# Perioperative Nutritional Support: A Review of Current Literature
## 6 Perioperative Nutritional Support in Non-Onological Pathology  
### Cardiac Surgery  
Malnutrition in Congestive Heart Failure (CHF) is not an isolated or unidirectional phenomenon. It is estimated that 50% of patients with CHF have malnutrition, and between 19 and 39% cachexia [124; 125]. CHF causes tissue hypoperfusion, creating and favoring a hypoxic environment and activation of the immune system with increased expression of pro-inflammatory cytokines (TNF\(\alpha\), IL-1, IL-6) that condition a situation of chronic inflammation that, in turn, as previously explained, causes an increase in catabolism and the appearance of sarcopenia and loss of muscle mass. TNF\(\alpha\) induces myocyte apoptosis and proteolysis (along with IL-6), while decreasing hepatic albumin synthesis and inhibiting appetite, synergistically with IL-1. IL-6 also inhibits hepatic albumin synthesis. On the other hand, these patient develop a resistance to insulin, along with a decrease in insulin-like growth factor 1 (IGF-1) and testosterone and dehydroepiandrosterone (DHEAS), which ultimately translates into a net increase in catabolism and a reduction in anabolic phenomena, along with a reduction in metabolic expenditure [126; 127; 128; 129; 130; 131; 132; 133]. Likewise, in CHF, the activation of various neurohormonal systems occurs. There is a chronic imbalance between the sympathetic and parasympathetic nervous systems, with a net increase in adrenaline and noradrenaline that induce catabolism. In addition, there is also activation of the renin-angiotensin-aldosterone system, with an increase in angiotensin II. Angiotensin II induces sarcopenia and loss of muscle mass by numerous mechanisms: Increased oxidative stress through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, decreased IGF-1 and increased pro-inflammatory cytokines (So it further worsens the pro-inflammatory situation), reduced appetite by direct effect on the central nervous system (CNS), alteration of metabolic expenditure by actions on adenosine monophosphate activated protein kinase (AMPK) and finally, but not least, decreased myocyte regeneration [126; 134; 135; 136; 137]. It should be remembered that the heart is mostly a muscular structure, so the tissue destruction generated by all exposed processes further worsens the situation of heart failure; in fact, sarcopenia itself is a cause of CHF, worsening cardiac mechanics, and is a factor of poor prognosis. Intestinal hypoperfusion and the presence of wall edema condition the appearance of maladaptive phenomena that cause not only a lower absorption of nutrients, but a whole plethora of digestive symptoms that worsen even more if possible the already delicate clinical situation of these patients [126; 133; 134; 135; 136; 137; 138; 139; 130]. Cardiac cachexia is defined as an unintentional and edema-free weight loss greater than 5% in the last 12 months (or a body mass index \(<\) 20) (Major criterion), accompanied by at least three of the following findings (Minor criteria): decreased muscle strength, fatigue, anorexia, low lean mass index or laboratory alterations such as elevated inflammatory markers (C-reactive protein or IL-6), hemoglobin \(<\) 12 g/dL or serum albumin \(<\) 3.2 g/dL [128; 129; 130; 135; 136; 137; 138; 139]. As we have previously anticipated, the appearance of this syndrome implies a worse prognosis in patients with CHF, with a mortality of 50% at 18 months, apart from a worse quality of life and functional capacity [125; 133; 134; 141; 142]. Thus, it is not surprising that patients who are going to undergo cardiac surgery are diagnosed with malnutrition in a high percentage (17-20% are at high risk of malnutrition and in some series, it reaches 46%, and even 50% in CHF) [143; 144; 145; 143; 14]. The presence of malnutrition is an independent risk factor for the appearance of postoperative complications and is associated with higher mortality and hospital stay [146; 149; 20; 38].