The main task of the respiratory system is to saturate the blood with oxygen..

Its implementation becomes possible thanks to a complex functional system, which is represented by the following structures:.

- controlling and managing the influence of the autonomic and central nervous systems;

- the frame of the chest, respiratory muscles, upper and lower airways, pulmonary parenchyma, which provide air ventilation;

- lungs, heart and vessels, which carry out gas exchange between blood and alveoli.

The result of the activity of this general system is normal or altered tension of oxygen and carbon dioxide in arterial blood..

Nutritional support for lung disease - a relatively new frontier in dietetics.

The results of the studies have shown that the main negative effect of protein-energy deficiency on the respiratory system is manifested in the structure and functions of the respiratory muscles, gas exchange and the degree of immune defense.. Less studied are the adverse effects of malnutrition on the architectonics of the lungs and its recovery after injury, on the production of surfactant.

In healthy people and patients with emphysema, there is a direct correlation between body weight and diaphragm weight. In addition, in patients with protein-energy deficiency, a decrease in the strength of the respiratory muscles was observed at the height of the maximum inspiratory and respiratory pressure.

Animal experiments have shown that insufficient amounts of proteins and calories lead to a decrease in the T-lymphocyte-dependent function of alveolar macrophages, despite their persisting neutrophil-dependent function..

Therefore, along with the general susceptibility to infectious diseases, malnourished patients may develop local immunity disorders of the lung mucosa.. In addition, there is a positive correlation between the nutritional status of patients and colonization of gram-negative bacteria in the mucous membrane of the lower respiratory tract..

Nutritional therapy for chronic obstructive pulmonary disease.

The majority of chronic lung diseases are pathophysiologically represented by the formation of obstructive or restrictive damage in the mechanics of external respiration (alone or in combination).

Protein-energy deficiency in chronic obstructive pulmonary diseases. The most common are chronic obstructive pulmonary disease (COPD), which affects 14% of adult men and 8% of women.. This term includes: emphysema, chronic bronchitis, and bronchial asthma.

Protein-energy deficiency is common among patients with COPD, accounting for, according to various studies, 19-25%. With progressive body weight loss in this group of patients, mortality is significantly (2 times) higher than in those patients who did not have weight loss.

In retrospective analysis, it was reasonably shown that individuals who had less than 90% of the ideal body weight at the beginning of the study, in general, had a higher mortality rate within 5 years, even after eliminating complications associated with lung dysfunction.

This effect was observed in patients with moderate obstruction (forced expiratory volume greater than 46% of the required volume) and in those who had severe obstruction (forced expiratory volume less than 35% of the required volume) - therefore, did not depend on lung function. Thus, progress in the treatment of COPD did not change the poor prognosis of concomitant protein-energy malnutrition..

Patients with chronic obstructive pulmonary disease with poor nutritional status have more pronounced respiratory failure and the absence of the classic symptoms of chronic bronchitis.

Possible pathophysiological mechanisms of protein-energy malnutrition in patients with chronic lung disease have been studied:.

- deterioration of the functions of the gastrointestinal tract;

- inadequate nutrition;

- an adaptive mechanism to reduce oxygen consumption (in order to reduce the work of the respiratory muscles);

- altered pulmonary and cardiovascular hemodynamics, limiting the supply of nutrients to other tissues;

- a state of increased metabolism.

Malnutrition in COPD patients is classically attributed to decreased food intake and increased energy expenditure secondary to high respiratory rate, in which resistive load increases and the efficiency of the respiratory muscles decreases..

Along with this, insufficient calorie intake can be during stress, surgery or infection, when the need for energy increases.

The research results showed that the real energy requirement in COPD patients with and without weight loss significantly exceeds the value calculated using the Harris-Benedict equation. Although these patients have an increased metabolism, they do not have the increased catabolism that occurs under stress with a predominance of fat oxidation.. Increased energy requirements may be associated with increased oxygen uptake by the respiratory muscles.

A higher level of energy consumption by the respiratory muscles to meet the need for it in daily life compared to healthy subjects, possibly maintains a state of hypermetabolism, and leads to progressive loss of body weight if calorie consumption exceeds their consumption.

