The concept of a critical oxygen delivery

In healthy tissues, decreases in oxygen delivery (QO_n) do not lower oxygen consumption (VO₂) because tissue O₂ extraction increases proportionately. When delivery is reduced below a critical threshold, VO₂ falls because tissue extraction exceeds a critical threshold, and cannot compensate for the reduction in delivery. In the adult respiratory distress syndrome and perhaps in septicemia, tissue extraction capacity is impaired, leading to O₂ supply dependency despite normal or increased overall delivery. This pathologic supply dependency could be caused by a loss in autoregulatory capacity, by disrupted blood flow distribution secondary to peripheral microembolization, or to other factors interfering with efficient tissue distribution of QO₂ with respect to VO₂. Alternatively, the increased VO₂ may be consumed in biochemical pathways not associated with ATP production, or in the production of oxygen radicals or hydrogen peroxide. To the extent this abnormal dependence of VO₂ on QO₂ reflects tissue hypoxia, clinical interventions which decrease systemic delivery should be evaluated with regard to possible deleterious effects on organ system function.