Clinical use of lactate monitoring in critically ill patients

Abstract

Increased blood lactate levels (hyperlactataemia) are common in critically ill patients. Although frequently used to diagnose inadequate tissue oxygenation, other processes not related to tissue oxygenation may increase lactate levels. Especially in critically ill patients, increased glycolysis may be an important cause of hyperlactataemia. Nevertheless, the presence of increased lactate levels has important implications for the morbidity and mortality of the hyperlactataemic patients. Although the term lactic acidosis is frequently used, a significant relationship between lactate and pH only exists at higher lactate levels. The term lactate associated acidosis is therefore more appropriate. Two recent studies have underscored the importance of monitoring lactate levels and adjust treatment to the change in lactate levels in early resuscitation. As lactate levels can be measured rapidly at the bedside from various sources, structured lactate measurements should be incorporated in resuscitation protocols.

Figure 1

Lactate at the cellular level. Usually not oxygen shortage per se, but acute energy requirements is a key determinant of lactate levels. a Under stable conditions, glucose is converted to pyruvate, generating 2 ATP, and pyruvate is then subsequently fully oxidized to CO₂ generating ~36 ATP. b Under stress, glycolysis can increase by a factor 100 to 1,000, provided that glucose is present and pyruvate is converted to lactate. Irrespective of optimal mitochondrial function and oxygenation, such a rate of pyruvate production will saturate the mitochondrial tricarboxylic acid cycle and oxidative phosphorylation (OxPhos). c During recovery, lactate is converted back to pyruvate and fully oxidized.

Figure 2

Lactate at the physiological level. The flexible use of glucose and lactate as fuels on the cellular level is mirrored at the organism level. All living tissues can consume glucose. From the glucose/lactate point of view, three sorts of tissues/cells exist: 1) cells that must produce lactate because they lack mitochondria, e.g., red blood cells; 2) tissues or cells that either produce or consume lactate depending on circumstances, i.e., all mitochondria-containing cells; 3) tissues that can perform gluconeogenesis and export glucose that is resynthesized from lactate. The liver and the kidneys can only perform gluconeogenesis and export glucose. Only this so-called Cori cycle (denoted by *) carries an energy penalty, whereas the other shuttles do not lead to “waste” of energy.

Figure 3

1,745 combined measurements of arterial pH and arterial lactate in 171 critically ill patients. Horizontal and vertical lines represent suggested definition of lactic acidosis [8]. For lactate levels ≥ 5.0 mmol/L, a significant linear regression analysis reveals a R² = 0.28 (p < 0.001).

Figure 4

Lactate levels and LDH levels in a patient with a lymphoma admitted to the ICU because of respiratory failure. Following diagnosis, treatment with chemotherapy was started. The effect of the first and second chemotherapy on lactate and LDH is shown.