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Objective: We previously reported in healthy volunteers that a cantaloupe melon extract chemically combined with wheat gliadin (melon extract/gliadin) and containing SOD, catalase and residual glutathione peroxidase (GPx), protected against DNA strand-break damage induced by hyperbaric oxygen (HBO), a well-established model of DNA damage resulting from oxidative stress. Aortic cross-clamping is a typical example of ischemia/reperfusion injury-related oxidative stress, and therefore we investigated whether this melon extract/gliadin would also reduce DNA damage after aortic cross-clamping and reperfusion., Design: Prospective, randomized, controlled experimental study., Setting: Animal laboratory., Patients and Participants: 18 anesthetized, mechanically ventilated and instrumented pigs., Interventions: After 14 days of oral administration of 1250 mg of the melon extract/gliadin (n=9) or vehicle (n=9), animals underwent 30 min of thoracic aortic cross-clamping and 4 h of reperfusion., Measurements and Results: Before clamping, immediately before declamping, and at 2 and 4 h of reperfusion, we measured blood isoprostane (immunoassay) and malondialdehyde concentrations (fluorimetric thiobarbituric acid test), SOD, catalase and GPx activities (spectrophotometric kits), NO formation (nitrate+nitrite; chemoluminescence), DNA damage in whole blood samples and isolated lymphocytes exposed to hyperbaric oxygen (comet assay). Organ function was also evaluated. Kidney and spinal cord specimen were analysed for apoptosis (TUNEL assay). The melon extract/gliadin blunted the DNA damage, reduced spinal cord apoptosis and attenuated NO release, however, without any effect on lipid peroxidation and organ function., Conclusions: Pre-treatment with the oral melon extract/gliadin may be a therapeutic option to reduce oxidative cell injury affiliated with aortic cross-clamping.

Diving accidents represent a departure from the routine practice of emergency physicians. The incidence of non-fatal diving accidents is reported as 1-2 per 10,000 dives. Apart from adequate intravenous hydration, oxygen is the only medication with a proven effect in the treatment of diving accidents. After a typical diving accident, administration of oxygen at an inspired concentration (F(I)O(2) 1.0) as high as possible is recommended. Many divers bring along their own oxygen administration systems to the diving sites and these are often better suited for the treatment of diving accidents than the oxygen systems of many emergency responders. Pressure regulators supplying low constant flow oxygen, nasal prongs and inhalation masks are inappropriate. When using artificial ventilation bags with face masks, an oxygen flow of at least 15 l/min should be used. Demand regulators are simple to use and able to deliver a F(I)O2 of 1.0. Their ease of use has earned them high marks in the emergency management of diving accidents and their similarity to standard diving equipment has also aided relatively widespread acceptance. Circulation breathing systems are more technologically complex oxygen delivery systems which permit CO2 absorption and re-breathing at low oxygen flow. In contrast to the demand modules, the likelihood of mistakes during their usage is higher. In diving accidents, the administration of normobaric oxygen, already begun in the field, is the most important therapy and should not be interrupted. Presented with an inadequate supplemental oxygen supply, the inspired oxygen concentration should not be decreased, rather the duration of the oxygen administration should be reduced. Hyperbaric oxygen therapy should be the mainstay of further treatment.

