The consequences of airway obstruction are varied and often manifest as: • An increase in resistance to air flow, especially when exhaling, causes air retention in the lungs and an increase in functional residual capacity, overstretching and distention of the lungs. Overstretching of the chest is accompanied by an increase in the work of breathing. • Decreased respiratory muscle effectiveness. A large degree of change in intrathoracic pressure is needed to change the volume of the lungs. Breathing is provided using even less effective respiratory muscles. • An increase in oxygen consumption and the formation of carbon dioxide, leading to hypoxemia, a decrease in pH, and the development of respiratory and metabolic acidosis. • Development of a mismatch between ventilation and perfusion, which leads to a drop in arterial oxygenation. Poorly perfused zones additionally increase the violation of CO2 removal. • Development of respiratory failure. Mostly obstructive types develop the following diseases: • bronchial asthma; • chronic obstructive pulmonary disease (COPD), which is based on chronic bronchitis, emphysema, or a combination thereof; • bronchiectatic disease. Bronchial asthma Bronchial asthma (BA) is a chronic, severe disease of a person’s lungs. Represents the most common allergic disease. BA suffer from 0.3-1% of the population. Causes of bronchial asthma: • internal (genetically determined defects in the form of hypersensitivity to the bronchial mucosa); • external (smoking, dust, toxic gases, plant pollen, etc.). Bronchial asthma (AD) is preceded by a state of predastma, characterized by the following symptoms. • Acute or chronic lung diseases with obstruction of the bronchi (asthmatic and obstructive bronchitis, acute pneumonia with obstruction, acute respiratory diseases with obstruction). • Extrapulmonary manifestations of altered reactivity. • Eosinophilia of blood and / or sputum. • Hereditary predisposition. If these signs are present, clinically severe bronchial asthma occurs in 70% of patients within 3 years. The fewer these signs, the less likely the development of this disease. Bronchial asthma accounts for 67-72% of bronchial obstructive conditions. Bronchial asthma is characterized by a pronounced change in external respiration (due to bronchial obstruction and impaired gas exchange between the external environment and the body). A mandatory sign of bronchial asthma is an attack of suffocation within a few hours. Respiratory distress in bronchial asthma often has an expiratory character and is accompanied by a feeling of chest compression. The chest is in the maximum inspiratory position (expands). Bronchial asthma can be caused by various etiological factors, the central position among them is occupied by allergens, mainly of infectious and pollen origin, as well as cold air, dust, physical activity, strong emotions, liberals (histamine, etc.), etc. The pathogenesis of an attack of bronchial asthma includes the following changes. • Recently, the role of bronchial hyperreactivity, pathogenetic factors of which are shown in Fig. 1, has been of great importance in the formation of obstructive syndrome. 29-3. • Another important pathogenetic factor of bronchial asthma is changes in the immunocompetent system, which is reflected in the modern classification of AD (infectious-allergic and non-infectious-allergic, or atopic). – In the immunodependent form of bronchial asthma, allergens entering the sensitized body interact with reagins (IgE) fixed on mast cells, endotheliocytes, smooth muscle cells, etc. Reagins realize their effect through the activation of G-proteins (which reduce the sensitivity of p-adrenoreceptors to adrenaline and norad) , mast cells, eosinophils, monocytes, lymphocytes and histiophages that secrete various FAs – 2% of allasthmatics develops an autoimmune variant of bronchial asthma – the most severe variant of the development of this disease. Various types of immunodeficiencies are of great importance in the development of AD. • A non-adrenergic and non-cholinergic system with the substance P, a vasoactive intestinal peptide (VIL), has a strong reducing or relaxing effect on the tone of the smooth muscles of the bronchi. So, bronchospasm may be due to increased bronchoconstrictive stimuli (increased cholinergic, a-adrenergic activity or the influence of substance P) or decreased p-adrenergic activity or VIP-release. • BA can be based on a drug mechanism, in particular aspirin. Aspirin asthma is characterized by intolerance to acetylsalicylic acid, bronchospasm and hay fever. The mechanism of the bronchoconstrictor action of acetylsalicylic acid is its ability to change the metabolism of arachidonic acid. With the activation of the lipoxygenase pathway of its metabolism, the formation of leukotrienes (including a slow-reacting substance) with a bronchospastic effect is enhanced.