Here's a review from Seminars in Respiratory and Critical Care Medicine. Free full text from Medscape is available here.
A few key points:
The microcirculation has diverse homeostatic functions which become severely altered in sepsis.
The microcirculation is the site where systemic inflammation and hemodynamic disturbance translates into organ failure.
The microcirculation is the interface between the macrocirculation and the cells. Total body oxygen delivery (DO2) may be fine while things are failing at the microcirculatory level. Microthrombi may be present or altered cellular processes may impair utilization of O2.
According to the article this state is associated with so called pathologic oxygen supply dependency in which 1) oxygen consumption varies directly with delivery over a wide range from subnormal to supranormal delivery and 2) there is an elevated DO2 threshold below which oxygen consumption becomes critically reduced. This led to efforts to raise DO2 to supranormal levels in critically ill patients. However, the very existence of such pathologic supply dependency has been in dispute for many years. Moreover, trials in the 1980s demonstrated a lack of benefit and possible harm from treatment regimens aimed at supranormal oxygen delivery. Clinical protocols aiming for high DO2 have been confused with early goal directed therapy, but they are fundamentally different.
The effects of standard sepsis treatment interventions on microcirculatory function are poorly understood.