Effect of in-water recompression with oxygen to 6 msw versus normobaric oxygen breathing on bubble formation in divers

Article (PDF Available)inArbeitsphysiologie 106(5):691-5 · June 2009with41 Reads
DOI: 10.1007/s00421-009-1065-y · Source: PubMed
Abstract
It is generally accepted that the incidence of decompression sickness (DCS) from hyperbaric exposures is low when few or no bubbles are present in the circulation. To date, no data are available on the influence of in-water oxygen breathing on bubble formation following a provocative dive in man. The purpose of this study was to compare the effect of post-dive hyperbaric versus normobaric oxygen breathing (NOB) on venous circulating bubbles. Nineteen divers carried out open-sea field air dives at 30 msw depth for 30 min followed by a 9 min stop at 3 msw. Each diver performed three dives: one control dive, and two dives followed by 30 min of hyperbaric oxygen breathing (HOB) or NOB; both HOB and NOB started 10 min after surfacing. For HOB, divers were recompressed in-water to 6 msw at rest, whereas NOB was performed in a dry room in supine position. Decompression bubbles were examined by a precordial pulsed Doppler. Bubble count was significantly lower for post-dive NOB than for control dives. HOB dramatically suppressed circulating bubble formation with a bubble count significantly lower than for NOB or controls. In-water recompression with oxygen to 6 msw is more effective in removing gas bubbles than NOB. This treatment could be used in situations of "interrupted" or "omitted" decompression, where a diver returns to the water in order to complete decompression prior to the onset of symptoms. Further investigations are needed before to recommend this protocol as an emergency treatment for DCS.
Eur J Appl Physiol
DOI 10.1007/s00421-009-1065-y
123
ORIGINAL ARTICLE
EVect of in-water recompression with oxygen to 6 msw versus
normobaric oxygen breathing on bubble formation in divers
Jean-Eric Blatteau · Jean-Michel Pontier
Accepted: 15 April 2009
© Springer-Verlag 2009
Abstract It is generally accepted that the incidence of
decompression sickness (DCS) from hyperbaric exposures
is low when few or no bubbles are present in the circula-
tion. To date, no data are available on the inXuence of in-
water oxygen breathing on bubble formation following a
provocative dive in man. The purpose of this study was to
compare the eVect of post-dive hyperbaric versus normo-
baric oxygen breathing (NOB) on venous circulating bub-
bles. Nineteen divers carried out open-sea Weld air dives at
30 msw depth for 30 min followed by a 9 min stop at
3 msw. Each diver performed three dives: one control dive,
and two dives followed by 30 min of hyperbaric oxygen
breathing (HOB) or NOB; both HOB and NOB started
10 min after surfacing. For HOB, divers were recompressed
in-water to 6 msw at rest, whereas NOB was performed in a
dry room in supine position. Decompression bubbles were
examined by a precordial pulsed Doppler. Bubble count
was signiWcantly lower for post-dive NOB than for control
dives. HOB dramatically suppressed circulating bubble for-
mation with a bubble count signiWcantly lower than for
NOB or controls. In-water recompression with oxygen to
6msw is more eVective in removing gas bubbles than
NOB. This treatment could be used in situations of “inter-
rupted” or “omitted” decompression, where a diver returns
to the water in order to complete decompression prior to the
onset of symptoms. Further investigations are needed
before to recommend this protocol as an emergency treat-
ment for DCS.
Keywords Diving · Decompression sickness · Bubble ·
In-water recompression
Introduction
Divers are at risk of decompression sickness (DCS) caused
by bubbles of inert gas that may evolve in the tissues or
blood due to supersaturation during decompression. It is
generally hypothesized that gas bubbles grow from pre-
existing nuclei attached to the vessel walls or by hydro-
dynamic cavitation resulting mainly from musculoskeletal
activity (Blatteau et al. 2006a, b). The detection of venous
circulating bubbles is considered as a valuable indicator of
decompression stress and used as a tool for validation of
the safety of decompression procedures. It is generally
accepted that the incidence of DCS is low when few or no
bubbles are present in the circulation (Nishi et al. 2003).
