acids were determined pre- and post-exposure. To manipulate blood plasma composition, half of the subjects obtained a fat-rich breakfast, while the other half got a fat-poor breakfast pre-dive. Eleven subjects obtained both. VGE scores measured with the precordial Doppler method were transformed to the logarithm of Kisman Integrated Severity Scores. With statistical analysis, including (partial) correlations, it could not be established whether γ as well as VGE scores are related to albumin, total protein or total cholesterol. With triglycerides and fatty acids correlations were also lacking, despite the fact that these compounds varied substantially. The same holds true for the paired differences between the two exposures of the 11 subjects. Moreover, no correlation between surface tension and VGE could be shown. From these findings and some theoretical considerations it seems likely that proteins lower surface tension rather than lipids. Since the findings are not in concordance with the classical surfactant hypothesis, reconsideration seems necessary.

High intensity cycling before SCUBA diving reduces post-decompression microparticle production and neutrophil activation.

BACKGROUND: Venous gas emboli (VGE) have traditionally served as a marker for decompression stress after SCUBA diving and a reduction in bubble loads is a target for precondition procedures. However, VGE can be observed in large quantities with no negative clinical consequences. The effect of exercise before diving on VGE has been evaluated with mixed results. Microparticle (MP) counts and sub-type expression serve as indicators of vascular inflammation and DCS in mice. The goal of the present study is to evaluate the effect of anaerobic cycling (AC) on VGE and MP following SCUBA diving. METHODS: Ten male divers performed two dives to 18 m for 41 min, one dive (AC) was preceded by a repeated-Wingate cycling protocol; a control dive (CON) was completed without exercise. VGE were analyzed at 15, 40, 80, and 120 min post-diving. Blood for MP analysis was collected before exercise (AC only), before diving, 15 and 120 min after surfacing. RESULTS: VGE were significantly lower 15 min post-diving in the AC group, with no difference in the remaining measurements. MPs were elevated by exercise and diving, however, post-diving elevations were attenuated in the AC dive. Some markers of neutrophil elevation (CD18, CD41) were increased in the CON compared to the AC dive. CONCLUSIONS: The repeated-Wingate protocol resulted in an attenuation of MP counts and sub-types that have been related to vascular injury and DCS-like symptoms in mice. Further studies are needed to determine if MPs represent a risk factor or marker for DCS in humans.

Can the oxygenator screen filter reduce gaseous microemboli?

Gaseous microemboli (GME) define small bubbles as < 200 microm in size. GME are reported to increase morbidity after cardiopulmonary bypass (CPB) and cardiac surgery. To prevent intrusion of GME into the systemic circulation during CPB, arterial line filtration is generally recommended. New trends in oxygenator design promote location of arterial filtration as an integral part of the oxygenator housing. The present experimental study aimed to evaluate the GME removal properties of an integrated arterial screen filter in a standard microporous oxygenator. The GME properties of Terumo Capiox FX25 with an integrated arterial screen filter was assessed in an experimental setup and compared with Capiox RX25, in which no arterial screen filter is present. A blood analog prime solution was recirculated using a roller pump at 4 and 6 L per minute flow rate, respectively, through a customized CPB circuit comprising oxygenator, reservoir, and connecting tubing. A controlled volume of air was introduced into the circuit. The GME activity was measured and computed using a Gampt BCC200 ultrasonic device placing one probe at the venous inlet and one other at the arterial outlet of the oxygenator. Transmembrane delta values of GME activity were used to calculate the removal efficacy based on counts and volume of GME. Use of screen filtration reduced the GME volume by 99.1% +/- .1% compared with 98.0% +/- .1% for controls at 4 L/min flow rate (p < .001). At 6 L/min, the reduction was 97.9% +/- .1% compared with 97.0% +/- .1% (p < .001). In contrast, the reduction of GME counts was less effective after screen filtration compared with controls: 89.6 +/- .6% versus 91.4 +/- .4% at 4 L/min and 55.6% +/- 1.6% versus 76.0% +/- 1.4% at 6 L/min, respectively (p < .001). The tested oxygenator with incorporated arterial screen filter reduced GME activity based on the calculated volume at the same time as counts of GME increased.

Bubbles in live-stranded dolphins.

