Diagnostic criteria for broncho-obstructive syndrome according to respiratory function data. Broncho-obstructive syndrome in adults and children. Pathogenesis of the formation of bronchial obstruction in children

Broncho-obstructive syndrome is not a disease, but a set of symptoms that cannot act as an independent diagnosis. The symptoms demonstrate a clear picture of problems of the respiratory system, namely, a violation of bronchial obstruction caused by either an organic or functional formation.

BOS (abbreviated name) is often diagnosed in children of an early age group. Approximately 5-50% of all children aged one to three years show some signs of broncho-obstructive syndrome. The doctor should pay attention to these symptoms and immediately begin to identify the cause of the biofeedback, and then prescribe the necessary diagnostic measures and appropriate treatment.

In children susceptible to allergic ailments, BOS is diagnosed more often - in approximately 30-50% of all cases. Also, this set of symptoms often manifests itself in young children who are exposed to repeated attacks of respiratory infections every year.

Kinds

Based on the degree of damage, four types of biofeedback are distinguished:

  • easy;
  • average;
  • heavy;
  • obstructive severe.

Each type is characterized by certain symptoms, and a manifestation such as cough is an integral sign of any type of biofeedback.

According to the degree of duration, acute, protracted, recurrent and continuously recurrent types of broncho-obstructive syndrome are distinguished.

  • the acute form is manifested by insidious symptoms and clinical aspects that prevail in the body for more than ten days;
  • protracted syndrome is characterized by an unexpressed clinical picture and long-term treatment;
  • in a recurrent form, symptoms can both appear and disappear without any reason;
  • finally, continuously relapsing biofeedback is characterized by visible remission and periodic manifestations of exacerbations.

Broncho-obstructive syndrome is of four types: allergic, infectious, hemodynamic and obstructive.

  • allergic biofeedback occurs due to an abnormal reaction of the body to taking certain substances;
  • infectious – as a result of penetration of pathogenic microorganisms into the body;
  • hemodynamic – due to low blood flow in the lungs;
  • obstructive – due to filling of the bronchial lumens with excessively viscous secretion.

Causes

Based on the underlying pathology, the causes of biofeedback can be divided into categories such as:

Gastrointestinal diseases include:

  • ulcers;
  • achalasia, chalasia and other problems with the esophagus;
  • diaphragmatic hernia;
  • tracheoesophageal fistula;
  • GES (or gastroesophageal reflux).

Respiratory system problems include:

  • bronchopulmonary dysplasia;
  • airway aspiration;
  • bronchiolitis obliterans;
  • infectious diseases of the respiratory tract;
  • congenital developmental anomalies;
  • bronchial asthma of various types.

Genetic and hereditary pathologies include cerebral palsy, cystic fibrosis, rickets, mucopolysaccharidosis, deficiency of proteins such as AAT, alpha-1 antithripsing, etc.

Solar radiation, polluted atmosphere, poor quality of drinking water - these and many other environmental factors negatively affect the body, weakening the immune system and making it very susceptible to various diseases.

Symptoms

There are many symptoms of broncho-obstructive syndrome.

Complications

With poor quality, untimely or incomplete treatment for broncho-obstructive syndrome, the following complications are most common:

  • acute heart failure;
  • life-threatening abnormalities in the heart rhythm;
  • paralytic state of the respiratory center;
  • pneumothorax;
  • with very frequent asthmatic attacks - the occurrence of secondary pulmonary emphysema;
  • pulmonary atelectasis;
  • formation of pulmonary acute heart;
  • asphyxia (suffocation), which occurs, for example, due to aspiration of viscous sputum from the lumens of the small bronchi.

Diagnostics

As mentioned above, broncho-obstructive syndrome is not a disease, but a kind of indicator of some kind of disturbance in the functioning of the body. This applies to both adults and children. As a result, before starting to treat the patient, the doctor must establish the true root cause of these symptoms, as well as make a correct diagnosis.
The fact is that bronchial obstruction can perfectly “disguise” itself as an acute respiratory infection like a common cold. That is why diagnosing solely clinical indicators is not enough; it is necessary to form an extensive examination of the patient.

As a rule, during biofeedback, the patient is prescribed the following diagnostic tests:

Treatment

Treatment includes several main areas, such as bronchodilator and anti-inflammatory therapy, as well as therapy aimed at improving the drainage activity of the bronchi. In order to increase the efficiency of the drainage function, it is important to carry out such procedures as:

  • mucolytic therapy;
  • rehydration;
  • massage;
  • postural drainage;
  • therapeutic breathing exercises.

Mucolytic therapy is aimed at thinning sputum and improving cough productivity. It is carried out taking into account such patient factors as age, severity of biofeedback, amount of sputum, etc. For ineffective cough and sticky sputum in children, oral and inhaled mucolytics are usually prescribed. The most popular among them are Ambrobene, Lazolvan, etc.
The combined use of mucolytic agents with expectorants is acceptable. They are often prescribed to children with a long-lasting, dry cough without sputum. Folk remedies also have a good effect - plantain syrup, coltsfoot decoction, etc. If a child is diagnosed with a moderate degree of BOS, he may be prescribed acetylcysteine; if it is severe, the baby should not take mucolytic drugs on the first day.

All patients, regardless of age and severity of broncho-obstructive syndrome, are prescribed antitussives.

Bronchodilator therapy

Bronchodilator therapy in children includes taking short-acting beta-2 antagonists, theophylline preparations
also short-acting and anticholinergic drugs.

Beta-2 antagonists produce a faster effect when administered via a nebulizer. Such drugs include Fenoterol, Salbutamol, etc. These drugs must be taken three times a day. They have minimal side effects, however, with long-term use of beta-2 antagonists, their therapeutic effect decreases.

Theophylline preparations include, first of all, Euphyllin. It is intended, first of all, to prevent bronchial obstruction in children. Eufillin has both positive and negative qualities. The advantages of this product include low cost, quick therapeutic results and a simple scheme of use. The disadvantages of aminophylline are numerous side effects.

Anticholinergics are drugs that block muscarinic M3 receptors. One of them is Atrovent, which is preferably taken through a nebulizer three times a day in the amount of 8-20 drops.

Anti-inflammatory therapy

Anti-inflammatory therapy is focused on suppressing the inflammatory course in the bronchi. The main drug in this group is Erespal. In addition to relieving inflammation, it is able to reduce bronchial obstruction in children and control the amount of mucus secreted. The product has an excellent effect when taken at the initial stage of the disease. Suitable for use by children of early age group.

To relieve inflammation in severe BOS, the doctor prescribes glucocorticoids. The preferred method of administration is, again, inhalation - the effect from it occurs quite quickly. Among glucocorticoids, Pulmicort is recognized as the most popular.

If a patient is diagnosed with allergic ailments, he is prescribed antihistamines. As antibacterial and antiviral therapy, the patient is prescribed a course of antibiotics.

If the patient is unable to breathe well on his own, he is given oxygen therapy through nasal catheters or a special mask.

– a complex of symptoms that is characterized by impaired patency of the bronchial tree of functional or organic origin. Clinically, it is manifested by prolonged and noisy exhalation, attacks of suffocation, activation of auxiliary respiratory muscles, and a dry or unproductive cough. The main diagnosis of broncho-obstructive syndrome in children includes the collection of anamnestic data, objective examination, radiography, bronchoscopy and spirometry. Treatment is bronchodilator pharmacotherapy with β2-adrenergic agonists, elimination of the leading etiological factor.

General information

Broncho-obstructive syndrome (BOS)– a clinical symptom complex that is characterized by narrowing or occlusion of bronchi of various calibers due to the accumulation of bronchial secretions, wall thickening, spasm of smooth muscles, decreased mobility of the lung or compression by surrounding structures. BOS is a common pathological condition in pediatrics, especially among children under 3 years of age. According to various statistics, against the background of acute diseases of the respiratory system, BOS occurs in 5-45% of cases. In the presence of a burdened medical history, this figure is 35-55%. The prognosis for biofeedback varies and directly depends on the etiology. In some cases, there is a complete disappearance of clinical manifestations against the background of adequate etiotropic treatment, in others there is a chronicity of the process, disability or even death.

Causes

The main reason for the development of broncho-obstructive syndrome in children is infectious diseases and allergic reactions. Among acute respiratory viral infections, bronchial obstruction is most often provoked by parainfluenza viruses (type III) and RS infection. Other probable causes: congenital heart defects and bronchopulmonary system, RDS, genetic diseases, immunodeficiency states, bronchopulmonary dysplasia, aspiration of foreign bodies, GERH, round helminths, hyperplasia of regional lymph nodes, neoplasms of the bronchi and adjacent tissues, side effects of medications.

In addition to the main causes of broncho-obstructive syndrome in children, there are contributing factors that significantly increase the risk of developing the disease and worsen its course. In pediatrics, these include a genetic predisposition to atopic reactions, passive smoking, increased reactivity of the bronchial tree and its anatomical and physiological characteristics in infancy, thymic hyperplasia, vitamin D deficiency, formula feeding, body mass deficiency, and intrauterine diseases. All of them are capable of enhancing each other’s influence on the child’s body and aggravating the course of broncho-obstructive syndrome in children.

Pathogenetically, broncho-obstructive syndrome in children can be caused by an inflammatory reaction of the bronchial wall, spasm of smooth muscles, occlusion or compression of the bronchus. The above mechanisms can cause narrowing of the bronchial lumen, impaired mucociliary clearance and thickening of secretions, swelling of the mucous membrane, destruction of the epithelium in large bronchi and its hyperplasia in small ones. As a result, deterioration of patency, lung dysfunction and respiratory failure develops.

