Consequences of chronic obstructive pulmonary disease. What is chronic obstructive pulmonary disease (COPD) Bronchial disease COPD

Pulmonary obstruction is a progressive disease of the broncho-pulmonary system, in which the air in the respiratory tract runs incorrectly. This is due to abnormal inflammation of the lung tissue in response to external stimuli.

This noncommunicable disease, it is not associated with the vital activity of pneumococci. The disease is widespread, according to WHO, 600 million people in the world suffer from pulmonary obstruction. Mortality statistics show that 3 million people die from the disease every year. With the development of megacities, this figure is constantly growing. Scientists believe that in 15-20 years the death rate will double.

The problem of the prevalence and incurability of the disease is the lack of early diagnosis. A person does not attach importance to the first signs of obstruction - cough in the morning and shortness of breath, which appears faster than in peers when performing the same physical activity. Therefore, patients seek medical care at the stage when it is already impossible to stop the pathological destructive process.

Risk factors and mechanism of disease development

Who is at risk of lung obstruction and what are the risk factors for the disease? Smoking comes first. Nicotine several times increases the likelihood of lung obstruction.

Occupational risk factors play an important role in the development of the disease. Professions in which a person is constantly in contact with industrial dust (ore, cement, chemicals):

• miners;
• builders;
• workers in the pulp processing industry;
• railroad workers;
• metallurgists;
• grain and cotton workers.

Atmospheric particles that can serve as a trigger in the development of the disease are exhaust gases, industrial emissions, industrial waste.

Also, hereditary predisposition plays a role in the occurrence of pulmonary obstruction. Internal risk factors include airway tissue hypersensitivity and lung growth.

The lungs produce special enzymes - protease and anti-protease. They regulate the physiological balance of metabolic processes, maintain the tone of the respiratory system. When there is a systematic and prolonged exposure to air pollutants (harmful air particles), this balance is disturbed.

As a result, the skeleton function of the lungs is impaired. This means that the alveoli (lung cells) collapse, lose their anatomical structure. Numerous bullae (formations in the form of vesicles) form in the lungs. Thus, the number of alveoli gradually decreases and the rate of gas exchange in the organ decreases. People begin to feel severe shortness of breath.

The inflammatory process in the lungs is a reaction to pathogenic aerosol particles and progressive airflow limitation.

Stages of development of pulmonary obstruction:

• tissue inflammation;
• pathology of small bronchi;
• destruction of the parenchyma (lung tissues);
• air flow limitation.

Symptoms of lung obstruction

Obstructive airways disease is characterized by three main symptoms: shortness of breath, cough, sputum production.

The first symptoms of the disease are associated with respiratory failure.. The person is out of breath. It is difficult for him to climb several floors. Going to the store takes more time, a person constantly stops to catch his breath. It becomes difficult to leave the house.

Development system of progressive dyspnea:

• initial signs of shortness of breath;
• difficulty breathing with moderate physical activity;
• gradual limitation of loads;
• a significant reduction in physical activity;
• shortness of breath when walking slowly;
• refusal of physical activity;
• persistent shortness of breath.

Patients with pulmonary obstruction develop a chronic cough. It is associated with partial obstruction of the bronchi. Cough is constant, daily, or intermittent, with ups and downs. As a rule, the symptom is worse in the morning and may appear during the day. At night, coughing does not bother a person.

Shortness of breath is progressive and persistent (daily) and only gets worse over time. It also increases with physical activity and respiratory diseases.

With obstruction of the lungs in patients, sputum discharge is recorded. Depending on the stage and neglect of the disease, mucus can be scanty, transparent or abundant, purulent.

The disease leads to chronic insufficiency respiration - the inability of the pulmonary system to provide high-quality gas exchange. Saturation (oxygen saturation of arterial blood) does not exceed 88%, at a rate of 95-100%. This is a life threatening condition. In the last stages of the disease, a person may experience apnea at night - suffocation, stopping lung ventilation for more than 10 seconds, on average it lasts half a minute. In extremely severe cases, respiratory arrest lasts 2-3 minutes.

In the daytime one feels severe fatigue, drowsiness, instability of the heart.

Lung obstruction leads to early disability and a reduction in life expectancy, a person acquires disability status.

Obstructive changes in the lungs in children

Pulmonary obstruction in children develops due to respiratory diseases, malformations of the pulmonary system, chronic pathologies of the respiratory system. Of no small importance is the hereditary factor. The risk of developing pathology increases in a family where parents constantly smoke.

Obstruction in children is fundamentally different from obstruction in adults. Blockage and destruction of the airways are the result of one of the nosological forms (a certain independent disease):

1. Chronical bronchitis. The child has a wet cough, wheezing of various sizes, exacerbations up to 3 times a year. The disease is a consequence of the inflammatory process in the lungs. The initial obstruction occurs due to excess mucus and sputum.
2. Bronchial asthma. Although bronchial asthma and chronic pulmonary obstruction are various diseases, in children they are interconnected. Asthmatics are at risk of developing obstruction.
3. bronchopulmonary dysplasia. This chronic pathology in babies during the first two years of life. The risk group includes premature and underweight children who have had SARS immediately after birth. In such infants, the bronchioles and alveoli are affected, the functionality of the lungs is impaired. Gradually, respiratory failure and oxygen dependence appear. There are gross changes in the tissue (fibrosis, cysts), the bronchi are deformed.
4. Interstitial lung diseases. This is a chronic hypersensitivity of lung tissue to allergenic agents. Develops by inhalation of organic dust. It is expressed by diffuse lesions of the parenchyma and alveoli. Symptoms - cough, wheezing, shortness of breath, impaired ventilation.
5. obliterating bronchiolitis. This is a disease of the small bronchi, which is characterized by narrowing or complete blockage of the bronchioles. Such obstruction in a child is predominantly manifested in the first year of life.. Reason: SARS adenovirus infection. Signs - unproductive, severe, recurrent cough, shortness of breath, weak breathing.

Diagnosis of lung obstruction

When a person contacts a doctor, an anamnesis (subjective data) is collected. Differential symptoms and markers of pulmonary obstruction:

• chronic weakness, decreased quality of life;
• unstable breathing during sleep, loud snoring;
• weight gain;
• increase in the circumference of the collar zone (neck);
• blood pressure is higher than normal;
• pulmonary hypertension (increased pulmonary vascular resistance).

The mandatory examination includes general analysis blood to exclude a tumor, purulent bronchitis, pneumonia, anemia.

A general urine test helps to exclude purulent bronchitis, in which amyloidosis is detected - a violation of protein metabolism.

A general sputum analysis is rarely done, as it is not informative.

Patients undergo peak flowmetry, a functional diagnostic method that evaluates the expiratory rate. This determines the degree of airway obstruction.

All patients undergo spirometry - a functional study of external respiration. Assess the rate and volume of breathing. Diagnosis is carried out on a special device - a spirometer.

During the examination, it is important to exclude bronchial asthma, tuberculosis, obliterating bronchiolitis, bronchiectasis.

