Mixed venous oxygen saturation (SvO2) - Pathophysiologic basis

Ref: Functional Hemodynamic monitoring by M.R. Pinsky, D. Payen

As DO2 (Oxygen delivery) is reduced - in critical illness by hypoxemia (hypoxic hypoxia), anemia ( anemic hypoxia), decreased cardiac output (stagnant hypoxia), or any combination thereof - oxygen consumption (VO2) is maintained by virtue of peripheral tissues taking up a greater fraction of the oxygen delivered.

At a sufficiently low level of delivery, approximately 7 ml/kg/min in this example - VO2 becomes dependent on DO2 and further reductions in DO2 are associated with a fall in VO2. This delivery-dependent limb of the VO2-DO2 relationship is characterized by lactic acidosis, organ dysfunction, physiologic instability and death.

As shown in the figure above, SvO2 falls as DO2 is diminished, reflecting tissue uptake being maintained, extraction fraction (VO2/DO2) rising, and arterio-venous content difference widening. SvO2 decreases because oxygen extraction increases. Thus, SvO2 can provide an early signal to determine the adequacy of delivery.

Oxygen extraction fraction (VO2/DO2) is not maximal at the critical delivery point - it continues to increase as DO2 falls below the critical point. However the increase in extraction fraction is not sufficient to maintain VO2, which becomes DO2 supply-dependent.

The rationale for a low SvO2 signalling inadequate DO2 is less clear in pathophysiologic processes associated with high output hypotension - sepsis, liver failure, pancreatitis, and other conditions marked by a systemic inflammatory response syndrome. In these conditions, once fluid resuscitation has taken place, the circulation is characterised by high flow, low systemic arterial pressure, and a high SvO2 despite an elevated oxygen consumption. It is also arguable that tissue hypoxia does not exist under these conditions, or at least is not the primary determinant of lactic acidosis. 

Nonetheless, it has been argued that while a high SvO2 may not guarantee absence of lactic acidosis or a risk for progression of organ failures, a low SvO2 signals inadequate resuscitation and has in fact been used as an endpoint for outcome studies assessing benefit from specific algorithms titrating therapy to this endpoint.