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PubMed2000

Medical supervision of sport diving in Scotland: reassessing the need for routine medical examinations.

BACKGROUND: The value of diving medicals in preventing incidents is uncertain and there has been only limited evaluation of the fitness to dive guidelines in a sport diving population. OBJECTIVE: To examine the need for routine diving medical examinations in the Scottish Sub-Aqua Club (SSAC) between 1991 and 1998. METHODS: A medical examination of all SSAC divers is performed at entry and then every one to five years based on their age and medical condition This information was analysed in terms of questionnaire findings and examination abnormalities. RESULTS: There were 2,962 medical forms available for analysis. Examination abnormalities were found in 174 subjects (5.9% of the population), with obesity affecting 75 subjects (2.5%). There was a linear increase in mean body mass index (r2 = 0.92), and a significant difference between 1991 and 1998 (mean (SD) of 24.1 (3.07) and 25.02 (3.4) respectively, p = 0.002) which was not related to age or sex distribution. There was also a significant increase in the prevalence of smokers (chi2 = 4.02, p = 0.045). The most common specialist referral was for evaluation of asthma, with hypertension and obesity as the next most common reasons. Most subjects were allowed to dive, with only 43 (25%) being failed outright. Overall, no examination abnormality alone caused a subject to be classified unfit to dive, and referrals were prompted by the answers in the questionnaire. CONCLUSIONS: No significant unexpected abnormalities were found on clinical examination in this population of sport divers. Conditions that prevented subjects from diving were detected by the questionnaire, and this prompted referral for further assessment by the medical advisors. Routine medical examinations were of little value.

Chi-Square Distribution↗
PubMed1981

Physiology of diving in marine mammals.

Natural dives are usually short and aerobic, involving swimming effort that is not energetically costly. Present evidence indicates few, if any, major biochemical enzyme adaptations that would promote an extended anaerobic capacity in marine mammals. We have discussed the lack of evidence for unusual biochemical adaptations for anaerobiosis and the importance and characteristics of natural aerobic dives. What explanation can we offer for the known capability of some marine mammals, such as Weddell seals and sperm whales, to remain submerged for over an hour? Attributes that serve them well for shorter dives are important also for long dives, such as: (a) a large total oxygen store relative to body size, and (b) parsimonious use of blood oxygen due to the lowered energy requirements of various organs. During long dives, some organs deplete their oxygen stores, become predominately dependent on anaerobic metabolism, and build up large quantities of lactate. The result is a degree of fatigue that leaves the animal incapable of further intense diving activities for some time. Consequently, long anaerobic dives are quite rare in nature.

Animals↗
PubMed1983

Diving responses in ducks after acute barodenervation.

The contribution of systemic arterial baroreceptors to the cardiovascular adjustments to diving has been investigated in unanesthetized ducks after acute baroreceptor denervation. Both intact and denervated ducks exhibited bradycardia on diving, although denervated ducks showed a lesser and more variable fall in heart rate. Hindlimb vascular resistance rose significantly in both intact and denervated ducks. Continuous stimulation of one depressor nerve, through miniature electrodes implanted on the cut central end, resulted in a diving bradycardia intermediate between that recorded in intact and denervated animals. Intermittent stimulation of the depressor nerve, for 20-s periods, at intensities high enough to cause a large fall in mean arterial pressure (MAP) predive caused a smaller reduction in MAP as a dive was prolonged, due to a large decline in the ability of the baroreceptor reflex to affect peripheral resistance. There was no change in the effect of stimulation on cardiac control before or during diving. The present experiments indicate that a barostatic reflex, which exerts its effects primarily through cardiac control and not control of total peripheral resistance, is active through the dive but that the majority of the diving response in ducks is independent of baroreceptor integrity.

Animals↗
PubMed1987

Adrenal gland denervation and diving in ducks.

The extreme elevation in plasma levels of free norepinephrine (NE) and free epinephrine (EP), which occurs during forced diving of ducks (Anas platyrhynchos), was studied before and after denervation of the adrenal glands. In intact animals both NE and EP concentration increased by up to two orders of magnitude in a 4-min dive but by a significantly lesser amount if the duck breathed O2 before the dive. Denervating the adrenal glands reduced the amounts of both catecholamines (CA) released during dives, plasma EP decreased to 10%, and NE to 50% of values obtained before denervation. Breathing O2 before a dive virtually eliminated CA release in denervates, indicating that hypoxia was the important non-neural releasing agent. Hypoxia was also the most important neural releasing agent compared with hypercapnia, acidosis, or hypoglycemia. Adrenal denervation did not cause significant changes in heart rate, blood pressure, arterial blood gas tensions, pH, or plasma glucose during dives, although denervation caused increased variation in some of these variables. In ducks CA release in dives is largely due to decreasing arterial O2 partial pressure, and full expression of the response is dependent on intact innervation of the adrenal gland.