Objective: To investigate the hemodynamic and metabolic effects of the peroxisome proliferator-activated receptor (PPAR)-gamma ligand and nuclear-factor (NF)-kappa B inhibitor 15-deoxy-Delta12,14-prostaglandin-J2 (15d-PGJ2) during long-term, hyperdynamic porcine endotoxemia., Design: Prospective, randomized, controlled experimental study with repeated measures., Setting: Investigational animal laboratory., Subjects: 19 anesthetized, mechanically ventilated and instrumented pigs., Interventions: At 12 h of continuous intravenous endotoxin and hydroxyethylstarch to keep mean arterial pressure (MAP)>60 mmHg, swine randomly received vehicle (control group, n=10) or 15-deoxy-Delta12,14-prostaglandin-J2 (15d-PGJ2 group, n=9; 1 microg kg(-1) min(-1) loading dose during 1 h; thereafter,0.25 microg kg(-1) min(-1) for 11 h)., Measurements and Results: Hemodynamic, metabolic and organ function parameters were assessed together with parameters of nitric oxide production and oxidative stress. 15d-PGJ2 prevented the endotoxin-induced progressive hypotension, due to a positive inotropic effect, which resulted in a significantly higher blood pressure during the treatment phase and prevented the rise in hepatic vein alanine-aminotransferase activity. It did not affect, however, any other parameter of organ function nor of nitric oxide production, proinflammatory cytokine release or lipid peroxidation (8-isoprostane)., Conclusions: 15d-PGJ2 stabilized systemic hemodynamics, due to improved myocardial performance, and resulted in an only transient effect on alanine-aminotransferase activity, without further beneficial effect on endotoxin-induced metabolic and organ function derangements. Low tissue 15d-PGJ2 concentrations and/or the delayed drug administration may explain these findings.

It is increasingly recognized that professional diving may elicit adverse long-term effects on the lungs, but conflicting results have been reported from distinct diving cohorts. This study reports the longitudinal change in lung function in professional divers who employ closed-circuit oxygen rebreathing apparatuses. All oxygen divers who attended the German Naval Medical Institute between 1994 and 1999 for regular medicals underwent spirometry and were entered if they had at least two follow-up examinations. Forced expiratory flows and volumes at baseline and at maximum follow up were compared. There were 39 divers who presented at least 3 times during a median period of 5.8 (2.7-8) yr. Forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) amounted to 4.86 +/- 0.62 L and 5.89 +/- 0.67 L at baseline, and 4.83 +/- 0.64 L and 5.87 +/- 0.69 L at maximum follow up, respectively. The change over time was statistically not significant. Substantial exposure to elevated oxygen partial pressure while diving is not associated with an accelerated decline in lung function. Factors other than hyperoxia (e.g., venous gas microemboli and altered breathing gas characteristics) may account for the long-term effects that have been found in professional divers.

Apnea diving is a fascinating example of applied physiology. The record for apnea diving as an extreme sport is 171 meters, 8:58 minutes. The short time beneath the surface induces profound cardiovascular and respiratory effects. Variations of blood-gas tensions result from the interaction of metabolism and the rapid sequence of compression and decompression. Decompression sickness is possible. Apnea divers can reach depths beyond the theoretic physiologic limit by using the lung-packing maneuver. Apnea divers exhibit a fall in heart rate, which can be trained and is an oxygen-conserving effect, but increases the incidence of ventricular arrhythmia.

This study aimed to establish epidemiological data on diving habits and outcome of subjects with respiratory diseases who are considered at increased risk for diving injuries. We conducted a cross-sectional demographics and prevalence study by distribution of an anonymous questionnaire with an issue of a widespread sport diving magazine. The questionnaire was designed to obtain medical and diving history data with an emphasis on respiratory diseases and complaints. The investigational population comprised sport scuba divers of any age and gender from Austria, Germany, and Switzerland. Two hundred and twenty-six male and 96 female divers sent completed questionnaires. Of the respondents 8.7 % indicated that they currently have asthma. Two thirds of asthmatics complained about regular dyspnoea. However, only 42.4 % used drugs relieving or controlling their symptoms regularly and 27.3 % used them in a prophylactic manner before diving. Five percent and 4.7 % of all divers reported a history of respiratory disease other than asthma or dyspnoea respectively. The divers with respiratory illness or complaints had logged a total of 17,386 dives. There were no cases of serious diving injuries. Despite the well-known limitations of postal surveys assessing self reported data, this study indicates that there is a population of subjects diving uneventfully with respiratory diseases that are considered medical contraindications to diving. These subjects deserve particular guidance on related risks and disease management.