Paul Bert is the Wrst to state that recompression using
oxygen is the optimal treatment for decompression injuries
and pointed out that this treatment was very eVective for
getting rid of the gas from vascular system (Bert 1878).
Vascular bubbles formed as a result of DCS continue to
grow for hours after their initial formation and mainly dam-
age the endothelium with numerous secondary eVects
related to biochemical or immunological responses devel-
oped with time (Francis and Mitchell 2003). There are two
theoretical considerations supporting recompression using
oxygen. First, the rapid removal of the bubbles from recom-
pression can prevent some of these secondary eVects and
avoid permanent tissue damage; and second there is the
advantage of increased inspired oxygen partial pressure
J.-E. Blatteau (&)
Ecole de Plongée Marine Nationale,
83800 Toulon Armées, France
e-mail: je.blatteau@infonie.fr
J.-M. Pontier
Département de Médecine,
Hyperbare Hôpital d’Instruction des Armées
Sainte-Anne, 83800 Toulon Armées, France
Eur J Appl Physiol
123
when pure oxygen is breathed, which can help counteract
the eVects of tissue hypoxia that may result from DCS-
induced endothelium damage.
Delay in starting treatment may inXuence results. It
appears that more severely injured divers are dependent on
the early treatment to maximize improvement (Ball 1993;
Moon and Gorman 2003) and that after 6 h or more, a fur-
ther hold-up of treatment does not inXuence outcome sig-
niWcantly (Stipp 2004; Ross et al. 2004). To achieve the
optimal outcome, the diver should be treated promptly and
longer delay than a few hours should be avoided.
The treatment of DCS remains a serious problem in
remote locations, especially in situations where the initia-
tion of a therapeutic recompression in a hyperbaric facility
may take several hours or days. In-water recompression
(IWR) is deWned as any attempt to treat or relieve suspected
symptoms of DCS by returning an aZicted diver to the
water. The published methods of IWR used pure oxygen
breathing for prolonged periods of time at a depth of 9 msw
(Edmonds 1999; Pyle 1999). IWR should be used in remote
localities as an immediate measure to stop the evolution of
DCS before evacuating the victim for subsequent treatment
to the nearest hyperbaric facility. However, there are many
problems associated with IWR that are well recognized by
both divers and medical advisers. Resulting from environ-
mental conditions, the risks of drowning and hypothermia
are the most often quoted, and pure oxygen breathing at
9 msw can also expose to acute oxygen toxicity. Moreover,
the IWR eVectiveness in comparison with standard recom-
pression techniques has not been assessed.
Actually, it is commonly accepted that normobaric oxy-
gen should be administered immediately after a DCS and
continued until the patient reaches the hyperbaric chamber.
This may signiWcantly reduce the symptoms for mild DCS,
but this initial treatment is not suYcient for patients with
severe neurological symptoms. The value of substituting
IWR for normobaric oxygen, in emergency treatment of
DCS has never been studied.
To date, no human clinical data are available on the
inXuence of in-water oxygen breathing on bubble formation
following a provocative dive. The purpose of this study was
to investigate whether oxygen breathing at 6 msw is more
eVective than normobaric oxygen in reducing post-dive
venous circulating bubbles.
Methods
Study population
Nineteen healthy military divers aged 23–48 years
(34 § 7 years, mean § SD), gave their written informed
consent to participate. All the subjects were trained divers
and none of them had experienced DCS in the past. Their
body mass index varied between 21.3 and 26.8 kg m
¡2
(24.2 § 1.4kgm
¡2
, mean § SD). All experimental proce-
dures were conducted in accordance with the declaration of
Helsinki.
Diving protocol
Scuba divers used open-circuit breathing air and were all
provided with the same diving material and thermal protec-
tion equipment (5 mm neoprene wetsuit). The dive protocol
consisted of an open-sea Weld dive to 30 msw (400 kPa)
breathing air for 30 min (sea temperature 15°C) with a
decompression rate of 15 msw min
¡1
and a 9-min stop at
3 msw (French Navy MN90 procedure). During bottom
time divers performed a constant Wn-swimming at a fre-
quency that was reproduced across all the dives. Each diver
performed three dives 3 days apart: one control dive, and
two dives followed by 30 min of hyperbaric (HOB) or
normobaric oxygen breathing (NOB); both HOB and NOB
started 10 min after surfacing. The divers did not do any
diving during the 3-day intermissions.