Classification

Depending on the pathogenesis of broncho-obstructive syndrome in children, the following forms of pathology are distinguished:

  1. Biofeedback of allergic origin. Occurs against the background of bronchial asthma, hypersensitivity reactions, hay fever and allergic bronchitis, Loeffler's syndrome.
  2. BOS caused by infectious diseases. Main causes: acute and chronic viral bronchitis, ARVI, pneumonia, bronchiolitis, bronchiectasis.
  3. BOS that developed against the background of hereditary or congenital diseases. Most often these are cystic fibrosis, α-antitrypsin deficiency, Kartagener and Williams-Campbell syndromes, GERH, immunodeficiency states, hemosiderosis, myopathy, emphysema and abnormalities of bronchial tubes.
  4. BOS resulting from neonatal pathologies. Often it is formed against the background of SDR, aspiration syndrome, stridor, diaphragmatic hernia, tracheoesophageal fistula, etc.
  5. Biofeedback as a manifestation of other nosologies. Broncho-obstructive syndrome in children can also be provoked by foreign bodies in the bronchial tree, thymomegaly, hyperplasia of regional lymph nodes, benign or malignant neoplasms of the bronchi or adjacent tissues.

According to the duration of the course, broncho-obstructive syndrome in children is divided into:

  • Spicy. The clinical picture is observed for no more than 10 days.
  • Protracted. Signs of bronchial obstruction are detected for 10 days or longer.
  • Recurrent. Acute biofeedback occurs 3-6 times a year.
  • Continuously relapsing. It is characterized by short remissions between episodes of prolonged biofeedback or their complete absence.

Symptoms of biofeedback in children

The clinical picture of broncho-obstructive syndrome in children largely depends on the underlying disease or factor that provokes this pathology. The general condition of the child in most cases is moderate, there is general weakness, moodiness, sleep disturbance, loss of appetite, signs of intoxication, etc. Direct biofeedback, regardless of the etiology, has characteristic symptoms: noisy loud breathing, wheezing that can be heard at a distance, a specific whistle when exhale.

Also observed is the participation of auxiliary muscles in the act of breathing, attacks of apnea, shortness of breath of an expiratory (more often) or mixed nature, dry or unproductive cough. With a prolonged course of broncho-obstructive syndrome in children, a barrel-shaped chest can form - expansion and protrusion of the intercostal spaces, horizontal movement of the ribs. Depending on the background pathology, fever, lack of body weight, mucous or purulent nasal discharge, frequent regurgitation, vomiting, etc. may also be present.

Diagnostics

Diagnosis of broncho-obstructive syndrome in children is based on the collection of anamnestic data, objective research, laboratory and instrumental methods. When interviewing the mother, a pediatrician or neonatologist focuses on possible etiological factors: chronic diseases, developmental defects, the presence of allergies, episodes of biofeedback in the past, etc. A physical examination of the child is very informative for broncho-obstructive syndrome in children. Percussion determines the increase in pulmonary sound up to tympanitis. The auscultatory picture is characterized by harsh or weakened breathing, dry, whistling, and in infancy - small-caliber wet rales.

Laboratory diagnostics for broncho-obstructive syndrome in children includes general tests and additional tests. In the CBC, as a rule, nonspecific changes are determined that indicate the presence of a focus of inflammation: leukocytosis, a shift in the leukocyte formula to the left, an increase in ESR, and, in the presence of an allergic component, eosinophilia. If it is impossible to establish the exact etiology, additional tests are indicated: ELISA to determine IgM and IgG to probable infectious agents, serological tests, a test to determine the level of chlorides in sweat if cystic fibrosis is suspected, etc.

Among the instrumental methods that can be used for broncho-obstructive syndrome in children, the most commonly used are chest radiography, bronchoscopy, spirometry, and less commonly, CT and MRI. X-ray makes it possible to see the enlarged roots of the lungs, signs of concomitant parenchymal damage, the presence of neoplasms or enlarged lymph nodes. Bronchoscopy allows you to identify and remove a foreign body from the bronchi, assess the patency and condition of the mucous membranes. Spirometry is carried out during long-term broncho-obstructive syndrome in children in order to assess the function of external respiration, CT and MRI - with low information content of radiography and bronchoscopy.

Treatment, prognosis and prevention

Treatment of broncho-obstructive syndrome in children is aimed at eliminating the factors causing obstruction. Regardless of the etiology, hospitalization of the child and emergency bronchodilator therapy using β2-adrenergic agonists are indicated in all cases. In the future, anticholinergic drugs, inhaled corticosteroids, and systemic glucocorticosteroids can be used. Mucolytic and antihistamines, methylxanthines, and infusion therapy are used as auxiliary drugs. After determining the origin of broncho-obstructive syndrome in children, etiotropic therapy is prescribed: antibacterial, antiviral, anti-tuberculosis drugs, chemotherapy. In some cases, surgery may be required. If there is anamnestic data indicating possible entry of a foreign body into the respiratory tract, emergency bronchoscopy is performed.

The prognosis for broncho-obstructive syndrome in children is always serious. The younger the child, the more severe his condition. Also, the outcome of biofeedback largely depends on the underlying disease. In acute obstructive bronchitis and bronchiolitis, as a rule, recovery is observed; hyperreactivity of the bronchial tree rarely persists. Biofeedback in bronchopulmonary dysplasia is accompanied by frequent acute respiratory viral infections, but often stabilizes by the age of two. In 15-25% of such children it transforms into bronchial asthma. Asthma itself can have a different course: a mild form goes into remission already at primary school age, a severe form, especially against the background of inadequate therapy, is characterized by a deterioration in the quality of life, regular exacerbations with death in 1-6% of cases. BOS against the background of bronchiolitis obliterans often leads to emphysema and progressive heart failure.

Prevention of broncho-obstructive syndrome in children involves eliminating all potential etiological factors or minimizing their impact on the child’s body. This includes antenatal fetal protection, family planning, medical and genetic counseling, rational use of medications, early diagnosis and adequate treatment of acute and chronic diseases of the respiratory system, etc.

S.L. Babak, L.A. Golubev, M.V. Gorbunova

Broncho-obstructive syndrome (BOS) is a clinical symptom complex caused by impaired air flow through the bronchi due to narrowing or occlusion of the airways with a subsequent increase in the resistance of the airways to the inhaled air flow.

Biofeedback is one of the pathophysiological disorders that can affect the outcomes and progressive course of many acute and chronic bronchopulmonary diseases. BOS, not being an independent nosological entity, can occur in various diseases of the lungs and heart, leading to obstruction of the airways. The main clinical manifestations of BOS are paroxysmal cough, expiratory shortness of breath and sudden attacks of suffocation. Based on clinical manifestations, biofeedback is usually divided into latent and pronounced clinical manifestations. According to the course, biofeedback is divided into acute (suddenly occurring) and chronic (permanent).
Functional changes in biofeedback are associated with a decrease in the main spirometric indicators, reflecting the degree of bronchial obstruction (BO) and the nature of the “air trap”, namely:

Forced expiratory volume in 1 second (FEV1);
FEV1/FVC ratio

These indicators are a diagnostic criterion for bronchial obstruction and serve to determine the severity of biofeedback.
Based on the severity of clinical and functional manifestations, BOS is divided into mild, moderate and severe.
The main clinical manifestations of BOS are shortness of breath, suffocation (refers to life-threatening conditions), paroxysmal cough, wheezing, noisy breathing. Symptoms are more noticeable with physical activity. Other manifestations of BOS - increased sweating, sleep disturbance, headache, confusion, convulsions - are detected in severe cases of the syndrome complex.

Variant forms of biofeedback
Spastic is the most common variant of BOS (>70% of all cases), the development of which is due to bronchospasm due to dysfunction in the systems of control of bronchial tone.
Inflammatory – the mechanism is caused by edema, infiltration of the airways, hyperemia of the bronchial membrane.
Discrinic - observed with excessive stimulation of enzymes of goblet cells and glands of the bronchial layer, leading to a deterioration in the properties of sputum, dysfunction of mucus formation and mucociliary transport.
Dyskinetic - bronchial patency is impaired due to congenital underdevelopment of the membranous part of the trachea and bronchi, which contribute to the closure of their lumen during inhalation.
Emphysematous - accompanied by collapse (collapse) of small bronchi due to reduction and loss of elasticity by the lungs.
Hemodynamic – occurs secondary to the background of hemodynamic disorders of the pulmonary circulation: with hypertension of the pre- and postcapillaries, congestion in the bronchial veins and with a hypertensive crisis in the pulmonary circulation.
Hyperosmolar - observed when there is a decrease in hydration of the mucous membranes of the bronchi (inhalation of cold air), when a high osmotic concentration on the surface of the cells causes irritation of the receptors and bronchospasm.
Bronchial obstruction is based on reversible (functional) and irreversible (organic) changes. The functional mechanisms of bronchial obstruction include spasm of smooth muscles, hypersecretion of mucus and swelling of the bronchial mucosa. Spasm of smooth muscles and hypersecretion of mucus occur as a result of exposure to irritating factors (pollutants, infectious agents) on the mucous membrane of the respiratory tract. In response to this, inflammatory mediators are released, which irritate the endings of the vagus nerve and promote the release of acetylcholine, which realizes its effect through muscarinic cholinergic receptors. Activation of these receptors causes cholinergic bronchoconstriction and hypersecretion. In the wall of the bronchi there is a sharp congestion of the microvasculature and an increase in their permeability. Thus, swelling of the mucous membrane and submucosal layer develops, their infiltration with mast cells, basophils, eosinophils, lymphoid and plasma cells.
The cough can be dry and productive. The initial period of the inflammatory or edematous process is characterized by a dry cough. The appearance of a productive cough indicates a violation of mucociliary clearance and bronchial drainage.
Among the infectious agents that most often cause obstructive syndrome are respiratory syncytial virus (about 50%), parainfluenza virus, mycoplasma pneumoniae, and less commonly, influenza viruses and adenovirus.