Adrenal Glands↗
PubMed1992

Baroreflex control of arterial blood pressure during involuntary diving in ducks (Anas platyrhynchos var.).

The dynamic role of arterial baroreceptors in control of mean arterial blood pressure (MAP), heart rate (HR), cardiac output (CO), hindlimb vascular (HLVR) and total peripheral (TPR) resistance responses to forced dives was investigated in acutely and chronically barodenervated ducks. To activate the baroreflex, the proximal end of one aortic nerve was stimulated electrically with bipolar electrodes that had been implanted under pentobarbital sodium anesthesia. Predive nerve stimulation caused CO to fall (by reducing HR; stroke volume remained constant), producing a decrease in MAP to half the prestimulation level. During diving (for 2.5-min periods) nerve stimulation did not affect HR and MAP after the first minute of submersion. Neither HLVR nor TPR contributed to the fall in MAP during aortic nerve stimulation before or during diving. The effects of nerve stimulation on HR and MAP were maintained to the end of dives in animals given 100% O2 to breathe before diving. In separate experiments, increasing arterial chemoreceptor input by perfusing one vascularly isolated carotid body with venous blood caused a reduction in the effects of aortic nerve stimulation on MAP. Arterial baroreceptors may thus act on HR to alter MAP early in the dive, but as the dive progresses the baroreflex is attenuated by an increase in peripheral chemoreceptor drive.

Animals↗
PubMed1997

Trigeminal and chemoreceptor contributions to bradycardia during voluntary dives in rats.

This study investigates the importance of chemoreceptive and trigeminal information during voluntarily initiated diving in rats. The heart rate responses to simulated diving are unaffected by chemoreceptor drive [McCulloch, P.F., and N. H. West. Am. J. Physiol. 263 (Regulatory Integrative Comp. Physiol. 32): R1049-R1056, 1992] but are reversibly eliminated by infusion of glutamate receptor antagonists into the spinal trigeminal nuclei [McCulloch, P. F., I. A. Paterson, and N. H. West. Am. J. Physiol. 269 (Regulatory Integrative Comp. Physiol. 38): R669-R677, 1995]. To investigate the role of chemoreceptor drive in conscious dives, rats were made hypercapnic, hyperoxic, or hypoxic predive. The role of trigeminal input was explored by infusing the glutamatergic antagonists D-2-amino-7-phosphoheptanoic acid and 6,7-dinitroquinoxaline-2,3-dione into the region of the trigeminal nuclei. The alteration of arterial blood gases predive had no effect on diving bradycardia. Trigeminal blockade reduced the intensity of the bradycardia but did not abolish it. Chemoreceptor input does not play a significant role in determining heart rate during conscious diving in rats. The attenuation, rather than abolition, of bradycardia on trigeminal blockade suggests either that we achieved incomplete blockade or that an additional spectrum of sensory inputs not present in simulated diving is important in determining the underwater heart rate during conscious diving in rats.

Animals↗
PubMed1998

Contribution of hypercapnia and trigeminal stimulation to cerebrovascular dilation during simulated diving.

We investigated the relative contribution of humoral (carbon dioxide) and neural (trigeminal stimulation) inputs in the cerebrovasodilatory response to simulated diving in the rat. The cerebral hemodynamic profile of rats was determined using the brain blood flow tracer N-[14C]isopropyl-p-iodoamphetamine. During a simulated dive response, cerebral vascular resistance (CVR) decreased 63.1%, resulting in a 1.5-fold increase in cerebral blood flow (CBF). To investigate the contribution of hypercapnia to the decrease in CVR during simulated diving, we measured CBF during simulated diving in rats with preexisting hypocapnia. To investigate the contribution of trigeminal input, we measured CBF during periods of trigeminal stimulation alone with continued ventilation. Preexisting hypocapnia abolished the cerebrovasodilatory response to simulated diving. Trigeminal stimulation alone did not produce a significant increase in CBF from control values in any brain region, suggesting that trigeminal input does not contribute to the cerebrovascular response to simulated diving in rats. These results suggest that the cerebrovasodilatory response observed during diving in small mammals is driven primarily by progressive hypercapnia associated with asphyxia.

