Chronic obstructive pulmonary diseases (COPD). COPD is a lung disease: treatment and symptoms, list of drugs Obstructive pulmonary disease

For effective treatment of chronic obstructive pulmonary disease (COPD) it is necessary.

Diagnostics

Bronchial asthma	COPD
Inflammation is localized in the small bronchi, without affecting the tissue of the lungs themselves	Inflammation is localized in the small bronchi, but spreads to the alveoli, destroying them and leading to the development of emphysema
Risk factors: allergens Family predisposition Common onset in children or young adults	Risk factors: smoking, occupational hazards Onset after age 35
Paroxysmal, reversible symptoms, lack of progression in mild forms	Steady increase in manifestations Often late diagnosis
Reversible bronchial obstruction according to spirometry	Irreversible bronchial obstruction according to spirometry

The main signs that help in the diagnosis of other lung diseases resembling COPD:

Disease	Characteristic signs
	Large volume of purulent sputum Frequent exacerbations Various dry and wet rales Signs of bronchiectasis on radiography or tomography
	Onset may be at a young age Characteristic radiological manifestations Detection of mycobacteria in sputum High prevalence of the disease in the region
Bronchiolitis obliterans	Starting in young people Presence of rheumatoid arthritis or acute gas poisoning
Diffuse panbronchiolitis	Onset in non-smoking men The majority have concomitant sinusitis (sinusitis, etc.) Specific signs on the tomogram
Congestive heart failure	Existing heart disease Characteristic wheezing in the lower parts of the lungs Spirometry shows no obstructive disorders

Treatment of COPD

Therapy is aimed at relieving symptoms, improving quality of life and exercise tolerance. In the long term, treatment aims to prevent the progression and development of exacerbations and reduce mortality.

Non-pharmacological treatment:

• to give up smoking;
• physical activity;
• vaccination against influenza and pneumococcal infection.

Drug treatment

The following groups of drugs are used in the treatment of stable COPD:

• bronchodilators;
• combination of bronchodilators;
• inhaled glucocorticoids (IGCS);
• combination of inhaled corticosteroids and long-acting bronchodilators;
• phosphodiesterase type 4 inhibitors;
• methylxanthines.

Let us remind you that a doctor must prescribe treatment; self-medication is unacceptable; Before starting therapy, you should read the instructions for use and ask your doctor any questions you may have.

• for moderate exacerbation - azithromycin, cefixime;
• for severe exacerbation - amoxiclav, levofloxacin.

If respiratory failure develops, oxygen and non-invasive ventilation are prescribed; in severe cases, treatment includes transfer to artificial ventilation.

Rehabilitation of patients

Pulmonary rehabilitation should last at least 3 months (12 sessions twice a week, lasting 30 minutes). It improves exercise capacity, reduces shortness of breath, anxiety and depression, prevents exacerbations and hospitalization, and has a positive effect on survival.

Rehabilitation includes treatment, physical training, nutritional correction, patient education, support from social workers and a psychologist.

The main thing in rehabilitation is physical training. They should combine strength and endurance exercises: walking, exercises with expanders and dumbbells, a step machine, cycling. Additionally, breathing exercises are used, including with the help of special simulators.

Nutrition correction consists of normalizing weight, sufficient amounts of protein, vitamins and microelements in the diet.

Patients need to be taught the skills to assess their condition, recognize deterioration and methods of correction, and also emphasize the need for ongoing treatment and monitoring by a doctor.

Read more about rehabilitation of patients with COPD

Chronic obstructive pulmonary disease (COPD) is an incurable pathology of the lower respiratory tract that leads to difficulty breathing. It is caused by constant inflammatory processes in the lungs, gradually leading to the degeneration of lung tissue. It is better known as “chronic obstructive bronchitis” or “pulmonary emphysema,” but according to the World Health Organization classification, these diseases are no longer used independently.

Definition of disease

Chronic obstructive pulmonary disease is a pathological inflammatory process in the lungs, the main consequence of which is the inability to breathe normally. A constant lack of oxygen in the body gradually leads not only to constant shortness of breath and painful coughing attacks. At the same time, physical activity decreases, since in the later stages even an attempt to climb a few steps on the stairs causes severe shortness of breath.

The insidiousness of the disease is that it can occur without a cough, which is why it is often diagnosed late.

The main symptoms of COPD are:

1. Dry cough. In the early stages, it may not appear, which complicates the early diagnosis of the disease. But more often than not, a mild cough without sputum is not taken seriously, which is why a person seeks help from a doctor too late.
2. Sputum. After some time, the cough becomes wet, with clear sputum being coughed up. In the later stages, the sputum becomes thick and abundantly secreted, often interspersed with pus.
3. Dyspnea. This is a symptom caused by a lack of oxygen in the body and a chronic inflammatory process in the lungs. It manifests itself at the last stage of COPD development, when changes in the lung tissue become irreversible. It can manifest itself with significant physical exertion, or with the weakest ARVI.

In addition, it provokes increased secretion of mucus in the bronchi, pulmonary hypertension, as well as various gas exchange disorders, as well as hemoptysis. Chronic obstructive pulmonary disease has the following main phases:

1. First. The disease itself is mild, often manifested only by rare bouts of coughing. At this stage, pathological changes in the lungs are almost invisible. At this stage, further development of the disease in some cases can be stopped with timely treatment.
2. Second. In the second stage, people most often begin to seek medical help. The cause is sharply manifested symptoms, such as cough with sputum and incipient shortness of breath. Pathological changes in the lungs become irreversible. After this, treatment can be aimed only at inhibiting painful symptoms.
3. Third. At the third, rather severe stage, the volume of air entering the lungs sharply decreases. This is associated with the development of obstructive phenomena, characterized by severe shortness of breath and coughing attacks with purulent sputum;
4. Fourth. The most severe stage, leading to complete loss of ability to work, and often posing a threat to life. It is at this stage that a pathology such as “pulmonary heart” appears and respiratory failure appears.

The development of chronic obstructive pulmonary disease is provoked by such main factors as:

• Long-term smoking;
• Polluted air in the house (for example, due to the use of solid fuel for heating);
• Low socio-economic status of the person or his family;
• Chronic infectious diseases of the lower respiratory tract (or);
• Adenoviral infection;
• Vitamin C deficiency in the body;
• Conditions of professional activity associated with the presence of dust and chemical vapors in the air (varnishes, paints, gases).

Another common cause of COPD is the so-called “passive smoking”. That is why health problems arise not only for the smoker himself, but also for all members of his family. This is especially dangerous for children, as it increases the risk of developing COPD in the future.

Proper and timely treatment of lower respiratory tract diseases in childhood helps prevent the development of COPD in adulthood.

General principles for prescribing drug therapy

Diagnosing chronic obstructive pulmonary disease is very simple. To do this, it is enough to perform spirometry and determine the volume of inhaled air. If such a diagnosis has already been made, full recovery is impossible. At the same time, competently carried out complex therapy aimed at strengthening the immune system and reducing symptoms.

Treatment of COPD can only be carried out with the help of medication and under the constant supervision of the attending physician. Self-medication in this case can lead to serious consequences, even life-threatening.

Complex drug therapy for COPD is aimed at:

• The need to prevent further development of the disease;
• Reducing the development of painful symptoms;
• The ability to prevent the development of complications;
• Preventing complications.

Proper drug therapy can prevent the development of all these problems and, if possible, improve the quality of life. What are the symptoms of influenza and ARVI, the differences between them are described in.

It is worth remembering that even the most modern and high-quality therapy cannot completely restore the affected tissue.

Treatment of COPD with drugs (list of drugs)

The basis of drug treatment is various drugs that help expand the bronchi and relax their muscles. First of all, these are drugs from the group of bronchodilators (bronchodilators). At each stage of the development of the disease, its own groups of medications are used, the volume of use of which is increasing.

All pharmacological agents used in the treatment of COPD are divided into those used in outpatient treatment and in hospital settings.

At the first stage (bronchodilators and inhalations)

At the initial stage of the disease, the doctor prescribes drugs from the group of bronchodilators. Depending on the severity of the disease, they can be used constantly or on demand during an exacerbation. For this, the following list of medications is used:

• Anticholinergics;
• β2-adrenergic agonists;
• Theophylline.

Most often they are prescribed in a course of 10–14 days during an exacerbation period. For COPD, the preferred method of administering the drug is inhalation, using modern.

Antibacterial drugs are used exclusively for infectious exacerbations of the disease.

Additionally, antioxidants with a mucolytic effect are used. Most often, a drug such as N-acetylcysteine ​​is used for this, used at a dosage of 600 milligrams per day. It can be used long-term, from 3 to 6 months, on an outpatient basis.

Bronchodilators for the second

In more severe stages, long-acting bronchodilators used by inhalation become the main drugs. Most often, these are quite expensive drugs, most often used for treatment in a hospital setting. These may be combination drugs such as:

• Salbutamol(100/200 mgk, 2 inhalations 2 times a day);
• Budesonide or Formoterol(160/4.5 mcg, applied 2 inhalations 2 times a day);
• Salmeterol (50 mcg, 1 inhalation 2 times a day).

They can be used both in a hospital setting and on an outpatient basis, under the constant supervision of a physician. At this stage, mucolytic drugs, such as Carbocisteine ​​or various iodine preparations, are used to facilitate coughing up sputum.

On third

Long-acting bronchodilators in combination with glucocorticosteroids also remain the basis of treatment. Treatment of COPD at this stage should be carried out. These drugs have a pronounced anti-inflammatory effect, and therefore are even more effective than for bronchial asthma. For this purpose, drugs such as Fluticasone propionate at a dosage of 1000 mcg/day can be used.

At a severe stage, drug treatment should be combined with oxygen therapy, or oxygen therapy.

The need for surgery

At the most severe, or fourth stage of COPD development, drug treatment of the disease is no longer enough. At this stage, a decision is often made about the need for surgical treatment. This helps to at least slightly improve lung function and reduce painful symptoms when drug treatments no longer give the desired result.

The decision about the need for surgical treatment has not been sufficiently studied. Therefore, it is used only in cases of threat to life.

In cases of severe pulmonary emphysema with severe shortness of breath, purulent sputum, and hemoptysis, bullectomy is used. This operation reduces shortness of breath and improves lung function. In addition, surgical treatment methods such as:

• Lung volume reduction surgery(reduces shortness of breath during the slightest physical exertion, for example when getting dressed or trying to walk a few meters);
• Lung transplantation(a radical treatment method that allows a patient with COPD to return to an almost full life).