Biofeedback treatment
The manifestation of biofeedback, regardless of etiology, requires the doctor to take urgent measures to eliminate bronchial obstruction by influencing its reversible component.
It should be noted that the reversibility of bronchial obstruction is determined by the degree of bronchial hyperreactivity (BHR). GRB is defined as the response of the bronchi to various chemical, physical or pharmacological stimuli, when bronchospasm develops in response to an influence that does not cause such a reaction in healthy individuals. The higher the GRB and the duration of exposure to the provocative agent, the more severe and life-threatening the biofeedback is.
In modern pulmonology, there are highly effective methods of delivering drugs directly to the bronchi. This technology is called inhalation nebulizer therapy (from the Latin nebulae - fog) therapy. Its characteristic feature is a high fraction (>80%) of particles ranging in size from 0.5 to 5 microns, which can easily reach the receptor zone in the small bronchi and quickly relieve bronchial obstruction.
The undeniable advantages of inhalation therapy in general are:

Effective creation of high concentrations of medications in the respiratory tract;
insignificant concentration of the drug in the blood;
rapid onset of action of drugs;
possibility of dose adjustment;
minimum systemic side effects.

The treatment tactics for biofeedback are quite clear and logical. To relieve bronchial obstruction, bronchodilators (bronchodilators) are used. Despite the differences in the mechanism of action of various bronchodilators, their most important property is the ability to eliminate spasm of the bronchial muscles and facilitate the passage of air into the lungs. All modern bronchodilators used for biofeedback therapy can be divided into several main groups:

Short- and long-acting B2 agonists;
short- and long-acting anticholinergics;
combination drugs;
methylxanthines.

Inhaled b2-agonists
Inhaled short-acting b2-agonists. This group includes two fairly selective b2-agonists - fenoterol and salbutamol. The main properties of this group of drugs are:

Relaxation of bronchial smooth muscles;
reduction of airway hyperresponsiveness;
improvement of mucociliary clearance of the bronchi;
decreased vascular permeability and plasma exudation;
reducing swelling of the bronchial mucosa;
stabilization of mast cell membranes, reducing the release of inflammatory mediators.

The advantages of these drugs are their rapid (within 3-5 minutes) and pronounced bronchodilator effect. The duration of action of the drugs is short, ranging from 3 to 6 hours, which is why they are classified as short-acting b2-agonists (SABA). Obviously, if it is necessary to effectively control the lumen of the bronchi within 24 hours, it is necessary to perform from 4 to 8 inhalations of SABA per day.
However, like any b2-agonists, drugs in this group have a large number of side effects, especially when used frequently (more than 4 times a day).
One of the serious side effects of b2-agonists is tremor due to the direct effect of the drug on b2-adrenergic receptors of skeletal muscles. Tremor is more often observed in elderly and senile patients. Tachycardia is often observed, either as a result of a direct effect on atrial beta-adrenergic receptors, or under the influence of a reflex response due to peripheral vasodilation through beta-receptors. Particular attention should be paid to prolongation of the QT interval, which can cause sudden death in patients with cardiovascular pathology. Less common and less severe complications include hypokalemia, hypoxemia, and irritability. In addition, short-acting b2-agonists are characterized by the phenomenon of tachyphylaxis - a rapid decrease in the therapeutic effect with repeated use of drugs.
Long-acting inhaled b2-agonists. Drugs in this group have a duration of action from 12 to 24 hours and are used as part of the basic therapy of diseases most often accompanied by biofeedback, such as bronchial asthma (BA). They are most effective when administered in combination with anti-inflammatory drugs – inhaled glucocorticosteroids (ICS). Today, the combination of LABA + ICS is recognized as an effective basic therapy for BA.
The most prominent representative of this group is formoterol fumarate (formoterol), which has the ability to relax bronchial smooth muscles, enhance mucociliary clearance, reduce vascular permeability and the release of mediators from mast cells and basophils, and provide long-term protection from factors leading to bronchospasm. However, there is insufficient evidence of the effect of formoterol on persistent inflammation in asthma; In addition, a number of studies have shown that with long-term use, the severity of the bronchodilator effect can vary greatly.
The undesirable effects of LABAs are not very different from those of CDBAs; they develop when the average daily recommended doses are exceeded and manifest themselves in the form of anxiety, skeletal muscle tremor, and stimulation of the cardiovascular system.

Inhaled M-anticholinergics
Inhaled short-acting M-anticholinergics. The main representative of this group, short-acting anticholinergic drugs (SDA), is ipratropium bromide (ipratropium), which has a pronounced bronchodilator effect.
The mechanism of bronchodilator action is due to the blockade of muscarinic cholinergic receptors, as a result of which the reflex narrowing of the bronchi caused by irritation of irritative cholinergic receptors is suppressed and the tone of the vagus nerve is reduced.
In almost all published guidelines on BA, anticholinergics are recognized as the “drugs of choice” for the treatment of this disease, as well as as additional bronchodilators for moderate and severe BOS in the elderly, senile and children.
The undeniable advantages of M-anticholinergics are:

Lack of cardiotoxic effect, which makes them “drugs of choice” for patients with cardiac and circulatory disorders, as well as in elderly patients;
absence of tachyphylaxis upon repeated use;
stable receptor activity (the number of M-cholinergic receptors does not decrease with age, unlike the number and activity of b2-adrenergic receptors);
rare side effects (dryness, bitter taste in the mouth).

The positive effects of anticholinergics are multifaceted and are not limited only to the bronchodilation effect. They are expressed in a decrease in the sensitivity of cough receptors, a change in the secretion of viscous sputum, and a decrease in oxygen consumption by the respiratory muscles. The positive features of ipratropium bromide include a long duration of action – up to 8 hours.
A conditional disadvantage of short-acting M-anticholinergics or short-acting anticholinergics (SAC) is the slow onset of action (30-60 minutes) after inhalation, which makes it difficult to quickly relieve symptoms of BOS.
Long-acting inhaled M-anticholinergics. The main representative of this group - long-acting anticholinergic drugs (LAADs) - is tiotropium bromide (tiotropium), which has a long-lasting and strong bronchodilator effect.
Tiotropium is advisable to use to eliminate BOS in “severe refractory asthma”, when high therapeutic doses of b2-agonists do not provide the desired bronchodilation and do not relieve BOS.

Combined bronchodilators
Short-acting inhaled combination bronchodilators. The main representative of this group - short-acting combined bronchodilators (SACDs) - is the combination of SABA (ipratropium 20 mcg) + SABA (fenoterol 50 mcg), which has become widespread in modern therapeutic practice under the commercial name "Berodual N" in the form of a metered-dose aerosol inhaler and "Berodual" in the form of a solution for inhalation (Boehringer Ingelheim, Germany).
The idea of ​​combining CDAC+CDBA is not new and has a long history. Suffice it to say about the high expectations from salbutamol + ipratropium, which have not yet found their widespread use. That is why we consider it necessary to note a number of features of combining fenoterol and ipratropium.
First, the M-anticholinergic ipratropium acts predominantly in the proximal bronchi, whereas the selective β2-agonist fenoterol acts predominantly in the distal bronchial tree. This leads to a “double effect” of bronchodilation, the possibility of reducing the dose of each drug to the minimum therapeutic level, and eliminates the possibility of third-party adverse events. Secondly, both substances have the same state of aggregation (aqueous solutions), which makes it possible to create a high respirable fraction during nebulizer therapy, and therefore effectively stop BOS.
It is justified to prescribe the drug Berodual for the relief of biofeedback in asthma in the following cases:

The presence of an altered b2 receptor in patients (genetic abnormality of the b2 receptor, consisting in the replacement of Gly at position 16 by Arg with the formation of the b2-APB16 Arg/Arg receptor genotype, which is not sensitive to any b2 agonists);
with a decrease in receptor b2 activity;
in the presence of pronounced manifestations of cardiovascular diseases;
with the phenomena of “night asthma” (a variant of asthma in which attacks of suffocation occur in the second half of the night against the background of bronchial obstruction caused by vagal activity);
with viral infections that can reduce the expression of the M2 gene and increase bronchial obstruction.

Of interest are randomized clinical trials examining the effectiveness of combination therapy compared with monotherapy with one of the components. Thus, in a randomized controlled crossover study, N. Gross et al. , which included 863 patients, combination therapy led to an increase in FEV1 by 24% compared with salbutamol monotherapy (p). Another study (a meta-analysis of two large 3-month studies in 1067 patients (E.J. Weber et al., 1999) demonstrated the advantage of combination therapy Biofeedback in patients with chronic obstructive pulmonary disease (COPD).It was found that with salbutamol monotherapy, the frequency of exacerbations of COPD (18%) and the number of days of exacerbations (770 person-days) were significantly higher than with combination therapy (12% and 554 person-days). ) (pThus, Berodual N was considered as a drug with a high cost/effectiveness ratio. Today, a fixed combination of a short-acting b2-agonist and ipratropium bromide (Berodual N) is included in international clinical guidelines for the treatment of patients with bronchial asthma COPD.
The undeniable proven advantages of Berodual N and Berodual solution for inhalation are:

Quick (5-10 minutes) and fairly long-lasting (6-8 hours) effect;
safe clinical profile (no cardiotoxic effects);
absence of tachyphylaxis;
no effect on mortality in elderly patients (unlike b2-agonists);
moderate anti-inflammatory effect (reducing the release of inflammatory mediators);
a more pronounced bronchodilatory response in combination than with each drug individually;
effective relief of acute BOS (with BA) and chronic BOS (with chronic obstructive pulmonary disease - COPD).

Methylxanthines
The main representative of this group is a bronchodilator, a purine derivative, called Theophylline (from Latin: theo-tea, phyllin-leaf). Theophylline has a weak bronchodilator effect, but has a positive effect on the respiratory muscles, improves sputum separation, and stimulates the respiratory center. This combination of positive properties, along with the availability of theophylline, once led to its widespread use.
The use of methylxanthines is accompanied by numerous side effects: nausea, vomiting, headache, agitation, gastroesophageal reflux, frequent urination, arrhythmia, tachycardia, etc. The drugs are used orally or parenterally.
Long-acting theophylline preparations have faded into the background. They are recommended in special cases to be used as an additional bronchodilator for biofeedback in patients with asthma and COPD with insufficient bronchodilation response from modern inhaled bronchodilator therapy.