For HOB, divers carried out in-water recompression to
6 msw at rest (160 kPa PO
2
). NOB was performed in a dry
room with a stable environmental temperature (20°C) in
supine position (Xow rate of 15 l/min, 100 kPa PO
2
).
Supine NOB was chosen to be as close to the underwater
weightlessness HOB for the similarity of increased cardiac
output and blood volume distribution within the body.
The order of the three dives was randomly allocated.
Divers were instructed to avoid physical exertion and div-
ing during the 2 days that preceded each trial.
Bubbles analysis
Decompression bubbles were examined by a pulsed Dopp-
ler device equipped with a 2 MHz probe on the precordial
area (MicroMaxx, Sonosite Inc, Bothell, WA). Monitoring
was performed by the same blinded operator 40, 60, and
80 min after surfacing in supine position for 3 min at rest
and after two lower limbs Xexions. The signal of bubbles
was graded according to the Spencer scale (Spencer 1976)
before to be converted into Kissman Integrated Severity
Score (KISS). This score takes into account the kinetics of
the bubbles at the diVerent recording times and was
assumed to be a meaningful linearized measure of post-
decompression intravascular bubble activity status that may
be treated statistically (Nishi et al. 2003).
Statistical analysis
All data are presented as mean § SD. For statistic process-
ing, we used the Sigmastat 3.0 software program (SPSS
Eur J Appl Physiol
123
inc., Chicago, IL, USA). Data were analyzed using non-
parametric statistics because of the small sample-size.
Comparisons for diVerence in bubble grade were evaluated
by Friedman test (repeated measures ANOVA on ranks)
and Tukey’s test for all pairwise multiple comparisons. The
level of signiWcance was set at P <0.05.
Results
None of the divers suVered from DCS after the dives or pre-
sented signs of CNS oxygen toxicity. The kinetics of the
bubble scores at 40, 60, and 80 min revealed a bubble peak
at 60 min for the control dives, whereas the bubble peak for
the two post-dive experimental conditions (HOB and NOB)
was observed at 40 min.
Kissman Integrated Severity Score bubble count was
signiWcantly diVerent in these three diVerent conditions
(P < 0.001) and signiWcantly lower for post-dive NOB than
for control dives. In-water recompression with oxygen to
6 msw (HOB) dramatically suppressed circulating bubble
formation. Bubble count was signiWcantly lower for post-
dive HOB than for the control dive and even the post-dive
NOB.
Discussion
The main Wnding in this study is that in-water recompres-
sion with oxygen to 6 msw is more eVective in removing
gas bubbles than air or even NOB.
Our results are in accordance with a previous study
including 17 pigs breathing air and submitted to a strenuous
dive to 600 kPa for 30 min (Mollerlokken et al. 2007). The
animals in the experimental group were recompressed in a
dry hyperbaric chamber to 160 kPa breathing 100% oxygen
while the control group remained at surface breathing air.
The recompression treatment was initiated an hour after the
provocative dive, when the number of vascular bubbles
were at peak values. Following recompression, the bubbles
in the pulmonary artery were rapidly reduced and no bub-
bles reappeared after ending the treatment. However, this
study did not compare the experimental group with a NOB
group and recompression was not performed in water but in
a dry hyperbaric chamber (Mollerlokken et al. 2007). There
is some evidence that immersion might enhance the rate at
which nitrogen is eliminated, however, exposure to cold
can limit this eVect. Indeed, cold results in the constriction
of peripheral circulatory vessels and decreased perfusion
reducing the eYciency of nitrogen elimination (Balldin and
Table 1 The individual bubble score (Spencer scale and KISS) after the experimental post-dive conditions (HOB and NOB) and control dives
The higher bubble score were seen with the control dives, however, two divers presented high bubble score with NOB (divers 2 and 6)
Bubble scores were closed to zero for HOB
Divers Control dives Post-dive NOB Post-dive HOB
40 min 60 min 80 min KISS 40 min 60 min 80 min KISS 40 min 60 min 80 min KISS
133342.12000 00010.39
233342.1233342.121111.56
333342.1222212.480000
422212.48111 1.560000
5110 1.17111 1.560000
622212.4833342.120000
733234.71100 0.390000
8120 6.63000 00000
9210 3.9000 00000
1033342.1232117.161000.39
1113331.98110 1.170000
12221 9.75121 7.020100.78
13111 1.56000 00000
14221 9.7532117.160000
1534370.9822212.480000
1633234.71120 6.631101.17
1733234.71000 00000
1833234.71000 00000
1932117.16000 00000
Eur J Appl Physiol
123
Lundgren 1972; Balldin 1973). Diving in 15° with 5 mm
wet suit would cause peripheral cooling. During the hyper-
oxic exposure, some diVerence may be related to the tem-
perature of the outer shell between NOB and HOB, where
at NOB peripheral perfusion may be higher.
