Hyperoxemia and hypoxemia impair cellular oxygenation: a study in healthy volunteers

Administration of oxygen therapy is common, yet there is a lack of knowledge on its ability to prevent cellular hypoxia as well as on its potential toxicity. Consequently, the optimal oxygenation targets in clinical practice remain unresolved. The novel PpIX technique measures the mitochondrial oxygen tension in the skin (mitoPO₂) which allows for non-invasive investigation on the effect of hypoxemia and hyperoxemia on cellular oxygen availability.

During hypoxemia, SpO₂ was 80 (77-83)% and PaO₂ 45(38-50) mmHg for 15 min. MitoPO₂ decreased from 42(35-51) at baseline to 6(4.3-9)mmHg (p < 0.001), despite 16(12-16)% increase in cardiac output which maintained global oxygen delivery (DO₂). During hyperoxic breathing, an FiO₂ of 40% decreased mitoPO2 to 20 (9-27) mmHg. Cardiac output was unaltered during hyperoxia, but perfused De Backer density was reduced by one-third (p < 0.01). A PaO₂ < 100 mmHg and > 200 mmHg were both associated with a reduction in mitoPO₂.

Hypoxemia decreases mitoPO₂ profoundly, despite complete compensation of global oxygen delivery. In addition, hyperoxemia also decreases mitoPO₂, accompanied by a reduction in microcirculatory perfusion. These results suggest that mitoPO₂ can be used to titrate oxygen support.