For local infiltration anesthesia

For local infiltration analgesia, a mixture is used containing 200— ml of a 0.25% solution of trimecain or lidocaine and 50-100 ml of a 5% solution of epsilon-aminocaproic acid. The mixture blocks not only different receptors of nerve structures, but also stabilizes cell membranes, including mast and intercellular interactions directly in the damage zone, around it and in distant organs due to local and resorptive actions. This explains antiarrhythmic, antihemorrhagic, anti-inflammatory and antibacterial effects. The solution is infiltrating step by step the skin, subcutaneous tissue, intercostal space, pre- and substernal space, the root of the lung and the tissue of the mediastinum. Local and conduction anesthesia takes no more than

7– min of the surgeon’s and anesthesiologist’s work, but in combination with central selective anesthesia and analgesia, it solves the most important task of intensive therapy of the operative period — to prevent nociceptive stimulation of stress-realizing systems, always accompanied by the development of energy-structural deficit and increased catabolism.

In addition to local anesthetics, the protective effect of anesthesia can be enhanced by pharmacological agonists and antagonists of humoral regulation factors, which play an extremely important role in the pathogenesis of stressful cell damage and determine the “price” of nonspecific adaptation. The potentiating analgesia effect was noted when gordox, dalargin, proglumide, calcium antagonists —finoptin and corinfar, antioxidants — tocopherol, glutamic acid, mafusol, methylpred izolone, and their combinations were introduced during the operation . In particular, the effectiveness of the combined use of sodium hydroxybutyrate (150 mg / kg), benzofurocain (10 mg / kg) and glutamic acid (in a volume equal to the volume of sodium hydroxybutyrate in ml . It has been established that the introduction of such a mixture 30 minutes before the operation leads to a subsequent decrease in oxygen consumption by the tissues, improves peripheral blood flow and increases cardiac output in patients with circulatory failure.

The presented data show the modern possibilities of managing the processes of nociception and antinociception and reflect the fundamental difference between the applied anesthesia scheme and classical NLA-II, which we currently do not use in thoracic surgery, refusing to use nitrous oxide, as well as other traditional inhalation anesthetics, which have little selective suppressive effect on the main functional life support systems and prevent the formation of urgent compensation systems. Studies have shown that the inclusion of nitrous oxide in the composition of the respiratory mixture at any stage of the operation very quickly — within 5– min leads to a significant decrease, often to critical values ​​(60 mm Hg) of the oxygen tension determined by the percutaneous method. We emphasize that the degree of hypoxia does not correspond to a decrease in the oxygen content in the breathing circuit,and is determined primarily by increasing the tone of the peripheral vessels and the deterioration of myocardial contractility. Circulatory hypodynamia and an increase in the central blood volume are preserved in the majority of patients after surgery, causing an overload of the pulmonary circulation, hypertension in the pulmonary capillaries and an increase of 2 times the volume of the extravascular fluid in the parenchyma of the lungs . The clinical manifestations of these changes depend on the functional reserves of the body and can vary from moderate disturbances in the function of external respiration, an increase in the amount of sputum, and a manifested picture of pulmonary edema. The insufficient antinociceptive ability of NLA-P is also indicated by an increase in the intensity of the oxygen regime. Violations of oxygen transport at all stages of its metabolism develop already during the operation and persist in the early postoperative period, leading to a rapid depletion of functional reserves and the breakdown of compensatory processes.

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