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Chronical bronchitis.

The criterion for the diagnosis of chronic bronchitis is a productive cough for most days of three consecutive months for at least two consecutive years. In the etiology of chronic bronchitis, smoking, air pollution, occupational exposure to dust, recurrent pulmonary infections, and hereditary factors play a role. Secretion of hypertrophied bronchial glands and swelling of the mucosa lead to airway obstruction. The term chronic asthmatic bronchitis can be used only when the main component of the disease is bronchospasm. The residual volume increases, but the OEL often remains normal. Often there is a pronounced intrapulmonary bypass and hypoxemia.
Chronic hypoxemia causes erythrocytosis, pulmonary hypertension and, ultimately, right-ventricular failure (cor pulmonale). Because of their appearance, patients with a similar symptom complex are often referred to as “blue bloaters”. With the progression of the disease, chronic hypercapnia gradually develops; the respiratory center becomes less sensitive to PaCO2, and oxygen inhalation can cause respiratory depression.
Emphysema. Emphysema is a pathological condition in which there is an irreversible expansion of the airways located distal to the terminal bronchioles, and the destruction of the alveolar septum. KT of the chest allows you to verify the diagnosis of emphysema. Senile emphysema (emphysema of the elderly), which affects the apex of the lungs, is isolated, is an age norm and has no clinical significance. Severe emphysema is almost always due to smoking. Less commonly, emphysema develops at a young age; its cause is a homozygous deficiency of Ct1 antitrypsin. Being a protease inhibitor, agantitrypsin prevents the excessive activity of proteolytic enzymes (mainly elastase) in the lungs. Proteases are produced by pulmonary neutrophils and macrophages during infection and contaminated air. The cause of emphysema during smoking can be a violation of the balance between proteases and antiproteases in sensitive individuals. Loss of elastic traction (which, due to radial traction, normally maintains the small airways in a straightened state); causes premature expiratory closure of the airways (dynamic compression of the airways). Emphysema is characterized by an increase in OO, FOB, OEL and the ratio of OO / OEL.

The destruction of pulmonary capillaries in the alveolar septa reduces the diffusion capacity of the lungs (Ch. 22) and inevitably leads to pulmonary hypertension in the terminal stages of the disease. In some cases, large cysts, or bullae, develop. A distinctive feature of emphysema is an increase in dead space. The oxygen tension in arterial blood is usually normal or only slightly reduced; PaCO2 also remains normal. During episodes of difficulty breathing, patients with emphysema often tighten their lips, creating an obstruction to exhalation, which slows the subsidence of the small airways (chap. 22). The presence of such an exhalation in combination with the absence of hypoxemia gave reason to call such patients "pink puffers".
Treatment. COPD treatment is mostly supportive. The most important event is smoking cessation. If the patient's airway obstruction is reversible (the criterion is an increase in 0OB1 by more than 15% after the appointment of a bronchodilator), then long-term treatment with bronchodilators is indicated. Very effective (32-adrenergic agonists and ipratropium; some clinicians consider ipratropium a bronchodilator of choice for emphysema. Long-term treatment with theophylline can give good results even in those patients who, when tested with bronchodilators, showed irreversible obstruction; the mechanism of action is probably associated with improved diaphragm function. Exacerbation of the disease often caused by bouts of bronchitis, which is manifested by a change in the properties of sputum; repeated courses of antibiotic therapy are indicated with a spectrum of action (for example, ampicillin, tetracycline, sulfametho-xazole-trimethoprim). In case of hypoxemia, oxygen therapy is recommended, but they should be done with great care. In case of chronic hypoxemia (PaO2 <55 mm Hg) and pulmonary hypertension, low-flow oxygen therapy is prescribed (1-2 l / min).
With an initial CO2 delay, oxygen therapy can lead to a dangerous increase in PaCO2; in these cases, PaO2 rises above bOmmrt. Art. may cause respiratory failure. There are two explanations for this phenomenon: elimination of the stimulating effect of hypoxia on the respiratory center and, more likely, suppression of hypoxic vasoconstriction (chap. 22). With right ventricular failure (cor pulmonale) to eliminate peripheral
rheumatic edema, diuretics are used; digoxin and vasodilators are not always effective. Physical therapy does not affect lung function, but improves the patient's self-awareness. According to some studies, the ability to increase MOD during exercise is inversely related to the risk of developing postoperative pulmonary complications.
Preoperative period. In COPD, preparation for a planned operation is carried out in accordance with the same principles as in bronchial asthma. When collecting an anamnesis, special attention is paid to the severity of shortness of breath, the presence of wheezing and the nature of sputum. OOBt <50% of the norm (1.2-1.5 L) usually corresponds to shortness of breath during physical exertion, while with QOB1 <25% of the norm (<1 L for men), shortness of breath occurs even with very little physical activity. Severe shortness of breath is also observed with a predominance of chronic bronchitis associated with a delay in CO2 and pulmonary hypertension. Thoroughly analyze data from studies of lung function, arterial blood gases, chest radiographs.