Animals↗
PubMed1998

Rapid brain cooling in diving ducks.

Hypothermia may limit asphyxic damages to the brain, and many small homeotherms have been shown to use anapyrexic strategies when exposed to asphyxic conditions. Larger homeotherms do not seem to use the same strategy, but could save oxygen and prevent hypoxic brain damage by employing selective brain cooling (SBC) in connection with asphyxia. To test the hypothesis that selective brain cooling may take place in connection with asphyxia, we have recorded brain [hypothalamic (THyp)] and body [colonic (TC)] temperatures and heart rates in four Pekin ducks during 5-min simulated (head submersion) diving in cold water (10 degrees C). Diving resulted in a drop in THyp (3.1 +/- 1.4 degrees C) that continued into the recovery period (P < 0.001). Restricting heat loss from the buccal cavity and eyes during diving compromised brain cooling in an additive manner. TC was not influenced by diving. Control cooling of the head with crushed ice during a 5-min period of undisturbed breathing had no effect on THyp. Warm water (35 degrees C) markedly reduced brain cooling, and dive capacity was reduced by approximately 14% (P < 0.05) compared with diving in water at 10 degrees C. The data suggest that SBC is used in ducks during diving, and we propose that this mechanism may enable the bird to save oxygen for prolonged aerobic submergence and to protect the brain from asphyxic damages.

Animals↗
PubMed1987

Simulated breath-hold diving to 20 meters: cardiac performance in humans.

Cardiac performance was assessed in six subjects breath-hold diving to 20 m in a hyperbaric chamber, while nonsubmersed or submersed in a thermoneutral environment. Cardiac index and systolic time intervals were obtained with impedance cardiography and intrathoracic pressure with an esophageal balloon. Breath holding at large lung volume (80% vital capacity) decreased cardiac index, probably by increasing intrathoracic pressure and thereby impeding venous return. During diving, cardiac index increased (compared with breath holding at the surface) by 35.1% in the nonsubmersed and by 29.5% in the submersed condition. This increase was attributed to a fall in intrathoracic pressure. Combination of the opposite effects of breath holding and diving to 20 m left cardiac performance unchanged during the dives (relative to the surface control). A larger intrathoracic blood redistribution probably explains a smaller reduction in intrathoracic pressure observed during submersed compared with nonsubmersed diving. Submersed breath-hold diving may entail a smaller risk of thoracic squeeze (lesser intrathoracic pressure drop) but a greater risk of overloading the central circulation (larger intrathoracic blood pooling) than simulated nonsubmersed diving.

Adult↗
PubMed1993

Arterial blood gas tensions during breath-hold diving in the Korean ama.

Korean female unassisted divers (cachido ama) breath-hold dive > 100 times to depths of 3-7 m during a work day. We sought to determine the extent of arterial hypoxemia during normal working dives and reasonable time limits for breath-hold diving by measuring radial artery blood gas tensions and pH in five cachido ama who dove to a fixed depth of 4-5 m and then continued to breath hold for various times after their return to the surface. Eighty-two blood samples were withdrawn from indwelling radial artery catheters during 37 ocean dives. We measured compression hyperoxia [arterial PO2 = 141 +/- 24 (SD) Torr] and hypercapnia (arterial PCO2 = 46.6 +/- 2.4 Torr) at depth. Mean arterial PO2 near the end of breath-hold dives lasting 32-95 s (62 +/- 14 s) was decreased (62.6 +/- 13.5 Torr). Mean arterial PCO2 reached 49.9 +/- 5.4 Torr. Complete return of these values to their baseline did not occur until 15-20 s after breathing was resumed. In dives of usual working duration (< 30 s), blood gas tensions remained within normal ranges. Detailed analysis of hemoglobin components and intrinsic oxygenation properties revealed no evidence for adaptive changes that could increase the tolerance of the ama to hypoxic or hypothermic conditions associated with repetitive diving.

2,3-Diphosphoglycerate↗
PubMed1997

Cardiovascular changes during deep breath-hold dives in a pressure chamber.