The purpose of the initial recompression treatment for
DCS is primarily to reduce the bubble formation and conse-
quently to diminish the mechanical eVects of the bubbles.
Vascular bubbles mainly damage the endothelium with
numerous secondary eVects, such as activation of leuko-
cytes, aggregation of thrombocytes and initiation of coagu-
lation (Francis and Mitchell 2003). The body regards
bubbles as foreign surfaces and responds to them some time
after the gas bubbles have been formed. Rapid removal of
the bubbles could prevent some of these secondary eVects
(Nossum et al. 1999, 2002). Despite a recompression treat-
ment, Mollerlokken et al. (2007) found no signiWcant diVer-
ence in survival time between the experimental and control
groups with, however, a trend towards better survival in
experimental group. Actually, this study observed that by
waiting for 1 h before starting the recompression treatment,
the removal of bubbles was not able to prevent arterial
endothelial damage. It was hypothesized that due to this
latency before the start of treatment, the endothelial func-
tion has already been impaired to a point where recompres-
sion to 160 kPa with oxygen for 60 min has little eVect.
Indeed, previous Wndings showed a relationship between
gas bubbles and mechanical endothelial damage related to
biochemical or immunological responses developed with
time (Nossum et al. 1999, 2002).
We hypothesized that delay in starting treatment could
inXuence results signiWcantly. Most of severe neurologic
DCS occur within a period of few minutes after surfac-
ing.(Francis and Mitchell 2003; Aharon-Peretz et al. 1993)
and in-water recompression should be performed immedi-
ately after the onset of symptoms (Edmonds 1999; Pyle
1999). In the present study, we chose a period of 10 min
after the provocative dive to provide a brief delay to pre-
pare the divers to IWR. The aim of our human study was
not to evaluate the eVect of recompression treatment on
DCS or endothelial damage. None of our divers presented
symptoms of DCS and we compare only vascular circulat-
ing bubbles in three diVerent situations. Actually, we
demonstrated a preventive eVect on bubble formation when
divers breath oxygen after surfacing and that this eVect is
better when divers return in water to 6 msw for 30 min.
Since it is generally accepted that the risk of DCS is low
when few or no bubbles are present in the circulation, this
treatment could be used to prevent DCS in situations of
“interrupted” or “omitted” decompression, where a diver
returns to the water in order to complete omitted decom-
pression prior to the onset of symptoms.
However, further experimental investigations are still
needed before a similar emergency treatment protocol for
DCS can be recommended. Published methods of IWR
involve victim returning underwater for a long period of
time i.e., 3 h (Edmonds 1999; Pyle 1999). But dehydration
and cold due to a long period of immersion can worsen
symptoms of DCS and acute oxygen toxicity is also related
to the duration of the exposition. In response to these
considerations, we have proposed a procedure for IWR at
190 kPa pressure with oxygen for only 1 h (Blatteau et al.
2006a, b). Indeed, previous data indicate that optimal pres-
sure to decrease elimination time for bubbles is 200 kPa,
and that additional pressure up to 400 kPa would not inXu-
ence this elimination time in pigs (Brubakk 2004). Another
Fig. 1 Experimental protocol
including one control dive and
two dives followed by 30 min of
hyperbaric (HOB) or normo-
baric oxygen breathing (NOB).
