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The Disparate Effects of Epinephrine and Norepinephrine on Hyperglycemia in Cardiovascular Surgery

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The Disparate Effects of Epinephrine and Norepinephrine on Hyperglycemia in Cardiovascular Surgery The Heart Surgery Forum #2018-2008 Online address: http://journal.hsforum.com 21 (6), 2018 [Epub December 2018] doi: 10.1532/hsf.2008 The Disparate Effects of Epinephrine and Norepinephrine on Hyperglycemia in Cardiovascular Surgery Daniel Phadke, BS, Jared P. Beller, MD, Curt Tribble, MD Division of Thoracic and Cardiovascular Surgery, Department of Surgery, University of Virginia, Charlottesville, Virginia, USA ABSTRACT apoptosis, immunologic modulation, vascular alteration, and impairment in wound healing [Girish 2014]. Hyperglycemia is a metabolic derangement that fre- Most cardiac surgery patients are managed with intrave- quently develops after cardiovascular surgery. The periop- nous inotropes in the early postoperative period. Although erative administration of inotropic and vasoactive agents, there are various institutional protocols and individual such as epinephrine and norepinephrine, are common in the preferences, common first-line agents include epinephrine management of cardiac surgery patients and are known to and norepinephrine. Although these agents are known to contribute to the development of postoperative hypergly- play a role in the development of postoperative hyperglyce- cemia. We hypothesized that hemodynamic support with mia, their different effects on hyperglycemia are currently epinephrine exacerbates postoperative hyperglycemia to a underrecognized and rarely discussed. The differences in greater degree than does treatment with norepinephrine. the specific mechanisms of each catecholamine’s action may This literature review outlines the mechanisms by which play an important role in how glucose is regulated in the epinephrine and norepinephrine alter glucose homeostasis, physiologically stressful postoperative state. We hypoth- while highlighting the significant differences in their effects esized that the use of norepinephrine in the perioperative on hepatic glucose mobilization and peripheral glucose uti- management of cardiac surgery patients is associated with lization. This review suggests that the use of epinephrine improved glucose control when compared to epinephrine. exacerbates postoperative hyperglycemia to a greater degree The purpose of this review is to outline the current evi- than does norepinephrine. dence to support that hypothesis. INTRODUCTION MATERIALS AND METHODS Hyperglycemia is a metabolic derangement commonly Data and information in this review were compiled by encountered and treated in everyday medical practice and using the NCBI’s PubMed electronic database using the fol- is associated with increased rates of morbidity and mortality lowing search queries: “epinephrine”, “norepinephrine”, in both medical and surgical settings [Gerstein 2014; Girish “glucose metabolism”, “cardiac surgery”, and “post-operative 2014; Ito 2014; Mulla 2014; Reddy 2014]. Disorders of glu- hyperglycemia”. Only peer-reviewed material was considered cose homeostasis have downstream effects on systemic and for inclusion in this review. Unpublished material, studies in cardiac-specific metabolic and inflammatory states, which preparation for publication, and any otherwise unpublished have been associated with adverse clinical outcomes [Furnary communications were not included. 2003]. Furthermore, abnormal glucose levels have been found to be an independent risk factor for adverse cardiovascular NORMAL GLUCOSE HOMEOSTASIS events, both in patients requiring coronary revasculariza- tion and those undergoing other cardiovascular procedures An intricate network of hormones and neuropeptides [Bartnik 2004a, Bartnik 2004b]. tightly regulate blood glucose concentrations under physi- After cardiac surgery, postoperative hyperglycemia is ologic conditions. These compounds are released primarily found in up to 80% of patients. Effective glycemic con- from the brain, pancreas, liver, intestine, adipose tissue, and trol is especially important in these patients because of muscle. This complex system allows for tight regulation of the significant association between stress hyperglycemia serum glucose levels under normal conditions. For example, and adverse outcomes. In the postoperative state, hyper- a decrease in plasma glucose as small as 20 mg/dL (from glycemia contributes to direct cellular toxicity, increased 90 to 70 mg/dL) will suppress pancreatic insulin release and decrease the uptake of glucose in certain parts of the brain Received March 23, 2018; received in revised form May 1, 2018; accepted May [Gerich 1988]. This results in activation of the sympathetic nervous system and leads to the secretion of counterregula- 5, 2018. tory hormones like glucagon, catecholamines, cortisol, and