After surgical treatment, a rehabilitation period begins, during which the person enters a stage of stable remission and returns to everyday life. It includes sanatorium treatment, as well as physical and social adaptation to a full life.

Chronic obstructive pulmonary disease is most often incurable, but with the right algorithm of actions you can live an almost full life. This allows you to reduce the frequency of exacerbations and extend periods of stable rehabilitation. To do this, the patient is recommended to follow these recommendations:

1. Regularly visit your doctor and strictly follow his instructions;
2. Follow a daily routine, sleep at least 8 hours;
3. Avoid unnecessary physical and emotional stress.

As with most pulmonary diseases, a complete and balanced diet rich in vitamins and microelements is of great importance.

One of the important components of a lifestyle with COPD is a high-calorie diet and strictly dosed physical activity.

It is easier to prevent such a serious disease as COPD than to treat it for a very long and difficult time. includes:

1. Complete smoking cessation;
2. and pneumococcal infection;
3. Timely treatment of infectious diseases of the respiratory tract;
4. Active lifestyle, including regular physical activity.

You should also avoid working in hazardous industries and, if necessary, use personal protective equipment.

Video

This video will tell you about the treatment of COPD.

conclusions

The most common cause of COPD is long-term smoking or frequent infectious diseases of the lower respiratory tract. Long-term persistent irritation of the bronchial tissues by chemical or mechanical irritants leads to a constant inflammatory reaction of the lungs. A particular danger is that the disease can develop slowly and practically asymptomatically. With timely prevention or drug treatment started as early as possible, the disease can be prevented. Find out about the treatment of smoker's cough at.

Chronic obstructive pulmonary diseases is a disease characterized by irreversible or partially reversible, progressive obstruction (impaired patency) of the bronchi. These are diseases that cause the air passages (bronchi) to become blocked or the small air sacs (alveoli) in the lungs to become damaged, causing difficulty breathing. Two main diseases; included in this group are emphysema and chronic bronchitis; Many people with chronic obstructive pulmonary disease experience both of these conditions.

Chronical bronchitis- This is a constant inflammation of the bronchi, leading to a constant cough with large amounts of mucus. When the cells lining the airways are irritated beyond a certain degree, the tiny cilia (hair-like projections) that normally catch and expel foreign objects stop working properly. Increased irritation leads to excessive mucus production, which clogs the air passages and causes severe coughing, characteristic of bronchitis. Bronchitis is considered chronic when the patient coughs with phlegm for three months, and this repeats for two years in a row.

Emphysema- This is the gradual damage to the lungs as a result of tissue destruction and loss of elasticity of the alveoli, in which oxygen enters the blood and carbon dioxide leaves it. If the lungs are damaged by chemicals in cigarette smoke, or as a result of persistent inflammation or chronic bronchitis, the thin walls of the alveoli can gradually become thicker, lose elasticity, and become much less functional. Loss of elasticity, often combined with narrowing of the small air passages in the lungs (sometimes completely blocking them), causes used air to be retained instead of being allowed to escape. Thus, the affected air sacs are unable to supply oxygen to the blood or remove carbon dioxide from it; this causes the shortness of breath characteristic of emphysema. Lung damage may progress until difficulty breathing becomes severe; from this point on, the disease becomes potentially life-threatening. Low levels of oxygen in the blood can lead to increased pressure in the pulmonary arteries (pulmonary hypertension), which in turn can prevent the right side of the heart from pumping blood through the lungs properly.

The development of chronic airway obstruction usually occurs gradually. Many years pass before symptoms appear, by which time the disease has already reached a significant stage. Lung damage is permanent, but in many cases it can be prevented by avoiding smoking. Chronic airway obstruction occurs two to three times more often in men than in women. COPD is considered a disease of the second half of life. The usual age of patients is over 40 years. Men get sick more often. The disease is more common in socially prosperous countries.

Symptoms

COPD is a very insidious disease characterized by a slow progressive course. From the actual onset of the disease to its manifestations, it takes from 3 to 10 years. Symptoms of COPD begin to appear only in the second stage of the disease.

Constant cough with mucus, especially in the morning (a sign of chronic bronchitis).

Chronic dry cough (a sign of emphysema).

In severe cases, symptoms of chronic obstructive pulmonary disease may include coughing up blood, chest pain, and a purple complexion.

Swollen legs and ankles from right heart failure (cor pulmonale).

Difficulty breathing.

Causes

Smoking is the most common cause of chronic obstructive pulmonary disease.

Air pollution may also be a contributing factor.

Industrial emissions or fumes containing chemicals can damage airways.

Repeated viral or bacterial lung diseases can thicken the walls of the bronchi, narrow the air passages, and stimulate excessive mucus production in the lungs.

Inherited deficiency of the enzyme alpha-1 antitrypsin can lead to damage to the walls of the alveoli.

People who are more susceptible to emphysema are those whose occupations regularly expose them to dust, chemicals, or other lung irritants, as well as those whose occupations require constant heavy use of the lungs, such as glassblowers or musicians who play wind instruments.

Young children living near smokers are more susceptible to chronic airway inflammation.

Diagnostics

A medical history and physical examination are necessary.

A saliva sample may be taken for analysis.

Blood tests from the artery and vein (to measure oxygen and carbon dioxide levels) are needed.

A chest x-ray is required.

Spirometry and other tests of lung function that measure breathing capacity and lung capacity are needed.

Measurements can be taken of the strength and efficiency of the heart muscle.

Treatment

Do not smoke; Avoid smoky rooms.

Drink more fluids to loosen mucus.

Avoid caffeine and alcohol as they are diuretics and can lead to dehydration.

Humidify the indoor air.

Avoid going outside on cold days or when the air is polluted, and avoid cold, wet weather. If bronchitis has reached an advanced stage and is incurable, you may want to consider moving to a warmer, drier climate.

Do not use cough suppressants. Coughing is necessary to clear accumulated mucus from the lungs, and suppressing it can lead to serious complications.

A viral respiratory tract infection can cause an exacerbation of the disease; Reduce your risk of infectious disease by minimizing contact with people with contagious respiratory illnesses and wash your hands frequently. Get vaccinated against flu and pneumonia annually.

A bronchodilator may be prescribed to widen the bronchial passages. In more serious cases, oxygen may be prescribed.

A doctor may prescribe antibiotics to treat or prevent bacterial lung infections, since patients with chronic obstructive pulmonary disease are more susceptible to them. Antibiotics must be taken for the entire prescribed period.

Your doctor may instruct you on how to clear mucus from your lungs by moving your head lower than your body.

Breathing exercises can be of some benefit.

In very serious cases where there is severe lung damage due to emphysema, a lung transplant may be performed (if the disease has weakened the heart, a heart and lung transplant is recommended).

1. Treatment of mild severity

At this stage, the disease, as a rule, has no clinical manifestations and does not require constant drug therapy. Seasonal vaccination against influenza and mandatory vaccination against pneumococcal infection once every five years are recommended (for example, with the PNEUMO 23 vaccine).

For severe symptoms of shortness of breath, short-acting inhaled bronchodilators may be used. Drugs Salbutamol, terbutaline, ventolin, fenoterol, berrotec. Contraindications: tachyarrhythmias, myocarditis, heart defects, aortic stenosis, decompensated diabetes mellitus, thyrotoxicosis, glaucoma. The drugs can be used no more than 4 times a day.

It is important to do inhalation correctly. If you have been prescribed such a drug for the first time, it is better to take the first inhalation with your doctor so that he can point out possible errors. The drug must be inhaled (injected into the mouth) precisely against the background of inhalation, so that it gets into the bronchi, and not just “down the throat”. After inhalation, you need to hold your breath at the height of inspiration for 5-10 seconds.

Separately in this group is the drug Berodual. Its distinctive features are the duration of action of at least 8 hours and a good severity of the therapeutic effect. The first two days of taking the drug may cause a reflex cough, which then goes away.

If there is a cough with sputum discharge, patients are prescribed Mucolytics (drugs that thin sputum).

Currently, there are a large number of drugs with this effect on the pharmaceutical market, but, in my opinion, preference should be given to drugs based on acetylcysteine.
For example, ACC (packages for preparing a solution for oral administration, effervescent tablets of 100, 200 and 600 mg), Fluimucil in effervescent tablets. The daily dose of drugs for an adult is 600 mg.

There is also a dosage form (acetylcysteine ​​solution for inhalation 20%) for inhalation using a nebulizer. A nebulizer is a device for converting liquid medicinal substances into aerosol form. In this form, the medicinal substance enters the smallest bronchi and alveoli and its effectiveness increases significantly. This method of administering drugs is preferable for patients with chronic diseases of the upper respiratory tract.

2. Treatment of moderate forms

Long-acting bronchodilators are added to the drugs used for stage 1 (mild) of the disease.

Serevent (salmeterol). Available in the form of a metered dose inhaler. The recommended daily dosage for adults is 50-100 mcg / 2 times a day. It is necessary to strictly monitor the inhalation technique.

Formoterol (foradil). Available in capsules containing powder for inhalation using a special device (handihaler). Recommended daily dosage is 12 mcg/2 times a day.

As an alternative, you can use Berodual regularly. If the drug is used in the form of a dosed aerosol, then take 2 inhalations (2 inhalations) of the drug three times a day: in the morning, at lunch and in the evening. The drug is also available as a solution for inhalation via a nebulizer. In this case, the recommended dosage for an adult is 30-40 drops through a nebulizer - 3 times a day.

A relatively new, but already proven drug from this group, Spiriva (tiotropium bromide). Spiriva is prescribed once a day and is available in capsules for inhalation using a special device. One of the most effective drugs for the treatment of COPD at present. Active use is limited only by a fairly high cost.

3. Severe treatment.

At this stage of the disease, constant anti-inflammatory treatment is necessary.

Inhaled glucocorticosteroids are prescribed in medium and high doses. Drugs: beclazone, becotide, benacort, pulmicort, flixotide, etc. They are usually produced in the form of metered aerosols for inhalation or in the form of solutions (pulmicort) for inhalation through a nebulizer.