Electrocardiogram, cardiac output, and blood lactate accumulation were recorded in three elite breath-hold divers diving to 40-55 m in a pressure chamber in thermoneutral (35 degrees C) or cool (25 degrees C) water. In two of the divers, invasive recordings of arterial blood pressure were also obtained during dives to 50 m in cool water. Bradycardia during the dives was more pronounced and developed more rapidly in the cool water, with heart rates dropping to 20-30 beats/min. Arrhythmias occurred, particularly during the dives in cool water, when they were often more frequent than sinus beats. Because of bradycardia, cardiac output decreased during the dives, especially in cool water (to <3 l/min in 2 of the divers). Arterial blood pressure increased dramatically, reaching values as high as 280/200 and 290/150 mmHg in the two divers, respectively. This hypertension was secondary to peripheral vasoconstriction, which also led to anaerobic metabolism, reflected in increased blood lactate concentration. The diving response of these divers resembles the one described for diving animals, although the presence of arrhythmias and large increases in blood pressure indicate a less perfect adaptation in humans.

Adult↗
PubMedDate not supplied

Diving injuries to the inner ear.

Most of the previous literature concerning otologic problems in compressed gas environments has emphasized middle ear barotrauma. With recent increases in commercial, military, and sport diving to deeper depths, inner ear disturbances during these exposures have been noted more frequently. Studies of inner ear physiology and pathology during diving indicate that the causes and treatment of these problems differ depending upon the phase and type of diving. Humans exposed to simulated depths of up to 305 meters without barotrauma or decompression sickness develop transient, conductive hearing losses with no audiometric evidence of cochlear dysfunction. Transient vertigo and nystagmus during diving have been noted with caloric stimulation, resulting from the unequal entry of cold water into the external auditory canals, and with asymmetric middle ear pressure equilibration during ascent and descent (alternobaric vertigo). Equilibrium disturbances noted with nitrogen narcosis, oxygen toxicity, hypercarbia, or hypoxia appear primarily related to the effects of these conditions upon the central nervous system and not to specific vestibular end-organ dysfunction. Compression of humans in helium-oxygen at depths greater than 152.4 meters results in transient symptoms of tremor, dizziness, and nausea plus decrements in postural equilibrium and psychomotor performance, the high pressure nervous syndrome. Vestibular function studies during these conditions indicate that these problems are due to central dysfunction and not to vestibular end-organ dysfunction. Persistent inner ear injuries have been noted during several phases of diving: 1) Such injuries during compression (inner ear barotrauma) have been related to round window ruptures occurring with straining, or a Valsalva's maneuver during inadequate middle ear pressure equilibration. Divers who develop cochlear and/or vestibular symptoms during shallow diving in which decompression sickness is unlikely or during compression in deeper diving, should be placed on bed rest with head elevation and avoidance of maneuvers which result in increased cerebrospinal fluid and intralabyrinthine pressure. With no improvement in symptoms after 48 hours, exploratory tympanotomy and repair of a possible labyrinthine window fistula should be considered. Recompression therapy is contraindicated in these cases...

Action Potentials↗
PubMed1994

Mechanisms of reduced pulmonary function after a saturation dive.

Deep saturation diving has been shown to have prolonged effects on pulmonary function. We wanted to assess the relative contribution of various factors that could contribute to these effects. Pulmonary function was, therefore, measured before and after 17 different saturation diving operations to depths of 5-450 m of sea water, corresponding to absolute pressures of 0.15-4.6 MPa. Four to fifteen divers participated in each operation. The measurements included static and dynamic lung volumes and flows, transfer factor of the lungs for carbon monoxide (TLCO), and closing volume. The dives were characterized by the cumulative hyperoxic and hyperbaric exposures, and the load of venous gas microemboli encountered during decompression was measured in 41 divers in three dives to 0.25, 1.2 and 3.7 MPa. TLCO was reduced by 8.3 +/- 7.0% mean +/- SD after the dives, this correlated with cumulative hyperoxic exposure and load of venous gas microembolism, independently of each other. Closing volume was increased and forced mid-expiratory flow rate reduced, in correlation with cumulative hyperoxic exposure. An increase in total lung capacity correlated with cumulative hyperbaric exposure. We conclude that hyperoxia, hyperbaria, and venous gas microembolism all contribute to the changes in pulmonary function after a single saturation dive, and all may explain some of the long-term effects of diving on pulmonary function.

