Article

Venous and Arterial Bubbles at Rest after No-Decompression Air Dives

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Abstract

During SCUBA diving, breathing at increased pressure leads to a greater tissue gas uptake. During ascent, tissues may become supersaturated, and the gas is released in the form of bubbles that typically occur on the venous side of circulation. These venous gas emboli (VGE) are usually eliminated as they pass through the lungs, although their occasional presence in systemic circulation (arterialization) has been reported and it was assumed to be the main cause of the decompression sickness. The aims of the present study were to assess the appearance of VGE after air dives where no stops in coming to the surface are required and to assess their potential occurrence and frequency in the systemic circulation. Twelve male divers performed six dives with 3 d of rest between them following standard no-decompression dive procedures: 18/60, 18/70, 24/30, 24/40, 33/15, and 33/20 (the first value indicates depth in meters of sea water and the second value indicates bottom time in minutes). VGE monitoring was performed ultrasonographically every 20 min for 120 min after surfacing. Diving profiles used in this study produced unexpectedly high amounts of gas bubbles, with most dives resulting in grade 4 (55/69 dives) on the bubble scale of 0-5 (no to maximal bubbles). Arterializations of gas bubbles were found in 5 (41.7%) of 12 divers and after 11 (16%) of 69 dives. These VGE crossovers were only observed when a large amount of bubbles was concomitantly present in the right valve of the heart. Our findings indicate high amounts of gas bubbles produced after no-decompression air dives based on standardized diving protocols. High bubble loads were frequently associated with the crossover of VGE to the systemic circulation. Despite these findings, no acute decompression-related pathology was detected.

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... Arterialization may also occur in individuals who do not possess PFO, when the quantity of VGE overwhelms the ability of the pulmonary circuit to trap and eliminate these bubbles (4). Investigations of arterialization at rest show incidents rates to range from 13 to 26% (11,16,18). Recent studies have used contrast bubbles to investigate intrapulmonary arterial-venous anastamoses (IPAVA) that allow blood to bypass the pulmonary microcirculation (24). ...
... Within 8 -15 min after surfacing, the divers were placed in the supine position where an ultrasonic probe connected to a Vivid q echographic scanner (GE, Milwaukee, WI) was used to obtain a clear apical four-chamber view of the heart. This position was monitored continuously until 30 min postsurfacing, and initial bubble images were recorded and scored on a scale of 0 to 5, with 4 being subdivided into 4A, 4B, and 4C, according to the method described by Eftedal and Brubakk (8), and later modified by Ljubkovic et al. (16). Next the subject was moved to a seating position where a bubble score was obtained again after approximately 2-3 min to observe the effect of the posture change on the bubble score. ...
... Regardless of these limitations, 65% of divers arterialized (exercise and rest) in the postdive period of our study. This proportion is much greater than is found in studies that examine these parameters for divers at rest, which range between 0 and 39% (16,18). Another study by Gerriets et al. (11) observed arterialization in 7 of 13 dives where VGE were present; however, five of these incidences were associated with PFO. ...
Article
Arterialization of venous gas emboli (VGE) after decompression from scuba diving has traditionally been associated with pulmonary barotraumas or cardiac defects such as the patent foramen ovale (PFO). Recent studies have demonstrated the right to left passage of emboli through intra-pulmonary arterial-venous anasthomoses (IPAVA) that allow blood to bypass the pulmonary microcirculation. These passages open up during exercise and the aim of this study is to see if exercise in a postdiving period increases the incidence of arterialization. After completing a dive, PFO-negative test subjects were monitored via trans-thoracic echocardiography (TTE) for bubble grade at rest. Subjects then completed an incremental cycle ergometry test to exhaustion under continuous TTE observation. Exercise was suspended if arterialization was observed and resumed when the arterialization cleared. Exercise continued and supplemental oxygen was provided and the time for arterialization to clear was compared to the first round when subjects were breathing room air. Out of 23 subjects, 3 arterialized at rest, 12 arterialized with exercise and 8 did not arterialize at all even during maximal exercise. The time for arterialization to clear with oxygen was significantly shorter than without (p = 0.035). Exercise after diving increased the incidence of arterialization from 13% at rest to 52%. This study shows that individuals are capable of arterializing through IPAVA and that the intensity at which these opens varies by individual. Basic activities associated with SCUBA diving such as surface swimming or walking with heavy equipment may be enough to allow the passage of VGE through IPAVA.
... Gas bubbles that occur after supersaturation and do not cause any symptoms are called "silent bubbles" and can be detected by Doppler imaging in venous circulation (13,16,17). Bubbles, depending on their numbers and sizes, can cause clinical signs and symptoms of DCS by causing mild or severe damage in any part of the body. ...
... Bubbles, depending on their numbers and sizes, can cause clinical signs and symptoms of DCS by causing mild or severe damage in any part of the body. DCS is a systemic disease with complex pathogenesis including the development of mechanical distortion, ischemia, hypoxia, vascular occlusion, increased capillary permeability with endothelial damage, plasma extravasation, hemoconcentration, platelet activation and aggregation, leukocyte-endothelial adhesion, ischemia reperfusion damage due to mechanical, embolic and biochemical effects of bubbles (13,14,17). It is seen in pilots, astronauts, compressed-air (caisson) workers and known as "bends" colloquially. ...
... Silent bubbles can also be seen after dives made according to the rules. In the presence of DCS, bubbles are usually found in high amounts (13,16,17). In a study conducted by the Divers Alert Network (DAN), venous gas bubbles were found with Doppler in 91% of divers after repeated dives at different depths, however DCS was not seen in any diver (19). ...
... Gas bubbles that occur after supersaturation and do not cause any symptoms are called "silent bubbles" and can be detected by Doppler imaging in venous circulation (13,16,17). Bubbles, depending on their numbers and sizes, can cause clinical signs and symptoms of DCS by causing mild or severe damage in any part of the body. ...
... Bubbles, depending on their numbers and sizes, can cause clinical signs and symptoms of DCS by causing mild or severe damage in any part of the body. DCS is a systemic disease with complex pathogenesis including the development of mechanical distortion, ischemia, hypoxia, vascular occlusion, increased capillary permeability with endothelial damage, plasma extravasation, hemoconcentration, platelet activation and aggregation, leukocyte-endothelial adhesion, ischemia reperfusion damage due to mechanical, embolic and biochemical effects of bubbles (13,14,17). It is seen in pilots, astronauts, compressed-air (caisson) workers and known as "bends" colloquially. ...
... Silent bubbles can also be seen after dives made according to the rules. In the presence of DCS, bubbles are usually found in high amounts (13,16,17). In a study conducted by the Divers Alert Network (DAN), venous gas bubbles were found with Doppler in 91% of divers after repeated dives at different depths, however DCS was not seen in any diver (19). ...
Article
Full-text available
Although patent foramen ovale (PFO) was anatomically depicted in 1513 by Leonardo da Vinci and described as a thromboembolism route in 1877, it has been ignored for a long time as a potential way to produce pathological conditions. The unifying hypothesis associated with multiple clinical issues, such as cryptogenic stroke, migraine and decompression sickness is that a particle, inert gas bubbles or chemical substance in the venous circulation bypasses the lungs and enters to the systemic circulation via PFO. In this review, current data on the status of PFO in diving medicine are discussed.
... 10 SCUBA diving can result in the formation of venous gas emboli, even when SCUBA divers adhere to recreational dive ascension rates and perform appropriate decompression stops on the ascent or perform no-decompression dives. 11 Due to the presence of a PFO, these venous gas emboli have the potential to bypass the pulmonary circuit and enter systemic and cerebral circulations resulting in neurological decompression symptoms. 11 Percutaneous closure of PFO has been shown to reduce the occurrence of SCUBA divers experiencing DCS, further supporting the link between the presence of PFO and DCS. 12 The prevalence of PFO has not been previously investigated in apnea diversa pervasive profession/sport, characterized by transient bouts of hydrostatic-and arterial hypertension subsequent to peripheral vasoconstriction. ...
... 11 Due to the presence of a PFO, these venous gas emboli have the potential to bypass the pulmonary circuit and enter systemic and cerebral circulations resulting in neurological decompression symptoms. 11 Percutaneous closure of PFO has been shown to reduce the occurrence of SCUBA divers experiencing DCS, further supporting the link between the presence of PFO and DCS. 12 The prevalence of PFO has not been previously investigated in apnea diversa pervasive profession/sport, characterized by transient bouts of hydrostatic-and arterial hypertension subsequent to peripheral vasoconstriction. This combination also increases central venous volume during deep dives, leading to an increase in central venous and right atrial pressures. ...
Article
Objectives During apnea diving, a patent foramen ovale (PFO) may function as a pressure relief valve under conditions of high pulmonary pressure, preserving left-ventricular output. However, PFO prevalence in apneic divers has not been previously reported. We aimed to determine the prevalence of PFO in apneic divers compared to non-diver controls. Design Cross Sectional Method Apnea divers were recruited from a training camp in Cavtat, Croatia and the diving community of Split, Croatia. Controls were recruited from the population of Split, Croatia and Eugene, Oregon, USA. Participants were instrumented with an intravenous catheter and underwent PFO screening utilizing transthoracic saline contrast echocardiography with and without the release of a Valsalva maneuver. Appearance of microbubbles in the left heart within 3 cardiac cycles indicated the presence of PFO. Lung function was measured with spirometry. Comparison of PFO prevalence was conducted using a chi-square analysis, p <0.05. Results Apnea divers had a significantly higher prevalence of PFO (19 of 36, 53%) compared to Controls (9 of 36, 25%)(X² (1, N = 72) = 5.844, p = .0156). Conclusion Why PFO prevalence is greater in apnea divers remains unknown, though hyperbaria during an apnea dive results in a translocation of blood volume centrally with a concomitant reduction in lung volume and alveolar hypoxia during ascent results in hypoxic pulmonary vasoconstriction. In combination, these conditions increase pulmonary arterial pressure, subsequently increasing right-atrial pressure allowing for right-to-left blood flow through a PFO which may be beneficial for preserving cardiac output and reducing capillary hydrostatic forces.
... Therefore, it remains to be determined whether other factors, such as risky diving behavior, body mass index (BMI), age, or sex, play a more important role [3][4][5][6]. On the other hand, reports that nitrogen bubbles can be detected in venous blood, even after a single conservative dive, raised the concern that divers with a right-to-left shunt might suffer from DCS even without violating decompression regimen [7,8]. These unpredictable events have been termed unprovoked DCS and are a potential threat to millions of recreational divers worldwide. ...
... It is of note, that even after a properly performed recreational dive a small number of VGE may be detected. Ljubkovic et al. found VGE after 80% of single nodecompression air dives [8]. It has been debated whether an unprovoked DCS might occur in some of these divers. ...
Article
Full-text available
Background: Patent foramen ovale (PFO), male sex, age, and body mass index (BMI) were all identified as potential risk factors of decompression sickness (DCS). It has been debated whether PFO might cause unprovoked DCS (i.e. without violation of decompression procedure) due to paradoxical embolization of venous gas emboli. To date, there are no data on the incidence or risk factors of unprovoked DCS. This study sought to evaluate the risk factors of unprovoked DCS in recreational divers. Methods: A total of 489 consecutive divers were screened for PFO between January 2006 and January 2014 by means of transcranial Doppler. All patients were prospectively included in the study registry. Survival analysis techniques were used to assess for risk factors for unprovoked DCS. Age, sex, BMI, PFO presence, and grade were analyzed. The total sum of dives was used as a measure of time. Results: The group performed a total of 169,411 dives (mean 346±636). Thirty-six (7%) of the divers suffered from an unprovoked DCS. The frequency of PFO was 97.2% in divers with a history of unprovoked DCS and 35.5% in controls (p<0.001). There was no difference in sex, age, BMI, or total number of dives between the respective groups. In the adjusted Cox proportional hazards model, PFO grade 3 was a major risk factor for unprovoked DCS; there was a slight protective effect of increasing age. Conclusions: We demonstrated that a high-grade PFO was a major risk factor for unprovoked DCS in recreational scuba divers.
... These bubbles either cause local tissue damage or embolize through venous blood (3). Small quantities of venous gas bubbles are believed to be common after most scuba diving (4,5). Although most divers remain asymptomatic, symptoms may occur with high bubble load (pulmonary gas embolism) or may be due to paradoxical embolism (arterialization of bubbles) in a diver with a transient right-to-left shunt. ...
... To test the effect of catheter-based PFO closure on the reduction of arterial bubbles, decompression dives according to the U.S. Navy Air Decompression Procedure 1996 (18) were used. This decompression procedure was previously reported to generate significant amounts of venous and arterial bubbles but no acute DCS symptoms (5,19). Two dive profiles were used. ...
