The main symptom is a long-term cough with sputum separation. In the initial period of the disease, exacerbations are observed in the cold season and are characterized by an increase in cough and an increase in the amount of sputum. In the presence of bronchopulmonary infection, patients develop fever or subfebrile condition, sputum becomes mucopurulent or purulent, impaired bronchial obstruction due to edema and inflammatory infiltration of the bronchial wall, bronchospasm, and accumulation of sputum with the formation of mucous plugs. When a blood test is observed leukocytosis and an increase in ESR. Over time, the cough becomes almost constant, episodes of bronchopulmonary infection become more frequent, shortness of breath joins. Exacerbations of the disease are more severe and longer. Unlike pulmonary emphysema, in which any episode of bronchopulmonary infection can be fatal, with exacerbation of chronic bronchitis, antibiotic therapy allows, as a rule, to achieve a rapid improvement in the patient’s condition. At the same time, the general condition improves, body temperature normalizes, the amount of sputum decreases, which gradually becomes mucous, dry wheezing and other signs of bronchial obstruction disappear. Another feature of chronic bronchitis that distinguishes it from emphysema is the rapid development of pulmonary hypertension, the severity of which increases with physical exertion. The cause of increased pressure in the pulmonary artery is considered to be a spasm of the pulmonary vessels in response to hypoxia, a violation of the rheological properties of blood against the background of secondary erythrocytosis. Long-term pressure overload of the right ventricle leads to the development of a pulmonary heart, decompensation of which is usually observed during exacerbations of chronic bronchitis as a result of an increase in the degree of airway obstruction and hypoxemia. In patients with a predominance of chronic bronchitis, body weight is increased, pronounced edematous syndrome and cyanosis are noted, in connection with which they are called “blue edema”. At rest, the respiratory rate is not significantly increased, auxiliary muscles in the act of breathing are clearly not involved. On examination, signs of severe emphysema are absent. Percussion sound is clear or slightly dull. Vesicular or hard breathing, exhalation is elongated. Scattered dry rales of various caliber are heard, in the lower parts of the lungs – inaudible moist small-bubbling rales that disappear after coughing and sputum discharge. The right border of the relative dullness of the heart is shifted. Accent II tone over the pulmonary artery. With decompensation of the pulmonary heart, in addition to edema, there is an increase in the liver, expansion of the jugular veins, accumulation of fluid in the cavities (ascites, hydrothorax, hydropericardium).
When radiography, the transparency of the lungs can be reduced, the pulmonary pattern is enhanced. As pulmonary hypertension increases, the shadow of the heart increases, and pulmonary arteries expand. On the ECG , signs of hypertrophy of the right atrium and ventricle are detected (an increase in the amplitude of tooth I in lead III and AVF, wave R in leads V1-2, the appearance of tooth S in leads K5-6, conduction disturbances in the right leg of the atrioventricular bundle). An electrocardiogram is a relatively insensitive method for diagnosing a pulmonary heart and in most cases does not reveal the initial hypertrophy of the right ventricle. To determine the wall thickness of the right ventricle and the size of its cavity during diastole in patients with COPD, echocardiography is increasingly being used. Signs of pulmonary hypertension during echocardiography are considered to be hypertrophy of the wall of the right ventricle (more than 5 mm), an increase in the amplitude of its movement, dilatation of the right ventricle (more than 25 mm with an increase in the ratio of the sizes of the right and left ventricles over 0.5). There are other methods for indirectly assessing pulmonary pressure, in particular rheography under conditions of a Valsalva test.
Unlike pulmonary emphysema, chronic obstructive pulmonary hypertension does not change significantly; VC and diffusion capacity are close to normal or moderately reduced. FEV1 and expiratory flow rate are sharply reduced. Ventilatron-perfusion disturbances in the absence of an increase in MOD lead to a decrease in PaO2, and an increase in PaCO2. Hypoxemia stimulates erythropoiesis and leads to secondary erythrocytosis. The main complication is ARF, due to an increase in the volume and (or) viscosity of sputum against a background of bronchopulmonary infection. In addition, ONE can cause pneumonia, left ventricular failure, pulmonary thromboembolism, the diagnosis of which is very difficult. Symptoms of menacing ONE are increasing shortness of breath, insomnia, agitation. Often, such patients are prescribed sedatives, which can contribute to the development of respiratory failure. Reliable criteria for the diagnosis of ODN in patients with COPD are considered to be a rapid decrease in RaO2 by 10-15 mm RT. Art. and pH below 7.30. A change in the latter indicator reflects the development of metabolic acidosis against the background of hypercapnia.