Detection of hypoxia at the cellular level

Abstract

Organ function is critically linked to the way tissues use available oxygen. In sepsis, tissue-related hypoxic injury is the result of hypoxemia and hypoperfusion and cytokine-mediated mitochondrial dysfunction termed cytopathic hypoxia. Organ dysfunction in sepsis is more likely related to derailment of the metabolic processes of cells to use available oxygen. Cellular dysoxia rather than hypoxia may be the most appropriate way of describing sepsis-related tissue injury. Lactate is a marker of aerobic mitochondrial dysfunction and anaerobic tissue metabolism and in some circumstances is considered the fuel of choice for certain tissues. The concept of cellular metabolic derangement or cytopathic hypoxia as a potential cause for multiorgan system dysfunction in sepsis may direct efforts to optimize outcome in septic patients from the classic targets of CO, tissue perfusion, DVo(2), and Vo(2) toward moderating sepsis-related early cytokine response, maximizing mitochondrial function, and using biomarkers to monitor treatment response.