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Possible Adverse Effects of Single Macronutrient on the Lung Tissue of Patients with ARDS

Carbohydrates and Lipids

High levels of intravenous CHO in TPN nutritional support increase body temperature [46], respiratory quotient, and VCO2, which in turn increase ventilatory demand, as seen in a small uncontrolled study [47] and in a small RCT [48]. It is nowadays becoming clearer that these effects are due to hyperalimentation, i.e., an excessive calorie load compared to metabolic needs (see later 11.4).

However, a prevalent CHO enteral feeding was associated with improved clinical outcomes [49] and with better muscle protein accretion compared with an isonitrogenous isocaloric high-fat feeding [50]. Then carbohydrates appear to be the preferential substrate in critical illness [51], because of a poor utilization of fat secondary to an impaired oxidation and inefficient transport between pools [52, 53].

Indeed, in healthy people, high-fat diets have been related to potential development of endotoxemia by causing changes to gastrointestinal barrier function or microbiota composition [54]. Hence, being patients with ARDS especially exposed to infectious complications, these considerations would argue against the use of high-fat diet in this population of patients.

Fatty acid chains differ by length, often categorized from short to long. Polyunsaturated fatty acids contain more than one double bond; depending on the location of the first double bond, they can be classified into w3, w6, or w9. Their relevance depends on their specific biological activity. More in details, long-chain w6 fatty acids (such as linoleic acid, LA, and gamma-linolenic acid, GLA) have been associated with pro-inflammatory phenotypes particularly dangerous in critically ill patients [55, 56]. Their supply also resulted in increased synthesis of vasodilating prostaglandins [57]; moreover, they can interfere with lung hemodynamics and with the V/Q regulation, which in turn may lead to worsened gas exchange due to resolution of hypoxic vasoconstriction in hypoventilated areas of a damaged lung [58, 59].

It has been reported that fatty acids from the w3 family (eicosapentaenoic, EPA, and docosahexaenoic acid, DHA), unlike w6, can modulate inflammatory processes [56]. Their use was associated with reduced availability of arachidonic acid, with a consequent shift in the production of cytokines from the highly pro-inflammatory four-series leukotrienes and dienoic prostaglandins to the less inflammatory five- series leukotrienes and trienoic prostaglandins [60]. Experimental w3 fatty acid supplementation was also associated with a restored permeability of injured alveolar-capillary membrane and with lower levels of tissue inflammation and apoptosis [61].

As for MCT, their higher DIT when compared to long-chain fats has already been mentioned, while we lack evidence as for any potential negative effect of w9 polyunsaturated fatty acids.


Protein administration increases minute ventilation more than expected for the increase in REE, suggesting a specific activity on ventilatory drive [62] that has to be taken into account when dealing with a patient with limited possibilities to increase work of breathing. In case of development of severe sepsis, particular attention has to be given to the risks of an enhanced supply of arginine, due to its pro-inflammatory characteristics [18].

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