Also, for this degree of severity of the disease, combination drugs containing both a long-acting bronchodilator and an inhaled corticosteroid can be used. Drugs: seretide, symbicort. Combination drugs are currently considered the most effective means of treating COPD of this severity.

If you have been prescribed a drug containing an inhaled corticosteroid, be sure to ask your doctor how to do the inhalation correctly. Improper procedure significantly reduces the effectiveness of the drug and increases the risk of side effects. After inhalation, be sure to rinse your mouth.

4. Extremely severe severity

In addition to the medications used for severe forms of the disease, oxygen therapy (regular inhalation of oxygen-enriched air) is added. For this purpose, in medical equipment stores or large pharmacies you can find both fairly large devices for home use and small cans that you can take with you on a walk and use when shortness of breath increases.

If the condition and age of the patient allows, surgical treatment is performed.
If the patient's condition is extremely severe, artificial ventilation may be required.

When an infection occurs, antibacterial agents are added to the therapy. The use of penicillin derivatives, cephalosporins, and fluoroquinolones is recommended. Specific drugs and their dosages are determined by the attending physician depending on the patient’s condition and the presence of concomitant diseases, for example, in case of liver and/or kidney pathology, the dosage is reduced.

Prevention

Don't smoke (smoking is the number one cause of chronic obstructive pulmonary disease).

Avoid spending a lot of time outside on days when the air is polluted.

Call your doctor if your symptoms become severe, such as if your shortness of breath or chest pain gets worse, your cough gets worse or you are coughing up blood, you have a fever, are vomiting, or your legs and ankles are more swollen than usual.

Make an appointment with your doctor if you have had a persistent cough with phlegm for the past two years or if you experience persistent shortness of breath.

Attention! Immediate medical attention is needed if your lips or face become bluish or purplish.

Version: MedElement Disease Directory

Other chronic obstructive pulmonary disease (J44)

Pulmonology

general information

Short description

(COPD) is a chronic inflammatory disease that occurs under the influence of various factors of environmental aggression, the main one of which is smoking. Occurs with predominant damage to the distal parts of the respiratory tract and parenchyma Parenchyma is a set of main functioning elements of an internal organ, limited by connective tissue stroma and capsule.
lungs, the formation of emphysema Emphysema - stretching (swelling) of an organ or tissue by air entering from the outside or by gas formed in the tissues
.

COPD is characterized by partially reversible and irreversible airflow limitation. The disease is caused by an inflammatory reaction, which differs from inflammation in bronchial asthma and exists regardless of the severity of the disease.

COPD develops in susceptible individuals and is manifested by cough, sputum production and increasing shortness of breath. The disease is steadily progressive, resulting in chronic respiratory failure and cor pulmonale.

Currently, the concept of “COPD” has ceased to be collective. Partially reversible airflow limitation associated with bronchiectasis is excluded from the definition of COPD. Bronchiectasis - expansion of limited areas of the bronchi due to inflammatory-dystrophic changes in their walls or abnormalities in the development of the bronchial tree
, cystic fibrosis Cystic fibrosis is a hereditary disease characterized by cystic degeneration of the pancreas, intestinal glands and respiratory tract due to blockage of their excretory ducts with viscous secretions.
, post-tuberculosis fibrosis, bronchial asthma.

Note. Specific approaches to the treatment of COPD in this subsection are presented in accordance with the views of leading pulmonologists of the Russian Federation and may not coincide in detail with the recommendations of GOLD - 2011 (- J44.9).

Classification

Classification of severity of airflow limitation in COPD(based on post-bronchodilator FEV1) in patients with FEV1/FVC<0,70 (GOLD - 2011)

Clinical classification of COPD by severity(used when it is impossible to dynamically monitor the state of FEV1/FVC, when the stage of the disease can be approximately determined based on the analysis of clinical symptoms).

Stage I. Mild COPD: the patient may not notice that his lung function is impaired; Chronic cough and sputum production are usually (but not always) present.

Stage II. Moderate COPD: at this stage, patients seek medical help due to shortness of breath and exacerbation of the disease. There is an increase in symptoms with shortness of breath that occurs during exercise. The presence of repeated exacerbations affects the quality of life of patients and requires appropriate treatment tactics.

Stage III. Severe COPD: characterized by a further increase in airflow limitation, increased shortness of breath, and the frequency of exacerbations of the disease, which affects the quality of life of patients.

Stage IV. Extremely severe COPD: at this stage, the quality of life of patients noticeably deteriorates, and exacerbations can be life-threatening. The disease becomes disabling. Characterized by extremely severe bronchial obstruction in the presence of respiratory failure. As a rule, the partial pressure of oxygen in arterial blood (PaO 2) is less than 8.0 kPa (60 mm Hg) in combination (or without) with an increase in PaCO 2 more than 6.7 kPa (50 mm Hg). Cor pulmonale may develop.

Note. Severity stage "0": Increased risk of developing COPD: chronic cough and sputum production; exposure to risk factors, lung function is not changed. This stage is considered as a pre-disease, which does not always develop into COPD. Allows you to identify patients at risk and prevent further development of the disease. In modern recommendations, stage “0” is excluded.

The severity of the condition without spirometry can also be determined and assessed over time according to some tests and scales. A very high correlation was noted between spirometric indicators and some scales.

Etiology and pathogenesis

COPD develops as a result of the interaction of genetic and environmental factors.

Etiology

Environmental factors:

Smoking (active and passive) is the main etiological factor in the development of the disease;

Smoke from combustion of biofuels for home cooking is an important etiological factor in underdeveloped countries;

Occupational hazards: organic and inorganic dust, chemical agents.

Genetic factors:

Alpha1-antitrypsin deficiency;

Currently, polymorphisms of the genes for microsomal epoxide hydrolase, vitamin D-binding protein, MMP12 and other possible genetic factors are being studied.

Pathogenesis

Airway inflammation in patients with COPD represents a pathologically exaggerated normal inflammatory response of the airways to long-term irritants (eg, cigarette smoke). The mechanism by which the enhanced response occurs is currently not entirely clear; It is noted that it may be genetically determined. In some cases, the development of COPD in non-smokers has been observed, but the nature of the inflammatory response in such patients is unknown. Due to oxidative stress and excess proteinases in the lung tissue, the inflammatory process further intensifies. This together leads to pathomorphological changes characteristic of COPD. The inflammatory process in the lungs continues even after smoking cessation. The role of autoimmune processes and persistent infection in the continuation of the inflammatory process is discussed.

Pathophysiology

1. Air flow limitation and air traps. Inflammation, fibrosis Fibrosis is the proliferation of fibrous connective tissue, occurring, for example, as a result of inflammation.
and hyperproduction of exudate Exudate is a protein-rich liquid that comes out of small veins and capillaries into surrounding tissues and body cavities during inflammation.
in the lumen of the small bronchi cause obstruction. As a result of this, “air traps” arise - an obstacle to the exit of air from the lungs during the exhalation phase, and then hyperinflation develops Hyperinflation - increased airiness detected by radiography
. Emphysema also contributes to the formation of “air traps” during exhalation, although it is more associated with gas exchange disorders than with a decrease in FEV1. Due to hyperinflation, which leads to a decrease in inspiratory volume (especially during physical activity), shortness of breath and limited exercise tolerance occur. These factors cause disruption of the contractility of the respiratory muscles, which leads to an increase in the synthesis of pro-inflammatory cytokines.
It is currently believed that hyperinflation develops already in the early stages of the disease and serves as the main mechanism for the occurrence of dyspnea on exertion.

2.Gas exchange disorders lead to hypoxemia Hypoxemia - low oxygen content in the blood
and hypercapnia Hypercapnia - increased levels of carbon dioxide in the blood and (or) other tissues
and in COPD are caused by several mechanisms. Transport of oxygen and carbon dioxide generally becomes worse as the disease progresses. Severe obstruction and hyperinflation in combination with impaired contractility of the respiratory muscles lead to increased load on the respiratory muscles. This increase in load, combined with a decrease in ventilation, can lead to the accumulation of carbon dioxide. Impaired alveolar ventilation and decreased pulmonary blood flow cause further progression of ventilation-perfusion ratio (VA/Q) impairment.

3. Hypersecretion of mucus, which leads to a chronic productive cough, is a characteristic feature of chronic bronchitis and is not necessarily associated with airflow limitation. Symptoms of mucus hypersecretion are not detected in all patients with COPD. In the presence of hypersecretion, it is caused by metaplasia Metaplasia is the persistent replacement of differentiated cells of one type with differentiated cells of another type while maintaining the main species of the tissue.
mucous membrane with an increase in the number of goblet cells and the size of the submucosal glands, which occurs in response to chronic irritating effects on the respiratory tract of cigarette smoke and other harmful agents. Hypersecretion of mucus is stimulated by various mediators and proteinases.

4. Pulmonary hypertension can develop already in the later stages of COPD. Its appearance is associated with hypoxia-induced spasm of the small arteries of the lungs, which ultimately leads to structural changes: hyperplasia Hyperplasia is an increase in the number of cells, intracellular structures, intercellular fibrous formations due to enhanced organ function or as a result of pathological tissue neoplasm.
intima and later hypertrophy/hyperplasia of the smooth muscle layer.
In the vessels, endothelial dysfunction and an inflammatory response similar to the reaction in the respiratory tract are observed.
An increase in pressure in the pulmonary circle can also be facilitated by depletion of pulmonary capillary blood flow during emphysema. Progressive pulmonary hypertension can lead to right ventricular hypertrophy and ultimately to right ventricular failure (cor pulmonale).

5. Exacerbations with increased respiratory symptoms in patients with COPD may be triggered by bacterial or viral infection (or a combination of both), environmental pollution and unidentified factors. With a bacterial or viral infection, patients experience a characteristic increase in the inflammatory response. During an exacerbation, there is an increase in the severity of hyperinflation and “air traps” in combination with a reduced expiratory flow, which causes increased shortness of breath. In addition, there is a worsening imbalance in the ventilation-perfusion ratio (VA/Q), which leads to severe hypoxemia.
Diseases such as pneumonia, thromboembolism and acute heart failure can simulate an exacerbation of COPD or aggravate its picture.

