Arterial Blood Gas Analysis in Breath-Hold Divers at Depth

Abstract

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 (HCO3−) 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.

Breath-Hold Diving – The Physiology of Diving Deep and Returning

“…ATA increases by 1 every 10 m gain of depth (i.e., 1 ATA on the surface and 11 ATA at 100 m). Blood gases collected at 40 m in breath-hold divers support the notion of hydrostatic-induced hyperoxia -see section Maximum Depth; (Bosco et al, 2018). These data also align with predicted P A O 2 across a simulated dive to 150 m (Ferretti, 2001).…”

“…Upon reaching maximum depth, the elevated hydrostatic pressure facilitates a peak in the partial pressure of arterial oxygen (PaO 2 ), due to the hyperbaric-induced increase in gas partial pressure and solubility (illustrated in Figure 1). In a recent study conducted at the "Y-40 THE DEEP JOY" pool in Italy, arterial blood gases were evaluated at a depth of 40 m in six breath-hold divers (Bosco et al, 2018). In four of the six divers, PaO 2 increased from 94 ± 6 mmHg on the surface to 263 ± 32 mmHg at 40 m. Intriguingly, two of the divers did not demonstrate the expected hyperoxia at depth (PaO 2 at 40 m was 68 ± 10 mmHg).…”

Nitric Oxide and Oxidative Stress Changes at Depth in Breath-Hold Diving

“…In BH-diving, this aspect may be the result of two different mechanisms. First, transient hypoxia, especially experienced in the ascent phase ( Bosco et al, 2018 , 2020 ), can reduce NOx due to reconversion to NO. Specifically, NO3 can be reduced to NO2 by several enzymes such as xanthine oxidase ( Li et al, 2003 ) and xanthine oxidoreductase ( Jansson et al, 2008 ).…”

Temporal changes in pulmonary gas exchange efficiency when breath‐hold diving below residual volume

“…Yet, it is still not clear whether lung squeeze can be attributed to the compression and alveolar collapse during descent, the cumulative strain and capillary stress failure under compression, or the decompression and reopening during ascent. Irrespective of exactly where this threshold occurs, exceeding such a limit is a major contributor to the incidence of pulmonary barotrauma -notably, pulmonary oedema, haemoptysis and an impairment in pulmonary gas exchange (Boussuges et al, 1999;Lindholm et al, 2008;Mijacika & Dujic, 2016;Schipke et al, 2019). This was well demonstrated by Lindholm et al (2008), who had divers perform dives at functional residual capacity to 5-6 m in a pool to show that diving to residual volume (RV) could lead to pulmonary oedema and haemoptysis.…”

“…For example, during submaximal effort dives, end‐tidal () has been measured below 40 mmHg following dives to 60+ m (Ferretti et al ., 1991; Lanphier & Rahn, 1963), and as low as ∼20 mmHg following more maximal effort static apnoeas (Lindholm & Lundgren, 2006). Likewise, arterial values of <63 mmHg have been reported upon surfacing (Qvist et al ., 1993), which can remain <80 mmHg for at least a couple minutes (Bosco et al., 2018; Bosco et al., 2020). Additionally, during maximal dry static apnoeas in elite divers, arterial and central venous have been shown to drop below 30 and as low as 20 mmHg, respectively, without syncope (Bain et al., 2016, 2017, 2018a; Willie et al., 2015).…”