Anaerobic metabolism at the cellular level occurs when oxygen transport and tissue oxygenation are compromised. This can be a result of hypoxemia, anemia, inadequate systemic blood flow, or a combination of these factors. Anaerobic metabolism leads to a rise in lactate levels, which therefore can be a marker of low cardiac output. Interpreting an elevated lactate level requires consideration of other markers of reduced perfusion. An elevated lactate level in isolation can be a consequence of increased glycogenolysis or inborn errors of metabolism. Similarly, poorly perfused tissue undergoing anaerobic metabolism may not mobilize lactate into the bloodstream until perfusion improves, with the rise of lactate level occurring after restoration of an adequate systemic blood flow.
Anaerobic metabolism is considerably less efficient than oxidative metabolism. A single glucose molecule generates only 2 ATP molecules while being metabolized to 2 pyruvate molecules via anaerobic glycolysis, whereas subsequent oxidative metabolism of the pyruvates via the tricarboxylic acid cycle yields 34 ATP. Furthermore, the glycolytic pathway contains an oxidative step that reduces the oxidized coenzyme NAD to NADH. To restore NAD for continued glycolysis, NADH must subsequently be reoxi-dized. Under aerobic conditions, this process usually occurs in the mitochondria (see equation 1) and generates ATP; however, in the absence of mitochondrial metabolism, oxidation of NADH to NAD must be coupled to the reduction of pyruvate to lactate. As this process usually accounts for less than 10% of normal myocardial metabolism, the amount of lactate formed is small. However, when oxidative metabolism is limited, such as during ischemia or hypoxia, the production of lactate may contribute to intracellular acidosis and possibly cellular K+ loss, although this is controversial