6. Systemic manifestations. Limiting air flow speed and especially hyperinflation negatively affect heart function and gas exchange. Circulating inflammatory mediators may contribute to muscle loss and cachexia Cachexia is an extreme degree of exhaustion of the body, characterized by sudden emaciation, physical weakness, decreased physiological functions, asthenic, and later apathetic syndrome.
, and can also provoke the development or aggravate the course of concomitant diseases (coronary heart disease, heart failure, normocytic anemia, osteoporosis, diabetes, metabolic syndrome, depression).

Pathomorphology

In the proximal airways, peripheral airways, lung parenchyma and pulmonary vessels in COPD, characteristic pathological changes are found:
- signs of chronic inflammation with an increase in the number of specific types of inflammatory cells in different parts of the lungs;
- structural changes caused by alternating processes of damage and recovery.
As the severity of COPD increases, inflammatory and structural changes increase and persist even after smoking cessation.

Epidemiology

Existing data on the prevalence of COPD have significant discrepancies (from 8 to 19%), due to differences in research methods, diagnostic criteria and approaches to data analysis. On average, the prevalence is estimated to be approximately 10% in the population.

Risk factors and groups

- smoking (active and passive) is the main and main risk factor; Smoking during pregnancy may place the fetus at risk through deleterious effects on intrauterine growth and lung development and possibly through primary antigenic effects on the immune system;
- genetic congenital deficiencies of certain enzymes and proteins (most often - antitrypsin deficiency);
- occupational hazards (organic and inorganic dust, chemical agents and smoke);
- male gender;
- age over 40 (35) years;
- socio-economic status (poverty);
- low body weight;
- low birth weight, as well as any factor that has an adverse effect on lung growth during fetal development and in childhood;
- bronchial hyperreactivity;
- chronic bronchitis (especially in young smokers);
- severe respiratory infections suffered in childhood.

Clinical picture

Symptoms, course

In the presence of cough, sputum production and/or shortness of breath, COPD should be suspected in all patients with risk factors for developing the disease. It should be kept in mind that chronic cough and sputum production can often be present long before the airflow limitation that leads to shortness of breath develops.
If the patient has any of these symptoms, spirometry should be performed. Each symptom alone is not diagnostic, but the presence of several of them increases the likelihood of having COPD.

Diagnosis of COPD consists of the following stages:
- information gleaned from a conversation with the patient (verbal portrait of the patient);
- data from an objective (physical) examination;
- results of instrumental and laboratory studies.

Studying a verbal portrait of the patient

Complaints(their severity depends on the stage and phase of the disease):

1. Cough is the earliest symptom and usually appears at the age of 40-50 years. During cold seasons, such patients experience episodes of respiratory infection, which at first are not associated by the patient and the doctor as one disease. The cough may be daily or intermittent; more often observed during the day.
In a conversation with the patient, it is necessary to establish the frequency of cough and its intensity.

2. Sputum, as a rule, is released in small quantities in the morning (rarely > 50 ml/day) and is mucous in nature. An increase in the amount of sputum and its purulent nature are signs of exacerbation of the disease. If blood appears in the sputum, another cause of cough should be suspected (lung cancer, tuberculosis, bronchiectasis). In a patient with COPD, streaks of blood in the sputum may appear as a result of a persistent hacking cough.
In a conversation with the patient, it is necessary to find out the nature of the sputum and its quantity.

3. Shortness of breath is the main symptom of COPD and for most patients it is a reason to consult a doctor. Often, the diagnosis of COPD is made at this stage of the disease.
As the disease progresses, shortness of breath can vary widely: from a feeling of lack of air during habitual physical activity to severe respiratory failure. Dyspnea during physical exertion appears on average 10 years later than cough (it is extremely rare that the disease debuts with shortness of breath). The severity of shortness of breath increases as pulmonary function decreases.
In COPD, the characteristic features of shortness of breath are:
- progression (constant increase);
- consistency (every day);
- increased during physical activity;
- increased with respiratory infections.
Patients describe shortness of breath as “increasing effort when breathing,” “heaviness,” “air starvation,” “difficulty breathing.”
In a conversation with the patient, it is necessary to assess the severity of shortness of breath and its relationship with physical activity. There are several special scales for assessing shortness of breath and other symptoms of COPD - BORG, mMRC Dyspnea Scale, CAT.

Along with the main complaints, patients may be concerned about the following: extrapulmonary manifestations of COPD:

Morning headache;
- drowsiness during the day and insomnia at night (a consequence of hypoxia and hypercapnia);
- weight loss and weight loss.

Anamnesis

When talking with a patient, it should be borne in mind that COPD begins to develop long before the appearance of severe symptoms and proceeds for a long time without significant clinical symptoms. It is advisable to clarify with the patient what he himself associates with the development of symptoms of the disease and their increase.
When studying the anamnesis, it is necessary to establish the frequency, duration and characteristics of the main manifestations of exacerbations and evaluate the effectiveness of previously carried out treatment measures. It is necessary to find out the presence of a hereditary predisposition to COPD and other pulmonary diseases.
If the patient underestimates his condition and the doctor has difficulty determining the nature and severity of the disease, special questionnaires are used.

A typical “portrait” of a patient with COPD:

Smoker;

Middle-aged or elderly;

Suffering from shortness of breath;

Having a chronic cough with sputum, especially in the morning;

Complaining of regular exacerbations of bronchitis;

Having partially (weakly) reversible obstruction.

Physical examination

The results of an objective examination depend on the following factors:
- degree of severity of bronchial obstruction;
- severity of emphysema;
- presence of manifestations of pulmonary hyperinflation (overdistension of the lungs);
- presence of complications (respiratory failure, chronic pulmonary heart disease);
- presence of concomitant diseases.

It should be borne in mind that the absence of clinical symptoms does not exclude the presence of COPD in a patient.

Examination of the patient

1. Appearance assessment the patient, his behavior, the reaction of the respiratory system to a conversation, movement around the office. Signs of severe COPD are pursed lips and a forced position.

2. Assessment of skin color, which is determined by a combination of hypoxia, hypercapnia and erythrocytosis. Central gray cyanosis usually indicates hypoxemia; if it is combined with acrocyanosis, then this usually indicates the presence of heart failure.

3. Chest examination. Signs of severe COPD:
- deformation of the chest, “barrel” shape;
- inactive when breathing;
- paradoxical retraction (retraction) of the lower intercostal spaces during inspiration (Hoover's sign);
- participation in the act of breathing of the auxiliary muscles of the chest and abdominal muscles;
- significant expansion of the chest in the lower sections.

4. Percussion chest. Signs of emphysema are a boxy percussion sound and drooping lower borders of the lungs.

5.Auscultatory picture:

Signs of emphysema: harsh or weakened vesicular breathing in combination with a low diaphragm;

Obstruction syndrome: dry wheezing, which intensifies with forced exhalation, combined with increased exhalation.

Clinical forms of COPD

In patients with moderate and severe disease, two clinical forms are distinguished:
- emphysematous (panacinar emphysema, “pink puffs”);
- bronchitis (centroacinar emphysema, “blue swelling”).

Identification of two forms of COPD has prognostic significance. In the emphysematous form, decompensation of the cor pulmonale occurs at later stages compared to the bronchitis form. A combination of these two forms of the disease is often observed.

According to clinical signs there are two main phases of COPD: stable and exacerbation of the disease.

Stable state - progression of the disease can only be detected with long-term follow-up of the patient, and the severity of symptoms does not change significantly over weeks or even months.

Exacerbation- deterioration of the patient’s condition, which is accompanied by an increase in symptoms and functional disorders and lasts at least 5 days. Exacerbations can have a gradual onset or manifest as a rapid deterioration of the patient’s condition with the development of acute respiratory and right ventricular failure.

The main symptom of exacerbation of COPD- increased shortness of breath. As a rule, this symptom is accompanied by a decrease in exercise tolerance, a feeling of constriction in the chest, the appearance or intensification of distant wheezing, an increase in the intensity of the cough and the amount of sputum, a change in its color and viscosity. In patients, indicators of external respiration function and blood gases significantly deteriorate: speed indicators (FEV1, etc.) decrease, hypoxemia and hypercapnia may appear.

There are two types of exacerbation:
- exacerbation, characterized by an inflammatory syndrome (increased body temperature, increased amount and viscosity of sputum, purulent nature of sputum);
- exacerbation, manifested by an increase in shortness of breath, increased extrapulmonary manifestations of COPD (weakness, headache, poor sleep, depression).

Highlight 3 degrees of severity of exacerbation depending on the intensity of symptoms and response to treatment:

1. Mild - symptoms increase slightly, exacerbation is controlled with bronchodilator therapy.

2. Moderate - exacerbation requires medical intervention and can be treated on an outpatient basis.

3. Severe - an exacerbation requires hospital treatment, is characterized by increased symptoms of COPD and the appearance or worsening of complications.

In patients with mild or moderate COPD (stages I-II), an exacerbation is usually manifested by increased shortness of breath, cough and an increase in sputum volume, which allows patients to be managed on an outpatient basis.
In patients with severe COPD (stage III), exacerbations are often accompanied by the development of acute respiratory failure, which requires intensive care in a hospital setting.

In some cases, in addition to severe, there are very severe and extremely severe exacerbations of COPD. In these situations, the participation of auxiliary muscles in the act of breathing, paradoxical movements of the chest, and the occurrence or worsening of central cyanosis are taken into account. Cyanosis is a bluish tint of the skin and mucous membranes caused by insufficient oxygen saturation of the blood.
and peripheral edema.

Diagnostics

Instrumental studies

1. Pulmonary function test- the main and most important method for diagnosing COPD. Performed to detect airflow limitation in patients with chronic productive cough, even in the absence of shortness of breath.

Main functional syndromes in COPD:

Impaired bronchial obstruction;

Changes in the structure of static volumes, disruption of the elastic properties and diffusion capacity of the lungs;

Decreased physical performance.

Spirometry
Spirometry or pneumotachometry are generally accepted methods for recording bronchial obstruction. When conducting studies, forced expiration in the first second (FEV1) and forced vital capacity (FVC) are assessed.

The presence of chronic airflow limitation or chronic obstruction is indicated by a post-bronchodilator decrease in the FEV1/FVC ratio of less than 70% of the predicted value. This change is recorded starting from stage I of the disease (mild COPD).
The post-bronchodilator FEV1 indicator has a high degree of reproducibility when the maneuver is performed correctly and allows you to monitor the state of bronchial patency and its variability.
Bronchial obstruction is considered chronic if it occurs at least 3 times within one year, despite therapy.