Bubble detection was performed
at 40, 60, and 80 min after sur-
facing
0
5
10
15
20
25
30
0 102030405060708090100110120130
time min
depth msw
bubble detection
HOB
NOB
Fig. 2 KISS bubble grades following control dive and post-dive expo-
sures with hyperbaric (HOB) or normobaric oxygen breathing (NOB).
A
sterisks denote P < 0.05 from control dives and dollar denotes
P < 0.05 from NOB
0
5
10
15
20
25
30
control
bubble score, KISS
*
*
§
HOB
NOB
Eur J Appl Physiol
123
important factor is that perfusion-dependent N
2
elimination
decreases secondary to vasoconstriction induced by
increasing oxygen pressures. Pure oxygen breathing
induced a small, insigniWcant (3.5%) decrease in nitrogen
yields, but further increases in oxygen pressure induced
signiWcant decreases in nitrogen yields, i.e.,¡8.9% for
200 kPa and ¡16.9% for 250 kPa (Anderson et al. 1991).
Protocols including a pressure up to 190 kPa breathing oxy-
gen for 1 h seem, however, a good compromise between
bubble reduction and nitrogen elimination. These proce-
dures should be tested in animal model of DCS immedi-
ately after the onset of DCS symptoms.
In conclusion, in-water recompression with oxygen to
6msw is more eVective in removing gas bubbles than
NOB. This treatment could be useful in situations of “inter-
rupted” or “omitted” decompression in order to prevent
DCS (Table 1; Figs. 1, 2).
ConXict of interest statement There is no Wnancial or other rela-
tionship that might be perceived as leading to a conXict of interest (i.e.,
aVecting author’s objectivity).
References
Aharon-Peretz J, Adir Y, Gordon CR, Kol S, Gal N, Melamed Y
(1993) Spinal cord decompression sickness in sport diving. Arch
Neurol 50:753–756
Anderson D, Nagasawa G, NorXeet W, Olszowka A, Lundgren C
(1991) O
2
pressures between 0.12 and 2.5 atm abs, circulatory
function, and N
2
elimination. Undersea Biomed Res 18(4):279–
292
Ball R (1993) EVect of severity, time to recompression with oxygen,
and re-treatment on outcome in forty-nine cases of spinal cord
decompression sickness. Undersea Hyperb Med 20(2):133–145
Balldin UI (1973) EVects of ambient temperature and body position on
tissue nitrogen elimination in man. Aerosp Med 44:365–370
Balldin UI, Lundgren CEG (1972) EVects of immersion with the head
above the water on tissue nitrogen elimination in man. Aerosp
Med 43:1101–1108
Bert P (1878) La Pression barométrique. Recherches de physiologie
expérimentale, Masson, Paris
Blatteau JE, Souraud JB, Gempp E, Boussuges A (2006a) Gas nuclei,
their origin, and their role in bubble formation. Aviat Space
Environ Med 77:1068–1076
Blatteau JE, Jean F, Pontier JM, Blanche E, Bompar JM, Meaudre E,
Etienne JL (2006) Decompression sickness accident management
in remote areas. Use of immediate in-water recompression ther-
apy. Review and elaboration of a new protocol targeted for a mis-
sion at Clipperton atoll. Ann Fr Anesth Reanim 25(8):874–883.
doi:10.1016/j.annfar.2006.04.007
Brubakk A (2004) Hyperbaric oxygen therapy: oxygen and bubbles.
Undersea Hyperb Med 31(1):73–79
Edmonds C (1999) Australian underwater oxygen treatment of DCS.