The diving fitness medical examination serves to show and reveal medical conditions that are a contraindication for diving or to evaluate the risk of preexisting conditions. For this reason, it should never have the character of a certification given as a matter of courtesy. Fitness to dive is given if the candidate is healthy and when there are no pathological findings. Even with deviations from the norm, diving is still possible, but with restrictions. Important organ systems for the diving fitness examination are the cardiovascular system, the respiratory organs and the ears. In addition, adequate eyesight is important. The German Society of Diving and Hyperbaric Medicine (GTOUM) has drawn up recommendations on the examination of scuba divers to assist the physician (www.gtuem.org).

Fundamentally, accident mechanisms during the isopression phase of diving are primarily dependent upon the partial pressures of the respiratory gases. An increased nitrogen partial pressure leads to compressed-air intoxication; an increased oxygen partial pressure while diving with oxygen-enriched gas mixtures can trigger an oxygen-induced convulsion. Elevated pCO2 can be provoked by inadequate breathing and/or physical exertion at greater diving depths. Through an adjusted diving behavior and observation of the limits, these problems could be easily avoided.

Barotraumas are caused by pressure differences. As described by Boyle's Law, barotraumas develop during the descent phase of diving (and much more rarely during the ascent). The most frequently affected are the ears and paranasal sinuses, in addition to the facial skin and eyes. The most important preventive measure is performing pressure compensation in the affected body cavities. Barotrauma is treated symptomatically.

A decompression accident occurs during uncontrolled dive ascent with diving equipment. Through the rapid decrease in the surrounding pressure, gas bubbles form in the blood and tissues. Depending upon the mechanism of onset, the decompression illness (DCI) is classified as decompression sickness (DCS) or arterial gas embolism (AGE). The therapy consists of administering, as quickly as possible, 100% oxygen as well as a volume substitution. The treatment is continued in a recompression chamber.

Scuba diving vacations in tropical surroundings belong to the repertoire of most divers. In addition to carefully making travel plans and taking care of the necessary vaccinations and appropriate malaria prophylaxis, the following points also must be observed. The flight itself affects diving safety. In particular, a too short time interval between diving and the return flight can lead to decompression problems. Because most of the diving areas are reached by ship, many divers need a prophylaxis against motion sickness. Moreover, external otitis occurs more frequently while diving in the tropics. Finally, there is potential danger from the sea inhabitants, primarily from scorpion fishes, Portuguese Man-of-Wars, box jellyfishes as well as cone snails.

Hyperbaric oxygen (HBO), e.g. pure oxygen breathing at supra-atmospheric pressures, represents a well-suited model for investigating oxidative stress-induced DNA damage as well as protective mechanisms. While the induction of heme oxygenase-1 (HO-1) seems to be crucial for this protection against this DNA damage, the role of nitric oxide (NO) remains unclear. HO-1 expression is a major regulator of the inducible NO synthase (iNOS), and therefore we investigated the effect of the interaction between HBO, NO, and HO-1 on DNA damage. Prior to exposure to HBO (3 h at 3 bar ambient pressure) rats randomly received vehicle (HBO alone, 1 mL 0.9% saline, n=8), the NO donor molsidomine (SIN-10, 40 mg/kg, n=8) or the HO-1 blocker tin-mesopophyrin (Sn-MP, 50 micromol/kg, n=8). Additional groups received SIN-10 without exposure to HBO, i.e. breathing air under normobaric conditions for 3h (SIN-10 alone, 40 mg/kg, n=6), vehicle without HBO (negative controls, n=6), and ethylmethanesulfonate without HBO (EMS, 200 mg/kg) (positive controls n=4). Immediately after the 3 h HBO or air breathing period blood was analysed for DNA strand breaks (tail moment in the alkaline comet assay) and nitrite+nitrate (chemoluminescence). Whereas the tail moment was ten-fold higher after EMS than in the negative controls, there was no effect of HBO nor SIN-10 alone. Together with HBO, pretreatment with SIN-10 doubled the tail moment, and Sn-MP increased it by 50%. In contrast to Sn-MP or HBO alone, SIN-10 resulted in a five-fold increase of nitrite+nitrate concentrations. We conclude that both HO-1 blockade and excess NO release promote DNA damage during HBO exposure in vivo. The effect of HO-1 inhibition is probably independent of the regulatory function of HO-1 for iNOS.