Treatment of the disease

The goals of treating obstructive lung disease are multifaceted and include the following steps:

• improvement in respiratory function of the lungs;
• constant monitoring of symptoms;
• increased resistance to physical stress;
• prevention and treatment of exacerbations and complications;
• stop the progression of the disease;
• minimizing the side effects of therapy;
• improving the quality of life;

The only way to stop the rapid destruction of the lungs is to completely stop smoking.

IN medical practice special programs have been developed to combat nicotine addiction in smokers. If a person smokes more than 10 cigarettes a day, then he is shown a drug course of therapy - short up to 3 months, long - up to a year.

Nicotine replacement treatment is contraindicated in such internal pathologies:

• severe arrhythmia, angina pectoris, myocardial infarction;
• circulatory disorders in the brain, stroke;
• ulcers and erosion of the digestive tract.

Patients are prescribed bronchodilator therapy. Basic treatment includes bronchodilators to widen the airways. The drugs are prescribed both intravenously and inhalation. When inhaled, the medicine instantly penetrates into the affected lung, has a quick effect, reduces the risk of developing negative consequences and side effects.

During inhalation, you need to breathe calmly, the duration of the procedure is an average of 20 minutes. With deep breaths, there is a risk of developing a strong cough and choking.

Effective bronchodilators:

• methylxanthines - Theophylline, Caffeine;
• anticholinergics - Atrovent, Berodual, Spiriva;
• b2-agonists - Fenoterol, Salbutamol, Formoterol.

In order to improve survival, patients with respiratory failure are prescribed oxygen therapy (at least 15 hours per day).

To thin the mucus, increase its discharge from the walls of the respiratory tract and expand the bronchi, a complex of drugs is prescribed:

• Guaifenesin;
• Bromhexine;
• Salbutamol.

To consolidate the treatment of obstructive pneumonia, rehabilitation measures are needed. Every day, the patient should conduct physical training, increase strength and endurance. Recommended sports are walking 10 to 45 minutes daily, stationary bike, lifting dumbbells. Nutrition plays an important role. It should be rational, high-calorie, contain a lot of protein. An integral part of the rehabilitation of patients is psychotherapy.

In our country, approximately one million people have chronic obstructive pulmonary disease. But it is possible that this figure is much higher.

The main reason occurrence of COPD is smoking. It doesn't matter if it's passive or active.

This lung disease is characterized by the progression and gradual loss of lung function. In this article, we will talk about the complications of COPD as well as preventive methods that will prevent the development of this disease.

COPD - the definition of the disease

According to statistics, they are more likely to get sick men after forty years. Chronic illness lung disease is one of the causes of disability and ranks fourth among the causes of death among the working population.

There are four stages depending on the forced expiratory volume and forced vital capacity of the lungs:

• Zero stage (stage of predisease). It is characterized by an increased risk of developing chronic obstructive pulmonary disease, but may not always pass into it. Signs: persistent cough with phlegm, but the lungs are still functioning.
• The first stage (the stage of light flow). You can detect minor obstructive disorders, there is a chronic cough with sputum.
• The second stage (the stage of moderate course). There is a progression of disorders.
• The third stage (the stage of severe course). When exhaling, there is an increase in airflow limitation.
• The fourth stage (the stage of extremely severe course). Manifested by a severe form of bronchial obstruction, there is a threat to life.

COPD development mechanism: tobacco smoke or another negative factor affects the vagus nerve receptors, which causes bronchospasm, stops the movement of their ciliated epithelium. Therefore, bronchial mucus cannot come out naturally, and its cells begin to produce even more mucus (defensive reaction). This is how chronic cough occurs. Many smokers think that nothing serious will happen, and they cough because of smoking.

But after a while, a chronic focus of inflammation develops, which clogs the bronchi even more. As a result of this, the alveoli are overstretched, which compress the small bronchioles, further disrupting the patency.

It should be remembered that at the beginning of the disease, the blockage is still reversible, since it occurs due to bronchospasm and mucus hypersecretion.

Therapy of the disease is aimed primarily at slowing down the progression of obstruction and the development of respiratory failure. Treatment helps to reduce the likelihood of exacerbations, and also makes them less severe and longer. Treatment helps to increase vital activity and increases. It is very important to eliminate the cause of the development of the disease.

Causes and treatment during an exacerbation

Nine out of ten cases of COPD are caused by smoking. Other factors affecting the development of the disease to a lesser extent include harmful production conditions (for example, inhalation of harmful gases), respiratory diseases transferred to childhood, bronchopulmonary pathologies, poor ecology.

The main occupational hazards are working with cadmium and silicon, metal processing, and combustion products also affect the development of COPD. Therefore, chronic obstructive pulmonary disease occurs in miners, railway workers, builders, workers in the pulp and paper and metallurgical industries, and agricultural workers.

Very rarely, people have a genetic predisposition to COPD. In this case, there is a lack of alpha-1-antitrypsin protein, which is produced by liver tissue. It is this protein that protects the lungs from damage by the enzyme elastase.

All of the above causes cause a chronic inflammatory lesion of the inner lining of the bronchi, resulting in impaired local bronchial immunity. There is a production of bronchial mucus, it becomes more viscous. Because of this, they create good conditions to activate pathogenic bacteria, bronchial obstruction occurs, lung tissues and alveoli change. As a person's condition worsens with COPD, swelling of the bronchial mucosa develops, smooth muscles spasm, a lot of mucus is produced, and the number of irreversible changes increases.

Symptoms and methods of diagnosis

At the initial stage of the disease, a periodic cough occurs. But the farther, the more often he worries (even at night).

When coughing, a small amount of sputum is secreted, the volume of which increases with exacerbation. Sometimes it may contain pus.

Another symptom of chronic obstructive pulmonary disease is shortness of breath. It can appear very late, even after a decade.

Patients with COPD are divided into two groups:

1. "Pink Puffers". These people are generally thin in build and suffer from shortness of breath, causing them to puff and puff out their cheeks. The skin becomes pink-gray.
2. "Bluish puffers". Usually these are overweight people. They suffer from a strong cough with phlegm, as well as swelling of the legs. Their skin has a blue tint.

The first group of patients has an emphysematous type of COPD. In this case, the main symptom is expiratory dyspnea (difficulty exhaling). Emphysema prevails over bronchial obstruction.

The second group has purulent inflammatory processes occurring in the bronchi and accompanied by symptoms of intoxication, cough with copious sputum (bronchitis type COPD). Bronchial obstruction is more pronounced than pulmonary emphysema.

Complications

Because COPD progresses over time, complications are sometimes unavoidable. But you can reduce the risk of their occurrence. To do this, sometimes you just need to quit smoking, avoid inhaling tobacco smoke and other chemical substances.

If the symptoms of COPD suddenly worsen, then they speak of an exacerbation of the disease. An exacerbation can be caused by infection, environmental pollution, and so on. It can occur up to several times a year.

Complications of chronic obstructive pulmonary disease include:

• Respiratory failure.
• Pneumothorax (air entering the pleural cavity).
• (pneumonia). May be caused by bacteria. Streptococcal pneumonia is considered the most common cause bacterial pneumonia in COPD.
• Blockage of blood vessels (thromboembolism).
• Deformation of the bronchi (bronchiectasis).
• Pulmonary hypertension ( high pressure in pulmonary artery).
• Pulmonary heart (thickening and expansion of the right parts of the heart with dysfunction).
• Lungs' cancer.
• Chronic heart failure, stroke.
• Atrial fibrillation (heart rhythm disorder).
• Depression. Emotional disorders may be associated with a decrease in the activity of life in general.