Article
Full-text available
Objectives This study sought to evaluate the effect of catheter-based patent foramen ovale (PFO) closure on the occurrence of arterial bubbles after simulated dives. Background PFO is a risk factor of decompression sickness in divers due to paradoxical embolization of bubbles. To date, the effectiveness of catheter-based PFO closure in the reduction of arterial bubbles has not been demonstrated. Methods A total of 47 divers (age 35.4 ± 8.6 years, 81% men) with a PFO (PFO group) or treated with a catheter-based PFO closure (closure group) were enrolled in this case-controlled observational trial. All divers were examined after a simulated dive in a hyperbaric chamber: 34 divers (19 in the PFO group, 15 in the closure group) performed a dive to 18 m for 80 min, and 13 divers (8 in the PFO group, 5 in the closure group) performed a dive to 50 m for 20 min. Within 60 min after surfacing, the presence of venous and arterial bubbles was assessed by transthoracic echocardiography and transcranial color-coded sonography, respectively. Results After the 18-m dive, venous bubbles were detected in 74% of divers in the PFO group versus 80% in the closure group (p = 1.0), and arterial bubbles were detected in 32% versus 0%, respectively (p = 0.02). After the 50-m dive, venous bubbles were detected in 88% versus 100%, respectively (p = 1.0), and arterial bubbles were detected in 88% versus 0%, respectively (p < 0.01). Conclusions No difference was observed in the occurrence of venous bubbles between the PFO and closure groups, but the catheter-based PFO closure led to complete elimination of arterial bubbles after simulated dives. (Nitrogen Bubble Detection After Simulated Dives in Divers With PFO and After PFO Closure; NCT01854281)
... Přesto i při dodržení těchto postupů v některých případech dojde k rozvoji DCS (nevyprovokovaná dekompresní příhoda). Malé množství dusíkových bublin vzniká běžně ve venózní krvi i po jednom ponoru při dodržení bezpečnostních předpisů (2,3). Většina takových příhod probíhá subklinicky, protože plicní kapilární filtr zachytí přítomné bubliny a umožní jejich postupné rozpuštění. ...
... Jako model dekompresního sestupu byl u kontrolní skupiny využit sestup do 18 m na 80 min (s dekompresní zastávkou po dobu 7 min v 3 m), který v naší práci generoval venózní bubliny u 74 % potápěčů a u 32 % potápěčů byly detekovány i bubliny arteriální. To je ve shodě s dříve popsaným faktem, že ke vzniku bublin dochází již po jednom ponoru i při dodržení dekompresního režimu (2,3). V kontrolní skupině došlo u jedné třetiny potápěčů s arteriálními bublinami k rozvoji příznaků DCS. ...
Article
Full-text available
Aim: The aim of this study was to compare the influence of transcatheter patent foramen ovale (PFO) closure and safe diving recommendations limiting bottom time and depth on the occurrence of arterial bubbles after simulated dives in a hyperbaric chamber. Methods: Forty-seven divers with a PFO were enrolled in this observational trial. Nineteen divers with PFO performed a decompression dive to 18m for 80 min (control group), 15 divers after a transcatheter PFO closure performed the same dive (group 1) and 13 divers with PFO performed a dive to the same depth for a non-decompression time of 51 min (group 2). In all divers venous and arterial bubbles were screened, venous bubbles by means of transthoracic echocardiography, arterial by means of transcranial Doppler ultrasonography. Results: Venous bubbles were detected in 74% divers in the control group, in 80% in group 1 (p=1.0) and in 31% in group 2 (p=0.03); arterial bubbles in 32% divers in control group, in 0% in group 1 (p=0.02), in 15% in group 2 (p=0.42). Conclusion: Safe diving recommendations avoiding decompression procedure led to the decrease in occurrence of venous bubbles but not the elimination of arterial bubbles in divers with PFO. Transcatheter PFO closure led to elimination of arterial bubbles. The results suggest that transcatheter PFO closure might be an effective treatment in prevention of DCS; the effectivity of the up-to-date safety recommendations used needs to be further tested, especially in longitudinal clinical studies.
... Obecně lze také snížit riziko vzniku bublin správnou přípravou na ponor (preconditio ning) pomocí hydratace a lehké fyzické zátěže bezprostředně před ponorem [27]. ficky detekovat i po běžných ponorech [7,8] (obr. 1). ...
... Při pobytu pod vodou dochází k ná růstu tlaku v pravé síni v důsledku redistri buce krve z periferie do hrudníku [17], potá pěči navíc v průběhu ponoru často opakovaně provádějí Valsalvův manévr (k vyrovnání tlaku ve středouší), v důsledku toho může dojít k intermitentnímu pravo levému zkratu skrze PFO. Výskyt určitého množství žilních bublin je přitom častý i po běžném rekreačním ponoru [8]. Proto se můžeme setkat u potá pěčů s PFO s projevy DCS i v případě, že ne došlo k porušení dekompresních pravidel [14]. ...
Article
Full-text available
Patent foramen ovale (PFO) is associated with increased risk of decompression sickness (DCS) in divers due to paradoxical embolization of nitrogen bubbles from the vein blood to the circulation through the PFO. Despite the high prevalence of PFO, many important questions, including optimal screening, risk stratification and management strategy, remain unanswered. Recently published data suggest possible effectiveness of PFO closure as well as conservative diving measures in preventing arterial gas embolization. This review aims to introduce the basic principles of physiology and patho-physiology of bubble formation and to summarize current literature on PFO and diving and review the possibilities of management of symptomatic divers.
... EMI were evaluated during a 'ground EMI test' as per avionic guidelines concerning the use of portable electronic devices on board aircrafts. 17 Some of the alternating current equipment was tested operationally by means of a special testing set (NAV402AP equivalent) in order to reproduce simulated flight conditions, thus ensuring EMI would not arise at any time. During in-flight echocardiography, the correct operation of the navigation, communications, identification and safety instruments of the aircraft was tested according to the above-cited avionics protocol. ...
... This is consistent with our equipment, although we acknowledge that recent research indicates that, with newer echocardiography devices, it is common to observe EB Grade 4 bubbles in asymptomatic divers. 17 Therefore, it would be more appropriate to use the 'expanded' EB grading scale with more modern devices to discriminate between the three groups more accurately. 18 Statistical analysis across the three groups showed that the diving exposure for the divers was similar, even though we recognise that it is difficult to standardize real-world diving. ...
Article
Inert gas accumulated after multiple recreational dives can generate tissue supersaturation and bubble formation when ambient pressure decreases. We hypothesized that this could happen even if divers respected the currently recommended 24-hour pre-flight surface interval (PFSI). We performed transthoracic echocardiography (TTE) on a group of 56 healthy scuba divers (39 male, 17 female) as follows: first echo - during the outgoing flight, no recent dives; second echo - before boarding the return flight, after a multiday diving week in the tropics and a 24-hour PFSI; third echo - during the return flight at 30, 60 and 90 minutes after take-off. TTE was also done after every dive during the week's diving. Divers were divided into three groups according to their 'bubble-proneness': non-bubblers, occasional bubblers and consistent bubblers. During the diving, 23 subjects never developed bubbles, 17 only occasionally and 16 subjects produced bubbles every day and after every dive. Bubbles on the return flight were observed in eight of the 56 divers (all from the 'bubblers' group). Two subjects who had the highest bubble scores during the diving were advised not to make the last dive (increasing their PFSI to approximately 36 hours), and did not demonstrate bubbles on the return flight. Even though a 24-hour PFSI is recommended on the basis of clinical trials showing a low risk of decompression sickness (DCS), the presence of venous gas bubbles in-flight in eight of 56 divers leads us to suspect that in real-life situations DCS risk after such a PFSI is not zero.
... The central place of bubbles as an inciting factor for DCS is widely accepted, yet most decompression procedures generate asymptomatic blood-borne bubbles (4,12,13). Inert gases inhaled while breathing are taken up by tissues in proportion to the ambient pressure, and when pressure is reduced, some of the gas released from tissues forms bubbles due to the presence of gas cavitation nuclei (6,33,34). Therefore, for the current study, we also measured intravascular gas bubbles after diving. ...
... These studies were conducted at rest and after arm or leg exercise to elicit bubble release from vascular margins, exactly as described in our previous report (25). Bubble grading employed a modified Brubakk scale that has been used in several studies (12). The grading system is as follows: 0, no bubbles; 1, occasional bubbles; 2, at least one bubble every four cardiac cycles; 3, at least one bubble every cardiac cycle; 4, continuous bubbling with modifiers [(a ϭ at least one bubble per cm 2 in all frames), (b ϭ at least three bubbles per cm 2 in all frames), or (c ϭ almost complete "whiteout" but individual bubbles can still be discerned)] and 5, whiteout where individual bubbles cannot be discerned. ...
Article
Full-text available
Predicated on evidence that diving-related microparticle generation is an oxidative stress response, this study investigated the role oxygen plays in augmenting production of annexin V-positive microparticles associated with open-water SCUBA diving and whether elevations can be abrogated by ascorbic acid. Following a cross-over study design, 14 male subjects ingested placebo and 2-3 weeks later ascorbic acid (2 g) daily for 6 days prior to performing either a 47 minute dive to 18 meters of sea water while breathing air (~222 kPa N2/59 kPa O2), or breathing a mixture of 60% O2/balance N2 from a tight-fitting face mask at atmospheric pressure for 47 minutes (~ 40 kPa N2/59 kPa O2). Within 30 minutes after the 18 meter dive in the placebo group, neutrophil activation and platelet-neutrophil interactions occurred, and total number of microparticles as well as sub-groups bearing CD66b, CD41, CD31, CD142 proteins or nitrotyrosine increased approximately 2-fold. No significant elevations occurred among divers after ingesting ascorbic acid, nor were elevations identified in either group after breathing 60% O2. Ascorbic acid had no significant effect on post-dive intravascular bubble production quantified by trans-thoracic echocardiography. We conclude that high pressure nitrogen plays a key role in neutrophil and microparticle-associated changes with diving and that responses can be abrogated by dietary ascorbic acid supplementation. Copyright © 2015, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology.
... The pressure excursion used here is slightly more aggressive (450 kPa) and two decompression stops were used, but significant bubbling that remains relatively high for most subjects until 60 min post-dive was found. A more recent study included one profile to 33 msw for 20 min in open sea and detected VGE with B-mode echocardiography assessed using a modified Eftedal and Brubakk grading system (Ljubkovic et al. 2011); however, only the median of the max VGE grade for the population was reported without details on time course or inter-subject variability. The median bubble grade observed 40 min post-surfacing was four (out of a maximum of five) and 10/12 of the divers tested did exhibit a grade 4 for this profile, with one subject arterializing also. ...
... In our counting method for VGE assessment, any count > 1 corresponds by definition to at least a grade 3 on this scale (3-at least one bubble per four cardiac cycles for more than one set of four cycles) and most of our subjects would fall into grade 4 (continuous bubbling). In this respect, our results are therefore consistent with those of Ljubkovic et al. for the same profile in cold water conditions (16-C-18-C, with thermal protection) (Ljubkovic et al. 2011). ...
Article
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Purpose: A reduction in ambient pressure or decompression from scuba diving can result in ultrasound-detectable venous gas emboli (VGE). These environmental exposures carry a risk of decompression sickness (DCS) which is mitigated by adherence to decompression schedules; however, bubbles are routinely observed for dives well within these limits and significant inter-personal variability in DCS risk exists. Here, we assess the variability and evolution of VGE for 2 h post-dive using echocardiography, following a standardized pool dive in calm warm conditions. Methods: 14 divers performed either one or two (with a 24 h interval) standardized scuba dives to 33 mfw (400 kPa) for 20 min of immersion time at NEMO 33 in Brussels, Belgium. Measurements were performed at 21, 56, 91 and 126 min post-dive: bubbles were counted for all 68 echocardiography recordings and the average over ten consecutive cardiac cycles taken as the bubble score. Results: Significant inter-personal variability was demonstrated despite all divers following the same protocol in controlled pool conditions: in the detection or not of VGE, in the peak VGE score, as well as time to VGE peak. In addition, intra-personal differences in 2/3 of the consecutive day dives were seen (lower VGE counts or faster clearance). Conclusions: Since VGE evolution post-dive varies between people, more work is clearly needed to isolate contributing factors. In this respect, going toward a more continuous evaluation, or developing new means to detect decompression stress markers, may offer the ability to better assess dynamic correlations to other physiological parameters.
... ▼ Diving with self-contained underwater breathing apparatus (SCUBA) is major physiological stress despite the common participation of recreational, industry and military personnel. For example, the impact of temperature, pressure, increased work of breathing, hyperoxia and psychological stress all have detrimental physiological consequences [22,25,35,42]. Following single or repetitive dives, impairment has been reported in systemic endothelial function [8,26,31], as well as cardiac and autonomic function [5,10,15]. ...
... The grading system used the following definition according to the modified scale by Eftedal and Brubakk: "0" no bubbles; "1" occasional bubbles; "2" at least one bubble per fourth heart cycle; "3" at least one bubble per heart cycle; "4" should continuous bubbling, with at least one bubble per cm 2 in all frames; and "5" for whiteout, where individual bubbles cannot be seen [13,37]. Recently, it was proposed that the rating of "4" should be subdivided as follows [22]: "4 A" continuous bubbling, with 1-2 bubbles per cm 2 in all frames (same as the current "4" grade); "4B" continuous bubbling, with at least 3 bubbles per cm 2 in all frames; "4C" almost complete whiteout in the right heart, but individual bubbles can still be discerned; and "5" complete whiteout. ...
Article
The effect that a SCUBA dive has on cerebral blood flow (CBF) at rest and during exercise is poorly understood. We examined the hypothesis that the altered hemodynamic parameters following a SCUBA dive will lead to differential changes in CBF at rest and during exercise. 16 divers completed a field-based study with a single dive at a depth of 18 m sea water with a 47-min bottom time. A follow-up laboratory based study was conducted - 1 week later. Intra-cranial velocities were measured with transcranial Doppler ultrasound (TCD) pre-dive, post-dive at rest and throughout incremental exercise until exhaustion. Following the dive at rest, middle cerebral artery velocity (MCAv) was elevated 15 and 30 min after surfacing (by 3.3±5.8 and 4.0±6.9 cm/s, respectively; p<0.05); posterior cerebral artery velocity (PCAv) was increased at 30 min after surfacing (by 3.0±4.5 cm/s; p<0.05). During exercise following the dive, both MCAv and PCAv increased up to 150W followed by a decrease towards baseline at 180W (p<0.05). We found no difference in CBV during exercise between field and laboratory studies (p<0.05). The novel finding of this study is the transient elevation in resting intra-cranial velocities within 30 min following a SCUBA dive. © Georg Thieme Verlag KG Stuttgart · New York.