Bubbles in supersaturated tissues and blood occur in beaked whales stranded near sonar exercises, and post-mortem in dolphins bycaught at depth and then hauled to the surface. To evaluate live dolphins for bubbles, liver, kidneys, eyes and blubber-muscle interface of live-stranded and capture-release dolphins were scanned with B-mode ultrasound. Gas was identified in kidneys of 21 of 22 live-stranded dolphins and in the hepatic portal vasculature of 2 of 22. Nine then died or were euthanized and bubble presence corroborated by computer tomography and necropsy, 13 were released of which all but two did not re-strand. Bubbles were not detected in 20 live wild dolphins examined during health assessments in shallow water. Off-gassing of supersaturated blood and tissues was the most probable origin for the gas bubbles. In contrast to marine mammals repeatedly diving in the wild, stranded animals are unable to recompress by diving, and thus may retain bubbles. Since the majority of beached dolphins released did not re-strand it also suggests that minor bubble formation is tolerated and will not lead to clinically significant decompression sickness.

The sitting position during neurosurgical procedures does not influence serum biomarkers of pulmonary parenchymal injury.

BACKGROUND: The sitting position during neurosurgical operations predisposes to air penetration through veins and the movement of the air through the pulmonary circulation. Contact of an air bubble with the endothelium can lead to acute lung injury. The presence of specific pulmonary proteins in the plasma such as surfactant protein D (SP-D) and Clara cell protein (CC16) is a biomarker of damaging processes at the air-blood barrier. The aim of our study was to examine the hypothesis that the level of investigated pulmonary biomarkers in plasma is higher in patients operated on in the sitting position. METHODS: The study included patients undergoing planned neurosurgical operations, who were divided into two groups: the sitting group (40 patients, operated on in the sitting position) and the supine group (24 patients, operated in the supine position). After the operation blood samples were drawn, centrifuged, frozen and stored until analyses were conducted. The determination of the SP-D and CC16 levels was performed using an ELISA test. Air embolism (VAE) was defined as a sudden drop in etCO2 of more than 2 mmHg and the presence of air bubbles in the aspirated blood from the central cannula. In all patients, the number of hospitalization days in the postoperative period was calculated. RESULTS: There were no differences in the average levels of SP-D between the groups (the mean in the sitting group was 95.56 ng/mL and the mean in the supine group was 101.21 ng/mL). The average levels of CC16 were similar in both groups as well (6.56 ng/mL in the sitting group and 6.79 ng/mL in the supine group). There was a statistically significant positive correlation between SP-D and CC16 values in both groups. VAE was diagnosed clinically in 12.5% of cases in the sitting group without a significant increase in SP-D and CC16 levels. On average, patients in both groups were discharged from the hospital within 9 days of surgery. CONCLUSION: The sitting position and intraoperative VAE during neurosurgical procedures do not affect the concentration of plasma biomarkers of pulmonary parenchymal injury such as SP-D and CC16.

Venous gas embolism after an open-water air dive and identical repetitive dive.

Decompression tables indicate that a repetitive dive to the same depth as a first dive should be shortened to obtain the same probability of occurrence of decompression sickness (pDCS). Repetition protocols are based on small numbers, a reason for re-examination. Since venous gas embolism (VGE) and pDCS are related, one would expect a higher bubble grade (BG) of VGE after the repetitive dive without reducing bottom time. BGs were determined in 28 divers after a first and an identical repetitive air dive of 40 minutes to 20 meters of sea water. Doppler BG scores were transformed to log number of bubbles/cm2 (logB) to allow numerical analysis. With a previously published model (Model2), pDCS was calculated for the first dive and for both dives together. From pDCS, theoretical logBs were estimated with a pDCS-to-logB model constructed from literature data. However, pDCS the second dive was provided using conditional probability. This was achieved in Model2 and indirectly via tissue saturations. The combination of both models shows a significant increase of logB after the second dive, whereas the measurements showed an unexpected lower logB. These differences between measurements and model expectations are significant (p-values < 0.01). A reason for this discrepancy is uncertain. The most likely speculation would be that the divers, who were relatively old, did not perform physical activity for some days before the first dive. Our data suggest that, wisely, the first dive after a period of no exercise should be performed conservatively, particularly for older divers.

In vitro evaluation of gaseous microemboli handling of cardiopulmonary bypass circuits with and without integrated arterial line filters.