Prevention

The main direction of prevention of chronic obstructive pulmonary disease is smoking cessation. Need to lead healthy lifestyle life, eat right and balanced, and strengthen the immune system.

Physical activity should include walking at a moderate pace, swimming in the pool and breathing exercises strengthening the respiratory muscles.

Do not forget about the timely treatment of any infectious diseases respiratory tract.

Those whose work involves exposure to harmful substances should be aware of safety precautions and the use of personal protective equipment.

COPD needs to be treated at an early stage. And in order to detect the problem in time, it is recommended to undergo a medical examination.

Unfortunately, the progression of COPD can lead to disability of the patient. An unfavorable outcome is possible with severe concomitant diseases, heart and respiratory failure, advanced age, bronchitis type of the disease.

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conclusions

It is a progressive disease. Cure him to the end on late stages it is impossible, so patients should lead a proper lifestyle, control symptoms, so that you can slow down the development of chronic obstruction.

COPD is dangerous for its complications. To prevent their occurrence, it is necessary proper treatment, the purpose of which is to slow down all progressive processes in the lungs, remove obstructions and exclude respiratory failure.

Patients with shortness of breath, chronic cough, and sputum production are tentatively diagnosed with COPD. What is this disease? This abbreviation stands for "chronic obstructive pulmonary disease". This disease is associated with an increased inflammatory response of the lung tissue to the action of inhaled particles or gases. The disease is characterized by progressive, irreversible (in the final stages) violation of bronchial patency.

Its distinctive feature is the progressive limitation of the air flow rate, which is confirmed only after spirometry - an examination that allows you to assess the state of pulmonary ventilation. Indicator FEV1(forced expiratory volume in the first minute) is an objective criterion for bronchial patency and the severity of obstruction. By size FEV1 evaluate the stage of the disease, judge the progression and evaluate the treatment.

Chronic obstructive pulmonary disease (COPD), what is it, how does it occur and what processes underlie it? Restriction of airflow velocity is caused by damage to the small bronchi (constriction of the bronchi develops -) and destruction of the parenchyma (occurs over time). The degree of prevalence of these two processes in the lung tissue is different in different patients, but one thing is common - it is chronic inflammation of the terminal airways that causes these changes. Common code this disease according to ICD-10 J44 (Other chronic obstructive pulmonary disease).

COPD develops in adults and most patients complain of shortness of breath, cough, and frequent winter colds. There are many reasons that cause this disease. One of the contributing factors is congenital pathology lung and chronic inflammatory diseases lung disease that begins in childhood continues into adolescents and progresses to COPD in adults. This disease in adults is the leading cause of death, so the study of this pathology is of great importance.

Information and teaching about COPD is constantly changing, the possibilities of the most effective treatment and increasing life expectancy. The problem is so urgent that in 1997 International group COPD experts decided to establish the Global COPD Initiative (GOLD). In 2001, the first report of the working group was published. Since then, the reports have been supplemented and republished annually.

The Global COPD Initiative monitors the disease and provides physicians with documents that form the basis for diagnosing and treating COPD. The data is useful not only for doctors, but also for students studying internal illnesses. It is especially necessary to rely on this document if a history of COPD is being written, since the document fully presents the causes of the disease, all stages of its development, and diagnosis. The medical history for therapy will be written correctly, since the document presents the clinic of the disease, the formulation of the diagnosis is proposed and detailed clinical recommendations for treatment are given. different groups patients depending on the severity of the disease.

Almost all documents of the Global COPD Initiative are available on the Internet in Russian. If there are none, then on the official website of GOLD you can find and download the document COPD recommendations gold 2015. The development of exacerbations is characteristic of chronic obstructive pulmonary disease. Gold 2015 defines: “COPD exacerbation is an acute condition characterized by worsening respiratory symptoms. This necessitates a change in the treatment regimen.”

An exacerbation aggravates the patient's condition and is the reason for seeking emergency help, and frequent exacerbations lead to a long-term deterioration in respiratory function. Taking into account possible causes, the presence of an exacerbation, the severity of the disease and an unspecified pathology with severe respiratory failure and chronic cor pulmonale, the COPD code for ICD-10 has several subgroups: J 44.0, J 44.1, J 44.8, J 44.9.

COPD pathogenesis

The pathogenesis is represented by the following mechanisms:

• irritants cause inflammatory process bronchopulmonary system;
• there is an enhanced response to the inflammatory process, the mechanisms of which are not sufficiently elucidated (may be genetically determined);
• the pathological response is expressed in the destruction of the lung tissue, which is associated with an imbalance between proteinases And antiproteinases (in the lung tissue there is an excess of proteinases that destroy the normal parenchyma);
• increased collagen formation (fibrosis), structural changes small bronchi and their narrowing (obstruction), which increases airway resistance;
• obstruction of the airways further prevents the exit of air during exhalation (created "air traps"), develops (increased airiness of the lung tissue due to incomplete emptying of the alveoli during exhalation), which in turn also leads to the formation of "air traps".

In patients with COPD, an increase in the concentrations of oxidative stress markers in sputum and blood is found. Oxidative stress increases with exacerbations. As a result of it and an excess of proteinases, the inflammatory process in the lungs is further enhanced. The inflammatory process continues even when the patient stops smoking. The severity of inflammation in the small bronchi, their fibrosis and the presence of exudate (sputum) are reflected in the degree of decrease in forced expiratory volume in the first second and the ratio FEV1/FZhEL.

Airflow limitation adversely affects the work of the heart and gas exchange. Disturbances in gas exchange lead to hypoxemia And hypercapnia . The transport of oxygen and carbon dioxide worsens as the disease progresses. The basis of exacerbations and progression of the disease is an inflammatory reaction. It begins with damage to the cells of the respiratory tract mucosa. Then specific elements are involved in the process (macrophages, neutrophils, activated interleukins , tumor necrosis factor, leukotriene B4 ). Moreover, the more pronounced the severity of the disease, the more active the inflammation, and its activity is a factor predisposing to exacerbations.

COPD classification

The international GOLD program of 2014 proposed a spirometric classification that reflects the severity (or stage) of obstruction.

But spirometric assessment is not enough, a clear assessment of symptoms and the risk of exacerbation in this patient is also necessary. In 2011, a comprehensive classification was proposed that takes into account the severity of symptoms and the frequency of exacerbations. In this regard, all patients in the international GOLD program are divided into 4 categories:

• A- low risk exacerbations, symptoms are not expressed, less than one exacerbation per year, GOLD 1-2 (according to spirometric classification).
• B - low risk of exacerbation, more symptoms than in the previous group, less than one exacerbation per year, GOLD 1–2 (spirometric classification).
• C - high risk of exacerbations, more than two exacerbations per year, GOLD 3-4.
• D - high risk of exacerbations, more symptoms than in group C, more than two exacerbations per year, GOLD 3-4.

IN clinical classification presented in more detail Clinical signs diseases that determine the severity.