... Normally these bubbles diffuse from the alveolar capillaries into the lungs to be expired out of the body through respiration. Doppler Ultrasound findings have shown repeatedly that bubbles are formed routinely on dives [2][3][4][5][6][7] and only sometimes does it result in DCS. This can happen when the ascent is too fast for instance, yielding big bubbles which get stuck in a blood vessel and/or too many bubbles which overload the filtering capacity of the lungs. ...
... They also urged for new decompression algorithms that would incorporate bubble dynamics directly (instead of compartment ratio considerations only) to be developed in light of these findings. They suggested asymptomatic bubble outcome of a dive measured ultrasonically as a way to measure the success of the decompression schedule since all dives result in some degree of bubbling [5,65]. ...
... Meanwhile, the continuous integration of microbubbles results in the formation of large bubbles, inducing more severe lung injury [4,5]. Bubbles can also cause angiospasms, which lead to tissue ischaemia, oedema and haemorrhage [6,7]. Thus, bubble formation is the primary factor in the pathogenesis of DCS [8]. ...
Article
To detect the ultrastructural changes in rabbits with type II decompression sickness (DCS), and study the therapeutic effects of hyperbaric oxygen (HBO). Twenty-seven male New Zealand rabbits were randomly divided equally into the DCS group, HBO treatment group and control group. Experimental models of each group were prepared. Lung apex tissues were harvested to prepare paraffin- and EPON812-embedded tissues. In the DCS group, macroscopic and histological examination revealed severe and rapid damage to lung tissue. Ultrastructural examination revealed exudation of red blood cells in the alveolar space. Type I alveolar epithelial cells exhibited retracted cell processes and swollen mitochondria, and type II cells showed highly swollen mitochondria and decrease in cytoplasmic lamellar bodies. Dilatation and congestion of capillary vessels were accompanied by swelling of endothelial cells and incomplete basement membrane. In the HBO treatment group, the findings were somewhat similar to those in the DCS group, but the extent of damage was lesser. Only a small amount of tiny bubbles could be seen in the blood vessels. Type I alveolar epithelia cells and endothelial cells of the capillaries illustrated slight shortening of cells, swollen cytoplasm and decreased cell processes. Type II alveolar epithelial cells showed slight swelling of the mitochondria, decreased vacuolar degeneration of lamellar bodies, and increase in the number of free ribosomes. Our microscopic and ultrastructural findings confirm that the lung is an important organ affected by DCS. We also confirmed that HBO can alleviate DCS-induced pulmonary damage.
... Individual subjects were scanned by the same technician team throughout the study, and bubble signals were graded in real time through consensus of the two evaluators. Grading employed a modified Brubakk scale that has been used in several studies (26,38). The grading system is as follows: 0 ϭ no bubbles; I ϭ occasional bubbles; II ϭ at least one bubble every four cardiac cycles; III ϭ at least one bubble every cardiac cycle; IV ϭ continuous bubbling with modifiers (a ϭ at least one bubble per cm 2 in all frames, b ϭ at least three bubbles per cm 2 in all frames, or c ϭ almost complete whiteout but individual bubbles can still be discerned); and V ϭ "whiteout", where individual bubbles cannot be discerned. ...
Article
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The study goal was to evaluate responses in humans following decompression from open-water SCUBA diving with the hypothesis that exertion underwater and use of a breathing mixture containing more oxygen and less nitrogen (enriched air nitrox, EAN) would alter annexin V-positive microparticles (MPs) production and size changes and neutrophil activation as well as their relationships to intravascular bubble formation. Twenty-four divers followed a uniform dive profile to 18 meters of sea water breathing air or 22.5 meters breathing 32% oxygen/68% nitrogen for 47 minutes either swimming with moderately heavy exertion underwater or remaining stationary at depth. Blood was obtained prior to and at 15 and 120 minutes post-dive. Intravascular bubbles were quantified by trans-thoracic echocardiography post-dive at 20 minute intervals for 2 hours. There were no significant differences in maximum bubble scores among the dives. MPs number increased 2.7-fold on average within 15 minutes after each dive; only the air-exertion dive resulted in a significant further increase to 5-fold over baseline at 2 hours post-dive. Neutrophil activation occurred after all dives. For the EAN-stationary at depth dive but not for other conditions the numbers of post-dive annexin V-positive particles above 1 µm in diameter were correlated with intravascular bubble scores (correlation coefficients ~ 0.9, p < 0.05). We conclude that post-decompression relationships among bubbles, MPs, platelet-neutrophil interactions and neutrophil activation appear to exist, but more study is required to improve confidence in the associations.
... Imbert et al. (2004) suggested a model in which, on initial decompression, tiny bubbles transverse the lung capillaries to the arterial side and continue to grow in the blood vessels of the nervous tissue. Other studies showed that with high density of venous bubbles, these can transverse to the systemic circulation even without a patent foramen ovale (Bakovic et al., 2008;Ljubkovic et al., 2011;Obad et al., 2007). The present study has demonstrated bubble formation on both sides of the circulation, with no need for a right-to-left shunt to move bubbles into the arterial systemic circulation. ...
Article
It has been shown that tiny gas nanobubbles form spontaneously on a smooth hydrophobic surface submerged in water. These nanobubbles were shown to be the source of gas micronuclei from which bubbles evolved during decompression of silicon wafers. We suggest that the hydrophobic inner surface of blood vessels may be a site of nanobubble production. Sections from the right and left atria, pulmonary artery and vein, aorta, and superior vena cava of sheep (n=6) were gently stretched on microscope slides and exposed to 1013kPa for 18h. Hydrophobicity was checked in the six blood vessels by advancing contact angle with a drop of saline of 71±19 degrees, with a maximum of about 110±7 degrees (mean±SD). Tiny bubbles ∼30μm in diameter rose vertically from the blood vessels and grew on the surface of the saline, where they were photographed. All of the blood vessels produced bubbles over a period of 80min. The number of bubbles produced from a square cm was: in the aorta, 20.5; left atrium, 27.3; pulmonary artery, 17.9; pulmonary vein, 24.3; right atrium, 29.5; superior vena cava, 36.4. More than half of the bubbles were present for less than 2min, but some remained on the saline-air interface for as long as 18min. Nucleation was evident in both the venous (superior vena cava, pulmonary artery, right atrium) and arterial (aorta, pulmonary vein, left atrium) blood vessels. This newly suggested mechanism of nucleation may be the main mechanism underlying bubble formation on decompression.
... In human scuba diving, GE is associated with breathing gas at increased pressure, which often leads to tissue gas supersaturation during ascent and the formation of venous gas emboli (VGE) 1 . VGE crossover to systemic arteries (arterialisation), mostly through the patent foramen ovale or the intrapulmonary arteriovenous anastomoses, causing a systemic gas embolism 28 . In sea turtles a cardiac right to left shunt occurs during the dive and the consequent apnoea. ...
Article
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Sea turtles that are entrapped in static and towed nets may develop gas embolism which can lead to severe organ injury and death. Trawling characteristics, physical and physiologic factors associated with gas-embolism and predictors of mortality were analysed from 482 bycaught loggerheads. We found 204 turtles affected by gas-embolism and significant positive correlations between the presence of gas-embolism and duration, depth, ascent rate of trawl, turtle size and temperature, and between mortality and ascent time, neurological deficits, significant acidosis and involvement of > 12 cardiovascular sites and the left atrium and sinus venosus-right atrium. About 90% turtles with GE alive upon arrival at Sea Turtle Clinic recovered from the disease without any supportive drug therapy. Results of this study may be useful in clinical evaluation, prognostication, and management for turtles affected by gas-embolism, but bycatch reduction must become a priority for major international organizations. According to the results of the present study the measures to be considered to reduce the catches or mortality of sea turtles for trawling are to be found in the modification of fishing nets or fishing operations and in greater awareness and education of fishermen.
... Movements were employed to mobilize gas bubbles presumably lodged or generated in the venous pathway. The bubbles were graded on a scale modifi ed from Eftedal and Brubbak [ 11 ] . The non-linear ordinal grading system was as follows: 0 -no bubbles; I -occasional bubbles; II -at least one bubble every 4 cardiac cycles; III -at least one bubble every cardiac cycle; IV -continuous bubbling with modifi ers [(a = at least one bubble.cm ...
Article
Acclimatization (an adaptive change in response to repeated environmental exposure) to diving could reduce decompression stress. A decrease in post-dive circulating venous gas emboli (VGE or bubbles) would represent positive acclimatization. The purpose of this study was to determine whether four days of daily diving alter post-dive bubble grades. 16 male divers performed identical no-decompression air dives on 4 consecutive days to 18 meters of sea water for 47 min bottom times. VGE monitoring was performed with transthoracic echocardiography every 20 min for 120 min post-dive. Completion of identical daily dives resulted in progressively decreasing odds (or logit risk) of having relatively higher grade bubbles on consecutive days. The odds on Day 4 were half that of Day 1 (OR 0.50, 95% CI: 0.34, 0.73). The odds ratio for a >III bubble grade on Day 4 was 0.37 (95% CI: 0.20, 0.70) when compared to Day 1. The current study indicates that repetitive daily diving may reduce bubble formation, representing a positive (protective) acclimatization to diving. Further work is required to evaluate the impact of additional days of diving and multiple dive days and to determine if the effect is sufficient to alter the absolute risk of decompression sickness.
... Active recreational SCUBA divers are estimated to represent 7 million people (PADI; Vann et al., 2005), with the biggest certifying agency, P.A.D.I, issuing over 500 000 certifications per year and the number of certified divers tripling in the last 20 years. Scuba diving per se, even when carried out according to standard rules, leads to bubble formation (Ljubkovic et al., 2011; Mollerlokken et al., 2011), which may be created in, or reach, the brain. Despite this, so far studies on the long-term effects of SCUBA diving have focused on professional, commercial and military diving and very few studies have looked at recreational SCUBA divers (Slosman et al., 2004). ...
... In spite of the correct usage of decompression tables, in individual cases divers may suffer from the effects of decompression sickness. Studies that use the Doppler method, showed very significant differences in the formation of bubbles among different people who were subjected to hyperbaric exposures of the same type [5,6]. For this reason, while planning the dive or hyperbaric exposure, it is necessary to consider the many factors that may influence the course of decompression. ...
Article
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In hyperbaric air exposures, the diver's body is subjected to an increased gas pressure, which simulates a real dive performed in water with the presence of hydrostatic pressure. The hyperbaric effect depends on pressure, its dynamics and exposure time. During compression, physical dissolution of inert gas in body fluids and tissues takes place. The decompression process should result in safe physiological disposal of excess gas from the body. However, despite the correct application of decompression tables we observe cases of decompression sickness. The study aim was to find factors affecting the safety of diving, with a particular emphasis on the diet, which thus far has not been taken into account. The study subjects were 56 divers. Before hyperbaric exposure, the following data were collected: age, height and weight; plus each divers filled out a questionnaire about their diet. The data from the questionnaires allowed us to calculate the approximate fat intake with the daily food for each diver. Moreover, blood samples were collected from each diver for analysis of cholesterol and triglycerides. Hyperbaric exposures corresponded to dives conducted to depths of 30 and 60 meters. After exposures each diver was examined via the Doppler method to determine the possible presence of microbubbles in the venous blood. Decompression stress was observed in 29 subjects. A high-fat diet has a direct impact on increasing levels of cholesterol and triglycerides in the blood serum. A high-fat diet significantly increases the severity of decompression stress in hyperbaric air exposures and creates a threat of pressure disease.
... Also, as in our recent studies, we found crossing of gas bubbles to systemic arterial side. These arterializations occurred more often after air dives as compared to nitrox (seven vs. two arterializations, respectively), which could be explained by the higher overall bubble load after air diving (Ljubkovic et al. , 2011. However, despite higher gas bubbling after air dives, nitrox diving had greater impact on endothelial function, as evidenced by signiWcantly reduced FMD response after nitrox diving. ...
Article
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Self-contained underwater breathing apparatus (SCUBA) diving is regularly associated with numerous asymptomatic changes in cardiovascular function. Freshwater SCUBA diving presents unique challenges compared with open sea diving related to differences in water density and the potential for dive locations at altitude. The aim of this study was to evaluate the impact of freshwater trimix diving at altitude on human cardiovascular function. Ten divers performed two dives in consecutive days at 294 m altitude with the surface interval of 24 h. Both dives were at a depth of 45 m with total dive time 29 and 26 min for the first and second dive, respectively. Assessment of venous gas embolization, hydration status, cardiac function and arterial stiffness was performed. Production of venous gas emboli was low, and there were no significant differences between the dives. After the first dive, diastolic blood pressure was significantly reduced, which persisted up to 24 h. Left ventricular stroke volume decreased, and heart rate increased after both dives. Pulse wave velocity was unchanged following the dives. However, the central and peripheral augmentation index became more negative after both dives, indicating reduced wave reflection. Ejection duration and round trip travel time were prolonged 24 h after the first dive, suggesting longer-lasting suppression of cardiac and endothelial function. This study shows that freshwater trimix dives with conservative profiles and low venous gas bubble loads can result in multiple asymptomatic acute cardiovascular changes some of which were present up to 24 h after dive.
... If the tissues become supersaturated during ascent, bubbles form. This can be observed sonographically in venous blood in most divers after a single properly performed dive (ie, without violation of the decompression regimen) (2,3). In divers with a PFO, these bubbles may embolize into systemic circulation, lodge into peripheral capillaries, and cause ischemic injury (4). ...
