Beyond global oxygen supply-demand relations: In search of measures of dysoxia

Abstract

Central to the management of the hemodynamically unstable patient are resuscitative therapies for circulatory shock and the hemodynamic monitoring used to guide such therapies. In this context, shock can be considered to reflect inadequate O2 utilization by the tissues, due to either inadequate O2 delivery or inadequate O2 uptake. Inadequate O2 delivery usually reflects either hypoperfusion or arterial desaturation, whereas impaired O2 utilization by the tissues reflects an abnormal O2 metabolism or dysoxia [1]. In the last 10 years increased attention has been directed at the assessment of O2 consumption and delivery in the critically ill patient using data derived from pulmonary arterial and systemic arterial catheterization. Initial clinical studies suggested that as O2 delivery was varied, O2 uptake co-varied in a similar fashion [2-4]. Since this phenomenon in critically ill patients was contrary to previously proposed mechanisms in the normal relation between O2 delivery and uptake, it was referred to as “pathological O2 supply dependency” [5].