In this classification, moderate severity corresponds to category B.

The course of the disease has the following phases:

• Remission.
• Aggravation.

A stable state (remission) is characterized by the fact that the severity of symptoms practically does not change for a long time (weeks and months).

An exacerbation is a period of deterioration in the condition, which is manifested by an increase in symptoms and a deterioration in the function of external respiration. Lasts 5 days or more. Exacerbations can begin gradually or rapidly with the development of acute respiratory failure.

COPD is a disease that combines many syndromes. To date, two phenotypes of patients are known:

• Emphysematous type (dyspnea predominates, patients have panacinar emphysema, according to appearance they are defined as "pink puffers").
• Bronchitis type (cough with sputum and frequent respiratory infections predominate, in patients, centroacinar emphysema is determined during the study, and in appearance these are “bluish edema”).

These types are isolated from patients with moderate to severe course. The selection of these forms is important for the prognosis. With emphysematous type cor pulmonale develops at a later date. Recently, further study of the disease has made it possible to identify other phenotypes: “female”, “COPD in combination with bronchial asthma”, “with rapid progression”, “with frequent exacerbations”, “α1-antitrypsin deficiency”, “young patients”.

Causes

The etiology (causes and conditions for the onset of the disease) is still being studied, but today it is well established that COPD develops through the interaction of genetic factors and adverse environmental factors. Among the main reasons are:

• Prolonged smoking. Most often, the incidence is directly dependent on this factor, but under equal conditions, the genetic predisposition to the disease matters.
• Genetic factor associated with severe hereditary deficiency α1-antitrypsin . deficit α1-antitrypsin causes destruction of lung tissue and the development of emphysema.
• Atmospheric air pollution.
• Air pollution in residential areas (heating with wood and bio-organic fuels in rooms with poor ventilation).
• Exposure to occupational factors (organic and inorganic dust, gas, smoke, chemicals, steam). In this regard, COPD is considered as an occupational disease in these patients.
• Bronchial asthma and chronic bronchitis in smokers, which increase the risk of developing COPD.
• Congenital pathology of bronchopulmonary structures. Intrauterine damage to the lungs, their improper development increases the risk of developing this disease in adults. Hypoplasia of the lungs along with other malformations of bronchopulmonary structures (sequestration of the lungs, defects in the wall of the trachea and bronchi, lung cysts, malformations of the veins and arteries of the lungs) are the cause of constant bronchopulmonary inflammation and the basis for a chronic inflammatory process. Lung hypoplasia - underdevelopment of the lung parenchyma, a decrease in the number of bronchial branches in combination with their defective wall. Lung hypoplasia usually develops at 6-7 weeks of embryo development.
• Cystic fibrosis. The disease manifests itself in early age, proceeds with purulent bronchitis and severe respiratory failure.

Risk factors include: family history, frequent respiratory tract infections in childhood, low birth weight, and age (aging of the airways and parenchyma resembles the processes that occur in COPD).

Symptoms of COPD

Chronic obstructive pulmonary disease is manifested by progressive shortness of breath, cough with sputum. The severity of these symptoms can change from day to day. The main symptoms of COPD in an adult are shortness of breath and feeling short of breath. It is shortness of breath that is the main cause of disability in patients.

Signs such as a persistent cough and sputum are often the first manifestations of the disease. chronic cough with sputum may appear many years before the development of bronchial obstruction. However, bronchial obstruction can develop without a previous chronic cough.

Auscultation reveals dry rales that occur on inhalation or exhalation. At the same time, the absence of wheezing does not exclude the diagnosis. Cough is most often underestimated by patients and is considered a consequence of smoking. At first, it is present periodically, and over time - every day and almost constantly. Cough in COPD may be without sputum, and its appearance in in large numbers indicates bronchiectasis. With exacerbation, sputum becomes purulent.

In severe and extremely severe cases, the patient develops fatigue, weight loss, lack of appetite, depression and anxiety. These symptoms are associated with the risk of exacerbations and have an unfavorable prognostic value. At strong cough coughs may appear, which are associated with a rapid increase in intrathoracic pressure when coughing. With a strong cough, ribs may occur. Edema lower extremities- a sign of the development of cor pulmonale.

The clinic distinguishes between different types: emphysematous and bronchitis. Emphysematous type - These are patients with reduced nutrition and they do not have cyanosis. The main complaint is shortness of breath and increased work of the respiratory muscles. The patient breathes superficially and exhales air through half-closed lips (“puffs”). The patient's posture is characteristic: in a sitting position, they tilt their torso forward and rest their hands on their legs, thereby facilitating their breathing. The cough is minor. Examination revealed emphysema. The gas composition of the blood is not very changed.

Bronchitis type - due to severe hypoxemia, patients are cyanotic and edematous due to heart failure ("cyanotic edema"). Shortness of breath is minor, and the main manifestation is coughing up sputum and signs of hypercapnia (tremor, headache, confused speech, constant anxiety). Examination reveals cor pulmonale.
Exacerbation of COPD is provoked by a bacterial or viral infection, adverse environmental factors. It is manifested by an increase in all symptoms, a deterioration in spirographic parameters and severe hypoxemia. Each exacerbation aggravates the course of the disease and is an unfavorable prognostic sign.

Analyzes and diagnosis of COPD

Diagnosis of the disease begins with a survey of the patient and the collection of complaints. Below are the main points to look out for and signs of the disease.

Instrumental and functional studies

• Spirometry. This is an important examination to determine the obstruction and its severity. Spirometry and post-bronchodilation spirometry are necessary to diagnose the disease and determine the severity. An FEV1/FVC ratio of less than 0.70 after administration of a bronchodilator (post-bronchodilation spirometry) confirms bronchial obstruction and the diagnosis. Spirometry is also a health assessment tool. Based on a threshold of 0.70, spirometric classification distinguishes into 4 degrees of severity of the disease.
• Plethysmography. Patients with this disease are characterized by air retention in the lungs (increased residual volume). Plethysmography measures total lung capacity and residual volume. As bronchial obstruction increases, hyperinflation develops (the total lung capacity, characteristic of emphysema, increases).
• Pulse oximetry. Shows the degree of saturation of hemoglobin with oxygen, after which conclusions are drawn about oxygen therapy.
• Radiography chest. Conducted to eliminate lung cancer , . During an exacerbation of COPD this method research is carried out to exclude all kinds of complications: pneumonia , pleurisy with effusion , pneumothorax . At mild degree COPD radiological changes are often not detected. As the disease progresses, emphysema (flat diaphragm, x-ray transparent spaces - bullae).
• Computed tomography is usually not performed, but if there is doubt about the diagnosis, the study reveals bullous changes and their prevalence. CT is necessary to resolve the issue of surgical intervention(decrease in lung volume).

The differential diagnosis of the disease depends on age. In children and young adults, with the exclusion of infectious diseases that occur with respiratory symptoms, the probable disease is bronchial asthma . COPD is more common in adults, however, differential diagnosis they should be carried out with bronchial asthma, which differs in clinical manifestations, history, but the main difference is the reversibility of bronchial obstruction in bronchial asthma. That is, the bronchodilation test during spirometry is positive. The main differential diagnostic signs are given in the table.