Article
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Objectives This paper sought to evaluate the occurrence of decompression sickness (DCS) after the application of a patent foramen ovale (PFO) screening and risk stratification strategy. Background PFO is associated with an increased risk of DCS. Recently, transcatheter closure was reported to reduce DCS occurrence in divers with a high-grade shunt. However, to date, there are no data regarding the effectiveness of any PFO screening and risk stratification strategy for divers. Methods A total of 829 consecutive divers (35.4 ± 10.0 years, 81.5% men) were screened for PFO by means of transcranial color-coded sonography in the DIVE-PFO (Decompression Illness Prevention in Divers with a Patent Foramen Ovale) registry. Divers with a high-grade PFO were offered either catheter-based PFO closure (the closure group) or advised conservative diving (high grades). Divers with a low-grade shunt were advised conservative diving (low grades), whereas those with no PFO continued unrestricted diving (controls). A telephone follow-up was performed. To study the effect of the screening and risk stratification strategy, DCS occurrence before enrollment and during the follow-up was compared. Results Follow-up was available for 748 (90%) divers. Seven hundred and 2 divers continued diving and were included in the analysis (mean follow-up 6.5 ± 3.5 years). The DCS incidence decreased significantly in all groups, except the controls. During follow-up, there were no DCS events in the closure group; DCS incidence was similar to the controls in the low-grade group (HR: 3.965; 95% CI: 0.558-28.18; P = 0.169) but remained higher in the high-grade group (HR: 26.170; 95% CI: 5.797-118.16; P < 0.0001). Conclusions The screening and risk stratification strategy using transcranial color-coded sonography was associated with a decrease in DCS occurrence in divers with PFO. Catheter-based PFO closure was associated with a DCS occurrence similar to the controls; the conservative strategy had a similar effect in the low-grade group, but in the high-grade group the DCS incidence remained higher than in all other groups.
... However, even when diving in line with recommendations for safe diving profi les with decompression stops, studies have shown bubble formation in the venous circulation. 7,8 Normally, these bubbles are fi ltered and exhaled by the lungs without causing DCS. 3 Both atrial septal defects 9 and persistent (patent) foramen ovale (PFO) 1,10-12 have been associated with an increased risk of DCS due to a right-to-left shunt of venous decompression bubbles into the arterial circulation. Moreover, it has been suggested that divers with PFO are more likely to suffer severe neurological forms of DCS and require longer treatment with hyperbaric oxygen therapy (HBOT). ...
Article
Introduction: Interatrial communication is associated with an increased risk of decompression sickness (DCS) in scuba diving. It has been proposed that there would be a decreased risk of DCS after closure of the interatrial communication, i.e., persistent (patent) foramen ovale (PFO). However, the clinical evidence supporting this is limited. Methods: Medical records were reviewed to identify Swedish scuba divers with a history of DCS and catheter closure of an interatrial communication. Thereafter, phone interviews were conducted with questions regarding diving and DCS. All Swedish divers who had had catheter-based PFO-closure because of DCS were followed up, assessing post-closure diving habits and recurrent DCS. Results: Nine divers, all with a PFO, were included. Eight were diving post-closure. These divers had performed 6,835 dives (median 410, range 140-2,200) before closure, and 4,708 dives (median 413, range 11-2,000) after closure. Seven cases with mild and 10 with serious DCS symptoms were reported before the PFO closure. One diver with a small residual shunt suffered serious DCS post-closure; however, that dive was performed with a provocative diving profile. Conclusion: Divers with PFO and DCS continue to dive after PFO closure and this seems to be fairly safe. Our study suggests a conservative diving profile when there is a residual shunt after PFO closure, to prevent recurrent DCS events.
... Phase 2 was further broken down into three parts: square dives between 18 and 51 msw corresponding to a PRT of 22, square dives between 18 and 54 msw corresponding to a PRT of 28, and multilevel dives that were a repetition of those considered the most interesting in phase 1 in which the residence time at the various levels was lengthened. For the square profiles, the depths were chosen to have some difference from one dive to the next, though in some cases the depth was chosen because data existed from human trials for that profile (Ljubkovic et al., 2011;Møllerløkken et al., 2011). For example, the 54 msw for 20 min at a PRT 28 dive was selected instead of a 51 msw dive). ...
Article
Results of a comprehensive effort to analyze commercially available dive computers and PC-based dive planners are reviewed. For this study 234 chamber test dives were carried out with profiles ranging from square to triangular, multilevel forward and multilevel reverse, to a maximum depth of 54 m. Air was the breathing medium for all dives. A first phase considered only no decompression dives, a second phase considered decompression dives at two levels of PRT (pressure root time) and a third phase considered repetitive dives with various surface intervals.
... 12 Small quantities of venous gas emboli (VGE) were confirmed by Doppler studies in 80-91% of scuba divers. 13,14 Most divers with VGE, however, remain asymptomatic, as these are effectively filtered by pulmonary circulation. Symptoms may occur either with high bubble load (i.e. ...
Article
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Patent foramen ovale (PFO) is associated with an increased risk of decompression sickness (DCS) in divers that results from a paradoxical embolization of nitrogen bubbles. The number of scuba divers worldwide is estimated in the millions, and the prevalence of PFO is 25%-30% in adults. It is interesting that despite these numbers, many important issues regarding optimal screening, risk stratification, and management strategy still remain to be resolved. Recently published data suggest the possible effectiveness of both PFO closure and conservative diving measures in preventing arterial gas embolization. This review aims to introduce the basic principles of physiology and the pathophysiology of bubble formation and DCS, summarize the current literature on PFO and diving, and review the possibilities of diagnostic workup and management. Copyright © 2015 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
... Decompression sickness (DCS) presents a health risk for deep sea divers and a constraint to space exploration and provocative diving operations. Bubbles are thought to play a role in pathophysiological responses mediating DCS, however, they are often produced without symptoms [1][2][3] . Therefore, additional etiological factors have been sought to explain DCS development. ...
Article
Full-text available
Production of blood-borne microparticles (MPs), 0.1–1 µm diameter vesicles, and interleukin (IL)-1β in response to high pressure is reported in lab animals and associated with pathological changes. It is unknown whether the responses occur in humans, and whether they are due to exposure to high pressure or to the process of decompression. Blood from research subjects exposed in hyperbaric chambers to air pressure equal to 18 meters of sea water (msw) for 60 minutes or 30 msw for 35 minutes were obtained prior to and during compression and 2 hours post-decompression. MPs and intra-particle IL-1β elevations occurred while at pressure in both groups. At 18 msw (n = 15) MPs increased by 1.8-fold, and IL-1β by 7.0-fold (p < 0.05, repeated measures ANOVA on ranks). At 30 msw (n = 16) MPs increased by 2.5-fold, and IL-1β by 4.6-fold (p < 0.05), and elevations persisted after decompression with MPs elevated by 2.0-fold, and IL-1β by 6.0-fold (p < 0.05). Whereas neutrophils incubated in ambient air pressure for up to 3 hours ex vivo did not generate MPs, those exposed to air pressure at 180 kPa for 1 hour generated 1.4 ± 0.1 MPs/cell (n = 8, p < 0.05 versus ambient air), and 1.7 ± 0.1 MPs/cell (p < 0.05 versus ambient air) when exposed to 300 kPa for 35 minutes. At both pressures IL-1β concentration tripled (p < 0.05 versus ambient air) during pressure exposure and increased 6-fold (p < 0.05 versus ambient air) over 2 hours post-decompression. Platelets also generated MPs but at a rate about 1/100 that seen with neutrophils. We conclude that production of MPs containing elevated concentrations of IL-1β occur in humans during exposure to high gas pressures, more so than as a response to decompression. While these events may pose adverse health threats, their contribution to decompression sickness development requires further study.
... DCS is a systemic pathophysiological process that occurs after tissues become supersaturated with nitrogen or other alternative gas used to dilute O 2 in breathing gas during deep-sea diving, high-altitude aviation, and space exploration. Although it is widely accepted that gas bubbles are an inciting factor for DCS, most decompression procedures generate asymptomatic blood-borne bubbles, thus prompting a search for additional factors (2,6,7). There is now considerable precedence that microparticles (MPs), cell-derived membrane vesicles with diameters of 0.1-1.0 ...
Article
We hypothesized that pathological changes associated with elevations in annexin V-positive microparticles (MPs) following high pressure exposures can be abrogated by ascorbic acid in a murine model. Mice exposed for 2 hours to 790 kPa air and euthanized at 2 or 13 hours post-decompression exhibited over 3-fold elevations in circulating MPs as well as sub-groups bearing Ly6G, CD41, Ter119, CD31, and CD142 surface proteins. There was evidence of significant neutrophil activation, platelet-neutrophil interactions and vascular injury to brain, omentum, psoas and skeletal muscles assessed as leakage of high molecular weight dextran. Prophylactic ascorbic acid (500 mg/kg IP) administration prevented all post-decompression neutrophil changes and vascular injuries. Ascorbic acid administration immediately after decompression abrogated most changes, but evidence of vascular leakage in brain and skeletal muscle at 13 hours post-decompression persisted. No significant elevations in these parameters occurred after injection of ascorbic acid alone. The findings support the idea that MPs production occurring with exposures to elevated gas pressure is an oxidative stress response and that anti-oxidants may offer protection from pathological effects associated with decompression. Copyright © 2015, Journal of Applied Physiology.
... The fall in environmental pressure normally causes a reduction in partial pressure of inspired inert gases (mainly nitrogen), which then diffuse from the tissues where they were dissolved at higher partial pressures and are carried by the blood to the lungs, where they are expired. Even under normal conditions, vascular gas emboli (VGE) frequently form at this stage [124,125], but DCS occurs only if certain local and general conditions are met, where bubbles may be trapped locally, occluding post-capillary venous vessels and/or compressing adjacent tissues and triggering inflammation and thrombosis [126]. If a structural or functional R-T-L shunt is present [127], bubbles can also be arterialised and, according to their size, also trapped in small arteries or arterioles [128][129][130]. ...
Article
Patent foramen ovale (PFO) is implicated in the pathogenesis of a number of medical conditions but to date only one official position paper related to left circulation thromboembolism has been published. This interdisciplinary paper, prepared with the involvement of eight European scientific societies, reviews the available evidence and proposes a rationale for decision making for other PFO-related clinical conditions. In order to guarantee a strict evidence-based process, we used a modified grading of recommendations, assessment, development, and evaluation (GRADE) methodology. A critical qualitative and quantitative evaluation of diagnostic and therapeutic procedures was performed , including assessment of the risk/benefit ratio. The level of evidence and the strength of the position statements were weighed and graded according to predefined scales. Despite being based on limited and observational or low-certainty randomised data, a number of position statements were made to frame PFO management in different clinical settings, along with suggestions for new research avenues. This interdisciplinary position paper, recog-nising the low or very low certainty of existing evidence, provides the first approach to several PFO-related clinical scenarios beyond left circulation thromboembolism and strongly stresses the need for fresh high-quality evidence on these topics.
... It is a risk associated with compressed gas diving and tunneling, high-altitude aviation, and space exploration. Gas bubbles, long thought to be an inciting factor for DCS, are often asymptomatic and may occur as a consequence of most decompression events (2,6,7). Hence, additional factors are involved in DCS pathophysiology. ...
Article
Circulating microparticle (MP) elevations due to high air pressure exposures, associated inflammatory changes and vascular injury may be due to oxidative stress. We hypothesized that these responses arise due to elevated nitrogen partial pressures and not because of high pressure oxygen. A comparison was made among high pressure air, normoxic high pressure nitrogen and high pressure oxygen for causing elevations of circulating annexin V-positive MPs, neutrophil activation and vascular injury assessed as leakage of high molecular weight dextran in a murine model. After mice were exposed for 2 hours to 790 kPa air there were over 3-fold elevations in total circulating MPs as well as sub-groups bearing Ly6G, CD41, Ter119, CD31, and CD142 surface proteins; evidence of neutrophil activation, platelet-neutrophil interactions and vascular injury to brain, omentum, psoas and skeletal muscles. Similar changes were found in mice exposed to high pressure nitrogen using a gas mix so that oxygen partial pressure was the same as that of ambient air; whereas none of these changes occurred after exposures to 166 kPa oxygen, the same partial pressure that occurs during high pressure air exposures. We conclude that nitrogen plays a central role in intra- and perivascular changes associated with exposure to high air pressure and these responses appear to be a novel form of oxidative stress. Copyright © 2015, Journal of Applied Physiology.
... Bubble scores were only slightly higher in DCI and, as other studies have since concluded, appeared to have limited diagnostic value. 8,48,52 Transcranial Doppler ultrasonography has been used to monitor cerebral embolization of bubbles from pulmonary barotrauma in a hospital setting, but is not practical in a field setting given its lack of a proven relationship to symptomatology and the exam's moderate time requirement. 57,80 Acute diaphragmatic rupture is possible in severe trauma. ...
Article
Introduction: Flights to high altitude can lead to exposure and unique pathology not seen in normal commercial aviation. Methods: This paper assesses the potential for point-of-care ultrasound to aid in management and disposition of injured crewmembers from a high altitude incident. This was accomplished through a systematic literature review regarding current diagnostic and therapeutic uses of ultrasound for injuries expected in high altitude free fall and parachuting. Results: While current research supports its utility in diagnostics, therapeutic procedures, and triage decisions, little research has been done regarding its utility in high altitude specific pathology, but its potential has been demonstrated. Discussion: An algorithm was created for use in high altitude missions, in the event of an emergency descent and traumatic landing for an unconscious and hypotensive pilot, to rule out most life threatening causes. Each endpoint includes disposition, allowing concise decision-making.Galdamez LA, Clark JB, Antonsen EL. Point-of-care ultrasound utility and potential for high altitude crew recovery missions. Aerosp Med Hum Perform. 2017; 88(2):128-136.