In a prospective, double-blind, randomised placebo-controlled study, we tested the hypothesis that a new formulation consisting of wheat gliadin chemically combined with a vegetal (thus orally effective) preparation of superoxide dismutase (SOD) allows to prevent hyperbaric oxygen (HBO)-induced oxidative cell stress. Twenty healthy volunteers were exposed to 100% oxygen breathing at 2.5 ATA for a total of 60 min. DNA strand breaks (tail moments) were determined using the alkaline version of the comet assay. Whole blood concentrations of reduced (GSH) and oxidised (GSSG) glutathione and F2-isoprostanes, SOD, glutathione peroxidase (GPx) and catalase (Cat) activities and red cell malondialdehyde (MDA) content were determined. After HBO exposure the tail moment (p = 0.03) and isoprostane levels (p = 0.049) were significantly lower in the group that received the vegetal formulation. Neither SOD and Cat nor GSH and GSSG were significantly affected by this preparation or HBO exposure. By contrast, blood GPx activity, which tended to be lower in the SOD-group already before the HBO exposure (p = 0.076), was significantly lower afterwards (p = 0.045). We conclude that an orally effective SOD-wheat gliadin mixture is able to protect against DNA damage, which coincided with reduced blood isoprostane levels, and may therefore be used as an antioxidant.

Diving with self-contained underwater breathing apparatus (scuba) has become a popular recreational sports activity throughout the world. A high prevalence of cardiovascular disorders among the population makes it therefore likely that subjects suffering from cardiovascular problems may want to start scuba diving. Although scuba diving is not a competitive sport requiring athletic health conditions, a certain medical fitness is recommended because of the physical peculiarities of the underwater environment. Immersion alone will increase cardiac preload by central blood pooling with a rise in both cardiac output and blood pressure, counteracted by increased diuresis. Exposure to cold and increased oxygen partial pressure during scuba diving will additionally increase afterload by vasoconstrictive effects and may exert bradyarryhthmias in combination with breath-holds. Volumes of gas-filled body cavities will be affected by changing pressure (Figure 1), and inert gas components of the breathing gas mixture such as nitrogen in case of air breathing will dissolve in body tissues and venous blood with increasing alveolar inert gas pressure. During decompression a free gas phase may form in supersaturated tissues, resulting in the generation of inert gas microbubbles that are eliminated by the venous return to the lungs under normal circumstances. Certain cardiovascular conditions may have an impact on these physiological changes and pose the subject at risk of suffering adverse events from scuba diving. Arterial hypertension may be aggravated by underwater exercise and immersion. Symptomatic coronary artery disease and symptomatic heart rhythm disorders preclude diving. The occurrence of ventricular extrasystoles according to Lown classes I and II, and the presence of atrial fibrillation are considered relative contraindications in the absence of an aggravation following exercise. Asymptomatic subjects with Wolff-Parkinson-White syndrome may be allowed to dive, but in case of paroxysmal supraventricular tachycardia they must refrain from diving. Pacemakers will fail with increasing pressure, but some manufacturers have proven their products safe for pressure equivalents of up to 30 m of seawater, so that patients may dive uneventfully when staying within the 0-20 m depth range. Significant aortic or mitral valve stenosis will preclude diving, whereas regurgitation only will not be a problem. Right-to-left shunts have increasingly gained attention in diving medicine, since they may allow venous gas microbubbles to spill over to the arterial side of the circulation enabling the possibility of arterial gas embolism. Significant shunts thus preclude diving. The highly prevalent patent foramen ovale is considered a relative contraindication only when following certain recommendations for safe diving (Table 2). Metabolic disorders are of concern, since adiposity is associated with both, higher bubble grades in Doppler ultrasound detection after scuba dives when compared to normal subjects, and an increased epidemiologic risk of suffering from decompression illness. In conclusion, cardiovascular aspects are important in the assessment of fitness to dive, and certain cardiovascular conditions preclude scuba diving. Any history of cardiac disease or abnormalities detected during the routine medical examination should prompt to further evaluation and specialist referral.