Adult↗
PubMed2006

The effect of myoglobin concentration on aerobic dive limit in a Weddell seal.

One physiological adaptation for prolonged dive duration in marine mammals is an elevated myoglobin (Mb) concentration in skeletal muscle. To determine the influence of Mb concentration on the aerobic dive limit (ADL), we modified a previously published model that simulated aerobic dives in a Weddell seal (Leptonychotes weddellii) and ran it for four Mb concentrations: 5, 27, 54 and 108 g Mb kg(-1) muscle representing 7%, 50%, 100% and 200%, respectively, of the normal Mb concentration in Weddell seal skeletal muscle. The model was run at increasing levels of muscular exertion and under postabsorptive and postprandial conditions to determine their effect on ADL. For each set of conditions, the model was also run at different levels of cardiac output (i.e. the dive response was varied) to determine the level of convective oxygen transport that optimized the ADL. In a postabsorptive state at a routine level of muscular exertion for a diving Weddell seal, a decrease in Mb concentration to 7% of normal caused a 39% decrease in the ADL (18 min to 11 min), while doubling the Mb concentration increased the ADL by 30% (18 min to 24 min). Under postprandial conditions at a routine level of muscular exertion, doubling the Mb concentration did not increase the ADL (12 min). The convective oxygen transport needed to meet the metabolic demands (Heat Increment of Feeding, HIF) of the splanchnic organs during digestion and assimilation required a cardiac output that was not optimal for the efficient use of muscle oxygen stores. This resulted in an over perfusion of the muscles and incomplete use of myoglobin-bound oxygen. As a result, the postprandial ADL was limited by the amount of oxygen stored in the blood, and increasing the Mb concentration had no effect on the ADL. We hypothesize that myoglobin concentration is optimized for the type and duration of dives routinely made by Weddell seals, and that a further increase may not increase the ADL for most free-ranging dives.

Animals↗
PubMed1997

Diving and swimming performance of white whales, Delphinapterus leucas: an assessment of plasma lactate and blood gas levels and respiratory rates.

The white whale Delphinapterus leucas is an exceptional diver, yet we know little about the physiology that enables this species to make prolonged dives. We studied trained white whales with the specific goal of assessing their diving and swimming performance. Two adult whales performed dives to a test platform suspended at depths of 5-300 m. Behavior was monitored for 457 dives with durations of 2.2-13.3 min. Descent rates were generally less than 2 m s-1 and ascent rates averaged 2.2-3 m s-1. Post-dive plasma lactate concentration increased to as much as 3.4 mmol l-1 (4-5 times the resting level) after dives of 11 min. Mixed venous PO2 measured during voluntary breath-holds decreased from 79 to 20 mmHg within 10 min; however, maximum breath-hold duration was 17 min. Swimming performance was examined by training the whales to follow a boat at speeds of 1.4-4.2 m s-1. Respiratory rates ranged from 1.6 breaths min-1 at rest to 5.5 breaths min-1 during exercise and decreased with increasing swim speed. Post-exercise plasma lactate level increased to 1.8 mmol l-1 (2-3 times the resting level) following 10 min exercise sessions at swimming speeds of 2.5-2.8 m s-1. The results of this study are consistent with the calculated aerobic dive limit (O2 store/metabolic rate) of 9-10 min. In addition, white whales are not well adapted for high-speed swimming compared with other small cetaceans.

Animals↗
PubMed1998

Effects of buoyancy on the diving behavior of northern elephant seals.

