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Lactic acidosis is characteristic of all forms of shock, including that due to systemic infection. It has been generally assumed that accumulation of excess lactate in patients with the systemic inflammatory response syndrome (SIRS) is due to hypoxia or inadequate delivery of oxygen to the tissues because of local or generalized ischemia. In the absence of sufficient oxygen, there is a shift from oxidative to anaerobic metabolism. Although lactate production provides a temporary source for muchneeded energy to the tissues, it is extremely inefficient and is associated with the rapid development of a severe metabolic acidosis. Maintenance of adequate tissue perfusion and oxygenation remains a key objective in the treatment of these patients.
In a provocative article in this issue of CHEST (see page 1301), Kellum and colleagues propose a very different scenario to explain the accumulation of lactic acid in patients who have acute lung injury associated with sepsis or pneumonia. The investigators found that lactate concentrations in the arterial blood slightly exceeded those in the mixed venous blood in each of nine patients with these abnormalities, but not in patients who had no evidence of lung injury. They cite literature that failed to show either tissue hvpoxia or systemic lactate production in animal or clinical studies of sepsis, and suggest that lactate generation by the lungs...