The delivery of gaseous microemboli (GME) by the cardiopulmonary bypass circuit should be minimized whenever possible. Innovations in components, such as the integration of arterial line filter (ALF) and ALFs with reduced priming volumes, have provided clinicians with circuit design options. However, before adopting these components clinically, their GME handling ability should be assessed. This study aims to compare the GME handling ability of different oxygenator/ALF combinations with our currently utilized combination. Five commercially available oxygenator/ALF combinations were evaluated in vitro: Terumo Capiox SX25RX and Dideco D734 (SX/D734),Terumo Capiox RX25R and AF125 (RX/AF125), Terumo FX25R (FX), Sorin Synthesis with 102 microm reservoir filter (SYN102), and Sorin Synthesis with 40 microm reservoir filter (SYN40). GME handling was studied by introducing air into the venous return at 100 mL/min for 60 seconds under two flow/ pressure combinations: 3.5 L/min, 150 mmHg and 5 L/min, 200 mmHg. Emboli were measured at three positions in the circuit using the Emboli Detection and Classification (EDAC) Quantifier and analyzed with the General Linear Model. All circuits significantly reduced GME. The SX/D734 and SYN40 circuits were most efficient in GME removal whilst the SYN102 handled embolic load (count and volume) least efficiently (p < .001). A greater number of emboli <70 microm were observed for the SYN102, FX and RX/AF125 circuits (p < .001). An increase in embolic load occurred with higher flow/pressure in all circuits (p < .001). The venous reservoir significantly influences embolic load delivered to the oxygenator (p < .001). The majority of introduced venous air was removed; however, significant variation existed in the ability of the different circuits to handle GME. Venous reservoir design influenced the overall GME handling ability. GME removal was less efficient at higher flow and pressure, and for smaller sized emboli. The clinical significance of reducing GME requires further investigation.

An explicitly multi-component arterial gas embolus dissolves much more slowly than its one-component approximation.

We worked out the growth and dissolution rates of an arterial gas embolism (AGE), to illustrate the evolution over time of its size and composition, and the time required for its total dissolution. We did this for a variety of breathing gases including air, pure oxygen, Nitrox and Heliox (each over a range of oxygen mole fractions), in order to assess how the breathing gas influenced the evolution of the AGE. The calculations were done by numerically integrating the underlying rate equations for explicitly multi-component AGEs, that contained a minimum of three (water, carbon dioxide and oxygen) and a maximum of five components (water, carbon dioxide, oxygen, nitrogen and helium). The rate equations were straight-forward extensions of those for a one-component gas bubble. They were derived by using the Young-Laplace equation and Dalton's law for the pressure in the AGE, the Laplace equation for the dissolved solute concentration gradients in solution, Henry's law for gas solubilities, and Fick's law for diffusion rates across the AGE/arterial blood interface. We found that the 1-component approximation, under which the contents of the AGE are approximated by its dominant component, greatly overestimates the dissolution rate and underestimates the total dissolution time of an AGE. This is because the 1-component approximation manifestly precludes equilibration between the AGE and arterial blood of the inspired volatile solutes (O2, N2, He) in arterial blood. Our calculations uncovered an important practical result, namely that the administration of Heliox, as an adjunct to recompression therapy for treating a suspected N2-rich AGE must be done with care. While Helium is useful for preventing nitrogen narcosis which can arise in aggressive recompression therapy wherein the N2 partial pressure can be quite high (e.g.∼5 atm), it also temporarily expands the AGE, beyond the expansion arising from the use of Oxygen-rich Nitrox. For less aggressive recompression therapy wherein nitrogen narcosis is not a significant concern, Oxygen-rich Nitrox is to be preferred, both because it does not temporarily expand the AGE as much as Heliox, and because it is much cheaper and more conservation-minded.

Decompression to altitude: assumptions, experimental evidence, and future directions.

Although differences exist, hypobaric and hyperbaric exposures share common physiological, biochemical, and clinical features, and their comparison may provide further insight into the mechanisms of decompression stress. Although altitude decompression illness (DCI) has been experienced by high-altitude Air Force pilots and is common in ground-based experiments simulating decompression profiles of extravehicular activities (EVAs) or astronauts' space walks, no case has been reported during actual EVAs in the non-weight-bearing microgravity environment of orbital space missions. We are uncertain whether gravity influences decompression outcomes via nitrogen tissue washout or via alterations related to skeletal muscle activity. However, robust experimental evidence demonstrated the role of skeletal muscle exercise, activities, and/or movement in bubble formation and DCI occurrence. Dualism of effects of exercise, positive or negative, on bubble formation and DCI is a striking feature in hypobaric exposure. Therefore, the discussion and the structure of this review are centered on those highlighted unresolved topics about the relationship between muscle activity, decompression, and microgravity. This article also provides, in the context of altitude decompression, an overview of the role of denitrogenation, metabolic gases, gas micronuclei, stabilization of bubbles, biochemical pathways activated by bubbles, nitric oxide, oxygen, anthropometric or physiological variables, Doppler-detectable bubbles, and potential arterialization of bubbles. These findings and uncertainties will produce further physiological challenges to solve in order to line up for the programmed human return to the Moon, the preparation for human exploration of Mars, and the EVAs implementation in a non-zero gravity environment.