Marine mammals experience radical seasonal changes in body composition, which would be expected to affect their buoyancy in the water. The aim of this study was to examine the relationship between such changes in buoyancy and diving behavior in northern elephant seals Mirounga angustirostris. This was achieved by modifying the buoyancy of 13 juvenile elephant seals translocated from Año Nuevo State Reserve, CA, USA, and released at various sites in Monterey Bay, CA, USA. The buoyancy of each seal was calculated and was increased or decreased using syntactic foam or lead weights, and their diving behavior was recorded as they returned to Año Nuevo. The seals were divided into three groups: increased buoyancy (B+), reduced buoyancy (B-) and control seals (Bc). Mean descent rates were 0.77+/-0.3 ms-1 for the B+ seals, 0.82+/-0.2 ms-1 for the control seals and 0.87+/-0.3 ms-1 for the B- seals, and were significantly different. Mean ascent rates for the three treatments were 0.82+/-0.3 ms-1 for the B+ seals, 0.86+/-0.3 ms-1 for the control seals and 0.82+/-0.3 ms-1 for the B- seals. All the B+ seals ascended faster than they descended, while four of the five B- seals descended faster than they ascended. There was a significant negative correlation between buoyancy and descent rate, with less buoyant seals descending faster than more buoyant seals. There was, however, no correlation between ascent rate and buoyancy. This suggests that seals may use negative buoyancy to drift passively during descent, but that all seals may swim continuously during ascent. There was a significant correlation between buoyancy and the drift descent rate of C-type drift dives, including upwards drift in the most buoyant seal. Buoyancy was not correlated with diving depth, trip duration, dive duration or surface-interval duration. This study demonstrates that buoyancy plays a significant role in shaping diving behavior in northern elephant seals and that elephant seals may adjust their behavior to suit their buoyancy, rather than adjusting their buoyancy to suit a dive. This study also validated the truncated cones method of calculating body composition in this species by comparing it with body composition determined using tritium dilution.

Adipose Tissue↗
PubMed2003

Airway reactivity and diving in healthy and atopic subjects.

BACKGROUND: The short- and long-term effects of self-contained underwater breathing apparatus (SCUBA) dives on airway responsiveness in nonasthmatic atopic subjects have not been systematically investigated. PURPOSE: To compare the effect of SCUBA diving at 50-m depth on lung function and airway responsiveness to methacholine (MCh) in atopic nonasthmatics and healthy subjects. METHODS: We studied 15 atopic nonasthmatic subjects and 15 controls who underwent the visit for the professional SCUBA-diving license at the Navy Medical Center, La Spezia, Italy. All subjects underwent spirometry and skin-prick test for common environmental allergens. MCh challenge was performed 24 h before, and 20 min and 24 h after a standardized SCUBA-dive test and after hyperbaric-chamber test. RESULTS: At 20 min, the provocative dose of MCh causing 20% fall of the forced expiratory volume at the first second (MCh PD20 - FEV1) was significantly reduced in atopic, asymptomatic subjects from 1712 x 2.6 microg (mean x geometric standard deviation) to 1202 x 2.2 microg (P < 0.0005) after the hyperbaric-chamber test and to 1204 x 2.3 microg (P < 0.005) after SCUBA diving. In healthy subjects, the baseline value of MCh PD20 was 2977 x 1.1 microg, and this value did not change significantly after the hyperbaric-chamber test (2575 x 1.4 microg) and after SCUBA dives (2553 x 1.4 microg, P > 0.1 for both comparisons). In atopic subjects, the MCh PD20 returned near to the baseline value 24 h after the hyperbaric-chamber test (1776 x 2.4 microg) and after the SCUBA test (1500 x 2.67 microg). No significant change in FEV1 was observed after the tests in both groups. CONCLUSION: SCUBA diving is associated with development of early airway hyperresponsiveness to MCh in atopic subjects.

Adult↗
PubMed2006

Hemodynamic changes induced by recreational scuba diving.

OBJECTIVE: Cardiac changes induced by scuba diving were investigated using Doppler echocardiography. MATERIAL AND METHODS: Ten healthy scuba divers dove to a mean depth of 34.3 +/- 2.7 m of sea water (113 +/- 9 feet) and a mean duration of 25.3 +/- 3.5 min. RESULTS: One hour after the dive, microbubbles could be detected in the right-heart chambers of all subjects. Left atrial and left ventricular (LV) diameters significantly decreased after the dive. Cardiac output, assessed by aortic blood flow, remained unchanged. Heart rate increased and stroke volume (SV) decreased after the dive. LV filling was assessed on transmitral profile. An increase of the contribution of the atrial contraction to LV filling was observed. Right cavity diameters were unchanged, but an increase of the right ventricular/right atrial gradient pressure was found. CONCLUSION: The diving profile studied promotes a rather important bubble grade in all volunteers. A significantly reduced cardiac diameters and SV was found by our hemodynamic study 1 h after diving. Two factors can explain these results: low volemia secondary to immersion, and venous gas embolism induced by nitrogen desaturation. Consequently, restoration of the water balance of the body should be considered in the recovery process after diving.

Adult↗