Bronchodilation test carry out:
- with short-acting β2-agonists (inhalation of 400 mcg salbutamol or 400 mcg fenoterol), assessment is carried out after 30 minutes;
- with M-anticholinergics (inhalation of ipratropium bromide 80 mcg), assessment is carried out after 45 minutes;
- it is possible to conduct a test with a combination of bronchodilators (fenoterol 50 mcg + ipratropium bromide 20 mcg - 4 doses).

To correctly perform a bronchodilator test and avoid distortion of the results, it is necessary to cancel the therapy in accordance with the pharmacokinetic properties of the drug taken:
- short-acting β2-agonists - 6 hours before the start of the test;
- long-acting β2-agonists - 12 hours;
- extended-release theophyllines - 24 hours before.

Calculation of FEV1 increase

by absolute increase in FEV1 in ml (the easiest way):

Disadvantage: this method does not allow one to judge the degree of relative improvement in bronchial patency, since the values ​​of neither the initial nor the achieved indicator in relation to the expected value are taken into account.

by the percentage ratio of the absolute increase in FEV1 to the initial FEV1:

Disadvantage: A small absolute increase will result in a high percentage increase if the patient has a low baseline FEV1.

- Method for measuring the degree of bronchodilation response as a percentage relative to the proper FEV1 [ΔOFEV1 proper. (%)]:

Method for measuring the degree of bronchodilation response as a percentage of the maximum possible reversibility [ΔOFV1 possible. (%)]:

Where OFV1 ref. - initial parameter, FEV1 dilate. - indicator after bronchodilation test, FEV1 should. - proper parameter.

The choice of method for calculating the reversibility index depends on the clinical situation and the specific reason for which the study is being carried out. The use of a reversibility indicator, which is less dependent on the initial parameters, allows for a more correct comparative analysis.

Marker of a positive bronchodilation response The increase in FEV1 is considered to be ≥15% of predicted and ≥200 ml. When such an increase is obtained, bronchial obstruction is documented as reversible.

Bronchial obstruction can lead to a change in the structure of static volumes towards hyperairiness of the lungs, the manifestation of which, in particular, is an increase in the total lung capacity.
To identify changes in the ratios of static volumes that make up the structure of the total lung capacity in hyperairiness and emphysema, body plethysmography and measurement of lung volumes by the method of diluting inert gases are used.

Bodyplethysmography
With emphysema, anatomical changes in the lung parenchyma (expansion of air spaces, destructive changes in the alveolar walls) are functionally manifested by an increase in the static extensibility of the lung tissue. There is a change in the shape and angle of the pressure-volume loop.

Measurement of the diffusion capacity of the lungs is used to identify damage to the pulmonary parenchyma due to emphysema and is performed after forced spirometry or pneumotachometry and determination of the structure of static volumes.

In emphysema, the diffusion capacity of the lungs (DLCO) and its ratio to the alveolar volume DLCO/Va are reduced (mainly as a result of destruction of the alveolar-capillary membrane, which reduces the effective area of ​​gas exchange).
It should be borne in mind that a decrease in the diffusion capacity of the lungs per unit volume can be compensated by an increase in the total capacity of the lungs.

Peak flowmetry
Determining the volume of peak expiratory flow (PEF) is the simplest, quick method for assessing the state of bronchial patency. However, it has low sensitivity, since in COPD, PEF values ​​can remain within the normal range for a long time, and low specificity, since a decrease in PEF values ​​can also occur in other respiratory diseases.
Peak flowmetry is used in the differential diagnosis of COPD and bronchial asthma, and can also be used as an effective screening method to identify a group at risk for developing COPD and to establish the negative impact of various pollutants Pollutant (pollutant) - one of the types of pollutants, any chemical substance or compound that is found in an object of the natural environment in quantities exceeding background values ​​and thereby causing chemical pollution
.

Determination of PEF is a necessary control method during exacerbations of COPD and especially at the rehabilitation stage.

2. Radiography chest organs.

An initial x-ray examination is carried out to exclude other diseases (lung cancer, tuberculosis, etc.) accompanied by clinical symptoms similar to COPD.
In mild COPD, significant radiographic changes are usually not detected.
In case of exacerbation of COPD, an X-ray examination is performed to exclude the development of complications (pneumonia, spontaneous pneumothorax, pleural effusion).

A chest x-ray can reveal emphysema. An increase in lung volume is indicated by:
- on a direct radiograph - a flat diaphragm and a narrow shadow of the heart;
- on the lateral radiograph there is flattening of the diaphragmatic contour and an increase in the retrosternal space.
The presence of bullae on an x-ray can confirm the presence of emphysema. Bulla - an area of ​​bloated, overstretched lung tissue
- are defined as radiolucent spaces greater than 1 cm in diameter with a very thin arcuate border.

3. CT scan chest organs are required in the following situations:
- when the existing symptoms are disproportionate to spirometric data;
- to clarify changes identified during chest x-ray;
- to assess indications for surgical treatment.

CT, especially high-resolution CT (HRCT) with 1 to 2 mm increments, has higher sensitivity and specificity for diagnosing emphysema compared with radiography. Using CT in the early stages of development, it is also possible to identify the specific anatomical type of emphysema (panacinar, centroacinar, paraseptal).

CT scans reveal a saber-shaped deformity of the trachea, which is pathognomonic for this disease, in many patients with COPD.

Since a standard CT examination is performed at the height of inspiration, when excessive airiness of areas of lung tissue is not noticeable, if COPD is suspected, CT tomography should be supplemented with expiratory tomography.

HRCT allows you to evaluate the fine structure of the lung tissue and the condition of the small bronchi. The condition of the lung tissue in case of impaired ventilation in patients with obstructive changes is studied under expiratory CT. When using this technique, HRCT is performed at the height of delayed expiration.
In areas of impaired bronchial patency, areas of increased airiness are identified - “air traps”, which lead to hyperinflation. This phenomenon occurs as a result of an increase in the compliance of the lungs and a decrease in their elastic traction. During exhalation, airway obstruction causes air retention in the lungs due to the patient's inability to exhale fully.
Indicators of the "air trap" (type IC - inspiratory capacity, inspiratory capacity) are more closely related to the condition of the airways of a patient with COPD than the FEV1 indicator.

Other studies

1.Electrocardiography in most cases, it allows to exclude the cardiac origin of respiratory symptoms. In some cases, an ECG can reveal signs of hypertrophy of the right heart during the development of cor pulmonale as a complication of COPD.

2.Echocardiography allows you to evaluate and identify signs of pulmonary hypertension, dysfunction of the right (and, if there are changes, the left) parts of the heart and determine the severity of pulmonary hypertension.

3.Exercise Study(step test). In the initial stages of the disease, disturbances in the diffusion capacity and gas composition of the blood may be absent at rest and appear only during physical activity. Exercise testing is recommended to objectify and document the degree of decrease in exercise tolerance.

A physical stress test is carried out in the following cases:
- when the severity of shortness of breath does not correspond to a decrease in FEV1 values;
- to monitor the effectiveness of therapy;
- for selecting patients for rehabilitation programs.

Most often used as a step test 6 minute walk test​which can be performed in an outpatient setting and is the simplest means for individual observation and monitoring of the course of the disease.

The standard 6-minute walk test protocol involves instructing patients about the purpose of the test, then asking them to walk down a measured hallway at their own pace, attempting to cover the maximum distance within 6 minutes. Patients are allowed to stop and rest during the test, resuming walking after resting.

Before the start and at the end of the test, shortness of breath is assessed using the Borg scale (0-10 points: 0 - no shortness of breath, 10 - maximum shortness of breath), SatO 2 and pulse. Patients stop walking if they experience severe shortness of breath, dizziness, pain in the chest or legs, and SatO2 decreases to 86%. The distance traveled in 6 minutes is measured in meters (6MWD) and compared with the proper 6MWD(i).
The 6-minute walk test is part of the BODE scale (see section "Prognosis"), which allows you to compare FEV1 values ​​​​with the results of the mMRC scale and body mass index.

4. Bronchoscopic examination used in the differential diagnosis of COPD with other diseases (cancer, tuberculosis, etc.) manifesting similar respiratory symptoms. The study includes examination of the bronchial mucosa and assessment of its condition, taking bronchial contents for subsequent studies (microbiological, mycological, cytological).
If necessary, it is possible to perform a biopsy of the bronchial mucosa and perform a bronchoalveolar lavage technique to determine the cellular and microbial composition in order to clarify the nature of the inflammation.

5. Quality of life study. Quality of life is an integral indicator that determines the patient’s adaptation to COPD. To determine the quality of life, special questionnaires are used (nonspecific questionnaire SF-36). The most famous questionnaire is The St.George’s Hospital Respiratory Questionnaire - SGRQ.

6. Pulse oximetry used to measure and monitor SatO 2 . It allows you to record only the level of oxygenation and does not allow you to monitor changes in PaCO 2. If SatO 2 is less than 94%, then a blood gas study is indicated.

Pulse oximetry is indicated to determine the need for oxygen therapy (if there is cyanosis or cor pulmonale or FEV1< 50% от должных величин).

When formulating the diagnosis of COPD, indicate:
- severity of the disease: mild (stage I), moderate (stage II), severe (stage III) and extremely severe (stage IV), exacerbation or stable course of the disease;
- presence of complications (cor pulmonale, respiratory failure, circulatory failure);
- risk factors and smoking index;
- in case of severe disease, it is recommended to indicate the clinical form of COPD (emphysematous, bronchitis, mixed).

Laboratory diagnostics

1. Blood gas study performed in patients with increasing shortness of breath, a decrease in FEV1 values ​​less than 50% of the predicted value, and in patients with clinical signs of respiratory failure or failure of the right heart.

Respiratory failure criterion(when breathing air at sea level) - PaO 2 less than 8.0 kPa (less than 60 mm Hg) regardless of the increase in PaCO 2. It is preferable to take samples for analysis by arterial puncture.

2. Clinical blood test:
- during exacerbation: neutrophilic leukocytosis with a band shift and an increase in ESR;
- with a stable course of COPD, there are no significant changes in the content of leukocytes;
- with the development of hypoxemia, polycythemic syndrome is observed (increased number of red blood cells, high Hb level, low ESR, increased hematocrit > 47% in women and > 52% in men, increased blood viscosity);
- detected anemia may cause the onset or worsening of shortness of breath.