COPD treatment

Chronic obstructive pulmonary disease occurs with periods of remission and exacerbations. Depending on this, the treatment will be different. Treatment is selected individually, and it differs in the main groups of patients (groups A, B, C, D, mentioned above). Application medicines reduces the severity of symptoms, reduces the frequency of exacerbations, reduces their severity, improves the general condition of the patient. As a result of treatment, exercise tolerance increases.

How and how to treat COPD? All drugs in the treatment of COPD can be divided into main groups:

• Bronchodilators. They increase the forced expiratory volume and change other indicators of spirometry. This is due to the relaxation of the muscles of the bronchi, which eliminates the obstacle to the removal of air. Bronchodilators can be used as needed or regularly. They are represented by different groups of drugs - β2-agonists ( short action and long). Inhaled short-acting β2-agonists are lifesaver drugs used for relief, while long-acting inhalers are used for long-term control of symptoms. Short-acting dosage preparations: (metered dose inhaler 100 mcg dose), (metered dose inhaler 100 mcg dose), Terbutaline (powder inhaler 400 mcg dose). Long-acting: formoterol (, Atimos , ), salmeterol ( sereventer ). Anticholinergic drugs: short acting based on ipratropium bromide (, Ipratropium Aeronative ) and long-acting with active substance thiotripium bromide (, Spiriva Respimat ). Combination of β2-agonists and M-anticholinergics:, Berodual N , Ipramol Steri-Neb , Ultibro Breezhaler . Methylxanthines (tablets and capsules, Teopec , ).
• Inhaled glucocorticosteroids:,.
• Inhalers with a combination of β2-agonists + glucocorticosteroids:, Zenhale .
• α1-antitrypsin replacement therapy. Young adults with severe α1-antitrypsin deficiency and established emphysema are candidates for replacement therapy. But this treatment is very expensive and not available in most countries.
• Mucolytic and antioxidant agents. Wide application these drugs are not recommended, however, in patients with viscous sputum, improvement is noted with the use of mucolytics (carbocysteine ​​and N-acetylcysteine). There is evidence that these drugs may reduce the frequency of exacerbations.

Most important points in the appointment of bronchodilators:

• Long-acting inhaled bronchodilators (both β2-agonists and M-anticholinergics) are the main drugs for maintenance treatment. The list of long-acting drugs is expanding to include 12-hour drugs ( Serevent , Atimos , Bretaris Genuair ) and 24-hour ( , Striverdi Respimat , Spiolto Respimat - combined).
• In the absence of the effect of monotherapy, a combination of a β2-agonist (short-acting or long-term) and an M-anticholinergic is prescribed.
• Inhaled bronchodilators are more effective than tablet forms and have less adverse reactions. has low efficiency and causes side effects, so it is used in cases where it is not possible to purchase expensive long-acting inhaler drugs. Many drugs are available for the nebulizer in the form of solutions. In patients with low inspiratory flow rates, the use of a nebulizer has advantages.
• Combinations of bronchodilators with different mechanisms of action are more effective in dilating the bronchi. Combined drugs: Berodual N , Spiolto Respimat , Ultibro Breezhaler , Anoro Ellipta , Duaklear Genuair , Spiolto Respimat .

When prescribing glucocorticoids, the following are taken into account:

• Limit the use of systemic glucocorticosteroids during an exacerbation to 5 days (dose 40 mg per day).
• The phenotype of COPD-asthma and the presence of eosinophils in sputum is a group of patients in which the use of corticosteroids (systemic and inhaled) is highly effective.
• An alternative to taking hormones orally during an exacerbation are inhaled forms of glucocorticosteroids. Long-term use of inhaled corticosteroids is not recommended, as they are less effective than the combination of β2-agonists + glucocorticoids: salmeterol / fluticasone ( Seretide , Salmecort , ), formoterol/budesonide ( , SymbicortTurbuhaler ), formoterol/beclomethasone (), formoterol/mometasone ( Zenhale ) fluticasone/vilanterol ( Relvar Ellipta - over long-acting).
• Long-term treatment with inhaled glucocorticoids is acceptable in severe or extremely severe form, frequent exacerbations, provided there is insufficient effect from long-acting bronchodilators. Long-term treatment with inhaled hormonal drugs is prescribed only according to indications, since there is a risk side effects(pneumonia, fractures).

The following treatment regimens for patients of various groups are proposed:

Patients in group A have mild symptoms and a low risk of exacerbations. Such patients are not indicated for the appointment of bronchodilators, however, sometimes they may need to use "on demand" short-acting bronchodilators.

In group B patients clinical picture moderate severity, but the risk of exacerbations is low. They are prescribed long-acting bronchodilators. In a particular patient, the choice of one or another drug depends on the effectiveness and relief of the condition after taking it.

With severe shortness of breath, they proceed to the next stage of treatment - a combination of long-acting bronchodilators of different groups. It is also possible to treat in combination short-acting bronchodilator + theophylline .

Group C patients have few complaints but a high risk of exacerbations. For the first line, inhaled hormonal drugs + long-acting β2-agonists (long-acting M-anticholinergics) are used. An alternative regimen is a combination of long-acting bronchodilators of two different groups.

Group D patients have a detailed picture of the disease and have a high risk of exacerbations. In the first line in these patients, inhaled corticosteroids + long-acting β2-agonists or long-acting M-anticholinergics are used. The second line of treatment is a combination of their three drugs: inhaled hormonal drug + β2-agonist (long-acting) + M-anticholinergic (long-acting).

Thus, in the moderate (II) stage, severe (III) and extremely severe (IV), one of the drugs is selected sequentially for regular use:

• M-anticholinergic short-acting -, AtroventH, Ipratropium Air .
• M-anticholinergic long-acting -, Incrus Ellipta , Spiriva Respimat .
• short-acting β2-agonists.
• Long acting β2 agonists: Atimos , Formoterol Easyhaler , sereventer , Onbrez Breezhaler , Striverdi Respimat .
• M-anticholinergic + β2-agonist.
• M-anticholinergic long-acting + theophyllines.
• Long-acting β2-agonists + theophyllines.
• Triple regimen: M-anticholinergic + inhaled β2-agonist + theophyllines or inhaled hormonal drug + β2-agonist (long-acting) + M-anticholinergic (long-acting).
• A combination of long-acting drugs, which are used constantly, and short-acting drugs - "on demand" are allowed if one drug is not enough to control dyspnea.

Forum, dedicated to the topic treatment, visited by patients with a disease of varying severity. They share their impressions of the drugs and come to the conclusion that the selection of the basic effective drug- a very difficult task for the doctor and the patient. Everyone is unanimous in the opinion that the winter period is very difficult to endure, and some do not go out at all.

In severe cases, during exacerbations, a combination of a hormone and a bronchodilator () is used three times a day, inhalation. Many point out that application of ACC facilitates the discharge of sputum and generally improves the condition. The use of an oxygen concentrator during this period is mandatory. Modern hubs are small in size (30-38 cm) and weight, suitable for stationary use and on the go. Patients choose to use a mask or a nasal cannula.

During remission, some take Erakond (alfalfa plant extract - a source of iron, zinc, flavonoids and vitamins) and many do breathing exercises according to Strelnikova in the morning and evening. Even patients with the third degree of COPD tolerate it normally and notice an improvement.