Decompression illness (DCI) is becoming more prevalent as more people engage in activities involving extreme pressure environments such as recreational scuba-diving. Rapid diagnosis and treatment offer these patients the best chance of survival with minimal sequelae. It is thus important that critical care physicians are able to evaluate and diagnose the signs and symptoms of DCI. The cornerstones of current treatment include the administration of hyperbaric oxygen and adjunctive therapies such as hydration and medications. However, managing patients in a hyperbaric environment does present additional challenges with respect to the particular demands of critical care medicine in an altered pressure environment. This article reviews the underlying pathophysiology, clinical presentation and therapeutic options available to treat DCI, from the intensivist's perspective.

Elite apnea divers have considerably extended the limits of dive depth and duration but the mechanisms allowing humans to tolerate the compression- and decompression-induced changes in alveolar gas partial pressures are still not fully understood. Therefore we measured arterial blood gas tensions and acid-base-status in two elite apnea divers during simulated wet dives lasting 3 : 55 and 5 : 05 minutes, respectively. Arterial pO2 followed the compression-(from 13.8/16.9 kPa before the dive to 30 kPa at the start of the bottom time) and decompression-induced (from 13.7/21.0 kPa to 3.3/4.9 kPa immediately after surfacing) variations of ambient pressure, while the arterial pCO2 remained within the physiologic range (3.0/3.9 kPa before diving vs. 5.7/5.9 kPa at the end of the bottom time), probably due to the CO2 storage capacity of the blood. These findings may help to explain why humans can sustain deep and long apnea dives without major increases in respiratory drive.

An increasing number of asthmatics participate in recreational scuba diving. This activity presents unique physical and physiological challenges to the respiratory system. This review addresses the susceptibility of divers with asthma to diving accidents, acute asthmatic attacks, and long-term exacerbation of their disease. Recommendations on fitness to dive with asthma and airway hyperresponsiveness are provided.

As the use of oxygen enhances the resorption of gas bubbles in decompression illness, it is recommended and generally accepted that the inspired oxygen concentration in emergency treatment of diving accidents has to be as close to 100% as possible. Therefore, several emergency oxygen devices are offered to the diving community but only with little data in literature on the efficacy of these devices. We tested four emergency oxygen devices with respect to efficacy of oxygen supply and breathing comfort at rest. Nine blinded volunteers had to breathe from the four systems with face mask and mouthpiece as well. Gases were measured with mass spectrometry during a 3 min interval from a capillary port close to the subject. The results showed that none of the systems was able to deliver 100% oxygen all the time, but in three systems inspiratory oxygen values were achieved, although in one system the nitrogen wash-out was slowed due to air contamination during inspiration. The fourth tested system frequently supplied the subjects simply with air while breathing at rest. We conclude from our study that it is difficult to achieve oxygen levels close to 100% in practice. Even in a perfectly working system, the interface between device and subject is a source of entrained air, especially when oxygen breathing has to be performed over a longer period of time. In addition, two of four systems had conceptional problems to supply the subjects with pure O2 during inspiration. None of the tested systems was perfectly designed to serve in such emergencies.

A 43-year-old female recreational scuba diver presented to the emergency department 1 hour after a rapid, uncontrolled ascent. Her presentation included progressing confusion, slow and slurred speech, and complaints of headache and hypesthesia over her forearms and anterior thighs bilaterally. Differential diagnosis included arterial gas embolism and decompression sickness. She underwent recompression therapy with US Navy Table 6 within 120 minutes of her ascent. After recompression therapy, the patient had signs and symptoms consistent with severe rhabdomyolysis, including creatine kinase levels of 36,000 U/L and myoglobinuria.

Hyperbaric oxygenation is achieved when a patient breathes 100 percent oxygen in an environment of elevated atmospheric pressure. Physiologically, this produces a directly proportional increase in the plasma volume fraction of transported oxygen which is readily available for cellular metabolism. A number of beneficial biochemical, cellular and physiologic effects result which account for the use of hyperbaric oxygen as an adjunctive therapy in the treatment of clostridial myonecrosis, crush injuries, compromised flaps, osteoradionecrosis and chronic problem wounds. Indications, modes of treatment, contraindications, side effects, costs and experimental and clinical results are presented. Overall, these data demonstrate that hyperbaric oxygen is no longer "a therapy in search of diseases". However, more randomized controlled clinical trials are necessary to demonstrate its efficacy.

