Concepts of “Tissue PO₂” In Relation to O₂ Delivery

Abstract

Resistance to O₂ diffusion is reflected in the difference in pO₂ between O₂ reservoirs of hemoglobin (Hb) and myoglobin. The very low normal myocyte pO₂ (less than one torr but adequate for optimal oxidative ATP synthesis) compared to venous pO₂ indicates that blood does not achieve equilibrium with tissue during its passage through capillaries. In the lung, diffusion rate of O₂ from alveolus to capillary is normally sufficient to achieve essential equilibrium. However, system-wide capillary pathology and reduced Hb saturation has been observed with distal local ischemia. In peripheral vascular disease (PVD) patients, we found a mean arterial pO₂ of 77 torr (normal over 90 torr).

Classical concepts based on “tissue pO₂” values derived from venous blood or oxygen electrodes inserted into tissue need re-evaluation. Readings of O₂ electrodes moved through tissue range widely from intracapillary levels down toward intracellular levels and do not reflect the pO₂ of any particular site. Intravenous pO₂ is the result of residual O₂ after incomplete diffusion out of capillaries during transit through a tissue, and is not an equilibrium value with some tissue pool.

The effect of HbO₂ p50 on oxygen release during the passage of blood through a capillary bed, generally judged on the basis of percentage percent saturation at “tissue pO₂”, should be judged on the basis of the change in p0₂ (the diffusion driving force) associated with a particular degree of HbO₂ saturation at a particular p50. The thesis that O₂ diffusion rate is a major determinant of oxygen delivery is supported by pO₂ responses to treatment of PVD that does not alter blood flow or p50.