Conclusion
Biofeedback accompanies many diseases, especially diseases of the respiratory system, such as bronchial asthma, COPD, ARVI, pneumonia, etc. All of them require appropriate medication correction.
The standard of treatment for BOS can be confidently considered to be inhaled drugs and the nebulizer method of their delivery, which allows creating the maximum concentration of the drug in the receptor zone and causing the maximum bronchodilator response in the absence of systemic action of the drug.
Various parts of the nervous system take part in the occurrence of BOS: sympathetic (b-receptors) and parasympathetic (M1-2 and M3 receptors). Quite often, it is clinically difficult to determine what predominates in the mechanism of bronchial obstruction: insufficient adrenergic stimulation or excessive vagal innervation. In this case, it is optimal to prescribe a combination of a short-acting b2-agonist and the M-anticholinergic ipratropium bromide (Berodual N).
We can confidently say that Berodual N in the form of a metered dose aerosol inhaler and Berodual solution for inhalation via a nebulizer are indicated for the prevention and symptomatic treatment of obstructive respiratory diseases with reversible bronchospasm, such as acute and chronic obstructive bronchitis, bronchial asthma, chronic obstructive pulmonary disease.

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1 BRONCHO-OBSTRUCTIVE SYNDROME AT THE PREHOSPITAL STAGE Practical recommendations for diagnosis, treatment and prevention Project Moscow, 2009

2 List of abbreviations: COPD chronic obstructive pulmonary disease BA bronchial asthma ICD X international classification of diseases 10th revision WHO World Health Organization (WHO World Health Organization) EMS emergency medical care FER external respiration function FEV 1 forced expiratory volume in the first second FVC forced vital capacity of the lungs PEF peak expiratory flow rate MEF minute volumetric expiratory flow rate PaCO 2 partial tension of carbon dioxide PaO 2 partial tension of oxygen SaO 2 oxygen saturation ECG electrocardiography ESR erythrocyte sedimentation rate IHD coronary heart disease HR heart rate RR respiratory rate BP arterial pressure GCS glucocorticosteroids ICS inhaled glucocorticosteroids HF heart failure 3

3 Introduction These recommendations are the result of a consensus of experts, based on a thorough analysis of research published in this area in the domestic and foreign literature over the past 10 years. These recommendations contain Russian data on the epidemiology of broncho-obstructive syndrome, its etiology and pathogenesis; separate sections are devoted to clinical, laboratory and instrumental diagnostics. There are separate chapters that include characteristics of individual classes of bronchodilators, analysis of actual practice in the treatment of broncho-obstructive syndrome, and indicators of the quality of patient management. The authors of the recommendations attempted to critically evaluate the validity of various approaches to the diagnosis and treatment of broncho-obstructive syndrome from the standpoint of evidence-based medicine. For this purpose, all presented recommendations were classified according to the level of evidence. This approach seems strictly justified for the development of an algorithm for the diagnosis and examination of patients with bronchial obstruction (Table 1). Table 1. Evidence criteria to support use in clinical practice guidelines Category of evidence Source of evidence Definition A Randomized controlled trials Evidence is based on well-designed randomized trials conducted on sufficient numbers of patients to obtain reliable results. Can be reasonably recommended for B C Randomized controlled trials Non-randomized clinical trials 4 broad applications Evidence is based on randomized controlled trials, but the number of patients included is insufficient for reliable statistical analysis Evidence is based on non-randomized clinical trials or studies performed on a limited number of patients D Expert opinion Evidence is based on a consensus developed by a group of experts on a specific problem

4 I. Epidemiology of COPD and asthma According to official statistics, currently the number of patients with COPD, bronchial asthma and status asthmaticus in the Russian Federation is 1 million people. However, in reality, the number of patients with chronic bronchial obstruction in our country is about 11 million people. These figures do not completely reflect the true prevalence of chronic broncho-obstructive syndrome, which is presumably much higher, which can be explained by the low rate of patients seeking medical care and insufficient diagnosis of the above diseases in their early stages of development [Dvoretsky L.I., 2005]. In addition, such a ten-million dollar gap between calculated and official data indicates the deepest gap between practical health care and the assumptions of scientists. COPD ranks third after cardio- and cerebrovascular pathologies in the structure of causes of mortality in Russia, and fourth in the world. Moreover, in the last few years there has been an increase in incidence, and in the coming decades a further increase in both morbidity and mortality from COPD is predicted. In order to confirm the above WHO postulates and determine the impact of COPD on the quality of life and prognosis of patients with various somatic pathologies, 6425 autopsy reports of patients (average age 68 years) who died from 2002 to 2007 were analyzed. in one of the large multidisciplinary emergency hospitals. The authors found that 903 patients (14%) suffered from COPD, which in 134 cases (15%) was the direct cause of death [Vertkin A.L., Skotnikov A.S., 2008]. Speaking about the prevalence of bronchial asthma, it should be noted that in Russia it is diagnosed in 5% of the adult population, as well as in 10% of children. Moreover, about 80% of adult patients develop it in childhood [Avdeev S.N., 2003]. The proportion of patients with bronchial asthma is about 3% of all EMS calls in Russia, and in approximately 2/3 of cases the reason for seeking medical help is complaints of shortness of breath or suffocation [Vertkin A.L., 2007]. 5

5 II. Definition and classification COPD is a disease characterized by progressive airflow limitation caused by an abnormal inflammatory response of lung tissue to pathogenic particles or gases. In turn, bronchial asthma is a disease that develops on the basis of chronic allergic inflammation of the bronchi [evidence level A], their hyperreactivity and is characterized by periodic attacks of difficulty breathing or suffocation as a result of widespread bronchial obstruction caused by bronchoconstriction, hypersecretion of mucus, swelling of the bronchial wall [Russian Respiratory Society, 2008]. Classification of COPD by severity 1. Mild FEV 1/FVC< 70% от должного ОФВ 1 80% от должного наличие или отсутствие хронических симптомов (кашель, мокрота) 2. Средняя ОФВ 1 /ФЖЕЛ < 70% от должного 50% ОФВ 1 < 80% от должных значений наличие или отсутствие хронических симптомов (кашель, одышка) 3. Тяжелая ОФВ 1 /ФЖЕЛ < 70% от должного 30% ОФВ 1 < 50% от должных значений в сочетании с хронической дыхательной недостаточностью (кашель, мокрота, одышка) 4. Крайне тяжелая ОФВ 1 /ФЖЕЛ < 70% ОФВ 1 30% от должного или ОФВ 1 < 50% от должного в сочетании с хронической дыхательной недостаточностью 6

6 Classification of bronchial asthma by severity 1. Intermittent course Short-term symptoms less than once a week Short exacerbations (from several hours to several days) Night symptoms less than 2 times a month Absence of symptoms and normal respiratory function between exacerbations Peak expiratory flow more than 80% from expected 2. Mild persistent course Symptoms from 1 time per week to 1 time per day Exacerbations can reduce physical activity and disrupt sleep Nighttime symptoms more than 2 times a month Peak expiratory flow is equal to or above 80% of expected 3. Moderate course Daily symptoms Exacerbations may lead to limitation of physical activity and sleep Nocturnal symptoms more than once a week Daily use of short-acting β 2 -agonists Peak expiratory flow 60 80% of predicted 4. Severe Constant presence of symptoms Frequent exacerbations Frequent nocturnal symptoms Limitation of physical activity due to symptoms asthma Peak expiratory flow less than 60% of predicted 7

7 Classification of the severity of exacerbation of bronchial asthma and COPD 1. Mild exacerbation physical activity preserved shortness of breath when walking colloquial speech sentences respiratory rate increased by 30% of the norm auxiliary muscles are not involved in the act of breathing wheezing in the lungs at the end of exhalation heart rate less than 100 per minute paradoxical pulse is absent or less than 10 mmHg. Art. peak expiratory flow after taking a bronchodilator more than 80% of the proper or individually best values ​​for the patient PEF variability less than 20% 2. Moderate exacerbation physical activity is limited shortness of breath when talking colloquial speech phrases respiratory rate is increased by 30 50% of the norm auxiliary muscles in the act of breathing usually loud whistling sounds are involved during the entire exhalation, heart rate per minute, paradoxical pulse mm. Hg peak expiratory flow is equal to or greater than 80% of the expected PEF variability is less than or equal to 30% 3. Severe exacerbation physical activity is sharply reduced or absent shortness of breath at rest spoken language individual words respiratory rate more than 30 per minute (50% higher than normal) accessory muscles in the act of breathing always involves loud wheezing sounds during exhalation and inhalation 8

8 heart rate more than 120 per minute, paradoxical pulse more than 25 mm Hg. Art. peak expiratory flow (PEF) after taking a bronchodilator is less than 60% of the expected PEF variability is more than 30% 4. Life-threatening exacerbation (status asthmaticus) physical activity is sharply reduced or there is no shortness of breath at rest spoken language there is no disorder of consciousness (stunning or stupor, maybe coma) respiratory rate increased or decreased participation of auxiliary muscles in the act of breathing paradoxical thoraco-abdominal movements wheezing no breathing superficial “silent” lung bradycardia absence of paradoxical pulsus (muscle fatigue) peak expiratory flow after taking a bronchodilator less than 33% of the expected PEF variability more than 30% III . Etiology and pathogenesis Bronchial asthma is a heterogeneous disease, and therefore it is difficult to distinguish between its etiological and pathogenetic components. The basis of bronchial asthma is increased nonspecific irritability of the tracheobronchial tract. This phenomenon serves as a cardinal sign of the disease and, probably, a trigger mechanism. As the disease process worsens and the severity of symptoms increases, the need for medications increases, the respiratory tract becomes increasingly sensitive to irritation and reacts even to nonspecific stimuli. Respiratory function becomes unstable with pronounced daily fluctuations. The main link in the pathogenesis of bronchial asthma is bronchial hyperreactivity, specific me- 9

