Stress hyperglycemia, cardiac glucotoxicity, and critically ill patient outcomes current clinical and pathophysiological evidence.

Abstract

Stress hyperglycemia is a transient increase in blood glucose during acute physiological stress in the absence of glucose homeostasis dysfunction. Its's presence has been described in critically ill patients who are subject to many physiological insults. In this regard, hyperglycemia and impaired glucose tolerance are also frequent in patients who are admitted to the intensive care unit for heart failure and cardiogenic shock. The hyperglycemia observed at the beginning of these cardiac disorders appears to be related to a variety of stress mechanisms. The release of major stress and steroid hormones, catecholamine overload, and glucagon all participate in generating a state of insulin resistance with increased hepatic glucose output and glycogen breakdown. In fact, the observed pathophysiological response, which appears to regulate a stress situation, is harmful because it induces mitochondrial impairment, oxidative stress‐related injury to cells, endothelial damage, and dysfunction of several cellular channels. Paradigms are now being challenged by growing evidence of a phenomenon called glucotoxicity, providing an explanation for the benefits of lowering glucose levels with insulin therapy in these patients. In the present review, the authors present the data published on cardiac glucotoxicity and discuss the benefits of lowering plasma glucose to improve heart function and to positively affect the course of critical illness.