Treatment for exacerbation of COPD

Exacerbation of COPD is regarded as an acute condition, which is characterized by worsening respiratory symptoms. Exacerbation in patients can be caused by viral infections and bacterial flora.

The systemic inflammatory process is assessed by biomarkers - the level of C-reactive protein and fibrinogen. Predictors of the development of frequent exacerbations in a patient are the appearance of neutrophils in the sputum and a high content of fibrinogen in the blood. Three classes of drugs are used to treat exacerbations:

• Bronchodilators. Of the bronchodilators in exacerbations, the most effective are short-acting inhaled β2-agonists in combination with short-acting M-anticholinergics. Intravenous administration of methylxanthines is the second line of treatment and is used only when short-acting bronchodilators are not effective enough in this patient.
• Glucocorticosteroids. In case of exacerbation, it is used in tablets in a daily dose of 40 mg. Treatment is carried out no more than 5 days. Tablet form is preferred. An alternative to taking hormones orally can be nebulizer therapy, which has a pronounced local anti-inflammatory effect.
• Antibiotics. Antibacterial therapy is indicated only for infectious exacerbation, which is manifested by increased shortness of breath, an increase in the amount of sputum and the appearance of a purulent sputum. Initially, empiric antibiotics are prescribed: aminopenicillins with clavulanic acid , macrolides or tetracyclines. After receiving the responses of the analysis to the sensitivity of the flora, the treatment is adjusted.

Antibiotic therapy takes into account the age of the patient, the frequency of exacerbations for Last year, FEV1 index and the presence of concomitant pathology. In patients under 65 years of age with an exacerbation frequency of less than 4 times a year and FEV1> 50%, either a macrolide is recommended ().

Azithromycin in the neutrophilic variant affects all components of inflammation. Treatment with this drug reduces the number of exacerbations by almost three times. If these two drugs are ineffective, the alternative is respiratory fluoroquinolone inside.

In patients over 65 years of age with exacerbations more than 4 times, with the presence of other diseases and with an FEV1 of 30-50% of the norm, protected aminopenicillin () or a respiratory fluoroquinolone () or a second-generation cephalosporin are offered as the drugs of choice. If the patient received more than 4 times in the previous year antibiotic therapy, FEV1 indicator<30% и постоянно принимал кортикостероиды, рекомендуется внутримышечно, или в высокой дозе levofloxacin , or a b-lactam antibiotic in combination with an aminoglycoside.

A new class of anti-inflammatory drugs (phosphodiesterase-4 inhibitors) is represented by roflumilast ( Daxas ). Unlike GCS, which only affect the level of eosinophils in the sputum, Daxas also affects the neutrophil link of inflammation. A course of treatment of four weeks reduces the number of neutrophils in sputum by almost 36%. In addition to the anti-inflammatory effect, the drug relaxes the smooth muscles of the bronchi and suppresses fibrosis. Some studies have shown efficacy in reducing the number of exacerbations. Daxas is prescribed to a certain group of patients who have the maximum effect: with frequent exacerbations (more than twice a day) and with a bronchitis type of disease.

Long term treatment roflumilast within a year, it reduces the frequency of exacerbations by 20% in the "COPD with frequent exacerbations" group. It is prescribed against the background of treatment with long-acting bronchodilators. The number of exacerbations can be significantly reduced with the simultaneous administration of corticosteroids and roflumilast. The more severe the course of the disease, the greater the effect in reducing the number of exacerbations against the background of such combined treatment.

The use of ACC Fluimycin and other drugs with the active substance acetylcysteine ​​also has an anti-inflammatory effect. Long-term therapy for a year and high doses (two tablets per day) reduces the number of exacerbations by 40%.

Treatment of COPD with folk remedies at home

As monotherapy, treatment with folk remedies will not bring results, given that COPD is a serious and complex disease. These funds must be combined with drugs. Basically, drugs with anti-inflammatory, expectorant and restorative effects are used.

In the initial stages of COPD, treatment with bear bile and bear or badger fat is effective. According to the recipe, you can take badger or pork internal fat (0.5 kg), aloe leaves crushed in a blender (0.5 kg) and 1 kg of honey. Everything is mixed and heated in a water bath (the temperature of the mixture should not rise above 37 C, so that the healing properties of honey and aloe are not lost). The mixture is taken in 1 tbsp. l. before meals three times a day.

Benefits will bring cedar resin, cedar oil and infusion of Icelandic moss. Icelandic moss is brewed with boiling water (a tablespoon of raw materials per 200 ml of boiling water, infused for 25-30 minutes) and taken 0.25 cups three times a day. The course of treatment can last up to 4-5 months with two-week breaks. In patients, sputum is easier to expectorate and breathing becomes freer, it is important that appetite and general condition improve. For inhalation and ingestion, decoctions of herbs are used: coltsfoot, plantain, oregano, marshmallow, St. John's wort, mint, calamus, thyme, St. John's wort.

The doctors

Medications

• Bronchodilators: Atimos , Incrus Ellipta , sereventer , Atrovent N , Ipratropium Air , Spiriva Respimat , Berodual N , Fenipra .
• Glucotricoids and glucocorticoids in combinations:, Salmecort , Symbicort , Turbuhaler , Zenhale , Relvar Ellipta .
• Antibiotics: / clavulanate , .
• Mucolytics:, Mukomist .

Procedures and operations

Pulmonary rehabilitation is a mandatory and integral part of the treatment for this disease. It allows you to gradually increase physical activity and its endurance. Various exercises improve well-being and increase the quality of life, have a positive effect on anxiety and often occur in patients. Depending on the condition of the patient, this may be:

• daily walking for 20 minutes;
• physical training from 10 to 45 minutes;
• training the upper muscle group using an ergometer or doing resistance exercises with weights;
• inspiratory muscle training;
• breathing exercises that reduce shortness of breath and fatigue, increase exercise tolerance;
• transcutaneous electrical stimulation of the diaphragm.

At the initial stage, the patient can exercise on an exercise bike and do exercises with light weights. Special breathing exercises (according to Strelnikova or Buteyko) train the respiratory muscles and gradually increase the volume of the lungs. A pulmonologist or a specialist in physical therapy should advise gymnastics, and you can also watch a video of breathing exercises for COPD.

Oxygen therapy

Short-term oxygen therapy is prescribed for a period of exacerbation of the disease, or in cases where there is an increase in oxygen demand, for example, when physical activity or during sleep, when hemoglobin oxygen saturation decreases. It is known that prolonged use of oxygen (more than 15 hours daily, including at night) increases the survival of patients with respiratory failure and hypoxemia at rest. This method remains the only one that can reduce mortality in the extremely severe stage. Long-term oxygen therapy is indicated only for some groups of patients:

• who are permanently hypoxemic PaO2 less than 55 mmHg Art. and there are signs of cor pulmonale;
• hypoxemia PaO2 less than 60-55 mm Hg. Art. and hypercapnia PaCO2 more than 48 mm Hg. Art. with the presence right ventricular hypertrophy and low breathing rates.