10 Causes of exacerbations of COPD and bronchial asthma The most common causes of exacerbations of COPD (pathogenic agents) are respiratory tract infections and atmospheric pollutants (level of evidence B), but the cause of a third of exacerbations cannot be identified. Data on the role of bacterial infection, which is believed to be the main cause of exacerbations, are conflicting. Conditions that may mimic exacerbations include pneumonia, congestive heart failure, pneumothorax, pleural effusion, pulmonary embolism, and arrhythmias. Triggers of exacerbations of bronchial asthma (sensitizing agents) can be tobacco smoke, medications and various foods, occupational hazards, house dust, animal hair, feathers and down of birds, pollen, and street dampness. In bronchial asthma, airflow limitation is often completely reversible (both spontaneously and under the influence of treatment), while in COPD it is not completely reversible and the disease progresses unless exposure to pathogenic agents is stopped. IV. Clinical symptoms and instrumental criteria of bronchial obstruction A description of an attack of bronchial asthma was given in the 30s of the 19th century by G.I. Sokolsky: “A person suffering from asthma, having just fallen asleep, wakes up with a feeling of tightness in the chest. This condition does not consist of pain, but it seems as if some kind of weight is placed on his chest, as if he is being pressed and suffocated by an external force... The man jumps out of bed, looking for fresh air. His pale face expresses melancholy and fear from strangulation... These phenomena, now increasing and now decreasing, continue until 3 or 4 o'clock in the morning, after which the spasm subsides and the patient can take a deep breath. With relief, he clears his throat and falls asleep tired.” Mandatory questions when interviewing a patient with suspected bronchial obstruction: Identify bronchial obstruction: “What is more difficult to do: inhale or exhale?” Identification of the expiratory nature of shortness of breath and the presence of clinical symptoms of respiratory failure indicate the presence of bronchial obstruction in the area of ​​the small airways, where there is bronchospasm, 11

11 hypersecretion of mucus and swelling of the mucous membrane, which indicates the presence of broncho-obstructive syndrome in the patient. Determine the presence of COPD: “Have similar attacks of suffocation ever occurred before and when did they appear for the first time in life?”, “Do you have a chronic cough, chronic shortness of breath or chronic discharge sputum?”, “Do you have any occupational hazards?”, “Do you smoke?”. The absence of a history of similar clinical symptoms in adult patients, a burdened allergic history, a long history of smoking and occupational hazards makes it possible to exclude chronic obstructive pulmonary disease and asthma and suspect broncho-obstruction caused by a foreign body, tumor or swelling of the larynx, in which difficulty in both inhalation and exhalation Carry out a differential diagnosis: “Do you have allergies?”, “Do you have shortness of breath at rest?”, “At what time do attacks most often develop?” The presence of hypersensitivity and sensitization to one or another group, and sometimes several groups of allergens, the presence of shortness of breath at rest, the suddenness of the development of an attack of suffocation and its occurrence mainly at night allows, based on one anamnesis, to assume that the patient has bronchial asthma and to distinguish it from COPD Assess the severity of the disease: “If suffocation did not occur for the first time, but appears periodically, how often does this happen?” Assess the severity of the exacerbation: “In the last two weeks, have you had to wake up at night due to difficulty breathing?” Nocturnal attacks of suffocation, as well as episodes of paroxysmal coughing in the morning, are characteristic of exacerbation of bronchial asthma, and their frequency and intensity make it possible to judge the severity of the disease. Adjust therapy: “Do you use medications to treat this condition? Is there always an effect from taking them? Information about the therapy received by the patient, as well as its effectiveness, allows the doctor providing emergency medical care to adjust the list of medications, their doses, frequency and route of administration. 12

12 Characteristic clinical manifestations of bronchial asthma are shortness of breath and suffocation, as well as the appearance of cough, wheezing and their disappearance spontaneously or after the use of bronchodilators and anti-inflammatory drugs. Exacerbation of bronchial asthma, requiring emergency care, can occur in the form of an acute attack or a prolonged state of bronchial obstruction. An acute attack of suffocation generally occurs suddenly, in some patients following certain individual precursors (sore throat, itchy skin, nasal congestion, rhinorrhea) at any time of the day, often at night, when the patient wakes up with a feeling of tightness in the chest and acute lack of air . The patient is not able to push out the air that is filling the chest, and in order to enhance exhalation, he sits up in bed, resting on it or on the knees of his legs lowered from the bed with straightened arms, or stands, leaning on a table or the back of a chair. With such a forced position of the body, the patient includes in the act of breathing not only the main, but also the auxiliary respiratory muscles of the shoulder girdle and chest. The patient’s face at the time of the attack is cyanotic, the veins in the neck are swollen. Already from a distance, whistling wheezing can be heard against the background of noisy, difficult exhalation. The chest appears as if frozen, in the position of maximum inspiration, with raised ribs, increased anteroposterior size, bulging supraclavicular fossae, and widened intercostal spaces. Auscultation reveals a sharp prolongation of exhalation and abundant various (wheezing, rough and musical) wheezing. At the end of the attack, a small amount of viscous mucous glassy sputum is difficult to pass. Examination and physical examination of a patient with bronchial obstruction: 1. Assess the general condition Anxiety, restlessness, feeling of “fear of death” and lack of air 2. Examine the patient Pale skin, central diffuse gray “warm” cyanosis, worsening with a coughing attack, swelling of the neck veins, forced “orthopnea” position, frequent arrhythmic shallow breathing, barrel chest 13

13 cell, increased intercostal spaces, bulging of the supraclavicular areas, participation of additional respiratory muscles in breathing 3. Conduct general thermometry The presence of high (remitting or hectic) fever is a symptom of purulent inflammatory and septic processes, and is not typical for bronchial asthma, characterized by chronic allergic inflammation in wall of the bronchi, but low-grade fever is possible 4. Assess the severity of respiratory failure Tachypnea, less often bradypnea, as well as an unproductive cough with glassy or mucous sputum 5. Assess hemodynamics: examination of the pulse (correct, incorrect), counting heart rate and blood pressure Tachycardia, moderate systolic hypertension, the possible appearance of a paradoxical pulse caused by a pronounced decrease in systolic blood pressure and the amplitude of pulse waves during inspiration, as a result of which the pulse in the peripheral arteries during inspiration may completely disappear 6. Palpation of the chest Decreased elasticity of the chest, bilateral weakening of vocal tremor 7. Comparative and topographic percussion of the lungs Box sound, the lower borders of the lungs are lowered, the upper ones are raised 8. Auscultation of the lungs Hard breathing, bilateral, dry, treble, whistling, buzzing scattered wheezing, intensifying or appearing with forced exhalation, not changing depending on the phase of breathing, decreasing after coughing, bilateral attenuation of bronchophony Disease control The rate of exhaled air flow depends on the degree of obstruction of the medium and large bronchi [Evidence Level A]. Obstructive breathing disorders are characterized by a decrease in the maximum volume of air exhaled during forced exhalation. This indicator is measured in liters per month.

14 kund of time, and the only available, handy device for determining it is a peak flow meter. Peak flowmetry is a method that allows on-site determination of the maximum volume of air exhaled during forced exhalation. For clarity, ease of use and efficiency of control over the state of the bronchial lumen, modern peak flow meters are equipped with a scale divided into three sectors: red, yellow and green, reflecting severe and moderate bronchial obstruction, as well as the absence thereof, respectively. Guided by the results obtained, the doctor, and sometimes the patient himself, decides on the severity of the next exacerbation and prescribes adequate therapy to stop it. Peak Flow Testing Technique For each measurement, the patient should be in the same position (sitting or standing), neutral neck position (neck not flexed) Set the needle to zero, hold the peak flow meter horizontally using both hands, while avoiding blocking the outgoing air from the peak flow meter, instruct the patient to breathe as deeply as possible Mouthpiece The peak flow meter is wrapped around the lips and teeth, avoid covering the opening of the mouthpiece with the tongue. Exhale air with maximum force, the force of exhalation is important, not the amount of exhaled air. Readings are taken into account only in the first second. Repeat this procedure three times and select the maximum value. Peak flow meter results, such as the percentage of reduction in peak flow meter. expiratory flow rate (EPF) from normal values ​​or the best individual indicator [level of evidence C] and the severity of bronchial asthma can be found in Table 2. Severity Symptoms Mild Moderate Severe Asthmatic status PEF* (% of normal or best individual indicator) > 80 % 50-70%< 50% < 30% 15

15 Severity Symptoms Mild Moderate Severe Status Asthma Frequency of bronchodilator use in the last 4-6 hours Not used or low or moderate doses used. The effectiveness is insufficient, the need for their use has increased. High doses were used. Therapy is ineffective PaCO 2 ** mm.Hg SaO 2 ** mm.Hg Table 2. Criteria for the severity of bronchial asthma PEF is used in adults and children over 5 years old ** currently determined mainly in the hospital V. Complications of broncho-obstructive syndrome Incorrect and untimely treatment of bronchial obstruction leads to a number of serious pulmonary and extrapulmonary complications: Pulmonary (pneumothorax, atelectasis, pulmonary failure) Extrapulmonary (pulmonary heart, heart failure) Long-term chronic obstructive pulmonary disease leads to the development of chronic pulmonary heart disease, one of the objective signs of which is changes on the ECG: In most cases, against the background of sinus rhythm, signs of hypertrophy of the right ventricle and atrium are noted. The earliest ECG changes, which at first may be transient and associated with worsening alveolar hypoxemia, are a rotation of the electrical axis of the heart to the right by more than 30 from the original. Often appear negative T waves in the right precordial leads, depression of the ST segment in leads II, III and avf, as well as varying degrees of blockade of the right bundle branch. Possible increase in the R wave in the left precordial leads of the qr or rsr type. In later stages, true rotation of the electrical axis is noted heart to the right from 90 to 180 and high R waves in the right precordial leads with or without negative T waves. 16