The presence of bull. COPD is often combined with heart diseases; therefore, it is necessary to assess the state of the cardiovascular system (Ch. 20).
Unlike bronchial asthma, after a short period of intensive preoperative preparation, only a very slight improvement in pulmonary function can be expected. Nevertheless, preoperative preparation, aimed at correcting hypoxemia, eliminating bronchospasm, reducing the amount and improving drainage of sputum, as well as treating infection, can reduce the risk of postoperative pulmonary complications; it is especially great if in the preoperative period indicators of pulmonary function are less than 50% of the due. At a high risk of complications, it is necessary to discuss with patients and the operating surgeon the likelihood of mechanical ventilation in the postoperative period.
Smoking cessation is indicated at least 6-8 weeks before surgery: this reduces the amount of sputum in the respiratory tract and possibly reduces the risk of pulmonary complications. Smoking increases sputum formation and worsens mucociliary clearance. Both gaseous and solid fractions of tobacco smoke deplete the supply of glutathione and vitamin C, which potentiates tissue damage by oxidants. Contained in

carbon monoxide (CO) increases the concentration of carboxyhemoglobin, and the products of the metabolism of nitrogen oxides increase methemoglobin. This means that quitting smoking at least 24 hours before surgery can theoretically increase the oxygen transport capacity of hemoglobin; note that this assumption is not confirmed by clinical studies. With changes in the nature of sputum, respiratory therapy (percussion massage and postural drainage) and antibiotic therapy, which reduce the formation of sputum and improve its drainage, have a positive effect. Bronchodilators and theophylline are used to treat bronchospasm. With moderate and severe disease in the perioperative period, there may be a need for corticosteroids. Before large operations, depleted patients are prescribed enhanced nutrition. Pulmonary hypertension is treated by optimizing oxygenation. In patients with corpulmonale, cardiac glycosides may be effective, especially with concomitant left ventricular failure.
Intraoperative period. In COPD, regional anesthesia is believed to be preferable to general, but high epidural or spinal anesthesia reduces pulmonary volumes, the activity of auxiliary respiratory muscles, and also suppresses coughing, which causes shortness of breath and prevents sputum discharge. The loss of proprioceptive impulse from the chest and the unusual position of the body on the operating table (for example, lithotomy or on the side) often increase shortness of breath with regional anesthesia in awake patients.
Preoxygenation prior to induction of anesthesia prevents the rapid decline in SaO2 often observed in COPD. In choosing anesthetics and performing anesthesia, they are guided by the principles described for patients with bronchial asthma. Unfortunately, inhaled anesthetics eliminate only the reversible component of obstruction - bronchospasm; even with deep inhalation anesthesia, pronounced expiratory airway obstruction may persist. In patients with moderate to severe illness, anesthetics cause respiratory depression to a greater extent than in people with healthy lungs. As with bronchial asthma, with COPD during mechanical ventilation, a regimen of large tidal volume and low respiratory rate is established to avoid the occurrence of an “air trap”. With severe bronchospasm and prolonged surgery (> 2 hours), the inhaled mixture is moistened. Large bullae and pulmonary hypertension -
contraindications to the use of nitrous oxide. Entering the cavity of the bulla, nitrous oxide increases its volume, which entails the risk of rupture and pneumothorax. Nitrous oxide increases pressure in the pulmonary artery, which is extremely undesirable for pulmonary hypertension. Inhaled anesthetics inhibit hypoxic vasoconstriction in the lungs, however, when using conventional doses, this effect has no clinical significance.
The analysis of arterial blood gases is indicated for prolonged interventions on the limbs, large operations on the organs of the abdominal cavity and all interventions on the organs of the chest cavity. Although pulse oximetry accurately detects a pronounced decrease in SaO2, direct measurement of PaO2 reveals less pronounced changes in intrapulmonary bypass. In addition, PaCO2 should be measured in order to properly set the ventilation parameters, as increasing dead space increases the gradient between PaCO2 and PiTCO2. Mechanical ventilation is carried out so as to maintain a normal pH in arterial blood. Normalization of PaCO2 in patients with preoperative CO2 retention leads to alkalosis (Ch. 30). The degree of invasiveness of hemodynamic monitoring is determined by the state of the cardiovascular system and the nature of the operation. In pulmonary hypertension, the CVP value reflects to a greater extent the function of the right ventricle, rather than the volume of circulating blood.
Sometimes after surgery it is difficult to determine at what point the endotracheal tube needs to be removed. The decision is made based on the ratio of the risks of bronchospasm and respiratory failure. So, in an awakened patient, before extubation, it is easy to assess the state of lung function, nevertheless, removal of the endotracheal tube in this case is associated with a risk of developing bronchospasm. Extubation with deep anesthesia reduces the likelihood of reflex bronchospasm, but is fraught with decompensation of breathing as a result of pulmonary dysfunction. At 00B1 <50%, the probability of transfer to prolonged mechanical ventilation is high, especially after operations on the organs of the chest cavity and the upper floor of the abdominal cavity. General criteria for extubation are discussed in chap. 5 and 50.