... Decompression sickness (DCS) is a risk associated with compressed-gas diving and tunneling, high-altitude aviation, and space exploration. Intravascular gas bubbles, thought to be an inciting factor for DCS, are common and often asymptomatic, so additional pathophysiological factors have been sought to explain development of the syndrome (13,31,32). There is now considerable evidence that microparticles (MPs), vesicles with diameters of~0.1-1.0 m that bud from the cell membrane surface, are elevated in association with simulated as well as bona fide underwater diving (36 -38, 46, 55, 56, 61). ...
Article
Inflammatory mediators are known to be elevated in association with decompression from elevated ambient pressure, but their role in tissue damage or overt decompression sickness is unclear. Circulating microparticles (MPs) are also know to increase and because interleukin (IL)-1β is packaged within these particles, we hypothesized that IL-1β was responsible for tissue injuries. Here, we demonstrate that elevations of circulating MPs containing up to 9-fold higher concentrations of IL-1β occur while mice are exposed to high air pressure (790 kPa), whereas smaller particles carrying proteins specific to exosomes are not elevated. MPs number and intra-particle IL-1β concentration increase further over 13 hours post-decompression. MPs also exhibit intra-particle elevations of tumor necrosis factor-α, caspase-1, inhibitor of κB kinase -β and -γ, and elevated IL-6 is adsorbed to the surface of MPs. Contrary to lymphocytes, neutrophil NLRP3 inflammasome oligomerization and cell activation parameters occur during high pressure exposure, and additional evidence for activation are manifested post-decompression. Diffuse vascular damage, while not apparent immediately post-decompression, was present 2 hours later and remained elevated for at least 13 hours. Prophylactic administration of an IL-1β receptor inhibitor or neutralizing antibody to IL-1β inhibited MPs elevations, increases of all MPs-associated pro-inflammatory agents, and vascular damage. We conclude that an auto-activation process triggered by high pressure stimulates MPs production and concurrent inflammasome activation, and IL-1β is a proximal factor responsible for further cytokine production and decompression-associated vascular injuries.
... Since nitrogen bubbles can be detected and observed using ultrasound (Doppler ultrasound monitoring and visual two-dimensional ultrasound imaging), it is assumed that decompression-induced vascular bubbles can be used as a measure of decompression stress and hence decompression safety (Mollerlokken et al. 2012;Eftedal et al. 2007). The link between detection of VGE by ultrasound and DCI was demonstrated by Ljubkovic et al. (2011). However, the extent of VGE is not strictly correlated with the severity of symptoms (Brubakk and Neuman 2003) and endothelial dysfunction (Germonpré and Balestra 2017). ...
Article
Full-text available
Decompression illness (DCI) is a complex clinical syndrome caused by supersaturation of respiratory gases in blood and tissues after abrupt reduction in ambient pressure. The resulting formation of gas bubbles combined with pulmonary barotrauma leads to venous and arterial gas embolism. Severity of DCI depends on the degree of direct tissue damage caused by growing bubbles or indirect cell injury by impaired oxygen transport, coagulopathy, endothelial dysfunction, and subsequent inflammatory processes. The standard therapy of DCI requires expensive and not ubiquitously accessible hyperbaric chambers, so there is an ongoing search for alternatives. In theory, perfluorocarbons (PFC) are ideal non-recompressive therapeutics, characterized by high solubility of gases. A dual mechanism allows capturing of excess nitrogen and delivery of additional oxygen. Since the 1980s, numerous animal studies have proven significant benefits concerning survival and reduction in DCI symptoms by intravenous application of emulsion-based PFC preparations. However, limited shelf-life, extended organ retention and severe side effects have prevented approval for human usage by regulatory authorities. These negative characteristics are mainly due to emulsifiers, which provide compatibility of PFC to the aqueous medium blood. The encapsulation of PFC with amphiphilic biopolymers, such as albumin, offers a new option to achieve the required biocompatibility avoiding toxic emulsifiers. Recent studies with PFC nanocapsules, which can also be used as artificial oxygen carriers, show promising results. This review summarizes the current state of research concerning DCI pathology and the therapeutic use of PFC including the new generation of non-emulsified formulations based on nanocapsules.
... The bubbles formed in the body after decompression have been accepted as a major cause of DCS, although the amount of bubbles does not correlate directly with the clinical manifestations of DCS (Bayne et al., 1985;Dunford et al., 2002). Increasing numbers of studies reveal that not only rapid decompression may cause bubble formation in the body, but a small number of bubbles may also be observed in the blood vessels after diving without protocol violation (Ljubkovic et al., 2011). Although clinical symptoms are not present in these divers, ultrasound examination shows repetitive regular diving can also cause acute interstitial lung edema, ...
Article
Full-text available
This study aimed to establish an animal model of decompression-induced lung injury (DILI) secondary to repetitive diving in mice and explore the role of macrophages in DILI and the protective effects of high-concentration hydrogen (HCH) on DILI. Mice were divided into three groups: control group, DILI group, and HCH group. Mice were exposed to hyperbaric air at 600 kPa for 60 min once daily for consecutive 3 d and then experienced decompression. In HCH group, mice were administered with HCH (66.7% hydrogen and 33.3% oxygen) for 60 min after each hyperbaric exposure. Pulmonary function tests were done 6 h after decompression; the blood was harvested for cell counting; the lung tissues were harvested for the detection of inflammatory cytokines, hematoxylin and eosin (HE) staining, and immunohistochemistry; western blotting and polymerase chain reaction (PCR) were done for the detection of markers for M1 and M2 macrophages. Our results showed that bubbles formed after decompression and repeated hyperbaric exposures significantly reduced the total lung volume and functional residual volume. Moreover, repetitive diving dramatically increased proinflammatory factors and increased the markers of both M1 and M2 macrophages. HCH inhalation improved lung function to a certain extent, and significantly reduced the pro-inflammatory factors. These effects were related to the reduction of M1 macrophages as well as the increase in M2 macrophages. This study indicates that repetitive diving damages lung function and activates lung macrophages, resulting in lung inflammation. HCH inhalation after each diving may be a promising strategy for the prevention of DILI.
... The fall in environmental pressure normally causes a reduction in partial pressure of inspired inert gases (mainly nitrogen), which then diffuse from the tissues where they were dissolved at higher partial pressures and are carried by the blood to the lungs, where they are expired. Even under normal conditions, vascular gas emboli (VGE) frequently form at this stage [124,125], but DCS occurs only if certain local and general conditions are met, where bubbles may be trapped locally, occluding post-capillary venous vessels and/or compressing adjacent tissues and triggering inflammation and thrombosis [126]. If a structural or functional R-T-L shunt is present [127], bubbles can also be arterialised and, according to their size, also trapped in small arteries or arterioles [128][129][130]. ...
Article
Patent foramen ovale (PFO) is implicated in the pathogenesis of a number of medical conditions but to date only one official position paper related to left circulation thromboembolism has been published. This interdisciplinary paper, prepared with the involvement of eight European scientific societies, reviews the available evidence and proposes a rationale for decision making for other PFO-related clinical conditions. In order to guarantee a strict evidence-based process, we used a modified grading of recommendations, assessment, development, and evaluation (GRADE) methodology. A critical qualitative and quantitative evaluation of diagnostic and therapeutic procedures was performed, including assessment of the risk/benefit ratio. The level of evidence and the strength of the position statements were weighed and graded according to predefined scales. Despite being based on limited and observational or low-certainty randomised data, a number of position statements were made to frame PFO management in different clinical settings, along with suggestions for new research avenues. This interdisciplinary position paper, recognising the low or very low certainty of existing evidence, provides the first approach to several PFO-related clinical scenarios beyond left circulation thromboembolism and strongly stresses the need for fresh high-quality evidence on these topics.
... 5,6 With the development of ultrasound technique, increasing studies reveal that not only rapid decompression may cause the production of bubbles in the blood and tissues, but there are a small amount of bubbles in the blood vessels of divers after diving without protocol violation. 7,8 Although clinical symptoms are not present in these divers, ultrasound examination shows the evidence of acute interstitial lung edema. 9,10 Macrophages derived from mononuclear phagocytes (MP) are an important participant in the inflammatory reaction. ...
Article
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Studies have shown that blood bubbles may be detectable and there is ultrasonic evidence of acute interstitial lung edema even after diving without protocol violation. Macrophages play a central role in the inflammation, and macrophage polarization is closely related to the pathogenesis some lung diseases. Available findings indicate that decompression may induce the production of pro-inflammatory cytokines, chemokines, and adhesion molecules in the blood and tissues, which are associated with the macrophage polarization, and hyperbaric treatment may exert therapeutic effects on decompression related diseases via regulating these factors. Thus, we hypothesize that the polarization of circulating and/or resident macrophages is involved in the pathogenesis of decompression induced lung injury.
... These bubbles can cause either local tissue damage or embolize through the blood (2). Small quantities of venous gas bubbles are common after recreational scuba diving (3,4). The occurrence of these bubbles is usually not associated with any clinical manifestation. ...
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Introduction: Patent foramen ovale (PFO) is a risk factor of decompression sickness (DCS). However, data on risk stratification of divers with a PFO are sparse. This study sought to evaluate the risk of neurological DCS (DCSneuro), based on the presence and grade of a right-to-left shunt (RLS). Methods: A total of 640 divers were screened for a RLS using TCD between 1/2006 and 4/2017. RLS was graded as low, medium, or high grade with two subgroups - after a Valsalva maneuver or at rest. Divers were questioned about their DCS history. Survival analysis techniques were used to assess risk factors for unprovoked DCS. Results: A RLS was found in 258 divers (40.3 %). 44 (17.1 %) divers with a RLS experienced DCSneuro compared to 5 (1.3 %) divers without a RLS (p <0.001). The proportion of DCSneuro increased from 4.6 % in the low-grade RLS subgroup to 57.1 % in the subgroup with high-grade RLS at rest. The hazard ratio for DCSneuro and RLS was11.806 (p <0.001). Conclusions: Divers with a RLS had a higher risk of DCSneuro and the risk increased with RLS grade. We suggest that TCD is an appropriate method for RLS screening and risk stratification in divers (Tab. 4, Fig. 2, Ref. 29).
... decompression sickness; myeloperoxidase; CD41; CD235; CD14; tissue factor; von Willebrand factor; platelet-endothelial cell-adhesion molecule DECOMPRESSION SICKNESS (DCS) is a risk associated with compressed gas diving, tunneling, high-altitude aviation, and space exploration. Gas bubbles, long thought to be the inciting factor for DCS, are common and often asymptomatic; hence, additional pathophysiological factors have been sought to explain the development of the syndrome (7,15,16). There is now considerable evidence that microparticles (MPs), cell-derived membrane vesicles with diameters of 0.1-1.0 ...
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Decompression sickness (DCS) is a systemic disorder assumed due to gas bubbles, but additional factors are likely to play a role. Circulating microparticles, vesicular structures with diameters of 0.1 to 1.0 µm, have been implicated but data in human divers has been lacking. We hypothesized that the number of blood-borne annexin V-positive microparticles (MPs) and neutrophil activation assessed as surface myeloperoxidase (MPO) staining would differ between SCUBA divers suffering from DCS versus asymptomatic divers. Blood was analyzed from 280 divers who had been exposed to maximum depths from 7 to 105 meters; 185 were control/asymptomatic divers and 90 were diagnosed with DCS. Elevations of MPs and neutrophil activation occurred in all divers but normalized within 24 hours in those who were asymptomatic. MPs bearing the following proteins: CD66b, CD41, CD31, CD142, CD235 and von Willebrand factor were between 2.4 and 11.7-fold higher in blood from divers with DCS versus asymptomatic divers matched for time of sample acquisition, maximum diving depth and breathing gas. Multiple logistic regression analysis documented significant associations (p<0.001) between DCS and MPs and for neutrophil MPO staining. Effect estimates were not altered by gender, body mass index, use of non-steroidal anti-inflammatory agents or emergency oxygen treatment, and modestly influenced by divers' age, choice of breathing gas during diving, maximum diving depth, and whether repetitive diving had been performed. There were no significant associations between DCS and number of MPs without surface proteins listed above. We conclude that MPs production and neutrophil activation exhibit strong associations with DCS. Copyright © 2015, Journal of Applied Physiology.
Article
Arterialization of venous gas emboli (VGE) formed after surfacing from SCUBA diving can become arterial gas emboli (AGE) through intrapulmonary arterial-venous anastomoses (IPAVAs) that open with exercise. METHODS: We recruited twenty PFO negative SCUBA divers and conducted a field and a laboratory study with the aims to investigate the appearance of AGE in intracranial vessels. At the field they performed a single dive to a depth of 18m sea water with a 47 min bottom time and a direct ascent to the surface. Transthoracic echocardiography was used to score VGE and AGE and transcranial Doppler was used to visualize middle (MCA) and posterior cerebral arteries (PCA) with automated objective bubble detection. Observations were conducted for 45 min post-dive at rest and at the laboratory after agitated saline injection at rest and throughout an incremental cycle supine exercise test until exhaustion and for 10 min of recovery. RESULTS: After resurfacing all divers presented endogenous VGE and arterialization was present in three divers. Saline contrast injection led to AGE in nine out of 19 subjects at rest. AGE that reached the cerebral arteries post-dive were recorded in 2 divers at 60W, 3 at 90W, 5 at 120W, 6 at 150W and 4 at 180W and in 3, 4, 5, 9 and 9 respectively after saline contrast injection in the lab. All divers had AGE grades of 1 or 2 and only single AGE reached the cerebral vasculature. CONCLUSION: These data suggest that few emboli of venous origin reach the brain through exercise-induced IPAVAs but cerebral embolization is not a high risk in the studied population.