16 It must be remembered that these changes on the ECG are largely masked by the descent of the diaphragm, an increase in the anteroposterior size of the chest and rotation of the more vertically located heart so that the right atrium and ventricle move anteriorly and the apex of the heart posteriorly. In such cases, the only “classical” electrocardiographic sign of cor pulmonale is often P-pulmonale, which, in this case, reflects a change in the anatomical position of the heart to a greater extent than hypertrophy of the right atrium. It is also necessary to know that the appearance of deep Q waves up to the QS wave in leads III and V 3.4, reminiscent of signs of cicatricial changes after myocardial infarction, is also characteristic of hypertrophy of the right heart. VI. Laboratory diagnostics and additional research methods In contrast to the operating conditions of the ambulance and its equipment, the clinic should be able to conduct spirometry, determine the patient's tidal volumes, chest x-ray, peripheral blood analysis and sputum examination. Thus, during an attack of bronchial asthma, in proportion to the degree of bronchial obstruction, the forced expiratory volume in the first second (FEV 1) and the peak expiratory flow (PEF), reflecting the state of the large bronchi, as well as the instantaneous volumetric flow rate (MOE-25% and MOE-75%) decrease in proportion to the degree of bronchial obstruction. ), demonstrating the condition of the small bronchi [Evidence Level D]. Timely implementation of this study allows each patient to be given an accurate diagnosis and ensure the appointment of adequate and safe therapy for bronchial obstruction [evidence level C]. An X-ray examination of the chest organs can provide information about the presence of infectious pulmonary complications, bronchiectasis, pulmonary emphysema, and atelectasis. In a general blood test, there may be either slight or massive eosinophilia (the number of eosinophils in microliters) and an increase in the number of neutrophils. ESR is usually normal. 17

17 In the patient’s sputum one can identify: Courshman spirals, whitish-transparent, corkscrew-shaped, convoluted tubular formations, which are “casts” of bronchioles, found, as a rule, at the time of bronchospasm. Charcot-Leyden crystals, smooth colorless crystals in the form of octahedrons, which consist of a protein that releases during the breakdown of eosinophils, which are present in large numbers during allergic inflammation. A large number of eosinophils (up to 50-90% of all leukocytes) VII. Features of diagnosing bronchial asthma in different age and professional groups Asthma in childhood Diagnosis of bronchial asthma in children often presents great difficulties, since episodes of wheezing and coughing are the most common symptoms of childhood diseases. Help in making a diagnosis is to clarify the family history and atopic background. Repeated attacks of night cough in practically healthy children almost certainly confirm the diagnosis of bronchial asthma. In some children, exercise triggers asthma symptoms. To make a diagnosis, it is necessary to study pulmonary function (PRF) with a bronchodilator, a spirometric test with physical activity, a mandatory allergy examination with determination of general and specific IgE, and skin tests. Bronchial asthma in older people In old age, not only the diagnosis of asthma is difficult, but also the assessment of the severity of its course. A thorough history taking, examination aimed at excluding other diseases accompanied by similar symptoms and, above all, ischemic heart disease with signs of left ventricular failure, as well as functional research methods, including ECG recording and X-ray examination, usually clarify the picture. To make a diagnosis, peak flowmetry is required to determine the morning and evening PEF for 2-3 weeks, as well as performing a respiratory function test with a test with a bronchodilator. 18

18 Occupational bronchial asthma It is known that many chemical compounds cause bronchospasm when present in the environment. They range from highly active low molecular weight compounds such as isocyanates, to known immunogens such as platinum salts, plant complexes and animal products. To make a diagnosis, a clear history is needed: the absence of symptoms before starting work, a confirmed connection between the development of asthma symptoms in the workplace and their disappearance after leaving the workplace. The diagnosis of bronchial asthma can be successfully confirmed by examining respiratory function indicators: measuring PEF at work and outside workplace, conducting specific provocative tests. It should be taken into account that even after the cessation of exposure to the damaging agent, the course of bronchial asthma persists and continues to worsen. Therefore, early diagnosis of occupational asthma, cessation of contact with the damaging agent, as well as rational pharmacotherapy are very important. VIII. Pathological anatomy The death of patients with asthma rarely coincides with an attack, therefore, regarding it, the material presented in the pathological literature is very small. Macroscopically, acute swelling of the lungs is noted, the lungs fill the entire chest cavity, very often imprints of the ribs are visible on the surface of the lungs. The height of the diaphragm is determined, as a rule, at the level of the 6th rib. The surface of the lungs is usually pale pink; when cut, the lungs are dark or gray-red. Pneumosclerosis, as a rule, is moderately expressed. A thickening of the walls of the bronchi protruding above the surface of the sections is revealed; almost all generations of the bronchi up to the respiratory bronchioles are filled with thick grayish-yellow glassy casts of sputum (bronchial secretions), which are squeezed out in the form of thin “worms”. The mucous membrane of the bronchi is hyperemic almost throughout. As a rule, pulmonary edema is pronounced; thromboembolism of the pulmonary artery and/or its branches sometimes occurs. 19

19 Histological examination in the dilated lumens of the bronchi reveals mucous plugs, layers of desquamated epithelium with an admixture of neutrophils, eosinophils, lymphocytes, almost complete exposure of the basement membrane, and sometimes Charcot-Leyden crystals are found. In the preserved epithelium there is an increased number of goblet cells. Infiltrates in the walls of the bronchi consist predominantly of eosinophils. Expansion and sharp congestion of the capillaries of the mucous membrane and submucosal layer are detected. The basement membrane is usually unevenly thickened to 5 μm; individual passages in it are often visible, perpendicular to the bronchial lumen, and focal resorption of individual sections of the basement membrane. The changes described above occur, as a rule, in those who died with a history of bronchial asthma of no more than 5 years. In patients with a long history of bronchial asthma, changes in the bronchi and lung tissue are mixed with elements of chronic productive inflammation. The remission phase is characterized by partial atrophy of the epithelium, sharp thickening and hyalinosis of the basement membrane, and pronounced lymphohistiocytic infiltration of the lamina propria of the mucous membrane. In some cases, Kurshman spirals, which are mucous casts of small bronchi, are found in the bronchial secretions. IX. Emergency therapy The doctor's tactics when treating an attack of bronchial obstruction have several general principles. 1. During the examination, the doctor needs to assess the severity of the exacerbation based on clinical data, determine the PEF (if a peak flow meter is available) 2. If possible, limit contact with causally significant allergens or triggers 3. Based on the medical history, clarify the previous treatment: bronchospasmolytic drugs, dosage routes and frequency of prescription, time of last drug intake, receipt of systemic corticosteroids for the patient and their dosage 4. Rule out complications (pneumonia, atelectasis, pneumothorax, etc.) 5. Provide emergency care depending on the severity of the attack 20

20 6. Assess the effect of therapy (shortness of breath, heart rate, blood pressure. Increase in PEF>15%). Modern care for patients with exacerbation of bronchial asthma and COPD involves the use of the following groups of drugs: 1. Selective short-acting β 2-agonists (salbutamol, fenoterol) 2. Anticholinergic drugs (ipratropium bromide) and the combination drug berodual (fenoterol + ipratropium bromide) 3 Glucocorticoids 4. Methylxanthines Selective β 2 -short-acting adrenergic receptor agonists Salbutamol (Ventolin) selective β 2 -adrenergic receptor agonist. The bronchodilator effect of salbutamol occurs within 4-5 minutes. The effect of the drug gradually increases to its maximum in a minute. The half-life is 3-4 hours and the duration of action is 4-5 hours. The drug is used using a nebulizer: 1 nebula with a volume of 2.5 ml contains 2.5 mg of salbutamol sulfate in saline solution. 1-2 nebulas (2.5-5.0 mg) are prescribed simultaneously for inhalation in undiluted form. If improvement does not occur, repeat inhalations of salbutamol 2.5 mg every 20 minutes for an hour. In addition, the drug is used in the form of a metered dose aerosol inhaler (2.5 mg per breath). Fenoterol is a selective short-acting β 2 -adrenergic receptor agonist. The bronchodilator effect occurs within 3-4 minutes and reaches its maximum effect by 45 minutes. The half-life is 3-4 hours, and the duration of action of fenoterol is 5-6 hours. The drug is applied using a nebulizer, 0.5-1.5 ml of fenoterol solution in saline solution for 5-10 minutes. If improvement does not occur, repeat inhalations of the same dose of the drug every 20 minutes. In addition, the drug is used in the form of a metered dose aerosol inhaler (100 mcg 1-2 breaths). It must be remembered that when using β 2 -agonists, hand tremors, agitation, headache, compensatory increase in heart rate, cardiac arrhythmias, and arterial hypertension are possible. 21

