Figure 1.

The impact of hydrostatic pressure (also referred to as the absolute pressure in atmospheres; ATA) on lung volume and arterial hypoxia during a simulated dive to 100 m. The hyperbolic nature of lung volume across a dive is due to the nonlinear pressure-volume relationship (calculated in accordance with Boyle’s Law). The temporary increase in lung volume immediately before the start of the dive coincides with lung packing, a maneuver employed by divers to increase the volume of oxygen in the lungs. In this example, with a total dive time of 205 s, the dive speed was set at 1 m/s, with a 5 s bottom time. The arterial oxygen content (CaO₂) and partial pressure of arterial oxygen (PaO₂) at the start of the dive were 20.3 mlO₂ dl⁻¹ and 97 mmHg, respectively. Lung packing was performed prior to immersion, thereby increasing lung volume by 10% above TLC, and facilitating a 10 mmHg increase in PaO₂. CaO₂ was calculated to be the product of Hb × 1.36(SaO₂/100) + 0.003(PaO₂) – and consisted of the following considerations: (1) Hb was assumed to be 15 g dl⁻¹, until the early portion of ascent (i.e., ~2 min into dive), when a 5% increase in oxygenated Hb occurred in the circulation (i.e., +0.75 g dl⁻¹) via splenic contraction. As discussed in the Ascent section, splenic contraction is presumed to occur during the latter phase of the dive to coincide with the onset of exercise and growing hypercapnia; (2) SaO₂ was 98–100% until the last 15 s of the dive when PaO₂ dropped below 100 mmHg, and SaO₂ was estimated off a right-shifted O₂ dissociation curve (Hall et al., 2011); (3) the solubility of O₂ dl⁻¹ of blood (i.e., 0.003) was assumed to remain constant and PaO₂ was calculated using the following steps – first the partial pressure of alveolar oxygen (P_AO₂) was calculated using a modified alveolar gas equation to account for hydrostatic pressure = F_ETO₂ (0.1444 during pre/post dive breathing and 0.16 during the dive due to lung packing) multiplied by the product of ATA × (760–47) – (PaCO₂/R). The partial pressure of arterial carbon dioxide (PaCO₂) pre-dive was 40 mmHg, and calculated to increase at a rate of 0.06875 mmHg sec⁻¹ (derived from PaCO₂ data during a static apnea in an elite breath-hold diver; Willie et al., 2015 as reviewed in Bain et al., 2018b), resulting in an end-dive PaCO₂ of 54 mmHg. R was assumed to remain constant at 0.9. 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_AO₂ across a simulated dive to 150 m (Ferretti, 2001). The metabolic uptake of oxygen during breath-holding was derived from data during static apneas (Willie et al., 2015; Bain et al., 2018b), and assumed to be steady across a dive, at a rate of 0.21205 mmHg sec⁻¹. This oxygen uptake was subtracted from P_AO₂. PaO₂ was assumed to mirror P_AO₂ until ascent, when an inefficiency of pulmonary gas exchange is expected to occur (Patrician et al., 2021b). In the latter portion of the dive, a widening of the a-A gradient was assumed to be 20 mmHg, which was based on measurements in divers diving beyond 100 m (Patrician et al., 2021a). PaO₂ within 5 s of surfacing was estimated to be 29.7 mmHg which, in trained breath-hold divers, is slightly above the theoretic limit of consciousness. However, most experienced divers are always conscious of the risk of shallow water blackout (see section: The last 10 m).