Animal experiments at great pressures are regularly undertaken to determine the limits of human exposure and thus ocean penetration. Ventilatory capacity is limited by restricted gas flow or increased work of breathing, both resulting from the effects of increased gas density or from pulmonary damage caused by the cooling effects on the lungs.
Hypoxia may be expected, as a result of such factors as an increased ‘diffusion dead space’ (caused by slowed diffusion of alveolar gases or incomplete mixing of fresh inspired gases and alveolar gases despite adequate inspired O2 pressure and overall pulmonary ventilation).
The Chouteau effect (a disputed concept) is apparent clinical hypoxia despite normal inspired O2 tension that, at least in goats, is rectified by a slight increase in the inspired O2 tension (i.e. normoxic hypoxia). It has been explained by both an alveolar-arterial diffusion abnormality and a non-homogenous mixing of alveolar gas at very high pressures. Saltzman2 has an alternative explanation, suggesting that at greater than 50 ATA there is decreased O2 uptake, with decreased pH and increasing acidosis. Thus, there is a block in the utilization or transport of O2.