21 Side effects are more expected in patients with diseases of the cardiovascular system, in older age groups and in children. Relative contraindications to the use of inhaled β 2 -agonists are thyrotoxicosis, heart defects, tachyarrhythmia and severe tachycardia, acute coronary pathology, decompensated diabetes mellitus, hypersensitivity to β 2 -agonists [evidence level A]. M-anticholinergics Ipratropium bromide (Atrovent) and Tiotropium bromide (Spiriva) are anticholinergic drugs with very low (no more than 10%) bioavailability, which makes the drugs well tolerated. They are used in case of ineffectiveness of β 2 -agonists, as additional agents to enhance their bronchodilator effect, as well as in case of individual intolerance to β 2 -agonists in patients with COPD. They are used by inhalation: ipratropium bromide enters the bronchi through a nebulizer in an amount of 1-2 ml (0.25-0.5 mg of substance). If necessary, the inhalation procedure is repeated after minutes. Another route of administration is a metered dose inhaler and spacer at a dose of 40 mcg [Evidence Level A]. Tiotropium bromide in the amount of 1 capsule is used through the HandiHaler inhaler. One capsule contains 18 mcg of tiotropium bromide. Combined drugs Berodual is a combined bronchospasmolytic drug containing two bronchodilators (fenoterol and ipratropium bromide). One dose of Berodual contains 0.05 mg of fenoterol and 0.02 mg of ipratropium bromide. Used with a nebulizer. To relieve an attack of bronchial obstruction, inhale 1-4 ml of Berodual solution for 5-10 minutes. The dose of the drug is diluted in saline solution. If improvement does not occur, repeat inhalation after 20 minutes. In addition, it is used using a metered-dose aerosol inhaler, 1-2 puffs at a time, if necessary, 2 more doses after 5 minutes, and subsequent inhalation should be carried out no earlier than 2 hours later (fenoterol + ipratropium bromide) [evidence level A]. 22

22 Inhaled glucocorticosteroids Budesonide (pulmicort) suspension for nebulizer in plastic containers of 2 ml (0.25-0.5 mg of substance). During biotransformation in the liver, budesonide forms metabolites with low glucocorticosteroid activity. Pulmicort nebulizer suspension can be diluted with saline and also mixed with solutions of salbutamol and ipratropium bromide. Adult dose to relieve an attack is 0.5 mg (2 ml), children's dose is 0.5 mg (1 ml) twice every 30 minutes. Systemic glucocorticosteroids Prednisolone is a dehydrated analogue of hydrocortisone and belongs to the synthetic glucocorticosteroid hormones. The half-life is 2-4 hours, the duration of action is hours. Administered parenterally to adults at a dose of at least 60 mg, to children parenterally or orally 1-2 mg/kg [evidence level A]. Methylprednisolone (metipred) is a non-halogen derivative of prednisolone that has greater anti-inflammatory (5 mg prednisolone is equivalent to 4 mg methylprednisolone) and significantly less mineralocorticoid activity. The drug is characterized by a short half-life, like prednisolone, and weaker stimulation of the psyche and appetite. Methylxanthines Theophylline is indicated for use in bronchial asthma for the purpose of stopping an attack in the absence of inhaled bronchodilators or as adjunctive therapy for severe or life-threatening bronchial obstruction [evidence level B]. When providing emergency care, the drug is administered intravenously, and the effect begins immediately and lasts up to 6-7 hours. The half-life in adults is 5-10 hours. About 90% of the administered drug is metabolized in the liver, metabolites and unchanged drug (7-13%) are excreted in the urine through the kidneys. Theophylline is characterized by a narrow therapeutic range, i.e. Even with a slight overdose of the drug, side effects may develop. The drug should not be used for bronchial asthma as a first-line drug [evidence level A]. Liver dysfunction, congestive heart 23

23 Insufficiency and old age slow down the metabolism of the drug and increase the risk of developing side effects, such as: decreased blood pressure, palpitations, cardiac arrhythmias, cardialgia, nausea, vomiting, diarrhea, headache, dizziness, tremor, convulsions. X. Nebulizer therapy in the prehospital setting The word "nebulizer" comes from the Latin word "nebula", which means "fog". A nebulizer is a device for converting liquid into an aerosol with particularly fine particles capable of penetrating primarily into the peripheral bronchi. The goal of nebulizer therapy is to deliver a therapeutic dose of the drug in aerosol form directly into the patient’s bronchi and obtain a pharmacodynamic response in a short period of time (5-10 minutes). Nebulizer therapy, creating high concentrations of the drug in the lungs, does not require coordination of inhalation with the act of inhalation, which has a significant advantage over metered-dose aerosol inhalers. The effectiveness of inhalation depends on the dose of the aerosol and is determined by a number of factors: the amount of aerosol produced; the characteristics of the particles; the ratio of inhalation and exhalation; the anatomy and geometry of the respiratory tract. Experimental data indicate that aerosols with a particle diameter are optimal for entry into the respiratory tract and, accordingly, recommended for use. 2-5 microns. Smaller particles (less than 0.8 microns) enter the alveoli, where they are quickly absorbed or exhaled, without remaining in the respiratory tract, without providing a therapeutic effect. That. a higher therapeutic index of medicinal substances is achieved, which determines the effectiveness and safety of the treatment. The main indications for the use of nebulizers at the prehospital stage of treatment: the need to use high doses of drugs; targeted delivery of the drug into the respiratory tract if complications occur when using regular doses of drugs and a high frequency of use of inhaled corticosteroids and other anti-inflammatory drugs 24

24 in children, especially in the first years of life, severity of the condition (lack of effective inspiration) patient preference It is widely known that systemic corticosteroids are successfully used to treat exacerbations of COPD and asthma. They shorten the time to remission and help restore lung function more quickly [Evidence Level A]. Their use should be considered at FEV 1< 50% от должного. Рекомендуется преднизолон в дозе 40 мг в сутки в течение 10 дней [уровень доказательности D]. Однако, в одном из широкомасштабных исследований показано, что будесонид в ингаляционной форме через небулайзер может быть альтернативой таблетированным ГКС при лечении обострения, не сопровождающегося ацидозом. Преимущества небулайзерной терапии [уровень доказательности А]: отсутствие необходимости в координации дыхания с поступлением аэрозоля возможность использования высоких доз препарата и получение фармакодинамического ответа за короткий промежуток времени непрерывная подача лекарственного аэрозоля с мелкодисперсными частицами быстрое и значительное улучшение состояния вследствие эффективного поступления в бронхи лекарственного вещества легкая техника ингаляций препараты для небулайзерной терапии применяют в специальных контейнерах, небулах, а также растворах, выпускаемых в стеклянных флаконах, что дает возможность легко, правильно и точно дозировать лекарственное средство Методика ингаляции посредством небулайзера: открыть небулайзер перелить жидкость из небулы или накапать раствор из флакона добавить физиологический раствор до нужного объема 2-3 мл собрать небулайзер, присоединить мундштук или лицевую маску выполнить ингаляцию до полного расходования раствора; Для первичной санитарной обработки небулайзера необходимо его разобрать, промыть насадки теплой водой с детергентом и просушить. 25

25 November Treatment of exacerbations of COPD at home Treatment of exacerbations of COPD at home involves increasing the dose and/or frequency of bronchodilator therapy [Evidence Level A]. If anticholinergic drugs have not been used before, they are included in therapy until the condition improves. In more severe cases, high-dose nebulizer therapy may be prescribed on an as-needed basis for several days if an appropriate nebulizer is available. However, after the acute episode has resolved, long-term use of a nebulizer for routine therapy is not recommended (Scheme 1). Scheme 1. Treatment of an attack of COPD at home Indications for hospitalization for examination and treatment of exacerbations of COPD: Significant increase in the intensity of symptoms, such as the sudden development of shortness of breath at rest Severe COPD preceding the exacerbation The emergence of new clinical manifestations (cyanosis, edema) Inability to stop the exacerbation with the initially used medications means 26

26 Serious concomitant diseases Diagnostic uncertainty New arrhythmias Old age Insufficient care at home The algorithm for prehospital pharmacotherapy for exacerbation of bronchial asthma is presented in Table 3, and daily therapy of the disease in Table 4. Severity of exacerbation Mild attack Moderate attack* Severe attack* Status asthmaticus** Drug therapy Salbutamol 2.5 mg (1 nebula) via nebulizer for 5-15 minutes or Berodual 1 ml (20 drops) via nebulizer for min. [level of evidence A] If the effect is unsatisfactory, repeat the same bronchodilator inhalation up to 3 times within an hour. Note: here and below, evaluate bronchodilator therapy after 20 minutes. Salbutamol 2.5-5.0 mg (1-2 nebulas) through a nebulizer for 5-15 minutes or Berodual 1-3 ml (20-60 drops) through a nebulizer for minutes. [level of evidence A] + prednisolone 60 mg IV or budesonide via nebulizer 1000 mcg over 5-10 minutes. [level of evidence A] Berodual 1-3 ml (20-60 drops) via nebulizer for minutes + prednisolone 120 mg IV + budesonide 2000 mcg via nebulizer for 5-10 minutes [level of evidence D] Salbutamol 5.0 mg (2 nebulas) via nebulizer over 5-15 minutes or Berodual 3 ml (60 drops) via nebulizer over minutes + prednisolone 120 mg IV + budesonide 2000 mcg via nebulizer over 5-10 minutes [evidence level A]. If ineffective, tracheal intubation, artificial ventilation, oxygen therapy [level of evidence D] Result Relief of attack 1. Relief of attack 2. Hospitalization in the therapeutic department Hospitalization in the therapeutic department Hospitalization in the intensive care unit Table 3. Emergency care algorithm for exacerbation of bronchial asthma * In the absence of nebulizers or at the persistent request of the patient, it is possible to administer aminophylline 2.4% solution 10.0-20.0 ml intravenously for 10 minutes ** If treatment is ineffective for severe exacerbation and there is a threat of respiratory arrest, it is possible to administer adrenaline to adults 0.1% - 0.5 ml (subcutaneous) [level of evidence B] 27

