Abstract

Pulmonary gas exchange in breath-hold diving (BHD) consists of a progressive increase in arterial PO2 and PCO2 (PaO2 and PaCO2) during descent. However, recent findings have demonstrated that PaO2 does not consistently rise in all subjects. This study aimed at verifying and explaining PaO2 derangements during BHD analyzing arterial blood gases and searching for pulmonary alterations with lung ultrasound. After ethical approval, 14 fit breath-hold divers were included. Experiments were performed in warm water (temperature: 31°C). We analyzed arterial blood gases immediately before, at depth, and immediately after a breath-hold dive - to -15 meters of fresh water (mfw) and -42 mfw. Signs of lung interstitial edema and atelectasis were searched simultaneously with a marinized lung ultrasound. In 5 subjects (-15 mfw) and 4 subjects (-42 mfw) the PaO2 at depth seems to decrease instead of increasing. PaCO2 and lactate showed slight variations. At depth, no lung ultrasound alterations were seen except in one subject (hypoxemia and B-lines at -15 mfw; B-lines at the surface). Lung interstitial edema was detected in 3 and 12 subjects after resurfacing from -15 mfw and -42 mfw, respectively. Two subjects developed hypoxemia at depth and a small lung atelectasis (a focal pleural irregularity of triangular shape, surrounded by thickened B lines) after resurfacing from -42 mfw. Current experiments confirmed that some BH divers can experience hypoxemia at depth. The hypothesized explanation for such a discrepancy is lung atelectasis, which could not be detected in all subjects probably due to limited time available at depth.

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