At the same time, clinical manifestations are also taken into account: shortness of breath at rest, cough, asthma attacks, lack of effectiveness from treatment, sleep disturbance, poor exercise tolerance. Oxygen delivery devices are: nasal cannula and Venturi masks. The latter are more acceptable oxygen devices, but they are not well tolerated by patients.

The gas flow is selected and changed by the doctor based on the saturation of the blood with oxygen. The duration of the sessions is determined by the principle "the longer the better" and they are necessarily held at night.

Oxygen therapy reduces shortness of breath, improves sleep, general well-being, hemodynamics, and restores metabolic processes. Holding it for several months reduces polycythemia and pressure in the pulmonary artery.

Ventilation support

Patients with extremely severe COPD require non-invasive ventilation, and a combination of long-term oxygen therapy and NIV (in the presence of daytime hypercapnia) is also possible. Ventilatory support increases survival but does not affect quality of life. For this purpose, devices with constant positive pressure during inhalation and exhalation are used.

Surgery

Lung volume reduction surgery is performed to reduce hyperinflation, improve lung function, and reduce shortness of breath. This operation also increases the elastic recoil of the lungs, increases the speed of exhaled air and exercise tolerance. It is indicated for patients with upper lobe emphysema and low exercise tolerance. Removal of the bulla, which does not take part in gas exchange, promotes the expansion of the nearby lung tissue. This type of surgery is palliative.

Diet

Diet therapy is aimed at:

• reduction of intoxication;
• improved regeneration;
• decrease in exudation in the bronchi;
• replenishment of losses of vitamins, proteins and mineral salts;
• stimulation of gastric secretion and improvement of appetite.

With this disease, it is recommended or. They fully provide the body's need for protein, fats and carbohydrates, activate immunological protection, increase the body's defenses and resistance to infections. These are diets with a high energy value (3000-3500 kcal and 2600-3000 kcal, respectively), they have an increased protein content - 110-120 g (more than half are proteins of animal origin - these are complete proteins).

This is due to the fact that the chronic purulent-inflammatory process is accompanied by the release of exudate, which contains protein in large quantities. The resulting loss of protein with sputum is eliminated by its increased consumption. In addition, in the course of the disease, many patients develop a lack of weight. The content of carbohydrates in diets is within the normal range. With an exacerbation, carbohydrates are reduced to 200-250 g per day. Diets are varied in terms of a set of products, they do not have special restrictions on cooking, if this is not dictated by the concomitant pathology of the gastrointestinal tract.

An increased content of vitamin products is provided. In the nutrition of such patients are important, FROM , IN Therefore, the diet is enriched with vegetables, juices, fruits, decoctions of wild rose and wheat bran, brewer's yeast, sea buckthorn, currants and other seasonal berries, vegetable oils and nuts, liver of animals and fish.

Vegetables, fruits, berries, juices, meat and fish broths help improve appetite, which is so important for patients with severe disease. You can eat all foods with the exception of fatty pork, duck and goose meat, refractory fats, hot spices. Salt restriction to 6 g reduces exudation, inflammation and fluid retention, which is important in cardiovascular decompensation.

Reducing the amount of fluid provides for cardiovascular decompensation. The diet must include foods with calcium (sesame seeds, milk and sour-milk products). Calcium has an anti-inflammatory and desensitizing effect. Especially necessary if patients receive hormones. The daily content of calcium is 1.5 g.

In the presence of severe shortness of breath, take light food in small portions. In this case, the protein should be easily digestible: cottage cheese, sour-milk products, boiled chicken or fish, soft-boiled eggs or scrambled eggs. If you are overweight, you need to limit simple carbohydrates (sweets, sugar, pastries, cookies, cakes, jams, etc.). The high standing of the diaphragm with obesity makes it difficult to already difficult breathing.

COPD prevention

With this disease, there is a specific prevention and prevention of complications that occur during the course of the disease.

Specific prevention:

• To give up smoking.
• Taking steps to improve the air quality in the workplace and at home. If it is impossible to achieve this under production conditions, patients must necessarily use personal protective equipment or decide on rational employment.

Prevention of complications:

• It is also important to stop smoking, which aggravates the course of the disease. In this, the strong-willed decision of the patient, the persistent recommendations of the doctor and the support of loved ones are of decisive importance. However, only 25% of patients can refrain from smoking.
• Prevention of exacerbations of the disease consists in vaccination against influenza and pneumococcal infection, which significantly reduces the risk of infectious diseases of the respiratory tract, which are the main factor provoking an exacerbation. It is recommended that every patient be vaccinated, which is most effective in the elderly and patients with severe forms of the disease. Influenza vaccines containing killed or inactivated live viruses are used. Influenza vaccine reduces mortality in COPD exacerbations by 50%. It also affects the reduction in the frequency of exacerbations against the background of the incidence of influenza. The use of pneumococcal conjugate vaccine (according to Russian specialists from Chelyabinsk) reduces the frequency of exacerbations by 4.8 times per year.
• Immunocorrective therapy, which reduces the time of exacerbation, increases the effectiveness of treatment and prolongs the period of remission. For the purpose of immunocorrection, drugs are used that contribute to the production of antibodies against the main pathogens: IRS-19 , . IRS-19 And Imudon - local preparations that are in contact with the mucous membranes of the upper respiratory tract for a short time. Broncho-Vaxom has a strong evidence base of effectiveness in the prevention of exacerbations of COPD. For prophylactic purposes, the drug is taken for a month, one capsule on an empty stomach. Then three courses are held for 10 days each month, with a break of 20 days. Thus, the entire prevention scheme lasts five months. The number of exacerbations of COPD is reduced by 29%.
• An important aspect remains pulmonary rehabilitation - breathing exercises, regular physical activity, hiking, yoga, and more.
• Exacerbations of COPD can be prevented by complex measures: physical rehabilitation, adequate basic treatment (taking a long-acting beta-blocker or long-acting M-anticholinergic) and vaccination. Despite the fact that the patient has a pathology of the lungs, he should be encouraged to physical activity and perform special exercises. Patients with COPD should lead as active a lifestyle as possible.

Consequences and complications of COPD

The following complications of the disease can be distinguished:

• Acute and chronic.
• Pulmonary hypertension . Pulmonary hypertension usually develops in the late stages due to hypoxia and the resulting spasm of the arteries of the lungs. As a result, hypoxia and spasm lead to changes in the walls of small arteries: hyperplasia (enhanced reproduction) intima (the inner layer of the vessel wall) and hypertrophy muscular layer of blood vessels. In small arteries, an inflammatory process is observed, similar to that in the respiratory tract. All these changes in the vascular wall lead to an increase in pressure in the pulmonary circle. Pulmonary hypertension progresses and eventually leads to right ventricular enlargement and right ventricular failure.
• Heart failure .
• Secondary polycythemia - an increase in the number of red blood cells.
• Anemia . It is registered more often than polycythemia. Most of the pro-inflammatory cytokines, adipokines, acute phase proteins, serum amyloid A, neutrophils, monocytes that are released during pulmonary inflammation play a role in the development of anemia. Significant in this is the inhibition of the erythroid germ, the violation of iron metabolism, the production of hepcidin by the liver, which inhibits the absorption of iron, deficiency in men, which stimulates erythropoiesis. Medications are important theophylline and ACE inhibitors inhibit the proliferation of erythroid cells.
• Pneumonia . The development of pneumonia in these patients is associated with a severe prognosis. The prognosis worsens if the patient has a cardiovascular pathology. At the same time, pneumonia, in turn, often leads to cardiovascular complications in the form of arrhythmia and pulmonary edema.
• Pleurisy .
• Thromboembolism .
• Spontaneous pneumothorax - accumulation of air in the pleural cavity, due to rupture of the lung tissue. In patients with COPD, the severity of pneumothorax is determined by a combination of processes: lung collapse, emphysema, and chronic inflammation. Even a slight collapse of the lung leads to a pronounced deterioration in the patient's condition.
• Pneumomediastinum - accumulation of air in the mediastinum, resulting from the rupture of the terminal alveoli.