Most studies demonstrate an adequate intake of calories, the need for which in patients with chronic obstructive pulmonary disease has been calculated or measured at rest.. However, the required number of calories for vigorous physical activity or intercurrent illness was not taken into account in order to assess their real adequacy for a given patient..

Attempting to increase calorie intake above normal (baseline) levels may be difficult in these patients due to respiratory and gastrointestinal distress.. Some of these symptoms (bloating, early satiety, anorexia) may be associated with the flattening of the phrenic muscle and its effect on the abdominal cavity..

In hypoxic patients with COPD, dyspnea may increase with food, which further limits the amount of food intake. Eating smaller, more frequent meals can alleviate some of these problems to some extent..

Studies in which malnourished patients with COPD were given food supplements to increase their total daily caloric intake demonstrated the difficulty of maintaining adequate caloric intake early in the study..

Increases in enteral supplementation have been accompanied by a tendency to decrease the amount of commonly consumed food. It has been shown that patients with chronic obstructive pulmonary disease and low body weight have the same energy requirements, as well as patients without weight loss.. But in the first group, a lower intake of calories was noted relative to their measured energy requirement..

Nutritional support.

With COPD, they expect to maintain the strength of the respiratory muscles, especially the diaphragm, their mass, as well as the ability to optimize the overall functioning of the patient's body..

Several studies have shown that consuming extra calories over 16 days leads to significant weight gain and an improvement in maximum respiratory pressure..

With a longer observation of patients with COPD, after 3 months of additional diet, an increase in body weight and other anthropometric data was noted, an increase in the strength of the respiratory muscles was observed, an improvement in general well-being and tolerance of 6-minute walking distances, as well as a decrease in the degree of shortness of breath. With a longer duration of additional nutrition, along with an increase in the weight of patients, there was a further improvement in the functions of the respiratory muscles..

The problem of adequate caloric intake in this patient population may be due to diet-induced thermogenesis: patients with reduced nutrition have been shown to have a greater increase in resting oxygen consumption after a meal than patients without chronic obstructive pulmonary disease..

In order to increase the positive nitrogen balance in patients with protein-energy malnutrition and COPD, recombinant growth hormone (0.05 mg / kg) was used subcutaneously daily for 3 weeks along with a balanced diet (35 kcal / kg).

While taking growth hormone, these patients showed improved nitrogen balance, increased body weight and increased maximum respiratory pressure compared to the first week when they received only a balanced diet.. Thus, the use of exogenous growth hormone can promote protein replenishment and synthesis, reducing the total amount of calories needed for anabolism..

There are no long-term studies that consider nutritional support as a criterion for improving the overall prognosis in patients with COPD. If survival is associated with weight gain, and this is the independent variable, and supplemental nutrition can improve and maintain body weight, then survival is expected to be associated with nutritional optimization in this population..

It is not clear what its potential effect on respiratory function could lead to an improvement in clinical results: immunocompetent, improved gas exchange, effect on reparative processes in the lung, or surfactant production. Despite the mixed results from short-term studies, the clinical rationale for supplementation in patients with chronic obstructive pulmonary disease is clear..

Because COPD patients have a limited respiratory reserve, a high carbohydrate diet is undesirable.. A diet high in fat is healthier. A study showed that a 5-day, low-carb diet in patients with COPD and hypercapnia resulted in lower arterial CO2 levels than a 5-day high-carb diet.. A significant functional parameter was assessed - a 12-minute walk.

The role of metabolic disorders of macro- and microelements in the formation of bronchial obstruction.

Electrolyte deficiency such as hypophosphatemia, hypokalemia, and hypocalcemia can adversely affect the function of the respiratory muscles. Improvement of diaphragm contractile function after phosphorus replenishment has been shown in patients with acute respiratory failure and hypophosphatemia.

This observation is especially typical for patients with chronic obstructive pulmonary disease who are indicated for mechanical ventilation, since they usually experience intracellular changes after correction of respiratory acidosis. Clinical manifestations of hypophosphatemia arise from depletion of intracellular phosphorus reserves, which, as a rule, accompanies chronic hypophosphatemia.

It has been reported that a sharp drop in serum calcium levels can also decrease the maximum contraction of the diaphragm..

A case of hypokalemic respiratory arrest, i.e. hypokalemic paralysis of the respiratory muscles, has been described.