Article
Laboratory and field investigations have demonstrated that intrapulmonary arteriovenous anastomoses (IPAVA) may provide an additional means for venous gas emboli (VGE) to cross over to the arterial circulation due to their larger diameter compared to pulmonary microcirculation. Once thought to be the primary cause of decompression sickness (DCS), it has been demonstrated that, even in large quantities, their presence does not always result in injury. Normally, VGE are trapped in the site of gas exchange in the lungs and eliminated via diffusion. When VGE crossover takes place in arterial circulation, they have the potential to cause more harm as they are redistributed to the brain, spinal column, and other sensitive tissues. The patent foramen ovale (PFO) was once thought to be the only risk factor for an increase in arterialization; however, IPAVAs represent another pathway for this crossover to occur. The opening of IPAVAs is associated with exercise and hypoxic gas mixtures, both of which divers may encounter. The goal of this review is to describe how IPAVAs may impact diving physiology, specifically during decompression, and what this means for the individual diver as well as the future of commercial and recreational diving. Future research must continue on the relationship between IPAVAs and the environmental and physiological circumstances that lead to their opening and closing, as well as how they may contribute to diving injuries such as DCS. © 2015, Wiley Periodicals, Inc.
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Alteration of breathing pattern ranging from an increase of respiratory rate to overt hyperventilation during and after SCUBA diving is frequently reported and is associated with intrathoracic fluid overload. This study was undertaken to assess breathing efficiency after diving and the association with damage of alveolar cells. Ventilation efficiency (VE/VCO2) during maximal cardiopulmonary exercise test (CPET) before and 2 h after a standard protocol dive has been analyzed in twelve professional males divers (39.5 ± 10.5 years). Furthermore, within 30 min from surfacing, subjects underwent blood sample for surfactant derived proteins (SPs) determination, while thoracic ultrasound was performed at 30, 60, 90 and 120 min. Dive consisted in a single quick descend to 18 m of sea water, a 47 min bottom stay and a direct ascent to the surface. CPET showed a preserved exercise performance with an increase of VE/VCO2 after diving (21.4 ± 2.9 vs. 22.9 ± 3.3, p < 0.05). Mature SP-B increased while other SPs were unchanged. Ultrasound lung comets (ULC) were high in the first post-dive evaluation with a significant, but not complete, progressive reduction at 120 min after surfacing. In conclusion we showed that, after a single dive, lung fluid increased with an increase of ventilation inefficiency and of the mature form of SP-B.
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Diving often causes the formation of 'silent' bubbles upon decompression. If the bubble load is high, then the risk of decompression sickness (DCS) and the number of bubbles that could cross to the arterial circulation via a pulmonary shunt or patent foramen ovale increase. Bubbles can be monitored aurally, with Doppler ultrasound, or visually, with two dimensional (2D) ultrasound imaging. Doppler grades and imaging grades can be compared with good agreement. Early 2D imaging units did not provide such comprehensive observations as Doppler, but advances in technology have allowed development of improved, portable, relatively inexpensive units. Most now employ harmonic technology; it was suggested that this could allow previously undetectable bubbles to be observed. This paper provides a review of current methods of bubble measurement and how new technology may be changing our perceptions of the potential relationship of these measurements to decompression illness. Secondly, 69 paired ultrasound images were made using conventional 2D ultrasound imaging and harmonic imaging. Images were graded on the Eftedal-Brubakk (EB) scale and the percentage agreement of the images calculated. The distribution of mismatched grades was analysed. Fifty-four of the 69 paired images had matching grades. There was no significant difference in the distribution of high or low EB grades for the mismatched pairs. Given the good level of agreement between pairs observed, it seems unlikely that harmonic technology is responsible for any perceived increase in observed bubble loads, but it is probable that our increasing use of 2D ultrasound to assess dive profiles is changing our perception of 'normal' venous and arterial bubble loads. Methods to accurately investigate the load and size of bubbles developed will be helpful in the future in determining DCS risk.
Article
The goals of this study were to investigate the difference in responses between a SCUBA dive preceded by aerobic exercise (EX) and a non-exercise control dive (CON), and further evaluate the potential relationship between venous gas emboli (VGE) and microparticles (MP). We hypothesized that exercise would alter the quantity and subtype of annexin V-positive MPs and VGE. Nineteen divers performed 2 dives to 18 m sea water for 41 min separated by at least 3 days, one of which was preceded by 60 min of treadmill interval exercise. Blood was obtained before exercise, before diving, and 15 min, 2, 4, and 24 h after surfacing. Intravascular bubbles were quantified by transthoracic echocardiography at 15, 40, 80, and 120 min. The median VGE remained unchanged between the 2 dives; however, there was a significant increase in VGE in the exercise dive at 40 and 80 min at rest. MPs were significantly elevated by approximately 2x at all time points following CON compared to EX. Markers of neutrophil and platelet activation were elevated by both dives and these elevations were attenuated in the EX dive. We conclude that some of the differences observed between the EX and CON related to MPs, platelet, and neutrophil activation provide additional insight to the potential protective benefits of exercise, however, further study is needed to understand the mechanism and true potential of these benefits.
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The presence of circulating gas bubbles and their influence on pulmonary and right heart hemodynamics was reported after uncomplicated self-contained underwater breathing apparatus (SCUBA) dive(s). Improvements in cardiac imaging have recently focused great attention on the right ventricle (RV). The aim of our study was to evaluate possible effects of a single air SCUBA dive on RV function using 2D speckle tracking echocardiography in healthy divers after single open sea dive to 18 meters of seawater, followed by bottom stay of 47 minutes with a direct ascent to the surface. Twelve experienced male divers (age 39.5 ± 10.5 years) participated in the study. Echocardiographic assessment of the right ventricular function (free wall 2 D strain, tricuspid annular planes systolic excursion [TAPSE], lateral tricuspid annular peak systolic velocity [RV s`] and fractional area change [FAC]) was performed directly prior to and 30, 60, 90 and 120 minutes after surfacing. Two-dimensional strain of all three segments of free right ventricular wall showed a significant increase in longitudinal shortening in post-dive period for maximally 26% (basal), 15.4% (mid) and 16.3% (apical) as well as TAPSE (11.6%), RV FAC (19.2%), RV S` (12.7%) suggesting a rise in systolic function of right heart. Mean pulmonary arterial pressure (mean PAP) increased post-dive from 13.3 mmHg to maximally 23.5 mmHg (P = .002), indicating increased RV afterload. Our results demonstrated that single dive with significant bubble load lead to increase in systolic function and longitudinal strain of the right heart in parallel with increase in mean PAP.
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Molecular oxygen (O2) is a vital element in human survival and plays a major role in a diverse range of biological and physiological processes. Although normobaric hyperoxia can increase arterial oxygen content (CaO2), it also causes vasoconstriction and hence reduces O2delivery in various vascular beds including the heart, skeletal muscle, and brain. Thus, a seemingly paradoxical situation exists in which the administration of oxygen may place tissues at increased risk of hypoxic stress. Nevertheless, with various degrees of effectiveness, and not without consequences, supplemental oxygen is used clinically in an attempt to correct tissue hypoxia (e.g. brain ischemia, traumatic brain injury, carbon monoxide poisoning, etc.), chronic hypoxemia (e.g. severe COPD, etc.), and to help with wound healing, necrosis, or reperfusion injuries (e.g. compromised grafts). Hyperoxia has also been used liberally by athletes in a belief that it offers performance enhancing benefits; such benefits also extend to hypoxemic patients both at rest and during rehabilitation. This review aims to provide a comprehensive overview of the effects of hyperoxia in humans from the 'bench-to-bedside'. The first section will focus on the basic physiological principles of partial pressure of arterial O2, CaO2, barometric pressure and how these changes lead to variation in regional O2delivery. The next section provides an overview of the evidence for and against the use of hyperoxia as an aid to enhance physical performance. The final section addresses pathophysiological concepts, clinical studies, and implications for therapy. The potential of O2toxicity and future research directions are also considered.
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Plasma gelsolin (pGSN) levels fall in association with diverse inflammatory conditions. We hypothesized pGSN would decrease due to the stresses imposed by high pressure and subsequent decompression, and repletion would ameliorate injuries in a murine decompression sickness (DCS) model. Research subjects were found to exhibit a modest decrease in pGSN level while at high pressure and a profound decrease after decompression. Changes occurred concurrent with elevations of circulating microparticles (MPs) carrying interleukin (IL)-1β. Mice exhibited a comparable decrease in pGSN after decompression along with elevations of MPs carrying IL-1β. Infusion of recombinant human (rhu)-pGSN into mice before or after pressure exposure abrogated these changes and prevented capillary leak in brain and skeletal muscle. Human and murine MPs generated under high pressure exhibited surface filamentous (F-) actin to which pGSN binds, leading to particle lysis. Additionally, human neutrophils exposed to high air pressure exhibit an increase in surface F-actin that is diminished by rhu-pGSN resulting in inhibition of MPs production. Administration of rhu-pGSN may have benefit as prophylaxis or treatment for DCS.
Article
Technical divers perform deep, mixed-gas 'bounce' dives, which are inherently inefficient because even a short duration at the target depth results in lengthy decompression. Technical divers use decompression schedules generated from modified versions of decompression algorithms originally developed for other types of diving. Many modifications ostensibly produce shorter and/or safer decompression, but have generally been driven by anecdote. Scientific evidence relevant to many of these modifications exists, but is often difficult to locate. This review assembles and examines scientific evidence relevant to technical diving decompression practice. There is a widespread belief that bubble algorithms, which redistribute decompression in favour of deeper decompression stops, are more efficient than traditional, shallow-stop, gas-content algorithms, but recent laboratory data support the opposite view. It seems unlikely that switches from helium- to nitrogen-based breathing gases during ascent will accelerate decompression from typical technical bounce dives. However, there is evidence for a higher prevalence of neurological decompression sickness (DCS) after dives conducted breathing only helium-oxygen than those with nitrogen-oxygen. There is also weak evidence suggesting less neurological DCS occurs if helium-oxygen breathing gas is switched to air during decompression than if no switch is made. On the other hand, helium-to-nitrogen breathing gas switches are implicated in the development of inner-ear DCS arising during decompression. Inner-ear DCS is difficult to predict, but strategies to minimize the risk include adequate initial decompression, delaying helium-to-nitrogen switches until relatively shallow, and the use of the maximum safe fraction of inspired oxygen during decompression.
Article
Circulating venous bubbles after dives are associated with symptoms of decompression sickness in adults. Up to now it is not known to what extent children and adolescents are subjected to a bubble formation during their shallow dives and if there are possible indications for that. The aim of this pilot study is to investigate whether bubbles and/or symptoms occur after standardised repeated dives performed by young divers. 28 children and adolescents (13.5±1.1 years) carried out two 25 min dives to a depth of 10 m with a 90 min surface interval. Before and after, echocardiographic data were recorded and evaluated with regard to circulating bubbles with an extended Eftedal-Brubakk-Scale by 2 different examiners. Bubbles were observed for a total of 6 subjects, Grade I (n=5) and Grade III (n=1). None of them showed any symptoms of decompression sickness. No differences were established regarding potential influencing factors on bubble formation between the groups with and without bubbles. The results indicate that even relatively shallow and short dives can generate venous bubbles in children and adolescents. To what extent this relates to the decompression sickness or clinical symptoms cannot be validated at this point.
Article
Hyperbaric oxygen (HBO2) became a mainstay for treating decompression sickness (DCS) because bubbles are associated with the disorder. Inflammatory processes including production of circulating microparticles (MPs) have now been shown to occur with DCS, leading to questions regarding pathophysiology and the role for HBO2. We investigated effects of HBO2 on mice exposed to 790 kPa air pressure for 2 h, which triggers elevations of MPs ladened with interleukin (IL)-1β that cause diffuse vascular injuries. Exposure to 283 kPa O2 (HBO2) inhibited MP elevations at 2 h postdecompression by 50% when applied either prophylactically or as treatment after decompression, and the MP number remained suppressed for 13 h in the prophylactic group. Particle content of IL-1β at 2 h postdecompression was 139.3 ± 16.2 [means ± SE; n = 11, P < 0.05) pg/million MPs vs. 8.2 ± 1.0 ( n = 15) in control mice, whereas it was 31.5 ± 6.1 ( n = 6, not significant vs. control (NS)] in mice exposed to HBO2 prophylactically, and 16.6 ± 6.3 ( n = 7, NS) when HBO2 was administered postdecompression. IL-1β content in MPs was similar in HBO2-exposed mice at 13 h postdecompression. HBO2 also inhibited decompression-associated neutrophil activation and diffuse vascular leak. Immunoprecipitation studies demonstrated that HBO2 inhibits high-pressure-mediated neutrophil nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 inflammasome oligomerization. Furthermore, MPs isolated from decompressed mice cause vascular injuries when injected into naïve mice, but if decompressed mice were exposed to HBO2 before MP harvest, vascular injuries were inhibited. We conclude that HBO2 impedes high-pressure/decompression-mediated inflammatory events by inhibiting inflammasome formation and IL-1β production. NEW & NOTEWORTHY High pressure/decompression causes vascular damage because it stimulates production of microparticles that contain high concentrations of interleukin-1β, and hyperbaric oxygen can prevent injuries.
