Over the past ten years, we have come to recognize a form of tissue hypoxia that is characterized by an inability of tissues to extract adequate oxygen from an otherwise adequate delivery. In normal tissues, oxygen consumption remains constant at a level determined by metabolic activity, unless delivery is reduced below some critical delivery threshold. Below this threshold, oxygen consumption falls with further reductions in delivery. However, in some states the ability of tissues to extract oxygen from the delivered supply becomes deranged, leading to a dependence of V̇O2 on delivery even at high levels of delivery. This may be viewed as an increase in the critical threshold of delivery. To date, such a defect in the peripheral extraction mechanisms has been identified only in patients with acute hypoxemic respiratory failure (ARDS), maintained on a ventilator with positive end-expiratory pressure (PEEP). Indeed, the defect in peripheral oxygen uptake in these patients was recognized when changes in the therapeutic level of PEEP were accompanied by changes in cardiac output, oxygen delivery, and V̇O2. Because we lack sufficient clinical data, we have no way of knowing whether this defect in peripheral O2 uptake is limited to patients with acute lung failure maintained on PEEP, or whether it may extend to patients with sepsis, trauma, or hypotension.
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Critical Care and Intensive Care Medicine
- Cardiology and Cardiovascular Medicine