3. Immunogram carried out to identify signs of immune deficiency with the steady progression of COPD.

4. Coagulogram carried out for polycythemia to select adequate disaggregating therapy.

5. Sputum cytology is carried out to identify the inflammatory process and its severity, as well as to identify atypical cells (given the advanced age of the majority of COPD patients, there is always oncological suspicion).
If there is no sputum, the method of studying induced sputum is used, i.e. collected after inhalation of hypertonic sodium chloride solution. The study of sputum smears with Gram staining allows for an approximate identification of the group affiliation (Gram-positive, gram-negative) of the pathogen.

6. Sputum culture carried out to identify microorganisms and select rational antibiotic therapy in the presence of persistent or purulent sputum.

Differential diagnosis

The main disease with which it is necessary to differentiate COPD is bronchial asthma.

Main criteria for differential diagnosis of COPD and bronchial asthma

Signs	COPD	Bronchial asthma
Age of onset	Typically over 35-40 years old	Most often children and young people 1
History of smoking	Characteristic	Uncharacteristic
Extrapulmonary manifestations of allergy 2	Uncharacteristic	Characteristic
Symptoms (cough and shortness of breath)	Constant, progresses slowly	Clinical variability, appear in paroxysms: throughout the day, day by day, seasonally
Family history of asthma	Uncharacteristic	Characteristic
Bronchial obstruction	Irreversible or irreversible	Reversible
Daily variability PSV	< 10%	> 20%
Bronchodilator test	Negative	Positive
Presence of cor pulmonale	Typically in severe cases	Uncharacteristic
Inflammation type 3	Neutrophils predominate, increased macrophages (++), increase CD8+ T lymphocytes	Eosinophils predominate, increased macrophages (+), increased CD+ Th2 lymphocytes, mast cell activation
Inflammatory mediators	Leukotriene B, interleukin 8, tumor necrosis factor	Leukotriene D, interleukins 4, 5, 13
Efficacy of therapyGKS	Low	High

1 Bronchial asthma can begin in middle and old age
2 Allergic rhinitis, conjunctivitis, atopic dermatitis, urticaria
3 The type of airway inflammation is most often determined by cytological examination of sputum and fluid obtained from bronchoalveolar lavage.

The following can provide assistance in doubtful cases of diagnosing COPD and bronchial asthma: signs identifying bronchial asthma:

1. An increase in FEV1 by more than 400 ml in response to inhalation of a short-acting bronchodilator or an increase in FEV1 by more than 400 ml after 2 weeks of treatment with prednisolone 30 mg/day for 2 weeks (in patients with COPD, FEV1 and FEV1/FVC as a result of treatment does not reach normal values).

2. Reversibility of bronchial obstruction is the most important differential diagnostic feature. It is known that in patients with COPD after taking a bronchodilator, the increase in FEV1 is less than 12% (and ≤200 ml) from the initial one, and in patients with bronchial asthma, FEV1, as a rule, exceeds 15% (and > 200 ml).

3. Approximately 10% of COPD patients also have signs of bronchial hyperresponsiveness.

Other diseases

1. Heart failure. Signs:
- wheezing in the lower parts of the lungs - during auscultation;
- significant decrease in left ventricular ejection fraction;
- dilatation of the heart;
- expansion of the contours of the heart, congestion (up to pulmonary edema) - on an x-ray;
- restrictive type disorders without airflow limitation - when studying pulmonary function.

2. Bronchiectasis. Signs:
- large volumes of purulent sputum;
- frequent association with bacterial infection;
- rough moist rales of different sizes - during auscultation;
- symptom of “drumsticks” (flask-shaped thickening of the terminal phalanges of the fingers and toes);

Expansion of the bronchi and thickening of their walls - on an x-ray or CT scan.

3. Tuberculosis. Signs:
- begins at any age;
- infiltration in the lungs or focal lesions - with radiography;
- high incidence in this region.

If pulmonary tuberculosis is suspected, the following is required:
- tomography and/or CT scan of the lungs;
- microscopy and culture of Mycobacterium tuberculosis sputum, including the flotation method;
- study of pleural exudate;
- diagnostic bronchoscopy with biopsy for suspected bronchial tuberculosis;
- Mantoux test.

4. Bronchiolitis obliterans. Signs:
- development at a young age;
- no connection with smoking has been established;
- contact with vapors, smoke;
- foci of reduced density during exhalation - on CT;
- rheumatoid arthritis is often present.

Complications

- acute or chronic respiratory failure;
- secondary polycythemia;
- chronic pulmonary heart disease;
- pneumonia;
- spontaneous pneumothorax Pneumothorax is the presence of air or gas in the pleural cavity.
;
- pneumomediastinum Pneumomediastinum is the presence of air or gas in the mediastinal tissue.
.

Treatment abroad

Get treatment in Korea, Israel, Germany, USA

Get advice on medical tourism

Treatment

Treatment goals:
- prevention of disease progression;
- relief of symptoms;
- increasing tolerance to physical activity;
- improving the quality of life;
- prevention and treatment of complications;
- prevention of exacerbations;
- reduction in mortality.

Main areas of treatment:
- reducing the influence of risk factors;
- educational programs;
- treatment of COPD in stable condition;
- treatment of exacerbation of the disease.

Reducing the influence of risk factors

Smoking
Smoking cessation is the first mandatory step in the COPD treatment program, as well as the single most effective way to reduce the risk of developing COPD and prevent progression of the disease.

The Tobacco Addiction Treatment Guide contains 3 programs:
1. Long-term treatment program with the goal of completely quitting smoking - intended for patients with a strong desire to quit smoking.

2. A short treatment program to reduce smoking and increase motivation to quit smoking.
3. Smoking reduction program designed for patients who do not want to quit smoking, but are ready to reduce its intensity.

Industrial hazards, atmospheric and household pollutants
Primary preventive measures consist of eliminating or reducing the influence of various pathogenic substances in the workplace. Secondary prevention is no less important - epidemiological control and early detection of COPD.

Educational programs
Education plays an important role in the treatment of COPD, especially education of patients to encourage them to quit smoking.
Key points of educational programs for COPD:
1. Patients must understand the nature of the disease and be aware of the risk factors leading to its progression.
2. Training must be adapted to the needs and environment of the individual patient, and must be appropriate to the intellectual and social level of the patient and those caring for him.
3. It is recommended to include the following information in training programs: smoking cessation; basic information about COPD; general approaches to therapy, specific treatment issues; self-management skills and decision-making during an exacerbation.

Treatment of patients with COPD in stable condition

Drug therapy

Bronchodilators are the basis of symptomatic treatment of COPD. All categories of bronchodilators increase exercise tolerance even in the absence of changes in FEV1. Inhalation therapy is preferred.
For all stages of COPD, it is necessary to exclude risk factors, annual vaccination with influenza vaccine and use short-acting bronchodilators as needed.

Short acting bronchodilators are used in patients with COPD as empirical therapy to reduce the severity of symptoms and limit physical activity. They are usually used every 4-6 hours. In COPD, regular use of short-acting β2-agonists as monotherapy is not recommended.

Long acting bronchodilators or their combination with short-acting β2-agonists and short-acting anticholinergics are prescribed to patients who remain symptomatic despite monotherapy with short-acting bronchodilators.

General principles of pharmacotherapy

1. In case of mild (stage I) COPD and the absence of clinical manifestations of the disease, regular drug therapy is not required.

2. For patients with intermittent symptoms of the disease, inhaled β2-agonists or short-acting M-anticholinergics are indicated, which are used as required.

3. If inhaled bronchodilators are not available, long-acting theophylline may be recommended.

4. Anticholinergic drugs are considered the first choice for moderate, severe and extremely severe COPD.

5. The short-acting M-anticholinergic (ipratropium bromide) has a longer-lasting bronchodilator effect compared to short-acting β2-agonists.

6. According to research, the use of tiotropium bromide is effective and safe in the treatment of patients with COPD. It has been shown that taking tiotropium bromide once a day (compared to salmeterol twice a day) leads to a more pronounced improvement in lung function and a decrease in shortness of breath.
Tiotropium bromide reduces the incidence of exacerbations of COPD with 1-year use compared to placebo and ipratropium bromide and with 6-month use compared to salmeterol.
Thus, tiotropium bromide, used once a day, seems to be the best basis for the combined treatment of stage II-IV COPD.

7. Xanthines are effective for COPD, but are “second-line” drugs due to their potential toxicity. For more severe disease, xanthines can be added to regular inhaled bronchodilator therapy.

8. In stable COPD, the use of a combination of anticholinergic drugs with short-acting β2-agonists or long-acting β2-agonists is more effective.
Nebulizer therapy with bronchodilators is indicated for patients with COPD stages III and IV. To clarify the indications for nebulizer therapy, PEF is monitored for 2 weeks of treatment; therapy continues even if the peak expiratory flow rate improves.

9. If bronchial asthma is suspected, trial treatment with inhaled corticosteroids is carried out.
The effectiveness of GCS in COPD is lower than in bronchial asthma, and therefore their use is limited. Long-term treatment with inhaled corticosteroids in patients with COPD is prescribed in addition to bronchodilator therapy in the following cases:

If the patient experiences a significant increase in FEV1 in response to this treatment;
- with severe/extremely severe COPD and frequent exacerbations (3 times or more in the last 3 years);
- regular (continuous) treatment with inhaled corticosteroids is indicated for patients with stages III and IV COPD with repeated exacerbations of the disease, requiring the use of antibiotics or oral corticosteroids at least once a year.
When the use of inhaled GCS is limited for economic reasons, it is possible to prescribe a course of systemic GCS (for no longer than 2 weeks) to identify patients with a pronounced spirometric response.

Systemic corticosteroids are not recommended for stable COPD.