Magnesium is of considerable interest to researchers. It was found that it activates adenylate cyclase, which catalyzes the formation of cAMP, inhibits the degranulation of mast cells and provides relaxation of the smooth muscles of the bronchi..

In patients with hypomagnesemia, obstructive dysfunctions of external respiration and hyperreactivity of the bronchi to histamine were found, which were completely or partially eliminated by the administration of magnesium preparations.. After intravenous administration, magnesium salts have a bronchodilator effect, stopping attacks of suffocation, increase the force of contraction of the respiratory muscles and reduce pulmonary hypertension in patients with bronchial asthma and other obstructive pulmonary diseases.

Increased attention to the relationship between micronutrients, vitamins and respiratory diseases. The dependence of the respiratory symptoms of bronchitis with the level of vitamin C in serum, zinc, copper, nicotinic acid was found..

Vitamin C is an antioxidant, and copper is an important cofactor for the enzyme lysyl oxidase, which is involved in the synthesis of elastic fibers and glycosaminoglycans that make up the structural component of the framework (basal tone) of the bronchi. Severe copper deficiency can lead to decreased elasticity of the bronchi.

Under artificially induced copper deficiency conditions in mammals, the development of primary emphysema was observed as a result of a sharp decrease in elastin in the lungs. The cause of an irreversible defect in the lung tissue is inactivation of the copper-containing enzyme lysyl oxidase, depression of superoxide dismutase and the associated intensification of lipid peroxidation..

Selective zinc deficiency leads to thymic hypoplasia, decreased thymoline activity and stimulates T-lymphocytes. It is believed that a change in the trace element composition of the blood is one of the reasons for the formation of secondary immunodeficiency states in diseases of the respiratory system.

Noteworthy are the data on the ability of trace elements to control the activity of lipid peroxidation and antioxidant protection. It is known that copper, zinc and manganese are part of superoxide dismutase, selenglutathione peroxidase. These enzymes are components of the intracellular antioxidant system.

Ceruloplasmin, one of the main extracellular antioxidants, belongs to the class of copper-containing proteins. Zinc, which forms chemical bonds with sulfhydryl groups of proteins, phosphate residues of phospholipids and carboxyl groups of sialic acids, has a membrane stabilizing effect. Copper and zinc deficiency leads to the accumulation of free radicals in the tissues. Excess ionized iron has a prooxidant effect.

In recent years, studies have shown that patients with COPD have a selenium deficiency associated with depression of the intracellular antioxidant glutathione peroxidase. Supplements of sodium selenite at a daily dose of 100 ?g for 14 days increase the activity of this enzyme and significantly reduce the clinical manifestations of bronchial obstruction.

Chronic lung disease may be associated with free radical damage when the lung's natural antioxidant defense system is suppressed (cigarette smoking) or insufficient (?-antitrypsin deficiency). Dietary micronutrient deficiencies may contribute to an increase in susceptibility to free radical damage and may be one of the factors that leads to excessive activation of lipid peroxidation..

Diet therapy for chronic obstructive pulmonary disease.

Diet therapy is aimed at reducing intoxication and increasing the body's defenses, improving the regeneration of the epithelium of the respiratory tract, reducing exudation in the bronchi. In addition, the diet provides for the replenishment of significant losses of proteins, vitamins and mineral salts, sparing the activity of the cardiovascular system, stimulation of gastric secretion, hematopoiesis.

For this purpose, it is recommended to prescribe a diet of a sufficiently high energy value (2600-3000 kcal) with an increased content of complete proteins - 110-120 g (of which at least 60% of animal origin), with a fat quota of 80-90 g and a carbohydrate content within the physiological.

It is planned to increase foods rich in vitamins, especially A, C, group B (decoctions of wheat bran and rose hips, liver, yeast, fresh fruits and vegetables, their juices), as well as calcium, phosphorus, copper and zinc salts.

The inclusion of vegetables, fruits, berries and juices from them, meat and fish broths contribute to an improvement in appetite.

Limiting table salt to 6 g has an anti-inflammatory effect, reduces exudation, fluid retention in the body and thereby prevents the development of cor pulmonale. The diet provides for the restriction of free fluid, which helps to reduce the amount of sputum secreted and a gentle regimen for the cardiovascular system.

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