27 Table 4. Daily basic therapy for bronchial asthma According to treatment effectiveness criteria, the response to therapy is considered: “good” if the patient’s condition is stable, shortness of breath and the amount of dry wheezing in the lungs has decreased, peak expiratory flow (PEF) has increased by 60 l/min (in children by 12-15% of the original) “incomplete” if the patient’s condition is unstable, the symptoms are expressed to the same degree, poor respiratory conductivity remains and there is no increase in PEF “bad” if the symptoms are expressed to the same degree or increase, and PEF worsens Indications for hospitalization for the treatment of exacerbations of bronchial asthma: Moderate and severe exacerbation Lack of response to bronchodilator therapy Patients at risk of death from bronchial asthma Threat of respiratory arrest Unfavorable living conditions The first actions that must be taken when admitting a patient to a hospital are to provide him with controlled oxygen therapy and determine the whether the exacerbation is life-threatening. If this is the case, the patient is immediately hospitalized in the intensive care unit. In other cases, the patient may receive therapy in the department. 28

28 Controlled oxygen therapy Oxygen therapy is the cornerstone of inpatient treatment for patients with exacerbation of COPD and asthma. Achieve an adequate level of oxygenation, i.e. PaO 2 > 8 kpa (60 mm Hg) or SaO 2 > 90%, mild in uncomplicated exacerbations, but CO 2 accumulation may occur unnoticed with minimal changes in symptoms. Arterial blood gases should be measured 30 minutes after the start of oxygen therapy to ensure adequate oxygenation without CO2 accumulation (acidosis). Venturi masks are more acceptable devices for controlled oxygen delivery than nasal cannulas, but they are often poorly tolerated by patients. Ventilation assistance The main goals of ventilation assistance in patients with exacerbation of COPD and asthma are to reduce mortality and morbidity rates, as well as reduce symptoms of the disease. Ventilation support includes both non-invasive ventilation using either negative or positive pressure devices, as well as traditional mechanical ventilation using an oro- or nasotracheal tube or through a tracheostomy. Non-invasive ventilation increases pH, decreases PaCO2, reduces the intensity of shortness of breath in the first 4 hours of treatment, and also shortens the length of hospitalization [evidence level A]. More importantly, mortality (or intubation rate if no mortality data is available) is reduced with this treatment. However, non-invasive ventilation cannot be used for all patients. Indications for non-invasive ventilation: Moderate to severe shortness of breath with use of accessory respiratory muscles and paradoxical movement of the abdomen Moderate to severe acidosis (ph 7.35) and hypercapnia (PaCO 2 > 6 kPa) Respiratory rate > 25 per minute Relative contraindications for non-invasive ventilation (any of these may be present): 29

29 Respiratory arrest Cardiovascular instability (hypotension, arrhythmias, myocardial infarction) Somnolence, inability of the patient to cooperate with medical personnel High risk of aspiration, viscous or copious bronchial secretions Recent facial or gastroesophageal surgery Craniofacial trauma, uncorrectable nasopharyngeal pathology Burns Patients, who, despite aggressive pharmacological therapy, experience increasing respiratory failure, as well as life-threatening acidotic changes and/or impaired mental function, are direct candidates for traditional mechanical ventilation. The three most widely used ventilation modes are assisted controlled ventilation, pressure support ventilation, and pressure support ventilation combined with intermittent mandatory ventilation. Indications for mechanical ventilation: Severe shortness of breath with use of accessory respiratory muscles Respiratory rate > 35 per minute Life-threatening hypoxemia (PaO 2< 5,3 кпа, или 40 мм рт. ст.) Тяжелый ацидоз (ph < 7,25) и гиперкапния (PaCO 2 >8 kPa, or 60 mm Hg. Art.) Respiratory arrest Drowsiness, impaired mental status Cardiovascular complications (hypotension, shock, heart failure) Other complications (metabolic abnormalities, sepsis, pneumonia, pulmonary embolism, barotrauma, massive pleural effusion) Failure of non-invasive ventilation or one of the criteria exceptions 30

30 November Typical errors in the treatment of bronchial obstruction at the prehospital stage: In real clinical practice, to relieve bronchial obstruction syndrome, drugs that are dangerous for use in a given clinical situation are very often unreasonably prescribed, namely: psychotropic drugs and, in particular, tranquilizers due to the possibility of respiratory depression for due to the central muscle relaxant effect, narcotic analgesics due to the danger of suppressing the respiratory center, antihistamines are not only ineffective, but can also aggravate bronchial obstruction by increasing the viscosity of sputum, non-steroidal anti-inflammatory drugs (“aspirin asthma”) [level of evidence B] it is necessary to know that repeated injections of aminophylline , as well as its use after adequate inhaled therapy with β 2 -agonists is fraught with the development of side effects (tachycardia, arrhythmias). simultaneous use of aminophylline and cardiac glycosides in conditions of hypoxemia is contraindicated due to the high risk of developing heart rhythm disturbances, including ventricular ones. The widespread use of adrenaline in bronchial asthma is also unjustified; this drug is indicated for the emergency treatment of anaphylactic shock or angioedema, and in bronchial asthma the risk of developing serious side effects outweighs the benefits. Antibiotics are effective when the volume and purulence of sputum increases in a patient with increased shortness of breath and cough [ Level of evidence B]. The choice of antibacterial drug should be made depending on the sensitivity of microorganisms, primarily S. pneumoniae and H. influenzae. 31


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1. Respiratory diseases:

Infectious and inflammatory diseases (bronchitis, bronchiolitis, pneumonia).

Allergic diseases (asthmatic bronchitis, bronchial asthma).

Bronchopulmonary dysplasia.

Malformations of the bronchopulmonary system.

Tumors of the trachea and bronchi.

2. Foreign bodies of the trachea, bronchi, esophagus.

3. Diseases of aspiration origin (or aspiration obstructive bronchitis) - gastroesophageal reflux, tracheoesophageal fistula, malformations of the gastrointestinal tract, diaphragmatic hernia.

4. Diseases of the cardiovascular system of congenital and acquired nature (CHD with hypertension of the pulmonary circulation, vascular anomalies, etc.)

5. Diseases of the central and peripheral nervous system.

6. Hereditary metabolic abnormalities.

7. Congenital and acquired immunodeficiency conditions.

8. Rare diseases: Lawrence-Moon-Bardet-Biedl syndrome, Kartagener syndrome, etc.

9. Other conditions: injuries and burns. Poisoning.

Impact of various physical and chemical environmental factors.

Compression of the trachea and bronchi of extrapulmonary origin.

3. From a practical point of view, depending on the etiological pathogenetic mechanisms, there are 4 variants of broncho-obstructive syndrome:

Infectious, developing as a result of viral and (or) bacterial inflammation in the bronchi and bronchioles;

Allergic, developing as a result of spasm and allergic inflammation of bronchial structures with a predominance of spastic phenomena over inflammatory ones;

Obstructive, observed during aspiration of a foreign body, with compression of the bronchi;

Hemodynamic, occurring in heart failure of the left ventricular type.

4. Manifestations of broncho-obstructive syndrome are of the same type, despite the variety of etiological factors and pathogenetic mechanisms of obstruction. Cardinal symptoms:

More often - expiratory shortness of breath due to increased resistance to air flow due to pathology of small and medium bronchi or the reflux of a small amount of stomach contents into the lumen of the bronchi (against the background of gastroesophageal reflux disease). Inspiratory dyspnea occurs less frequently with pathology of the large bronchi, trachea or heart;

Choking as an extreme degree of acute respiratory failure (refers to life-threatening conditions);

Paroxysmal cough with sputum (or without it);

Noisy breathing (whisking);

Distant wheezing.

More rare manifestations of broncho-obstructive syndrome are symptoms of hypercapnia (increase in pCO2): headache, sleep disturbance, increased sweating, tremor: in severe cases - confusion, convulsions and even hypercapnic coma.


5. Obstructive syndrome is observed with such forms of respiratory allergosis as bronchial asthma atopic in nature. Obstruction in this disease is manifested mainly by spasm of small bronchi and bronchioles (tonic type) and to a lesser extent by hypersecretion and edema. Heredity burdened with allergic diseases, a burdened personal allergic history (skin manifestations of allergies, “minor” forms of respiratory allergosis - allergic rhinitis, laryngitis, tracheitis, bronchitis, intestinal allergosis), the presence of a connection between the occurrence of the disease and a causally significant allergen and the absence of such a connection with infection, positive effect of elimination, recurrence of attacks, their uniformity.

The clinical picture is characterized by the following signs: absence of intoxication, distant wheezing, expiratory shortness of breath with the participation of auxiliary muscles; mainly wheezing and a few wet wheezes are heard in the lungs, the number of which increases after relief of bronchospasm. An attack occurs, as a rule, on the first day of exacerbation of the disease and is eliminated in a short time with adequate therapy (salbutamol, Berotek, etc.). The cardinal signs of bronchial asthma are an attack of suffocation, eosinophilia of blood and sputum, the presence of allergic or polypous rhinosinusitis, a positive test for detection of hidden bronchospasm. The same criteria, as well as the results of an allergological examination, are used for the differential diagnosis of bronchial asthma with asthma-like bronchospasm in carcinoid syndrome, irritation of the trachea or bronchi by a foreign body, compression by a tumor, enlarged lymph nodes, or aortic aneurysm.

6. COPD- diffuse progressive inflammation of the bronchi, not associated with local or generalized damage to the lungs and manifested by cough. It is customary to speak of the chronic nature of the process if a productive cough, not associated with any other disease, continues for at least 3 months a year for 2 years in a row.

The main cause of COPD is prolonged smoking, repeated inhalation of dust (in working conditions, for example in textile, wool, tobacco factories), irritating gases, disintegration aerosols, disaggregation. The etiological significance of unfavorable climatic conditions and microclimate (large fluctuations in temperature and humidity, air pollution) is undeniable.

What distinguishes COPD from bronchial asthma is, first of all, the absence of asthma attacks - COPD is characterized by constant coughing and shortness of breath. In the bronchial variant of COPD, the difference between morning and evening peak flow measurements is reduced (variability less than 15%), the irreversible component of bronchial obstruction predominates, in bronchial asthma it is increased (variability more than 20% indicates increased bronchial reactivity), in addition, COPD is not characterized by concomitant allergic diseases, eosinophilia of blood and sputum.