Treatment regimen with bronchodilators at various stages of COPD without exacerbation

1. At the mild stage (I): treatment with bronchodilators is not indicated.

2. At moderate (II), severe (III) and extremely severe (IV) stages:
- regular use of short-acting M-anticholinergics or
- regular use of long-acting M-anticholinergics or
- regular use of long-acting β2-agonists or
- regular use of short- or long-acting M-anticholinergics + short- or long-acting inhaled β2-agonists or
- regular use of long-acting M-anticholinergics + long-acting theophyllines or
- inhaled long-acting β2-agonists + long-acting theophyllines or
- regular use of short- or long-acting M-anticholinergics + short- or long-acting inhaled β2-agonists + theophyllines
long acting

Examples of treatment regimens at various stages of COPD without exacerbation

All stages(I, II, III, IV)
1. Elimination of risk factors.
2. Annual vaccination with influenza vaccine.
3. If necessary, inhale one of the following drugs:

Salbutamol (200-400 mcg);
- fenoterol (200-400 mcg);
- ipratropium bromide (40 mcg);

Fixed combination of fenoterol and ipratropium bromide (2 doses).

Stages II, III, IV
Regular inhalations:
- ipratropium bromide 40 mcg 4 times a day. or
- tiotropium bromide 18 mcg 1 time / day. or
- salmeterol 50 mcg 2 times a day. or
- formoterol "Turbuhaler" 4.5-9.0 mcg or
- formoterol "Autohaler" 12-24 mcg 2 times a day. or
- fixed combination of fenoterol + ipratropium bromide 2 doses 4 times a day. or
- ipratropium bromide 40 mcg 4 times a day. or tiotropium bromide 18 mcg 1 time / day. + salmeterol 50 mcg 2 times a day. (or formoterol "Turbuhaler" 4.5-9.0 mcg or formoterol "Autohaler" 12-24 mcg 2 times a day or ipratropium bromide 40 mcg 4 times a day) or
- tiotropium bromide 18 mcg 1 time per day + orally theophylline 0.2-0.3 g 2 times per day. or (salmeterol 50 mcg 2 times a day or formoterol "Turbuhaler" 4.5-9.0 mcg) or
- ormoterol "Autohaler" 12-24 mcg 2 times a day. + orally theophylline 0.2-0.3 g 2 times/day. or ipratropium bromide 40 mcg 4 times a day. or
- tiotropium bromide 18 mcg 1 time / day. + salmeterol 50 mcg 2 times a day. or formoterol "Turbuhaler" 4.5-9.0 mcg or
- formoterol "Autohaler" 12-24 mcg 2 times a day + orally theophylline 0.2-0.3 g 2 times a day.

Stages III and IV:

Beclomethasone 1000-1500 mcg/day. or budesonide 800-1200 mcg/day. or
- fluticasone propionate 500-1000 mcg/day. - with repeated exacerbations of the disease, requiring the use of antibiotics or oral corticosteroids at least once a year, or

Fixed combination of salmeterol 25-50 mcg + fluticasone propionate 250 mcg (1-2 doses 2 times / day) or formoterol 4.5 mcg + budesonide 160 mcg (2-4 doses 2 times / day) the same indications, as for inhaled corticosteroids.

As the disease progresses, the effectiveness of drug therapy decreases.

Oxygen therapy

The main cause of death in patients with COPD is acute respiratory failure. In this regard, correction of hypoxemia with oxygen is the most reasonable method of treating severe respiratory failure.
In patients with chronic hypoxemia, long-term oxygen therapy (LOT) is used, which helps reduce mortality.

VCT is indicated for patients with severe COPD if the possibilities of drug therapy have been exhausted and the maximum possible therapy does not lead to an increase in O 2 above the limit values.
The goal of DCT is to increase PaO 2 to at least 60 mm Hg. at rest and/or SatO 2 - at least 90%. DCT is not indicated for patients with moderate hypoxemia (PaO 2 > 60 mm Hg). Indications for VCT should be based on gas exchange parameters, which were assessed only during the stable condition of patients (3-4 weeks after an exacerbation of COPD).

Indications for continuous oxygen therapy:
- RaO 2< 55 мм рт.ст. или SatO 2 < 88% в покое;
- RaO 2 - 56-59 mm Hg. or SatO 2 - 89% in the presence of chronic cor pulmonale and/or erythrocytosis (hematocrit > 55%).

Indications for “situational” oxygen therapy:
- decrease in RaO 2< 55 мм рт.ст. или SatO 2 < 88% при физической нагрузке;
- decrease in RaO 2< 55 мм рт.ст. или SatO 2 < 88% во время сна.

Destination modes:
- O2 flow 1-2 l/min. - for most patients;
- up to 4-5 l/min. - for the most severely ill patients.
At night, during physical activity and during air travel, patients should increase their oxygen flow by an average of 1 L/min. compared to the optimal daily flow.
According to international studies MRC and NOTT (from nocturnal oxygen therapy), VCT is recommended for at least 15 hours a day. with breaks not exceeding 2 hours in a row.

Possible side effects of oxygen therapy:
- violation of mucociliary clearance;
- decreased cardiac output;
- decrease in minute ventilation, carbon dioxide retention;
- systemic vasoconstriction;
- pulmonary fibrosis.

Long-term mechanical ventilation

Noninvasive ventilation is performed using a mask. Helps improve the gas composition of arterial blood, reduce hospitalization days and improve the quality of life of patients.
Indications for long-term mechanical ventilation in patients with COPD:
- PaCO 2 > 55 mm Hg;
- PaCO 2 within 50-54 mm Hg. in combination with nocturnal desaturation and frequent episodes of hospitalization of the patient;
- shortness of breath at rest (respiratory rate > 25 per minute);
- participation in breathing of auxiliary muscles (abdominal paradox, alternating rhythm - alternation of thoracic and abdominal types of breathing.

Indications for artificial ventilation of the lungs in acute respiratory failure in patients with COPD

Absolute readings:
- stopping breathing;
- severe disturbances of consciousness (stupor, coma);
- unstable hemodynamic disorders (systolic blood pressure< 70 мм рт.ст., ЧСС < 50/мин или >160/min);
- fatigue of the respiratory muscles.

Relative readings:
- respiratory rate > 35/min;
- severe acidosis (arterial blood pH< 7,25) и/или гиперкапния (РаСО 2 > 60 mmHg);
- RaO 2 < 45 мм рт.ст., несмотря на проведение кислородотерапии.
- ineffectiveness of non-invasive ventilation.

Protocol for the management of patients with exacerbation of COPD in the intensive care unit.
1. Assessment of the severity of the condition, radiography of the respiratory organs, blood gas composition.
2. Oxygen therapy 2-5 l/min., at least 18 hours/day. and/or non-invasive ventilation.
3. Repeated control of the gas composition after 30 minutes.
4. Bronchodilator therapy:

4.1 Increasing the dosage and frequency of administration. Ipratropium bromide solution 0.5 mg (2.0 ml) via oxygen nebulizer in combination with solutions of short-acting β2-agonists: salbutamol 5 mg or fenoterol 1.0 mg (1.0 ml) every 2-4 hours.
4.2 Combination of fenoterol and ipratropium bromide (Berodual). Berodual solution 2 ml through a nebulizer with oxygen, every 2-4 hours.
4.3 Intravenous administration of methylxanthines (if ineffective). Eufillin 240 mg/hour. up to 960 mg/day. IV at an administration rate of 0.5 mg/kg/h. under ECG control. The daily dose of aminophylline should not exceed 10 mg/kg of the patient’s body weight.
5. Systemic corticosteroids intravenously or orally. Orally - 0.5 mg/kg/day. (40 mg/day for 10 days), if oral administration is not possible - parenterally up to 3 mg/kg/day. A combined route of administration, intravenous and oral administration, is possible.
6. Antibacterial therapy (orally or intravenously for signs of bacterial infection).
7. Anticoagulants subcutaneously for polycythemia.
8. Treatment of concomitant diseases (heart failure, cardiac arrhythmias).
9. Non-invasive ventilation.
10. Invasive pulmonary ventilation (IVL).

Exacerbation of COPD

1. Treatment of exacerbation of COPD on an outpatient basis.

In case of mild exacerbation, an increase in the dose and/or frequency of taking bronchodilators is indicated:
1.1 Anticholinergic drugs are added (if not previously used). Preference is given to inhaled combination bronchodilators (anticholinergic drugs + short-acting β2-agonists).

1.2 Theophylline - if it is impossible to use inhaled forms of drugs or their insufficient effectiveness.
1.3 Amoxicillin or macrolides (azithromycin, clarithromycin) - for bacterial exacerbations of COPD.

For moderate exacerbations, along with increased bronchodilator therapy, amoxicillin/clavulanate or second generation cephalosporins (cefuroxime axetil) or respiratory fluoroquinolones (levofloxacin, moxifloxacin) are prescribed for at least 10 days.
In parallel with bronchodilator therapy, systemic corticosteroids are prescribed in a daily dose of 0.5 mg/kg/day, but not less than 30 mg of prednisolone per day or another systemic corticosteroid in an equivalent dose for 10 days, followed by discontinuation.

2. Treatment of exacerbation of COPD in an inpatient setting.

2.1 Oxygen therapy 2-5 l/min, at least 18 hours/day. with monitoring of blood gas composition after 30 minutes.

2.2 Bronchodilator therapy:
- increasing the dosage and frequency of administration; solutions of ipratropium bromide - 0.5 mg (2 ml: 40 drops) through a nebulizer with oxygen in combination with solutions of salbutamol (2.5-5.0 mg) or fenoterol - 0.5-1.0 mg (0.5- 1.0 ml: 10-20 drops) - “on demand” or
- fixed combination of fenoterol and anticholinergic agent - 2 ml (40 drops) through a nebulizer with oxygen - “on demand”.
- intravenous administration of methylxanthines (if ineffective): aminophylline 240 mg/hour to 960 mg/day. IV at an administration rate of 0.5 mg/kg/h. under ECG control.

2.3 Systemic corticosteroids intravenously or orally. Orally 0.5 mg/kg/day. (40 mg/day of prednisolone or other SCS in an equivalent dose for 10 days), if oral administration is not possible - parenterally up to 3 mg/kg/day.

2.4 Antibacterial therapy (orally or intravenously for signs of bacterial infection):

2.4.1 Simple (uncomplicated) exacerbation: drug of choice (one of the following) orally (7-14 days):
- amoxicillin (0.5-1.0 g) 3 times/day.
Alternative drugs (one of the following) by mouth:
- azithromycin (500 mg) 1 time/day. according to the scheme;
- amoxicillin/clavulanate (625) mg 3 times/day. or (1000 mg) 2 times/day;
- cefuroxime axetil (750 mg) 2 times/day;
- clarithromycin SR (500 mg) 1 time/day;
- clarithromycin (500 mg) 2 times/day;

- moxifloxacin (400 mg) 1 time/day.