Decompression injuries are potentially life-threatening incidents, generated by a rapid decline in ambient pressure. Although typically seen in divers, they may be observed in compressed air workers and others exposed to hyperbaric environments. Decompression illness (DCI) results from liberation of gas bubbles in the blood and tissues. DCI may be classified as decompression sickness (DCS) or arterial gas embolism (AGE), depending on where the gas bubbles lodge. DCS occurs after longer exposures to a hyperbaric environment with correspondingly larger up-take of inert gas. DCS may be classified into type 1 with cutaneous symptoms and musculoskeletal pain only or type 2 with neurologic and/or pulmonary symptoms as well. AGE usually results from a pulmonary barotrauma, and with cerebral arterial involvement, the symptoms are similar to a stroke. The most important therapy, in the field, is oxygen resuscitation with the highest possible concentration and volume delivered. The definitive treatment is rapid recompression with hyperbaric oxygen therapy. Additional therapeutic measures are discussed.

Although many studies are available concerning the treatment of sudden deafness using hyperbaric oxygenation, only a few of these deal with tinnitus. The aim of the present study was to evaluate the therapeutic use of hyperbaric oxygenation in cases of tinnitus. A total of 193 patients, having undergone primary intravenous hemorheologic therapy, were treated with hyperbaric oxygenation. Tinnitus was evaluated before, after ten sessions and after 15 sessions using a tinnitus questionnaire. Additionally, an audiometric examination was performed. Measurable improvements of the tinnitus occurred in 22% of the patients, whereas a moderate improvement was seen in 17% of cases. 10.4% showed an excellent improvement and tinnitus disappeared completely in two patients. The improvement rate decreased in those cases where the time from onset of tinnitus exceeded 40 days. In conclusion, hyperbaric oxygenation seems to be a moderately effective additional treatment in the therapy of tinnitus after primary hemorheologic therapy, provided the time from onset of tinnitus is less than 1 month.

Background: Perioperative hypothermia is common and likely contributes to morbidity, but the efficacy of prophylactic fluid warning has hardly been analyzed systematically. We tested the hypothesis that the use of an infusion/blood warmer, based on the principle of countercurrent heat exchange, reduces incidence and degree of severe hypothermia following aortic surgery., Methods: In a prospective randomized investigation of patients (n = 50) undergoing elective abdominal aortic aneurysm surgery, all fluids/blood products (approx. 3500 ml) administered intraoperatively were infused either (n = 25) via countercurrent-like heat exchangers (Hotline Level 1 Technologies Inc.) or without (n = 25) taking special precautions (infusions stored at 21 degrees C, blood products heated to 37 degrees C in a water bath). Anaesthesia was standardized using a thiopentone, fentanyl, vecuronium induction sequence, and maintained by isoflurane in N2O/O2., Results: The perioperative decrease of oesophageal temperature (-0.35 degree C +/- 0.4) in the group managed with heat exchangers was significantly smaller (P < 0.0001) than in the control group (-1.5 degrees C +/- 0.54), and oesophageal temperature at the end of surgery was considerably higher (35.1 degrees C +/- 0.45 vs. 34.2 degrees C +/- 0.7; P < 0.0001). Furthermore, while postoperative hypothermia below 34.5 degrees C was observed in 16 patients (incidence: 64%) of the control group, it occurred in only 2 patients (incidence: 8%) managed with heat exchangers (P < 0.001)., Conclusions: The efficacy of fluid/blood warmers has hitherto only been evaluated in bench tests. Our results demonstrate that the use of heat exchangers alone, while not completely preventing hypothermia, markedly reduces the incidence of severe perioperative hypothermia, and lessens its degree during abdominal aortic aneurysm surgery.

