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Introduction: Full-face-masks (FFM) prevent the diver's face from cold and can support nasal breathing underwater. The aim of the study was to evaluate the effect of the use of FFMs on lung function and wellbeing., Methods: Twenty-one, healthy, non-asthmatic divers performed two cold-water dives (4⁰C, 25 min, 10 metres' depth) - one with a FFM and the other with a standard scuba regulator (SSR). Spirometry was performed before and after each dive and well-being and cold sensation were assessed after the dives., Results: Significant decreases in forced vital capacity (FVC), forced expiratory volume in one second (FEV₁) and midexpiratory flow at 75% of FVC (MEF₇₅) occurred after both FFM and SSR dives. Changes in FVC and FEV₁ did not differ significantly between FFM and SSR dives. However, the mid-expiratory flows measured at 50% and 25% of FVC (MEF₅₀ and MEF₂₅) were significantly lower 10 minutes after the FFM dive compared to 10 minutes after the SSR dive. The wellbeing and cold sensation of the divers were significantly improved with FFM dives compared to SSR dives., Conclusions: Cold-water dives during wintertime can be associated with airway narrowing. During cold-water dives, the use of a FFM appears to reduce the cold sensation and enhance the well-being of the divers. However, a FFM does not appear to prevent airway narrowing in healthy, non-asthmatic subjects.

Introduction: In-water resuscitation has recently been proposed in the European resuscitation guidelines. Initiation of mechanical ventilation underwater might be considered when an immediate ascent to the surface is impossible or dangerous. The present study evaluated the feasibility of such ventilation underwater., Methods: A resuscitation manikin was ventilated using an Interspiro® MK II full-face mask or with an Oxylator® ventilator via a facemask or a laryngeal tube, or with mouth-to-tube inflation. Tidal volumes achieved by the individual methods of ventilation were assessed. The ventilation tests were performed during dives in the wet compartment of a recompression chamber and in a lake. Ventilation was tested at 40, 30, 20, 12, 9 and 6 metres' depth., Results: Ventilation was impossible with the cuffed mask and only sufficient after laryngeal intubation for a small number of breaths. Laryngeal tube ventilation was associated with the aspiration of large amounts of water and the Oxylator failed during the ascent. Efficient ventilation with the MK II full-face mask was also possible only for a short period. An absolutely horizontal position of the manikin was required for successful ventilation, which is likely to be difficult to achieve in open water. Leakage at the sealing lip of the full-face mask and the cuff of the laryngeal tube led to intrusion of water and resulted in subsequent complete failure of ventilation., Conclusions: The efficacy of underwater ventilation seems to be poor with any of the techniques trialed. Water aspiration frequently makes ventilation impossible and might foster emphysema aquosum-like air trapping and, therefore, increase the risk of pulmonary barotrauma during ascent. Because the limitations of underwater ventilation are substantial even under ideal conditions, it cannot be recommended presently for real diving conditions.

Hyperbaric oxygen (HBO) therapy is used for the treatment of a variety of diseases, but also leads to oxidative stress as a result of increased formation of reactive oxygen species. The consequences may be damage to the lung, the central nervous system and the genome. The oxidative attack on DNA causes, among other damage, single and double strand breaks. Using the comet assay, a well-established genotoxicity test, it was possible to show that a single HBO exposure leads to increased levels of DNA strand breaks in a close dose-effect relationship. On the other hand, it was possible to demonstrate that these strand breaks are repaired rapidly and that, in repeated HBO exposures, DNA strand breaks occur only after the first treatment, not subsequent ones, indicating an induction of protective mechanisms. In healthy organisms, DNA repair and antioxidant mechanisms maintain a steady-state level of damage with minimal risk to the cell or the whole organism, but it cannot be excluded that HBO might lead to a significant mutational burden in situations where antioxidant defence is deficient or overwhelmed. The administration of antioxidants draws an ambivalent picture; Vitamin C, E or even N-acetylcysteine seems to be ineffective to prevent HBO-induced genotoxicity, whereas the orally effective vegetal superoxide dismutase (SOD, Glisodin®) is effective, and, thus, may play a role in the prevention of oxidative DNA damage.