2.4.2 Complicated exacerbation: drug of choice and alternative drugs (one of the following) IV:
- amoxicillin/clavulanate 1200 mg 3 times/day;
- levofloxacin (500 mg) 1 time/day;
- moxifloxacin (400 mg) 1 time/day.
If you suspect the presence of Ps. aeruginosa for 10-14 days:
- ciprofloxacin (500 mg) 3 times/day. or
- ceftazidime (2.0 g) 3 times a day.

After IV antibacterial therapy, one of the following drugs is prescribed orally for 10-14 days:
- amoxicillin/clavulanate (625 mg) 3 times/day;
- levofloxacin (500 mg) 1 time/day;
- moxifloxacin (400 mg) 1 time/day;
- ciprofloxacin (400 mg) 2-3 times/day.

Forecast

The prognosis for COPD is conditionally unfavorable. The disease progresses slowly and steadily; as it develops, the patients’ ability to work is steadily lost.
Continued smoking usually contributes to the progression of airway obstruction, leading to early disability and shortened life expectancy. After quitting smoking, the decline in FEV1 and disease progression slow down. To alleviate the condition, many patients are forced to take medications in gradually increasing doses for the rest of their lives, and also use additional medications during exacerbations.
Adequate treatment significantly slows down the development of the disease, up to periods of stable remission for several years, but does not eliminate the cause of the development of the disease and the resulting morphological changes.

Among other diseases, COPD is the fourth leading cause of death in the world. Mortality depends on the presence of concomitant diseases, the age of the patient and other factors.

BODE method(Body mass index, Obstruction, Dyspnea, Exercise) provides a combined score that predicts subsequent survival better than any of the above indicators taken separately. Currently, research into the properties of the BODE scale as a tool for quantitative assessment of COPD is ongoing.

Risk of complications, hospitalization and mortality in COPD

Severity according to the GOLD spirometric classification

Number of complications per year

Number of hospitalizations per year - the patient is able to take long-acting bronchodilators (β2-agonists and/or anticholinergic drugs) in combination with or without inhaled corticosteroids; Short-acting inhaled β2-agonists should be taken no more frequently than every 4 hours; The patient is able (if he was previously treated as an outpatient) to move around the room independently; The patient is able to eat and can sleep without frequent awakenings due to shortness of breath; Clinical stability for 12-24 hours; Stable arterial blood gas values ​​for 12-24 hours; The patient or home care provider fully understands the correct dosage regimen; Issues of further monitoring of the patient have been resolved (for example, visits to the patient by a nurse, supply of oxygen and food); - the patient, family and doctor are confident that the patient can successfully manage at home. Global strategy for the diagnosis, treatment and prevention of chronic obstructive pulmonary disease (revision 2011) / trans. from English edited by Belevsky A.S., M.: Russian Respiratory Society, 2012 Longmore M., Wilkinson Y., Rajagopalan S. Oxford Handbook of Clinical Medicine / ed. prof. Doctor of Medicine Sciences Shustova S.B. and Ph.D. honey. Sciences Popova I.I., M.: Binom, 2009 Ostronosova N.S. Chronic obstructive pulmonary disease (clinic, diagnostics, treatment and examination of working capacity), M.: Academy of Natural Sciences", 2009 Chuchalin A.G. Pulmonology. Clinical guidelines, M.: GEOTAR-Media, 2008 http://lekmed.ru/info/literatura/hobl.html wikipedia.org (Wikipedia) Information Patients with COPD, as a rule, are treated on an outpatient basis, without issuing a certificate of incapacity for work. Criteria for disability in COPD(Ostronosova N.S., 2009): 1. COPD in the acute stage. 2. The emergence or worsening of respiratory failure and heart failure. 3. The occurrence of acute complications (acute or chronic respiratory failure, heart failure, pulmonary hypertension, cor pulmonale, secondary polycythemia, pneumonia, spontaneous pneumothorax, pneumomediastinum). The period of temporary disability ranges from 10 days or more, and the following factors are taken into account: - phase and severity of the disease; - state of bronchial patency; - the degree of functional disorders of the respiratory and cardiovascular systems; - complications; - nature of work and working conditions. Criteria for discharging patients to work: - improvement of the functional state of the bronchopulmonary and cardiovascular systems; - improvement of indicators of exacerbation of the inflammatory process, including laboratory and spirometric indicators, as well as the X-ray picture (with associated pneumonia). Patients are not contraindicated from working in an office environment. Work activity factors that negatively affect the health status of patients with COPD: - unfavorable weather conditions; - contact with toxic substances that irritate the respiratory tract, allergens, organic and inorganic dust; - frequent travel, business trips. Such patients, in order to prevent recurrence of exacerbations of COPD and complications, should be employed according to the conclusion of the clinical expert commission (CEC) of the medical institution for various periods (1-2 months or more), and in some cases referred for medical and social examination (ITU). When referring for a medical and social examination, disability (moderate, severe or severe) is taken into account, primarily associated with dysfunction of the respiratory (DNI, DNII, DNIII) and cardiovascular systems (CI, CHII, CHIII), as well as professional history of the patient. With mild severity during an exacerbation, the estimated period of temporary disability in patients with COPD is 10-12 days. With moderate severity, temporary disability in patients with COPD is 20-21 days. For severe severity - 21-28 days. In extremely severe cases - more than 28 days. The average period of temporary disability is up to 35 days, of which inpatient treatment is up to 23 days. With I degree of DN shortness of breath in patients occurs with previously available physical effort and moderate physical stress. Patients indicate shortness of breath and cough, which appears when walking quickly or climbing uphill. On examination, slight cyanosis of the lips, tip of the nose, and ears is noted. Respiratory rate - 22 breaths per minute; FVD changed slightly; Vital vital capacity decreases from 70% to 60%. There is a slight decrease in arterial blood oxygen saturation from 90% to 80%. In case of II degree of respiratory failure (DNII) shortness of breath occurs during normal exertion or under the influence of minor physical stress. Patients complain of shortness of breath when walking on level ground, fatigue, and cough. Examination reveals diffuse cyanosis, hypertrophy of the neck muscles, which take an auxiliary part in the act of breathing. Respiratory rate - up to 26 breaths per minute; there is a significant change in respiratory function; Vital life capacity decreases to 50%. Arterial blood oxygen saturation decreases to 70%. In case of III degree of respiratory failure (DNIII) shortness of breath occurs with the slightest physical exertion and at rest. Severe cyanosis and hypertrophy of the neck muscles are noted. Pulsation in the epigastric region and swelling of the legs may be detected. Respiratory rate - 30 breaths per minute and above. X-ray reveals a significant enlargement of the right heart. FVD indicators are sharply deviated from the proper values; Vital vital capacity - below 50%. Arterial blood oxygen saturation decreases to 60% or lower. The ability to work of patients with COPD without respiratory failure outside the acute stage was preserved. Such patients have access to a wide range of jobs in favorable conditions. Extremely severe COPD with exacerbations 5 times a year characterized by the severity of clinical, radiological, radionuclide, laboratory and other indicators. Patients experience shortness of breath of more than 35 breaths per minute, cough with purulent sputum, often in large quantities. X-ray examination reveals diffuse pneumosclerosis, emphysema, and bronchiectasis. FVD indicators are sharply deviated from normal values, vital capacity is below 50%, FEV1 is less than 40%. Ventilation indicators are reduced from normal. Capillary blood circulation is reduced. ECG: severe overload of the right heart, conduction disturbances, blockade of the right bundle branch, changes in the T wave and displacement of the ST segment below the isoline, diffuse changes in the myocardium. As the disease progresses, changes in biochemical blood parameters - fibrinogen, prothrombin, transaminase - increase; the number of red blood cells and hemoglobin content in the blood increases due to increasing hypoxia; the number of leukocytes increases; possible appearance of eosinophilia; ESR increases. In the presence of complications in patients with COPD with concomitant diseases from the cardiovascular system (coronary heart disease, stage II arterial hypertension, rheumatic heart defects, etc.), neuropsychiatric, the duration of inpatient treatment increases to 32 days, and the total duration - to 40 days. Patients with rare, short-term exacerbations with DHI need a job according to the conclusion of the CEC. In cases where exemption from the above factors will entail the loss of a qualified profession with a constant speech load (singers, lecturers, etc.) and strain on the respiratory apparatus (glassblowers, brass band musicians, etc.), patients with COPD are subject to referral to MSE for establishment of disability group III due to moderate limitation of life activity (according to the criterion of limitation of work activity of the first degree). Such patients are prescribed light physical labor in non-contraindicated production conditions and mental labor with moderate psycho-emotional stress. For severe, frequent, prolonged exacerbations of COPD with DNII, CHI or DNII-III, CHIIA, CHIIB Patients should be referred to MSE to determine their II disability group due to severe limitations in life activity (according to the criteria of II degree limitation of abilities for self-care and movement and II degree labor activity). In some cases, work in specially created conditions, at home, may be recommended. Significantly expressed disorders of the respiratory and cardiovascular systems: DNIII in combination with CHIII(decompensated cor pulmonale) define disability group I due to pronounced limitation of life activity (according to the criterion of limited ability to self-care, movement - III degree), clinical changes, morphological disorders, decreased external respiratory function and developing hypoxia. Thus, to correctly assess the severity of COPD, the duration of temporary disability, clinical and work prognosis, and conduct effective medical and social rehabilitation, a timely comprehensive examination of patients is necessary to determine the state of bronchial obstruction, the degree of functional disorders of the respiratory and cardiovascular systems, complications, and concomitant diseases. , nature of work and working conditions. Attention! By self-medicating, you can cause irreparable harm to your health. The information posted on the MedElement website and in the mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Guide" cannot and should not replace a face-to-face consultation with a doctor. Be sure to contact a medical facility if you have any illnesses or symptoms that concern you. The choice of medications and their dosage must be discussed with a specialist. Only a doctor can prescribe the right medicine and its dosage, taking into account the disease and condition of the patient’s body. The MedElement website and mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Directory" are exclusively information and reference resources. The information posted on this site should not be used to unauthorizedly change doctor's orders. The editors of MedElement are not responsible for any personal injury or property damage resulting from the use of this site.