Selective vulnerability of the inner ear to decompression sickness in divers with right-to-left shunt: the role of tissue gas supersaturation.

Inner ear decompression sickness has been strongly associated with the presence of right-to-left shunts. The implied involvement of intravascular bubbles shunted from venous to arterial circulations is inconsistent with the frequent absence of cerebral symptoms in these cases. If arterial bubbles reach the labyrinthine artery, they must also be distributing widely in the brain. This discrepancy could be explained by slower inert gas washout from the inner ear after diving and the consequent tendency for arterial bubbles entering this supersaturated territory to grow because of inward diffusion of gas. Published models for inner ear and brain inert gas kinetics were used to predict tissue gas tensions after an air dive to 4 atm absolute for 25 min. The models predict half-times for nitrogen washout of 8.8 min and 1.2 min for the inner ear and brain, respectively. The inner ear remains supersaturated with nitrogen for longer after diving than the brain, and in the simulated dive, for a period that corresponds with the latency of typical cases. It is therefore plausible that prolonged inner ear inert gas supersaturation contributes to the selective vulnerability of the inner ear to short latency decompression sickness in divers with right-to-left shunt.

Venous air embolism induces both platelet dysfunction and thrombocytopenia.

BACKGROUND: In vitro, air bubbles can induce platelet activation and platelet to air bubble binding. We therefore tested in vivo the hypothesis that venous air embolism (VAE) induces (1) platelet dysfunction and (2) thrombocytopenia. METHODS: Adult swine (60.8+/-3.9 kg; n=8) were anaesthetized, mechanically ventilated, and placed in a semi-upright position. Air boli (0.5-80 ml) were injected randomly via an ear vein, and arterial blood was sampled after cumulative air dosages of 0, 80, 160, and 240 ml. Coagulation was assessed by impedance aggregometry, rotational thrombelastometry, whole blood count, plasmatic coagulation variables, and fibrinogen, d-dimer, protein C, and antithrombin plasma concentrations, respectively. RESULTS: VAE induced a 47% decrease in platelet count (303 vs. 160 nl(-1); P<0.001) over the dose range assessed, with haematocrit being unaltered. Furthermore, VAE-impaired platelet aggregation induced by adenosine diphosphate, arachidonic acid, collagen, and the thromboxan analogue U46619 over the dose range assessed independent of thrombocytopenia. (P<0.05 vs. baseline). In contrast, rotational thrombelastometry alone was quite insensitive in detecting VAE-induced coagulation changes, showing only at near lethal air dosages a prolonged clot formation time following activation with tissue factor, contact activator, and during spontaneous coagulation (P<0.05 vs. baseline). CONCLUSIONS: VAE induces both a dose-dependent decrease in platelet count and a marked decrease in platelet aggregation, independent of thrombocytopenia (P<0.05 vs. baseline).

Nitrogen Washout and Venous Gas Emboli During Sustained vs. Discontinuous High-Altitude Exposures.

INTRODUCTION: The frequency of long-duration, high-altitude missions with fighter aircraft is increasing, which may increase the incidence of decompression sickness (DCS). The aim of the present study was to compare decompression stress during simulated sustained high-altitude flying vs. high-altitude flying interrupted by periods of moderate or marked cabin pressure increase.METHODS: The level of venous gas emboli (VGE) was assessed from cardiac ultrasound images using the 5-degree Eftedal-Brubakk scale. Nitrogen washout/uptake was measured using a closed-circuit rebreather. Eight men were investigated in three conditions: one 80-min continuous exposure to a simulated cabin altitude of A) 24,000 ft, or four 20-min exposures to 24,000 ft interspersed by three 20-min intervals at B) 20,000 ft or C) 900 ft.RESULTS: A and B induced marked and persistent VGE, with peak bubble scores of [median (range)]: A: 2.5 (1-3); B: 3.5 (2-4). Peak VGE score was less in C [1.0 (1-2), P < 0.01]. Condition A exhibited an initially high and exponentially decaying rate of nitrogen washout. In C the washout rate was similar in each period at 24,000 ft, and the nitrogen uptake rate was similar during each 900-ft exposure. B exhibited nitrogen washout during each period at 24,000 ft and the initial period at 20,000 ft, but on average no washout or uptake during the last period at 20,000 ft.DISCUSSION: Intermittent reductions of cabin altitude from 24,000 to 20,000 ft do not appear to alleviate the DCS risk, presumably because the pressure increase is not sufficient to eliminate VGE. The nitrogen washout/uptake rate did not reflect DCS risk in the present exposures.Ånell R, Grönkvist M, Eiken O, Gennser M. Nitrogen washout and venous gas emboli during sustained vs. discontinuous high-altitude exposures. Aerosp Med Hum Perform. 2019; 90(6):524-530.