Article
The pathogenesis of predominantly neurological decompression sickness (DCS) is multifactorial. In SCUBA diving, besides gas bubbles, DCS has been linked to microparticle release, impaired endothelial function, and platelet activation. This study focused on vascular damage and its potential role in the genesis of DCS in breath-hold diving. Eleven breath-hold divers participated in a field study comprising eight deep breath-hold dives with short surface periods and repetitive breath-hold dives lasting for 6 h. Endothelium-dependent vasodilation of the brachial artery, via flow-mediated dilation (FMD), and the number of microparticles (MPs) were assessed before and after each protocol. All measures were analyzed by two-way within-subject ANOVA (2 × 2 ANOVA; factors: time and protocol). Absolute FMD was reduced following both diving protocols (p < 0.001), with no interaction (p = 0.288) or main effect of protocol (p = 0.151). There was a significant difference in the total number of circulating MPs between protocols (p = 0.007), where both increased post-dive (p = 0.012). The number of CD31+/CD41- and CD66b+ MP subtypes, although different between protocols (p < 0.001), also increased by 41.0% ± 56.6% (p = 0.050) and 60.0% ± 53.2% (p = 0.045) following deep and repetitive breath-hold dives, respectively. Both deep and repetitive breath-hold diving lead to endothelial dysfunction that may play an important role in the genesis of neurological DCS.
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Techniques for ultrasonic assessment of decompression stress continue to evolve in concert with technological development. While aural Doppler remains a staple, imaging techniques are gaining in popularity. Current initiatives to increase the resolution of three-dimensional and dual-frequency imaging hold promise to expand our monitoring capabilities. An appreciation of the limitations and strengths of ultrasonic assessment is important to interpret existing work on decompression and to appropriately design new studies.
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Although decompression procedures have been improved over the years, decompression still remains a significant problem in diving. While there is universal agreement that the basic problem of decompression is gas coming out of solution, forming bubbles when pressure is reduced, the exact mechanism of decompression injury is not known. Furthermore, the wide variety of clinical symptoms and the significant difference in individual susceptibility makes identification of the mechanisms involved difficult. Using ultrasound, vascular gas bubbles have been detected in most decompressions, and these bubbles can act on the endothelial lining of blood vessels resulting in impaired endothelial function. Normal endothelial function is a major indicator of cardiovascular health and thus a reduction in vascular bubble formation and hence the risk of endothelial injury is an important goal in decompression. Even if vascular gas bubbles may not be the only adverse effect of decompression, vascular gas bubbles and their adverse effects on the endothelium may be a useful model for decompression injury. This review claims that endothelial dysfunction may be a possible main mechanism for neurological decompression injuries and describes some of the effects of vascular gas bubbles on the endothelium. Furthermore, as the formation of vascular gas bubbles can be significantly influenced by physical exercise and the use of nitric oxide, a novel approach to reducing the risk of decompression injury is suggested.
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Persistent foramen ovale (PFO) is found in 9.2--32% of echocardiographic examinations. The gold standard for the detection of a PFO is transoesophageal echocardiography (TEE) and the mostly used provocation test is the Valsalva manoeuvre. The aim of our study was to evaluate the effectiveness of the Valsalva manoeuvre compared to other provocation tests by simultaneous haemodynamic measurements of the right and left atrial pressure. Fifty patients underwent Swan-Ganz catheterization. Right atrial pressure and pulmonary capillary wedge pressure, which corresponds to the left atrial pressure, were measured simultaneously. The following manoeuvres were compared: the Valsalva manoeuvre, coughing, deep inspiration and expiration pressures of 20 mmHg, 40 mmHg and 60 mmHg. The main objective of our study was to compare the occurrence of pressure gradients (right atrial pressure> left atrial pressure). For further quantification mean gradients, time duration of pressure overlap, as well as products of mean gradients and overlap time were analysed. During the Valsalva manoeuvre a significant pressure gradient could be observed in 84% of the patients, followed by an expiration pressure of 60 mmHg (82%), inspiration (78%), expiration pressure of 40 mmHg (76%), coughing (75%) and an expiration pressure of 20 mmHg (62%). Comparing the mean gradients and the products of mean gradients and overlap time duration during the different manoeuvres, we could detect the significantly best results with the Valsalva manoeuvre. The Valsalva manoeuvre might be the most effective test to provoke a right-to-left atrial shunt for the detection of a PFO during echocardiographic examinations.
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Gas bubbles from decompression and gas embolization lead to endothelial dysfunction and mechanical injury in the pig, rabbit and lamb. In the study presented here, 0.01 ml air/min/kg was infused through a catheter into the jugular vein in 12 rabbits for 60 min. The endothelial response was measured using tension measurements in the blood vessel wall, and morphological changes where quantified using light microscopy and image processing. Percent lung water content was calculated and used to estimate the severity of pulmonary oedema. The infusion led to a significant decrease in the acetylcholine-mediated endothelial-dependent vasodilatation in the pulmonary artery 6 h after the infusion (6-h group, n = 6). A decrease in substance-P-mediated endothelial-dependent vasodilatation was also detected. No changes where seen in a group of rabbits examined 1 h after infusion (l-h group, n=6). The impaired endothelial-dependent vasodilatation caused by the bubbles is probably biochemical in origin, since no visible changes were seen in the endothelial layer. A significant increase in polymorphonuclear neutrophils was observed in the 6-h group compared to the l-h group. This study demonstrates that small numbers of bubbles, corresponding to "silent bubbles", lead to an impairment of the endothelial-dependent vasoactive response.
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Paradoxical arterializations of venous gas emboli can lead to neurological damage after diving with compressed air. Recently, significant exercise-induced intrapulmonary anatomical shunts have been reported in healthy humans that result in widening of alveolar-to-arterial oxygen gradient. The aim of this study was to examine whether intrapulmonary shunts can be found following strenuous exercise after diving and, if so, whether exercise should be avoided during that period. Eleven healthy, military male divers performed an open-sea dive to 30 m breathing air, remaining at pressure for 30 min. During the bottom phase of the dive, subjects performed mild exercise at approximately 30% of their maximal oxygen uptake. The ascent rate was 9 m/min. Each diver performed graded upright cycle ergometry up to 80% of the maximal oxygen uptake 40 min after the dive. Monitoring of venous gas emboli was performed in both the right and left heart with an ultrasonic scanner every 20 min for 60 min after reaching the surface pressure during supine rest and following two coughs. The diving profile used in this study produced significant amounts of venous bubbles. No evidence of intrapulmonary shunting was found in any subject during either supine resting posture or any exercise grade. Also, short strenuous exercise after the dive did not result in delayed-onset decompression sickness in any subject, but studies with a greater number of participants are needed to confirm whether divers should be allowed to exercise after diving.
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Most decompression procedures induce the formation of asymptomatic venous gas bubbles. They can be classified as "silent bubbles," which are asymptomatic compared to paradoxical arterialization of venous gas emboli, which can lead to serious neurologic damage. The penetration of such gas bubbles into the arterial circulation is due to pulmonary barotrauma, intrapulmonary (I-P) passage after massive bubble formation ("chokes"), or intracardiac shunting. Venous gas bubbles can be monitored and graded with echocardiographic scanning. We believe this is the first case to be reported of a recreational diver who, after surfacing from a dive, developed grade 5 ("white-out") venous gas bubbles in the right heart with evidence of I-P shunt at rest without any symptoms of decompression sickness. Grade 4 gas bubbles were found on the left side of the heart, indicating significant I-P shunting even at rest. We observed venous bubbles crossing through the I-P shunt during post-dive recovery at rest in a diver who developed "white out" of venous bubbles. Previously, the maximum bubble grade 5 had been observed in experimental animals, but not in humans. Moreover, a significant bubble grade was found on the left side of the heart, indicating a need for further studies to investigate the mechanisms of post-dive changes in peripheral and central circulation.
Article
Purpose. To determine whether spectral Doppler measurements obtained from bilateral uterine, arcuate, radial, and spiral arteries in early gestation correlate with adverse pregnancy outcome. Methods. One hundred five pregnant women underwent transvaginal Doppler sonographic examination of uteroplacental circulation at 6-12 weeks' gestation. Resistance index (RI) and pulsatility index (PI) of bilateral uterine, arcuate, radial, and spiral arteries were measured. Diameters of gestational sac (GS) and yolk sac, crown-rump length (CRL), GS-CRL difference, and GS/CRL ratio were also recorded. Correlation was made with pregnancy outcome. Results. Sixteen women developed adverse pregnancy outcome. In these women, right uterine artery PI and RI were significantly higher than in women with normal obstetrical outcome. Spiral artery PI and RI values were also higher, but the difference was not statistically significant. GS-CRL difference, GS/CRL ratio, and yolk sac diameters were significantly lower in this group. Conclusion. Transvaginal Doppler examination can detect hemodynamic changes in uteroplacental circulation associated with subsequent adverse pregnancy outcome. (C) 2007 Wiley Periodicals, Inc.
Article
Paradoxical arterializations of venous gas emboli can lead to neurological damage after diving with compressed air. Recently, significant exercise-induced intrapulmonary anatomical shunts have been reported in healthy humans that result in widening of alveolar-to-arterial oxygen gradient. The aim of this study was to examine whether intrapulmonary shunts' can be found following strenuous exercise after diving and, if so, whether exercise should be avoided during that period. Eleven healthy, military male divers performed an open-sea dive to 30 in breathing air, remaining at pressure for 30 min. During the bottom phase of the dive, subjects performed mild exercise at similar to 30% of their maximal oxygen uptake. The ascent rate was 9 m/min. Each diver performed graded upright cycle ergometry up to 80% of the maximal oxygen uptake 40 min after the dive. Monitoring of venous gas emboli was performed in both the right and left heart with an ultrasonic scanner every 20 min for 60 min after reaching the surface pressure during supine rest and following two coughs. The diving profile used in this study produced significant amounts of venous bubbles. No evidence of intrapulmonary shunting was found in any subject during either supine resting posture or any exercise grade. Also, short strenuous exercise after the dive did not result in delayed-onset decompression sickness in any subject, but studies with a greater number of participants are needed to confirm whether divers should be allowed to exercise after diving.
Article
Aims: Persistent foramen ovale (PFO) is found in 9·2–32% of echocardiographic examinations. The gold standard for the detection of a PFO is transoesophageal echocardiography (TEE) and the mostly used provocation test is the Valsalva manoeuvre. The aim of our study was to evaluate the effectiveness of the Valsalva manoeuvre compared to other provocation tests by simultaneous haemodynamic measurements of the right and left atrial pressure. Methods: Fifty patients underwent Swan-Ganz catheterization. Right atrial pressure and pulmonal capillary wedge pressure, which corresponds to the left atrial pressure, were measured simultaneously. The following manoeuvres were compared: the Valsalva manoeuvre, coughing, deep inspiration and expiration pressures of 20 mmHg, 40 mmHg and 60 mmHg. The main objective of our study was to compare the occurrence of pressure gradients (right atrial pressure) left atrial pressure). For further quantification mean gradients, time duration of pressure overlap, as well as products of mean gradients and overlap time were analysed. Results: During the Valsalva manoeuvre a significant pressure gradient could be observed in 84% of the patients, followed by an expiration pressure of 60 mmHg (82%), inspiration (78%), expiration pressure of 40 mmHg (76%), coughing (75%) and an expiration pressure of 20 mmHg (62%). Comparing the mean gradients and the products of mean gradients and overlap time duration during the different manoeuvres, we could detect the significantly best results with the Valsalva manoeuvre. Conclusions: The Valsalva manoeuvre might be the most effective test to provoke a right-to-left atrial shunt for the detection of a PFO during echocardiographic examinations.
Article
SCUBA diving is associated with generation of gas emboli due to gas release from the supersaturated tissues during decompression. Gas emboli arise mostly on the venous side of circulation, and they are usually eliminated as they pass through the lung vessels. Arterialization of venous gas emboli (VGE) is seldom reported, and it is potentially related to neurological damage and development of decompression sickness. The goal of the present study was to evaluate the generation of VGE in a group of divers using a mixture of compressed oxygen, helium, and nitrogen (trimix) and to probe for their potential appearance in arterial circulation. Seven experienced male divers performed three dives in consecutive days according to trimix diving and decompression protocols generated by V-planner, a software program based on the Varying Permeability Model. The occurrence of VGE was monitored ultrasonographically for up to 90 min after surfacing, and the images were graded on a scale from 0 to 5. The performed diving activities resulted in a substantial amount of VGE detected in the right cardiac chambers and their frequent passage to the arterial side, in 9 of 21 total dives (42%) and in 5 of 7 divers (71%). Concomitant measurement of mean pulmonary artery pressure revealed a nearly twofold augmentation, from 13.6 ± 2.8, 19.2 ± 9.2, and 14.7 ± 3.3 mmHg assessed before the first, second, and the third dive, respectively, to 26.1 ± 5.4, 27.5 ± 7.3, and 27.4 ± 5.9 mmHg detected after surfacing. No acute decompression-related disorders were identified. The observed high gas bubble loads and repeated microemboli in systemic circulation raise questions about the possibility of long-term adverse effects and warrant further investigation.
Article
Thesis (doctoral)--Katholieke Universiteit van Nijmegen.
If P1 is the pressure breathed by men for a prolonged period, and P2 is the pressure to which it is just safe to decompress rapidly, then assuming the volume of tissue gas released upon decompression is critical, it is predictable from theoretical considerations that there is a relation between P1 and P2 of the form P1 = aP2 + b, where a and b are constants. The use of men as experimental subjects confirms this theoretical prediction for the case where mixtures of oxygen and helium are breathed. By assuming that the same critical volume of released gas provokes mild attacks of decompression sickness when air, or other respirable gases are breathed, the relevant values of a and b can be deduced, and the values accord well with the known facts for such gases. This analysis also offers an explanation for the changes in signs and symptoms of decompression sickness which can follow changes in the nature of the exposure to pressure.