In five subjects we examined the effect of exercise on the pattern of central venous (right atrial) N2 tensions (PVN2) after ascent from simulated non-decompression dives. The dives consisted of exposure to air at 3 bar for 20 min with 10 min of exercise (workload 75 W) at depth to achieve near-complete N2 saturation of the muscles. After the dive the subjects rested or, on another day, exercised for 30 min (workload 100 W) starting 10 min after completing the ascent. Blood samples taken every 10 min until the 60th min and 90 min after the dive were analyzed for PVN2 using a manometric Van Slyke apparatus. The amount of N2 eliminated was estimated from the PVN2 by adapting the Fick principle. Immediately after the ascent, PVN2 were 950 +/- 39 and 942 +/- 27 mmHg, respectively, in the rest and experiment series. In the rest experiments PVN2 continuously decreased to 606 +/- 8 mmHg 90 min after the dive, remaining significantly higher (P < 0.05) than before the dive. Exercise caused the PVN2 to increase beyond the corresponding levels of the rest experiments (P < 0.05 at 20 and 30 min exercise). After the exercise PVN2 rapidly declined, reaching predive levels 60 min after the ascent. Exercise increased N2 elimination to 970 +/- 143 ml, whereas it had been 311 +/- 61 ml (P < 0.05) in the corresponding phase of the rest experiments. We conclude that if extensive supersaturation and bubble formation can be avoided, such as probably was the case in our shallow non-decompression dives, exercise after the ascent accelerates N2 elimination.

We report a case of transient circulatory depression due to inadvertent apnea of a subject during decompression from a stimulated dive. The dive consisted of exposure to air at 5 bar and subsequent decompression stops. Arterial blood pressure and a lead II ECG were recorded continuously. During decompression from 1.6 to 1.3 bar, the subject inadvertently held his breath. Arterial pressure fell rapidly from 120/80 to 60/53 mmHg within 20 s. Recognizing that the subject held his breath, one of the supervisors ordered him to resume breathing, and arterial blood pressure was restored rapidly. This circulatory depression was probably due to reduced stroke volume such as described for the syncope of ascent: with the subject retaining his breath, the expanding lung volume increased intrathoracic pressure resulting in impaired venous return.

In 5 subjects arterial and central venous nitrogen partial pressures (PN2) were measured after decompression from a chamber dive following a decompression schedule for scuba diving. The simulated dives consisted of exposure to air at 6 bar for 30 min corresponding to a depth of 50 m. Afterward the subjects were decompressed with decompression stops at 2.5, 2.2, 1.9, 1.6, and 1.3 bar with a total decompression time of 67 min. In 3 of the subjects the measurements were repeated after they had exercised (workload 75 W) during bottom time. Immediately after decompression and every 40 min until Minute 240 arterial and central venous blood samples were analyzed for PN2 using a manometric Van Slyke apparatus. Venous PN2 remained elevated until 160 min after decompression, indicating still incomplete nitrogen washout for at least 2 h after decompression had been accomplished. We did not find any difference in PN2 values after decompression from dives at rest and after exercise. Applying a computer program based on a wide range of theoretical tissue half-times nitrogen elimination proved to be consistent with Haldanian theories when using our decompression profile. Our data confirm that nitrogen elimination is prolonged after decompression from simulated dives at rest and after exercise.

In five subjects arterial and central venous nitrogen partial pressures (PN2) were measured after decompression from a chamber dive following a decompression schedule for scuba diving. The simulated dives consisted of exposure at rest to air at 6 bar for 30 min. corresponding to a depth of 50 m. Afterwards the subjects were decompressed with decompression stops at 2.5, 2.2, 1.9, 1.6 and 1.3 bar with a total decompression time of 73 min. Immediately after decompression and every 40 min. until the 240th min. arterial and central venous blood samples were analyzed for PN2 using a manometric Van Slyke apparatus. Venous PN2 remained elevated until 160 min. after decompression indicating still incomplete nitrogen wash-out at least two hours after decompression had been accomplished. Bubble formation is discussed as a cause for prolonged nitrogen elimination. Our data confirm that nitrogen elimination is prolonged after decompression from simulated dives at rest.