Cardiac troponin I elevation after orogenital sex during pregnancy.

BACKGROUND: Venous air embolism due to orogenital sex in pregnancy is an uncommon clinical event. CASE: A previously healthy, 29-week pregnant woman presented to the emergency room unconscious 1 hour after engaging in orogenital sex with her partner. The cardiology service was consulted due to troponin elevation. Assessment was that the patient had likely suffered an air embolism with associated troponin leak. CONCLUSION: Although a rare clinical event, air embolism from air insufflation of the vagina can result in troponin elevation and should be considered in the differential diagnosis in pregnant patients with a history of orogenital sex.

Blood platelet count and bubble formation after a dive to 30 msw for 30 min.

INTRODUCTION: Previous human studies reported that platelet count (PC) is decreased following decompression. Platelet aggregation and adherence to the bubble surface has been demonstrated in severe decompression sickness (DCS). The present study was designed to clarify the relationship between post-dive changes in blood PC and the level of bubble formation in divers. METHODS: There were 40 healthy experienced divers who were assigned to 1 experimental group (N = 30) with an open-sea air dive to 30 msw for 30 min in field conditions and 1 control group (N = 10) without hyperbaric exposure. Bubble grades were monitored with a pulsed Doppler according to the Spencer scale and Kissman integrated severity score (KISS). Blood samples for red blood cell counts (RBC), hematocrit (Hct), and PC were taken 1 h before and after exposure in two groups. RESULTS: None of the divers developed any signs of DCS. In two groups, the results showed significant increase in RBC count and Hct related with hemoconcentration and no change in PC. Divers with a high KISS score (39 +/- 5.8; mean +/- SD) presented a significantly more pronounced percent fall in PC than divers with a lower KISS score. We found a significant correlation between the percent fall in PC after a dive and the bubble KISS score. DISCUSSION: The present study highlighted a relationship between the post-dive decrease in PC and the magnitude of bubble level after decompression. Our primary result is that the post-dive decrease in PC could be a predictor of decompression severity after diving.

Recompression during decompression and effects on bubble formation in the pig.

INTRODUCTION: There is a relationship between gas bubble formation in the vascular system and serious decompression sickness. Hence, control of the formation of vascular bubbles should allow safer decompression procedures. METHODS: There were 12 pigs that were randomly divided into an experimental group (EXP) and a control group (CTR) of 6 animals each. The pigs were compressed to 500 kPa (5 ATA) in a dry hyperbaric chamber and held for 90 min bottom time breathing air. CTR animals were decompressed according to a modified USN dive profile requiring four stops. EXP followed the same profile except that a 5-min recompression of 50 kPa (0.5 ATA) was added at the end of each of the last three decompression stops before ascending to the next stop depth. RESULTS: All CTR animals developed bubbles, compared with only one animal in EXP. The number of bubbles detected during and after the dive was 0.02 +/- 0.02 bubbles x cm(-2) in CTR, while the number of bubbles detected in EXP were 0.0009 +/- 0.005 bubbles x cm(-2); the difference was highly significant. CONCLUSION: By brief recompression during late decompression stops, the amount of bubbles was reduced. Our findings give further support for a gas phase model of decompression.

Intravenous perfluorocarbon emulsion increases nitrogen washout after venous gas emboli in rabbits.

Intravenous perfluorocarbon emulsion (IV-PFC) has been shown to provide hemodynamic protection from gas embolism (Venous-VGE or arterial-AGE). The objective of this study was to investigate the mechanism of PFC protection from controlled VGE by quantifying the effects of IV-PFC emulsion on pulmonary elimination of nitrogen (N2). All rabbits received an intravenous pretreatment of PFC emulsion (Oxygent, 2.7 g/kg) or saline, then either a continuous room air infusion (0.25 ml/kg for 10 minutes) or a bolus of air (0.8 ml/kg within 10 seconds) through the femoral vein. Expiratory N2 peaked higher with PFC infusion immediately after air injection. The recovery to baseline of end tidal N2 was faster for PFC-treated animals (40 +/- 4.7 vs. 58 +/- 6.5 minutes). In PFC-treated animals, expired CO2, O2, arterial pressure and central venous pressure returned to baseline faster than the saline group. This study demonstrated that PFC increased pulmonary N2 washout. Correspondingly, PFC treatment better preserved the animals' hemodynamics after VGE injury. The use of IV-PFC promises to be a breakthrough non-recompression therapy for gas embolism in the treatment of Decompression Sickness (DCS) and in surgery.