Hyperglycemia as an effect of cardiopulmonary bypass: intra-operative glucose management

Abstract

Cardiopulmonary bypass (CPB) is associated with surgical stress, hypothermia, hyperoxia, enhancement of neuroendocrine outflow, and administration of glucogenic catecholamines that are associated with glucogonolysis and glucogenesis that result in hyperglycemia. The hyperglycemic state during CPB has been associated with adverse outcomes, such as infection, neurological impairment, cardiac dysfunction, prolonged hospitalization, and higher mortality rates. This report justifies vigilant monitoring of blood glucose levels and a rational protocol for the treatment of hyperglycemia of all open heart surgical patients that may improve post-CPB surgical outcomes.

Figure 1.

Pancreatic β cell. Glucose (G) is transported into the β cell by the glucose transporter, GLUT2. The resulting generation of ATP closes the K⁺_ATP channel and induces membrane depolarization and Ca²⁺ influx. This Ca²⁺ stimulates the gene expression, synthesis, and secretion of insulin and C-peptide. The stimulation of the α₂-receptor inhibits the Ca²⁺ influx and thus insulin synthesis.

Figure 2.

Hepatocyte. Glucose (G) is transported into the hepatocyte by the glucose transporter, GLUT2. Insulin receptor stimulation induces the formation of glycogen. Stimulation of either the β₂-adrenergic or glucagon receptors induces cyclic-adenosine monophosphate (cAMP) and thereby protein kinase A (PKA). PKA activates glycogen phosphorylase (GPa) that induces the production of glucose from glycogen.

Figure 3.

Muscle. Glucose (G) is transported into muscle by the insulin-sensitive glucose transporter, GLUT4. Either insulin receptor or α₁-receptor stimulation can cause the translocation of the GLUT4 from the cytosol to the membrane. The glucose can be converted into ATP by the citric acid cycle or to glycogen. Increased free fatty acids inhibit the glucose conversion to ATP. Glucagon receptor stimulation induces cyclic-adenosine monophosphate (cAMP) and thereby protein kinase A (PKA). PKA activates glycogen phosphorylase (GPa) that produces glucose from glycogen.