In: Key E and Spencer MP (eds) In-water recompression. Pro-
ceedings for the 48th workshop of the Undersea and Hyperbaric
Medical Society, pp 2–15
Francis TJR, Mitchell SJ (2003) Pathophysiology of decompression
sickness. In: Brubbak AO, Neuman TS (eds) The Bennett and
Elliot’s physiology and medicine of diving, 5th edn. WB
Saunders, London, pp 530–556
Moon RE, Gorman DF (2003) Treatment of the decompression disor-
ders. In: Brubbak AO, Neuman TS (eds) The Bennett and Elliot’s
physiology and medicine of diving, 5th edn. WB Saunders,
London, pp 600–650
Nishi RY, Brubakk AO, Eftedal OS (2003) Bubble detection. In:
Brubakk AO, Neuman TS (eds) Bennett and Elliot’s physiology
and medicine of diving, 5th edn. WB Saunders, London, pp 501–
529
Nossum V, Koteng S, Brubakk A (1999) Endothelial damage by bub-
bles in the pulmonary artery of the pig. Undersea Hyperb Med
26(1):1–8
Nossum V, Hjelde A, Brubakk A (2002) Small amounts of venous gas
embolism cause delayed impairment of endothelial function and
increase polymorphonuclear neutrophil inXammation. Eur J Appl
Physiol 86:209–214. doi:10.1007/s00421-001-0531-y
Pyle RL (1999). Keeping up with the times: application of technical
diving practices for in-water recompression. In: Key E, Spencer
MP (eds) In-water recompression. Proceedings for the 48th work-
shop of the undersea and hyperbaric medical society, pp 74–88
Ross JAS, Trevett AJ, Forbes RF, Rae CK, Sheehan C (2004) The
treatment of decompression illness arising from diving around the
Orkeny islands October 1991–June 2003. Undersea Hyperb Med
31(3):354
Spencer MP (1976) Decompression limits for compressed air deter-
mined by ultrasonically detected blood bubbles. J Appl Physiol
40:229–235
Stipp W (2004) The inXuence of time to hyperbaric oxygen treatment
on the outcome of neurological decompression illness in divers.
Undersea Hyperb Med 31(3):353
Mollerlokken A, Nossum V, Hovin W, Gennser M, Brubakk A (2007)
Recompression with oxygen to 160 kPa eliminates vascular bub-
bles, but does not prevent endothelium damage. Eur J Underwater
Hyperbaric Med 8(1, 2):11–16
    • "We present data suggesting that venous gas emboli incurred from scuba diving, as measured with a validated semi-quantitative echocardiographic protocol, can be effectively reduced to zero with in-water recompression . This pilot study replicates the same results as those of Blatteau [13], strongly suggesting that IWR is more effective than NBO 2 in reducing VGE. We believe this is the first investigation of IWR used to attempt a reduction in established VGE compared to VGE prophylaxis . "
    [Show abstract] [Hide abstract] ABSTRACT: Decompression sickness is a potentially fatal illness. Optimal treatment is dry recompression with hyperbaric oxygen. In-water recompression (IWR) offers expedited treatment but has insufficient evidence to recommend it as a treatment option. This trial compares IWR to standard surface oxygen treatment using 2D echocardiography as the semi-quantitative measurement for inert gas loading. Divers were randomly assigned to either IWR or normobaric oxygen (NBO2). A provocative dive profile to 33.5 meters for 25 minutes was used to stimulate bubble formation. After 60 minutes on the surface, bubble scoring was obtained using 2D echocardiography. Divers underwent either the IWR or NBO2 treatment for 82 minutes. Echocardiography was then repeated. Pre-treatment mean bubble counts were 28.1 bpf (bubbles per echo frame), [+/-13.2 to 43.0 95% CI] for IWR, and 18.3 bpf [+/-0.0 to 39.6 95% CI] for NBO2. After treatment, mean bubble score dropped to 0.1 bpf [+/-0.0 to 0.2 95% CI] (p<0.01) and 1.8 bpf [0.0 to 3.8 95% CI] (p=0.103) respectively. IWR vs. NBO2 reduction of bubble counts was 99.7% vs. 90.1%; however, this was not found to be statistically significant. IWR reduced the central VGE load compared to NBO2, suggesting that IWR is a viable emergency treatment when a recompression chamber is unavailable.