Article
Mongrel dogs weighing 15-25 kg and anesthetized with thiopental-gamma-hydroxybutyric acid were used to investigate the effects of pulmonary gas embolism on pulmonary arterial pressure (Pap), systemic arterial pressure (Pa) and cardiac output (Q). Pulmonary gas embolism was produced either by venous injecton or by venous infusion. The most marked effect of pulmonary gas embolism on circulation was an increase in Pap which returned to the original level after stopping the gas administration. 1. After gas injection Pap rose to a maximum within 30--60 s. The extent of this rise in Pap showed a positive correlation with the volume of the injected gas. The kind of gas (oxygen, helium, neon, nitrogen, air), however, did not influence the extent of the rise in Pap, but did influence the time of return of Pap to the original level. Carbon dioxide showed an exceptional behavior in that it had almost no effect on Pap at all. P a hardly changed with the volume of the gas injections (20--60 ml injected within 1 s); Q was not measured after gas injection (the direct Fick method is not usable in this situation). 2. Gas infusion caused a slow rise of Pap, its steepness and extent depending on the rate of infusion and on the physical properties of the infused gas. When the right ventricle was able to maintain its output, a constant level of Pap was reached after 10--15 min. In this circulatory steady state Pap appeared to be a measure of the degree of embolization. However, this relationship no longer held when the right ventricle failed as evidenced by a fall in Pap, Pa and Q. It may be concluded that pulmonary gas embolism produces a transient partial obstruction in the pulmonary circulation and that the performance of the right ventricle determines the maximum degree of embolization compatible with a sufficient circulation.
Article
The dose-response relationship for decompression magnitude and venous gas emboli (VGE) formation in humans was examined. Pressure exposures of 138, 150, and 164 kPa (12, 16, and 20.5 ft of seawater gauge pressure) were conducted in an underwater habitat for 48 h. The 111 human male volunteer subjects then ascended directly to the surface in less than 5 min and were monitored for VGE with a continuous-wave Doppler ultrasound device over the precordium or the subclavian veins at regular intervals for a 24-h period. No signs or symptoms consistent with decompression sickness occurred. However, a large incidence of VGE detection was noted. These data were combined with those from our previously reported experiments at higher pressures, and the data were fit to a Hill dose-response equation with nonlinear least-squares or maximum likelihood routines. Highly significant fits of precordial VGE incidences were obtained with the Hill equation (saturation depth pressure at which there is a 50% probability of detectable VGE [D(VGE)50] = 150 +/- 1.2 kPa). Subclavian monitoring increased the sensitivity of VGE detection and resulted in a leftward shift [D(VGE)50 = 135 +/- 2 kPa] of the best-fit curve. We conclude that the reduction in pressure necessary to produce bubbles in humans is much less than was previously thought; 50% of humans can be expected to generate endogenous bubbles after decompression from a steady-state pressure exposure of only 135 kPa (11 ft of seawater). This may have significant implications for decompression schedule formulation and for altitude exposures that are currently considered benign. These results also imply that endogenous bubbles arise from preexisting gas collections.
Article
30 patients with a history of decompression sickness were examined for the presence of patent foramen ovale by bubble contrast, two-dimensional echocardiography and colour flow doppler imaging. With bubble contrast, 11 (37%) of the patients had right-to-left shunting through a patent foramen ovale during spontaneous breathing. 61% of a subset of 18 patients with serious signs and symptoms had shunting. This number was significantly higher than the 5% prevalence seen with the same diagnostic technique in 176 healthy volunteers. The presence of patent foramen ovale seems to be a risk factor for the development of decompression sickness in divers.
Article
The prevalence of right-to-left interatrial shunts was determined by contrast echocardiography in a blind comparison of 61 divers who had had decompression sickness, divided into four predetermined clinical subgroups, and a control group of 63 who had not. The prevalence of shunt was 15/63 in the controls and did not differ significantly in 24 divers with onset of neurological symptoms more than 30 minutes after surfacing (4/24) or 6 with joint pain only (1/6). In divers who had neurological symptoms within 30 minutes of surfacing the prevalence of shunt was 19/29, significantly higher. Rashes soon after surfacing were related to shunts but late rashes were not.
Article
The occurrence of intravascular bubbles in arteries and veins has been studied using pulsed Doppler ultrasound in six subjects who performed two ascending excursions each from 300 to 250 meters of seawater (msw) during a heliox saturation dive. Following decompression, high-intensity reflections could be observed not only in the venous system but also in the arteries, most notably in the carotid artery. Intravascular bubbles were more numerous during the first ascent than during the second. The arterial bubbles most probably come from the venous side of the circulation, indicating that the pulmonary filter is not as effective as previously thought during saturation diving.
Article
In our experience, it is easier to identify gas bubbles in ultrasonic images than in aural Doppler signals. To verify this, we asked 27 observers with no previous training to estimate the quantity of gas bubbles in video tapes containing sequences of ultrasound images recorded during decompression experiments. The amount of bubbles was graded according to a non-linear grading system with six levels. The results obtained were compared to evaluations performed on-site by a trained observer. Approximately 70% of the evaluations performed by the untrained observers agreed completely with the on-site gradings, and more than 95% agreed within 1 grade unit. The strength of agreement can be described by use of the weighted kappa statistic, and we have compared the agreement in our study with agreement obtained in a previous study using Doppler signals for bubble detection. We find that in grading bubble signals in images, untrained observers perform equally as well as trained observers grading bubbles in Doppler signals. We conclude that ultrasonic imaging offers a useful and cost-effective alternative to Doppler systems for detection and quantification of intravascular gas bubbles.
Article
Neurologic injury subsequent to decompression from diving may be due to paradoxical arterialization of venous gas emboli. Of 40 divers who performed 53 open water dives after being tested for a patent foramen ovale (PFO), arterial gas emboli were detected in 7 of 13 dives, which resulted in venous bubbles. In five of these seven dives, there was evidence of a PFO by contrast transcranial Doppler sonography, indicating an increased risk of arterializing venous bubbles in divers with a PFO.
Article
We have previously shown in a rat model that a single bout of high-intensity aerobic exercise 20 h before a simulated dive reduces bubble formation and after the dive protects from lethal decompression sickness. The present study investigated the importance of these findings in man. Twelve healthy male divers were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa min(-1) breathing air and remaining at pressure for 80 min. The ascent rate was 9 m min(-1) with a 7 min stop at 130 kPa. Each diver underwent two randomly assigned simulated dives, with or without preceding exercise. A single interval exercise performed 24h before the dive consisted of treadmill running at 90% of maximum heart rate for 3 min, followed by exercise at 50% of maximum heart rate for 2 min; this was repeated eight times for a total exercise period of 40 min. Venous gas bubbles were monitored with an ultrasonic scanner every 20 min for 80 min after reaching surface pressure. The study demonstrated that a single bout of strenuous exercise 24h before a dive to 18 m of seawater significantly reduced the average number of bubbles in the pulmonary artery from 0.98 to 0.22 bubbles cm(-2)(P= 0.006) compared to dives without preceding exercise. The maximum bubble grade was decreased from 3 to 1.5 (P= 0.002) by pre-dive exercise, thereby increasing safety. This is the first report to indicate that pre-dive exercise may form the basis for a new way of preventing serious decompression sickness.
Article
We hypothesized that increasing exercise intensity recruits dormant arteriovenous intrapulmonary shunts, which may contribute to the widened alveolar-arterial oxygen difference seen with exercise. Twenty-three healthy volunteers (13 men and 10 women, aged 23-48 yr) with normal lung function and a wide range of fitness (mean maximal oxygen uptake = 126% predicted; range = 78-200% predicted) were studied by agitated saline contrast echocardiography (4-chamber apical view). All 23 subjects had normal resting contrast echocardiograms without evidence of intracardiac or intrapulmonary shunting. However, with cycle ergometer exercise, 21 of 23 (91%) of the subjects showed a delayed (>3 cardiac cycles) appearance of contrast bubbles in the left heart. This pattern is consistent with passage of contrast bubbles through the pulmonary circulation. Because the contrast bubbles are known to be significantly larger than pulmonary capillaries, we propose that they are traveling through direct arteriovenous intrapulmonary shunts. In all cases, the intrapulmonary shunting developed at submaximal oxygen uptakes [%maximal oxygen uptake = 59 +/- 20 (SD)] and once evident persisted at all subsequent work rates. Within 3 min of exercise termination, the contrast echocardiograms with bubble injection showed no evidence of intrapulmonary shunting. These dynamic shunts will contribute significantly to the widened alveolar-arterial oxygen difference seen with exercise. They may also act as a protective parallel vascular network limiting the rise in regional pulmonary vascular pressure while preserving cardiac output during exercise.
Article
During and after decompression from dives, gas bubbles are regularly observed in the right ventricular outflow tract. A number of studies have documented that these bubbles can lead to endothelial dysfunction in the pulmonary artery but no data exist on the effect of diving on arterial endothelial function. The present study investigated if diving or oxygen breathing would influence endothelial arterial function in man. A total of 21 divers participated in this study. Nine healthy experienced male divers with a mean age of 31 +/- 5 years were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa min(-1) breathing air and remaining at pressure for 80 min. The ascent rate during decompression was 9 kPa min(-1) with a 7 min stop at 130 kPa (US Navy procedure). Another group of five experienced male divers (31 +/- 6 years) breathed 60% oxygen (corresponding to the oxygen tension of air at 280 kPa) for 80 min. Before and after exposure, endothelial function was assessed in both groups as flow-mediated dilatation (FMD) by ultrasound in the brachial artery. The results were compared to data obtained from a group of seven healthy individuals of the same age who had never dived. The dive produced few vascular bubbles, but a significant arterial diameter increase from 4.5 +/- 0.7 to 4.8 +/- 0.8 mm (mean +/- s.d.) and a significant reduction of FMD from 9.2 +/- 6.9 to 5.0 +/- 6.7% were observed as an indication of reduced endothelial function. In the group breathing oxygen, arterial diameter increased significantly from 4.4 +/- 0.3 mm to 4.7 +/- 0.3 mm, while FMD showed an insignificant decrease. Oxygen breathing did not decrease nitroglycerine-induced dilatation significantly. In the normal controls the arterial diameter and FMD were 4.1 +/- 0.4 mm and 7.7 +/- 0.2.8%, respectively. This study shows that diving can lead to acute arterial endothelial dysfunction in man and that oxygen breathing will increase arterial diameter after return to breathing air. Further studies are needed to determine if these mechanisms are involved in tissue injury following diving.
Article
After decompression from dives, bubbles are frequently observed in the right ventricular outflow tract and may lead to vascular damage, pulmonary arterial hypertension and right ventricular overload. No data exist on the effect of open sea diving on the pulmonary artery pressure (PAP). Eight professional divers performed an open sea air dive to 30 msw. Before and postdive a Doppler echocardiographic study was undertaken. Systolic pulmonary artery pressure (SPAP) was estimated from measurement of peak flow velocity of the tricuspid regurgitant jet; the ratio between pulmonary artery acceleration times (AccT) and right ventricular ejection time (RVET) was used as an estimate of the mean PAP. No evidence of either patent foramen ovale or intra-pulmonary shunt was found in any subject postdive after performing a Valsalva maneuver. SPAP increased from 25 +/- 3 to 33 +/- 2 mmHg and AccT/RVET ratio decreased from 0.44 +/- 0.04 to 0.3 +/- 0.02 20 min after the dive, respectively. Pulmonary vascular resistance increased from 1.2 +/- 0.1 to 1.4 +/- 0.1 Woods Units. Postdive right ventricle end-diastolic and end-systolic volumes were increased for about 19% (P = 0.001) and 33% (P = 0.001) and right ejection fraction decreased about for 6% (P = 0.001). Cardiac output decreased from 4.8 +/- 0.9 (l min(-1)) to 4.0 +/- 0.6 at 40 min postdive due to decreases in heart rate and stroke volume. This study shows that a single open sea dive may be associated with right heart overload due to increased pressure in the pulmonary artery.
Article
Diving-induced acute alterations in cardiovascular function such as arterial endothelial dysfunction, increased pulmonary artery pressure (PAP) and reduced heart function have been recently reported. We tested the effects of acute antioxidants on arterial endothelial function, PAP and heart function before and after a field dive. Vitamins C (2 g) and E (400 IU) were given to subjects 2 h before a second dive (protocol 1) and in a placebo-controlled crossover study design (protocol 2). Seven experienced divers performed open sea dives to 30 msw with standard decompression in a non-randomized protocol, and six of them participated in a randomized trial. Before and after the dives ventricular volumes and function and pulmonary and brachial artery function were assessed by ultrasound. The control dive resulted in a significant reduction in flow-mediated dilatation (FMD) and heart function with increased mean PAP. Twenty-four hours after the control dive FMD was still reduced 37% below baseline (8.1 versus 5.1%, P = 0.005), while right ventricle ejection fraction (RV-EF), left ventricle EF and endocardial fractional shortening were reduced much less (approximately 2-3%). At the same time RV end-systolic volume was increased by 9% and mean PAP by 5%. Acute antioxidants significantly attenuated only the reduction in FMD post-dive (P < 0.001), while changes in pulmonary artery and heart function were unaffected by antioxidant ingestion. These findings were confirmed by repeating the experiments in a randomized study design. FMD returned to baseline values 72 h after the dive with pre-dive placebo, whereas for most cardiovascular parameters this occurred earlier (24-48 h). Right ventricular dysfunction and increased PAP lasted longer. Acute antioxidants attenuated arterial endothelial dysfunction after diving, while reduction in heart and pulmonary artery function were unchanged. Cardiovascular changes after diving are not fully reversed up to 3 days after a dive, suggesting longer lasting negative effects.
Article
We report a case of right-to-left intrapulmonary (IP) shunting of venous gas bubbles at a high level of exercise after diving. The diagnosis was made using a 4-chamber view of the heart via echocardiography during exercise. This case is the first in which we could find evidence of IP shunt recruitment during exercise after diving, and the bubble grade was the highest ever seen in our laboratory. Venous bubbles crossing over through IP shunts during exercise after diving is a very rare event. © 2007 Wiley Periodicals, Inc. J Clin Ultrasound, 2007