Relative hypoxemia at depth during breath-hold diving investigated through arterial blood gas analysis and lung ultrasound.

Pulmonary gas exchange in breath-hold diving (BHD) consists of a progressive increase in arterial partial pressures of oxygen ([Formula: see text]) and carbon dioxide ([Formula: see text]) during descent. However, recent findings have demonstrated that [Formula: see text] does not consistently rise in all subjects. This study aimed at verifying and explaining [Formula: see text] 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 m of fresh water (mfw) and -42 mfw. Signs of lung interstitial edema and atelectasis were searched simultaneously with a marinized lung ultrasound. In five subjects (-15 mfw) and four subjects (-42 mfw), the [Formula: see text] at depth seems to decrease instead of increasing. [Formula: see text] 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 to -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.NEW & NOTEWORTHY During breath-hold diving, arterial partial pressure of oxygen ([Formula: see text]) and arterial partial pressure of carbon dioxide ([Formula: see text]) are believed to increase progressively during descent, as explained by theory, previous end-tidal alveolar gas measurements, and arterial blood gas analysis in hyperbaric chambers. Recent experiments in real underwater environment found a paradoxical [Formula: see text] drop at depth in some divers. This work confirms that some breath-hold divers can experience hypoxemia at depth. The hypothesized explanation for such a discrepancy is lung atelectasis, as suggested by lung ultrasound findings.

Comparison between Arterial Blood Gases and Oxygen Reserve Index™ in a SCUBA Diver: A Case Report.

Hypoxia and hyperoxia are both worrisome issues potentially affecting SCUBA divers, but validated methods to monitor these two conditions underwater are still lacking. In this experiment, a volunteer SCUBA diver was equipped with a pulse oximeter to detect peripheral oxygen saturation (SpO2) and a device to monitor the oxygen reserve index (ORi™). ORi™ values were compared with arterial blood oxygen saturation (SaO2) and the partial pressure of oxygen (PaO2) obtained from the cannulated right radial artery at three steps: at rest out of water; at -15 m underwater after pedaling on a submerged bike; after resurfacing. SpO2 and ORi™ mirrored the changes in SaO2 and PaO2, confirming the expected hyperoxia at depth. To confirm the potential usefulness of an integrated SpO2 and ORi™ device, further studies are needed on a broader sample with different underwater conditions and diving techniques.

Delayed Neurological Sequelae Successfully Treated with Adjuvant, Prolonged Hyperbaric Oxygen Therapy: Review and Case Report.

Carbon Monoxide (CO) intoxication is still a leading cause of mortality and morbidity in many countries. Due to the problematic detection in the environment and subtle symptoms, CO intoxication usually goes unrecognized, and both normobaric and hyperbaric oxygen (HBO) treatments are frequently administered with delay. Current knowledge is mainly focused on acute intoxication, while Delayed Neurological Sequelae (DNS) are neglected, especially their treatment. This work details the cases of two patients presenting a few weeks after CO intoxication with severe neurological impairment and a characteristic diffused demyelination at the brain magnetic resonance imaging, posing the diagnosis of DNS. After prolonged treatment with hyperbaric oxygen, combined with intravenous corticosteroids and rehabilitation, the clinical and radiological features of DNS disappeared, and the patients' neurological status returned to normal. Such rare cases should reinforce a thorough clinical follow-up for CO intoxication victims and promote high-quality studies.

Arterial blood gases in divers at surface after prolonged breath-hold.

PURPOSE: Adaptations during voluntary breath-hold diving have been increasingly investigated since these athletes are exposed to critical hypoxia during the ascent. However, only a limited amount of literature explored the pathophysiological mechanisms underlying this phenomenon. This is the first study to measure arterial blood gases immediately before the end of a breath-hold in real conditions. METHODS: Six well-trained breath-hold divers were enrolled for the experiment held at the "Y-40 THE DEEP JOY" pool (Montegrotto Terme, Padova, Italy). Before the experiment, an arterial cannula was inserted in the radial artery of the non-dominant limb. All divers performed: a breath-hold while moving at the surface using a sea-bob; a sled-assisted breath-hold dive to 42 m; and a breath-hold dive to 42 m with fins. Arterial blood samples were obtained in four conditions: one at rest before submersion and one at the end of each breath-hold. RESULTS: No diving-related complications were observed. The arterial partial pressure of oxygen (96.2 ± 7.0 mmHg at rest, mean ± SD) decreased, particularly after the sled-assisted dive (39.8 ± 8.7 mmHg), and especially after the dive with fins (31.6 ± 17.0 mmHg). The arterial partial pressure of CO2 varied somewhat but after each study was close to normal (38.2 ± 3.0 mmHg at rest; 31.4 ± 3.7 mmHg after the sled-assisted dive; 36.1 ± 5.3 after the dive with fins). CONCLUSION: We confirmed that the arterial partial pressure of oxygen reaches hazardously low values at the end of breath-hold, especially after the dive performed with voluntary effort. Critical hypoxia can occur in breath-hold divers even without symptoms.

Arterial Blood Gas Analysis in Breath-Hold Divers at Depth.

The present study aimed to evaluate the partial pressure of arterial blood gases in breath-hold divers performing a submersion at 40 m. Eight breath-hold divers were enrolled for the trials held at "Y-40 THE DEEP JOY" pool (Montegrotto Terme, Padova, Italy). Prior to submersion, an arterial cannula in the radial artery of the non-dominant limb was positioned. All divers performed a sled-assisted breath-hold dive to 40 m. Three blood samplings occurred: at 10 min prior to submersion, at 40 m depth, and within 2 min after diver's surfacing and after resuming normal ventilation. Blood samples were analyzed immediately on site. Six subjects completed the experiment, without diving-related problems. The theoretically predicted hyperoxia at the bottom was observed in 4 divers out of 6, while the other 2 experienced a reduction in the partial pressure of oxygen (paO2) at the bottom. There were no significant increases in arterial partial pressure of carbon dioxide (paCO2) at the end of descent in 4 of 6 divers, while in 2 divers paCO2 decreased. Arterial mean pH and mean bicarbonate ( HCO 3 - ) levels exhibited minor changes. There was a statistically significant increase in mean arterial lactate level after the exercise. Ours was the first attempt to verify real changes in blood gases at a depth of 40 m during a breath-hold descent in free-divers. We demonstrated that, at depth, relative hypoxemia can occur, presumably caused by lung compression. Also, hypercapnia exists at depth, to a lesser degree than would be expected from calculations, presumably because of pre-dive hyperventilation and carbon dioxide distribution in blood and tissues.