Hemodynamic Consequences of Severe Lactic Acidosis in Shock States

Abstract

High lactate concentration with low pH is systematically considered as a marker of severity in critically ill patients and is also a biological marker of tissue oxygen debt irrespective of the initial hypoxic or dysoxic trigger. Lactic acidosis is not only the cause and consequence of reduced cardiac contractility and vascular hyporesponsiveness that arise due to the administration of vasopressors during shock state, but it also displays protective effects against shock-induced cytokine storm. In view of these antagonist effects, the most recent septic shock guideline recommends against the prescription of symptomatic treatment for pH above 7.15 while issuing no recommendation for pH levels < 7.15. This work, based on a critical and personal appraisal of the literature, will describe how lactic acidosis increases during shock, its deleterious effects on the cardiovascular system including its counterintuitive protective effects, and finally the literature on which the various therapeutic options are based.