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Introduction: To prevent extensive pulmonary lesions in submerged oxygen divers lung function like the forced vital capacity (FVC) or the diffusing capacity for carbon monoxide (DL,co) are used to monitor pulmonary oxygen toxicity (POT). As the diffusing capacity for nitric oxide (DL,no) measures more accurately the membrane diffusing capacity compared to DL,co we hypothesized that DL,no is superior in monitoring the onset of physiological changes indicative of POT as compared to DL,co or FVC., Method: 26 healthy divers (mean age 30.7 ± 6.2 years) made two submerged dives to 190 kPa for 1 h on two randomized separate days, whilst breathing 100% oxygen or compressed air. FVC, DL,no, DL,co and alveolar volume (VA ) were measured 6 times during a 26-h period., Results: Up to 8 h no significant differences in outcomes were found between the oxygen and air dives. However, at 8 h after the oxygen dives there was a significant reduction in DL,no, DL,co and VA as compared with air dives. In contrast, the reduction in FVC was significantly greater after the air dive. At 22 h there were no longer differences in outcomes between the dives., Conclusions: These data show that DL,no and DL,co are significantly reduced 8 h after submerged oxygen dives as compared to similar air dives. Together with the reduction in VA this may be indicative of interstitial edema as an early sign of POT. Our data warrant validation of the superiority of DL,no and DL,co over FVC in the practical monitoring of divers., (© 2013 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd.)

Rationale: Breathing oxygen with a partial pressure of >50 kPa causes pulmonary oxygen toxicity (POT), resulting in a decrease in vital capacity (VC) and in diffusing capacity for carbon monoxide (DLco). As submersion is thought to potentiate POT, we hypothesized that submerged oxygen divers are at increased risk for POT., Objective: To compare changes in lung function after submerged (wet) and non-submerged (dry) oxygen dives., Method: Thirteen healthy male divers (mean ± SD: 25 ± 2 years, 184 ± 7 cm, 85 ± 10 kg) made a dry and a wet dive to 150 kPa for 3 h, during which they breathed 100% oxygen. At baseline, within 1 and 4 h after their dives, spirometry and diffusing capacity were measured. Data were analysed with ANOVA using Bonferroni correction and paired t-tests., Results: Compared with baseline, there was a significant reduction in DLco (-1·6 mmol kPa(-1) min(-1)) after a wet oxygen dive but not after a dry dive. In addition, relative to baseline, there was a significant difference in ΔDLco and ΔVC when comparing wet and dry oxygen dives., Conclusion: Diffusing capacity is more impaired after a wet oxygen dive than after a dry one. This suggests that wet oxygen divers are at increased risk for POT. Monitoring studies during daily practice of professional divers are mandatory to determine the exact operational relevance of the present findings., (© 2011 The Authors. Clinical Physiology and Functional Imaging © 2011 Scandinavian Society of Clinical Physiology and Nuclear Medicine.)

Objective: Levels of glucose and lactate were measured in the brain by means of microdialysis in order to evaluate the effects of ventilator-induced hypocapnia and hypercapnia on brain metabolism in healthy non-brain-traumatized animals., Design and Setting: Prospective animal study in a university laboratory., Subjects: Eight adult Landrace/Yorkshire pigs., Interventions: The microdialysis probe was inserted in the brain along with a multiparameter sensor and intracranial pressure (ICP) probe. The animals were ventilated in a pressure-controlled mode according to the open lung concept with an inspired oxygen fraction of 0.4/1.0. Starting at normoventilation (PaCO(2) +/-40 mmHg) two steps of both hypercapnia (PCO(2) +/- 70 and 100 mmHg) and hypocapnia (PaCO(2) +/- 20 and 30 mmHg) were performed. Under these conditions, brain glucose and lactate levels as well as brain oxygen (PbrO(2)), brain carbon dioxide (PbrCO(2)), brain pH (brpH), brain temperature and ICP were measured., Results: At hypercapnia (PaCO(2) = 102.7 mmHg) there were no significant changes in brain glucose and lactate but there was a significant increase in PbrCO(2), PbrO(2) and ICP. In contrast, at hypocapnia (PCO(2) = 19.8 mmHg) there was a significant increase in brain lactate and a significant decrease in both brain glucose and PbrCO(2)., Conclusions: Hypocapnia decreases brain glucose and increases brain lactate concentration, indicating anaerobic metabolism, whereas hypercapnia has no influence on levels of brain glucose and brain lactate.

Based on a literature search, an overview is presented of the pathophysiology of venous and arterial gas embolism in the experimental and clinical environment, as well as the relevance and aims of diagnostics and treatment of gas embolism. The review starts with a few historical observations and then addresses venous air embolism by discussing pulmonary vascular filtration, entrapment, and the clinical occurrence of venous air emboli. The section on arterial gas embolism deals with the main mechanisms involved, coronary and cerebral air embolism (CAE), and the effects of bubbles on the blood-brain barrier. The diagnosis of CAE uses various techniques including ultrasound, perioperative monitoring, computed tomography, brain magnetic resonance imaging and other modalities. The section on therapy starts by addressing the primary treatment goals and the roles of adequate oxygenation and ventilation. Then the rationale for hyperbaric oxygen as a therapy for CAE based on its physiological mode of action is discussed, as well as some aspects of adjuvant drug therapy. A few animal studies are presented, which emphasize the importance of the timing of therapy, and the outcome of patients with air embolism (including clinical patients, divers and submariners) is described.

Objective: To investigate the effect of hyperbaric conditions on brain oxygenation, intracranial pressure and brain glucose/lactate levels in healthy non-brain-traumatized animals., Design and Setting: Prospective animal study in a hyperbaric chamber., Subjects: Twelve adult Landrace/Yorkshire pigs., Interventions: The animals were normoventilated in a pressure-controlled mode according to the open lung concept first at normobaric pressures (FiO2 of 0.4 and 1.0) and subsequently in the hyperbaric chamber at 1.9 and 2.8 bar (both at an FiO2 of 1.0). Under these conditions brain oxygen tension and intracranial pressure were recorded and brain glucose/lactate levels were measured by microdialysis., Results: At normobaric conditions, increasing the FiO2 from 0.4 (baseline) to 1.0 resulted in a significant increase in brain oxygen tension from 33 +/- 14 to 63 +/- 28 mmHg (P<0.05). Compared with baseline, both hyperbaric conditions (at an FiO2 of 1.0) led to a significant increase in brain oxygen tension to 151 +/- 65 mmHg (P<0.001) at 1.9 bar and to 294 +/- 134 mmHg (P<0.001) at 2.8 bar., Conclusions: If there is a need for increased oxygenation in the brain, then one way to achieve this is to apply hyperbaric conditions at 100% oxygen. Compared with an atmospheric pressure with a FiO2 of 0.4, a nine-fold increase (900%) in PbrO2 values can be reached by increasing the FiO2 to 1.0 and the pressure to 2.8 bar. In this study, hyperbaric oxygen pressure in the brain did not lead to changes in intracranial pressure or in brain glucose/lactate levels.