    Full-text · Article · Apr 2016
    • "the results from the present study confirm that oxygen breathing during decompression dramatically decreases the amount of bubbles after an air dive to 30 msw for 30 min breathing air. these results are in accordance with previous studies in an animal model of DcS (Mollerlokken et al. 2007) and in human divers (Blatteau and Pontier 2009). Several hypotheses can be considered to explain how the reduction of circulating bubbles may be attributable to oxygen breathing during decompression stop. "
    [Show abstract] [Hide abstract] ABSTRACT: We highlighted a relationship between decompression-induced bubble formation and platelet micro-particle (PMP) release after a scuba air-dive. It is known that decompression protocol using oxygen-stop accelerates the washout of nitrogen loaded in tissues. The aim was to study the effect of oxygen deco-stop on bubble formation and cell-derived MP release. Healthy experienced divers performed two scuba-air dives to 30 msw for 30 min, one with an air deco-stop and a second with 100 % oxygen deco-stop at 3 msw for 9 min. Bubble grades were monitored with ultrasound and converted to the Kisman integrated severity score (KISS). Blood samples for cell-derived micro-particle analysis (AnnexinV for PMP and CD31 for endothelial MP) were taken 1 h before and after each dive. Mean KISS bubble score was significantly lower after the dive with oxygen-decompression stop, compared to the dive with air-decompression stop (4.3 ± 7.3 vs. 32.7 ± 19.9, p < 0.001). After the dive with an air-breathing decompression stop, we observed an increase of the post-dive mean values of PMP (753 ± 245 vs. 381 ± 191 ng/μl, p = 0.003) but no significant change in the oxygen-stop decompression dive (329 ± 215 vs. 381 +/191 ng/μl, p = 0.2). For the post-dive mean values of endothelial MP, there was no significant difference between both the dives. The Oxygen breathing during decompression has a beneficial effect on bubble formation accelerating the washout of nitrogen loaded in tissues. Secondary oxygen-decompression stop could reduce bubble-induced platelet activation and the pro-coagulant activity of PMP release preventing the thrombotic event in the pathogenesis of decompression sickness.
    Full-text · Article · Feb 2014
  • [Show abstract] [Hide abstract] ABSTRACT: Effect of in-water oxygen prebreathing at different depths on decompression-induced bubble formation and platelet activation in scuba divers was evaluated. Six volunteers participated in four diving protocols, with 2 wk of recovery between dives. On dive 1, before diving, all divers breathed normally for 20 min at the surface of the sea (Air). On dive 2, before diving, all divers breathed 100% oxygen for 20 min at the surface of the sea [normobaric oxygenation (NBO)]. On dive 3, before diving, all divers breathed 100% O2 for 20 min at 6 m of seawater [msw; hyperbaric oxygenation (HBO) 1.6 atmospheres absolute (ATA)]. On dive 4, before diving, all divers breathed 100% O2 for 20 min at 12 msw (HBO 2.2 ATA). Then they dove to 30 msw (4 ATA) for 20 min breathing air from scuba. After each dive, blood samples were collected as soon as the divers surfaced. Bubbles were measured at 20 and 50 min after decompression and converted to bubble count estimate (BCE) and numeric bubble grade (NBG). BCE and NBG were significantly lower in NBO than in Air [0.142+/-0.034 vs. 0.191+/-0.066 (P<0.05) and 1.61+/-0.25 vs. 1.89+/-0.31 (P<0.05), respectively] at 20 min, but not at 50 min. HBO at 1.6 ATA and 2.2 ATA has a similar significant effect of reducing BCE and NBG. BCE was 0.067+/-0.026 and 0.040+/-0.018 at 20 min and 0.030+/-0.022 and 0.020+/-0.020 at 50 min. NBG was 1.11+/-0.17 and 0.92+/-0.16 at 20 min and 0.83+/-0.18 and 0.75+/-0.16 at 50 min. Prebreathing NBO and HBO significantly alleviated decompression-induced platelet activation. Activation of CD62p was 3.0+/-0.4, 13.5+/-1.3, 10.7+/-0.9, 4.5+/-0.7, and 7.6+/-0.8% for baseline, Air, NBO, HBO at 1.6 ATA, and HBO at 2.2 ATA, respectively. The data show that prebreathing oxygen, more effective with HBO than NBO, decreases air bubbles and platelet activation and, therefore, may be beneficial in reducing the development of decompression sickness.
    Full-text · Article · Feb 2010
Show more