Correspondence: Curtis G. Tribble, MD, Department of Surgery, University growth hormone [Gerich 1988]. These substances will act to of Virginia School of Medicine, PO Box 800300, Charlottesville, VA 22908; increase the release of glucose into the plasma in order to 1-434-924-2145 (e-mail: [email protected]). achieve a state of normoglycemia. E522 The Disparate Effects of Epinephrine and Norepinephrine on Hyperglycemia in Cardiovascular Surgery—Phadke et al EPINEPHRINE receptors in the liver, which leads to increased cyclic adenos- ine monophosphate (cAMP) and stimulation of protein kinase Effect of Epinephrine on Glucose Regulation A followed by activation of phosphorylase kinases [Rui 2014]. Epinephrine is a naturally occurring catecholamine The initial studies on the kinetics of these interactions utilized released in response to a number of physiologic stimuli. infusions of epinephrine and glucagon in a canine model in These stimuli are generally grouped into one of 4 categories: which insulin levels were held constant [Dufour 2009]. These physical, psychological, social, and cardiovascular/metabolic studies led to the understanding that a certain refractoriness [Kvetnansky 2009]. The characterization of epinephrine and to stable levels of glucose rapidly develops, whereas additional its effects began in the nineteenth century when the first elevations of glucose levels could be achieved through either reports of the cardiovascular effects of a then unknown adre- an additional stimulus or an alteration in the concentration of nal extract were published [Oliver 1895]. Shortly thereafter, the hormones being studied. As a result of these early stud- the compound itself was isolated and its structure identified ies, as well as more contemporary research, 2 conclusions [Abel 1897; Takamine 1901]. can be drawn: (1) that the steady state achieved is not due to A relationship between epinephrine and glucose metabo- depletion of glycogen or substrate for gluconeogenesis, but lism has long been appreciated, but over time, the charac- rather is due to an alteration in sensing, and (2) that a non- terization of the specific mechanisms of its action has devel- cAMP–mediated pathway for epinephrine’s influence may oped in a stepwise fashion. Initially, a rise in blood glucose in exist [Sacca 1978]. response to epinephrine was attributed to increased hepatic The initial increase in hepatic-derived serum glucose glycogen breakdown. This early understanding of the effects is mediated first through glycogenolysis and subsequently of epinephrine on glucose regulation relied on studies that through increases in the rate of gluconeogenesis [Dufour utilized supraphysiologic serum concentrations of this cat- 2009]. Initially, gluconeogenesis remains at a basal rate, and echolamine. This approach limited a complete understand- epinephrine exerts its effects primarily through enhanced ing of epinephrine’s specific mechanism of action because the breakdown of glycogen. However, after approximately resultant hyperglycemia was mediated via both alpha- and 60 minutes of infusion of epinephrine, glycogenolysis slows beta-adrenergic pathways [Antonis 1967]. Subsequent experi- and gluconeogenesis rapidly increases, leading to a 4:1 ratio ments helped to show that, in addition to its powerful influ- in favor of production (gluconeogenesis) over breakdown ence on hepatic glucose production, epinephrine also exerts (glycogenolysis). Thus, epinephrine has a profound effect on its influence through other routes, including attenuation of net glucose production by the liver, both through glycoge- peripheral utilization of glucose and enhanced gluconeogen- nolysis and gluconeogenesis, but the relative contributions of esis [Sherwin 1984]. these pathways vary over time. In addition, epinephrine was found to have signifi- cant effects on glucose regulation via the potentiation of Epinephrine’s Interaction with Insulin and Peripheral responses to other stress hormones. The synergism between Glucose Uptake epinephrine and both glucagon and cortisol contributes to Insulin serves to stimulate glucose utilization and its the profound systemic perturbations in glycemic control that removal from the bloodstream, whereas epinephrine is known follow physiologic stresses such as cardiopulmonary bypass to attenuate the effects of insulin. Early work in this arena and major surgery. Eigler et al demonstrated this principle was carried out by Walaas and colleagues, who created an iso- in a canine model in which isolated infusions of glucagon, lated rat diaphragm preparation and were the first to demon- epinephrine, or cortisol resulted in only mild or insig- strate epinephrine’s ability to block insulin-stimulated muscle nificant elevations in plasma glucose concentration [Eigler uptake in vitro [Walaas 1950]. The key observation in their 1979]. However, the increase
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