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Chronical bronchitis.

    In recent years, due to the deteriorating environmental situation, the prevalence of smoking, and a change in the reactivity of the human body, there has been a significant increase in the incidence of chronic non-specific lung diseases (COPD). The term KNZL was adopted in 1958 in London at a symposium convened by the pharmaceutical group Ciba. He combined such diffuse diseases
  2. Chronical bronchitis
    Chronic bronchitis is a chronic disease characterized by diffuse inflammatory damage to the respiratory tract with excessive secretion of mucus in the bronchial tree and sclerotic changes in the deeper layers of the bronchial wall, manifested by productive cough, persistent rales of various sizes in the lungs (for 3 months), in the presence of exacerbations at least two times per
  3. Chronical bronchitis
    Chronic bronchitis is a disease common among smokers and residents of megacities affected by smog (a mixture of fog, smoke and soot). The diagnosis of chronic bronchitis is made when a persistent cough with sputum production lasts for at least 3 months in 2 years. With simple chronic bronchitis, cough with sputum without signs of airway obstruction is noted
  4. Chronical bronchitis
    Chronic bronchitis is a progressive diffuse inflammation of the bronchi, not associated with local or generalized lung damage, manifested by cough. You can talk about chronic bronchitis if the cough lasts for 3 months in the 1st year - 2 consecutive years. Etiology. The disease is associated with prolonged irritation of the bronchi by various harmful factors (inhalation of air contaminated
    - diffuse inflammatory lesion of the bronchial tree, caused by prolonged irritation of the bronchi by various harmful agents, having a progressive course and characterized by impaired mucus formation and drainage function, which is manifested by cough, sputum separation and shortness of breath According to the WHO recommendation, bronchitis can be considered chronic if the patient coughs up phlegm on
  6. Chronical bronchitis
    Chronic bronchitis is a progressive, diffuse inflammation of the bronchi, not associated with local or generalized lung damage, manifested by coughing. You can talk about chronic bronchitis if the cough lasts for 3 months in 1 year 2 years in a row. The disease is associated with prolonged irritation of the bronchi by various harmful factors (smoking, inhalation of air contaminated with dust,
    On patency of the bronchi: obstructive and non-obstructive. According to the level of damage: proximal - up to 5-6 generation of bronchi. Purulent and catarrhal. Obstructive bronchitis. If distal, then the main symptom is associated with an air trap (when inhaling, the air enters the alveoli, during exhalation the bronchi are shortened, take the form of a corrugated tube and the air does not pass back, the volume increases
  8. Chronic bronchitis in children
    Protocol code: 04-042 Profile: pediatric Stage: hospital Purpose of stage: 1. clarification of the diagnosis and elimination of the inflammatory process in the bronchi; 2. relief of symptoms of respiratory failure, general intoxication; 3. FEV1 recovery. Duration: 11 days ICD codes: J40 Bronchitis, unspecified as acute or chronic J41.0 Simple chronic bronchitis J41.1 Mucopurulent
  9. Chronical bronchitis
    CHRONIC Bronchitis (CB) is a diffuse inflammatory lesion of the bronchial tree caused by prolonged irritation of the airways by volatile pollutants and / or (less commonly) damage by viral and bacterial agents, accompanied by hypersecretion of the mucus, impaired cleansing function of the bronchi, which is manifested by persistent or intermittent cough and sputum discharge.
  10. Chronic bronchitis and emphysema
    Chronic bronchitis is a disease characterized by chronic or recurrent excessive secretion of mucus in the bronchi, leading to the appearance of a productive cough with annual exacerbations of up to 3 months or more in recent years. Emphysema is a disease caused by an increase in the air space of the end bronchioles as a result of destructive changes in their walls. Distinguish
  11. CHRONIC Bronchitis and Pulmonary Emphysema
    Chronic bronchitis is a disease characterized by chronic or recurrent excessive secretion of mucus in the bronchi, leading to the appearance of a productive cough with annual exacerbations of up to 3 months or more in recent years. Emphysema is a disease caused by an increase in the air space of the end bronchioles as a result of destructive changes in their walls. Distinguish
  12. Chronic bronchitis (code J 41, J 44)
    Definition Chronic bronchitis is a diffuse, progressive non-allergic inflammatory lesion of the bronchial tree associated with prolonged irritation of the airways by harmful agents, usually characterized by a restructuring of the secretory apparatus of the mucous membrane, as well as sclerotic changes in the deeper layers of the bronchial wall and peribronchial tissue,
    бронхов и бронхиол.Этиология и патогенез. Инфекция. ХБ может развиваться на почве острого бронхита или воспаления легких. Важную роль в его развитии имеет длительное раздражение слизистой бронхов химическими веществами, пыль, курение.В начале заболевания слизистая полнокровна, местами гипертрофирована, слизистые железы в состоянии гиперплазии. В дальнейшем воспаление распространяется на
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