Patients with COPD develop comorbidities: metabolic syndrome muscle dysfunction, lungs' cancer , depression . Comorbidities have an impact on mortality rates. Inflammatory mediators circulating in the blood exacerbate ischemic heart disease , anemia And diabetes .

Forecast

It is assumed that COPD by 2020 will come out on the 3rd place among the causes of death. The increase in mortality is associated with an epidemic of smoking. In patients, a decrease in airflow limitation is associated with an increased number of exacerbations and a reduced life expectancy. Because each exacerbation reduces lung function, worsens the patient's condition and increases the risk of death. Even one exacerbation almost halves the forced expiratory volume in the first second.

In the first five days of an exacerbation of the disease, the risk increases significantly arrhythmias , acute coronary syndrome , and sudden death. The number of subsequent exacerbations increases rapidly, and the periods of remission are significantly reduced. If between the first and second exacerbation five years can pass, then in the future between the eighth and ninth - about two months.

It is important to predict the frequency of exacerbations, as this affects the survival of patients. Due to respiratory failure, which develops with severe exacerbations, the mortality rate increases significantly. The following relationship has been traced: the more exacerbations, the worse the prognosis. Thus, exacerbation is associated with a poor prognosis and it is important to avoid it.

How long do patients with this diagnosis live? Life expectancy in COPD is affected by severity, comorbidities, complications, and the number of exacerbations of the underlying disease. The age of the patient is also important.

How long can you live with stage 4 COPD? It is difficult to answer this question unequivocally, and all of the above factors must be taken into account. You can refer to the statistics: this is an extremely severe degree of the disease and with an exacerbation 2 times a year, mortality within 3 years occurs in 24% of patients.

At grade 3, how long do patients with this disease live? Under the same conditions, mortality within 3 years occurs in 15% of patients. Even in the absence of frequent exacerbations, GOLD 3 and GOLD 4 patients are at greater risk of death. Concomitant diseases aggravate the course of the disease and often cause death.

List of sources

• Zinchenko V. A., Razumov V. V., Gurevich E. B. Occupational chronic obstructive pulmonary disease (COPD) is a missing link in the classification of occupational lung diseases (a critical review). In: Clinical aspects of occupational pathology / Ed. Doctor of Medical Sciences, Professor V. V. Razumov. Tomsk, 2002, pp. 15–18
• Global strategy for the diagnosis, treatment and prevention of chronic obstructive pulmonary disease (revised 2014) / Per. from English. ed. A. S. Belevsky.
• Chuchalin A. G., Avdeev S. N., Aisanov Z. R., Belevsky A. S., Leshchenko I. V., Meshcheryakova N. N., Ovcharenko S. I., Shmelev E. I. Russian Respiratory Society . Federal clinical guidelines for the diagnosis and treatment of chronic obstructive pulmonary disease // Pulmonology, 2014; 3:15–54.
• Avdeev S. Systemic effects in patients with COPD // Vrach. - 2006. - No. 12. - P. 3-8.

So, “COPD is characterized by airflow limitation that is not completely reversible. Airflow limitation is usually progressive and is caused by an abnormal reaction of the lungs to exposure to various noxious particles and gases. Next are the key points. It means clinical picture : prolonged cough, sputum production, shortness of breath, increasing as the disease progresses; in the terminal stage - severe respiratory failure and decompensated cor pulmonale. Pathophysiological mechanisms we : obstructive type of violation of the ventilation function of the lungs, mucociliary dysfunction, deposition of neutrophils in the respiratory mucosa, bronchial remodeling and damage to the lung parenchyma. And finally morpho logical changes : chronic progressive inflammatory process of the airways and lung parenchyma (especially respiratory bronchioles), existing regardless of the severity of the disease.

The term "chronic obstructive bronchitis" did not satisfy the fact that this pathology was previously regarded as a process occurring mainly in the bronchi, which determined a somewhat frivolous attitude towards this disease. Despite the fact that the process primarily occurs in the bronchi, they are not the only springboard on which pathology develops.

Recall the definition chronic obstructive bronchitis - a disease characterized by chronic diffuse inflammation of the bronchi, leading to a progressive obstructive ventilation disorder and manifested by cough, shortness of breath and sputum production, not associated with damage to other systems and organs. COB is characterized by progressive airway obstruction and increased bronchoconstriction in response to nonspecific stimuli.

Given the above, the term "COPD" is preferable to "chronic obstructive bronchitis", because in case of a disease, not only the bronchi are involved in the pathological process, but all the functional and structural elements of the lung tissue without exception (alveolar tissue, vascular bed, pleura, respiratory muscles). ). Understanding and knowledge of the features of this pathology makes us consider "COPD" as a term that more fully and deeply describes this disease.

In this way, COPD is characterized a progressive increase in irreversible obstruction as a result of pollutant-induced chronic inflammation, which is based on gross morphological changes in all lung tissue structures involving the cardiovascular system and respiratory muscles. COPD leads to limited physical performance, disability of patients and in some cases death.

The term COPD, taking into account all stages of the disease, includes chronic obstructive bronchitis, chronic purulent obstructive bronchitis, pulmonary emphysema, pneumosclerosis, pulmonary hypertension, chronic cor pulmonale. Each of the terms - "chronic bronchitis", "emphysema", "pneumosclerosis", "pulmonary hypertension", "cor pulmonale" - reflects only the peculiarity of the morphological and functional changes that occur in COPD.

The appearance in clinical practice of the term "COPD" is a reflection of the basic law of formal logic - "one phenomenon has one name."

According to the International Classification of Diseases and Causes of Death of the 10th revision, COPD is coded according to the code of the underlying disease that led to the development of COPD - chronic obstructive bronchitis (code 491) and sometimes bronchial asthma (code 493).

Epidemiology.

It has been established that the prevalence of COPD in the world among men and women in all age groups is 9.3 and 7.3 per 1000 population, respectively.

COPD is one of the most common diseases in which mortality continues to increase.

Etiology.

COPD is defined by the disease that caused it. COB is based on a genetic predisposition, which is realized as a result of prolonged exposure to the bronchial mucosa of factors that have a damaging (toxic) effect. In addition, several loci of mutated genes associated with the development of COPD have been discovered so far in the human genome. First of all, this is a deficiency of α1-antitrypsin - the basis of the antiprotease activity of the body and the main inhibitor of neutrophil elastase. In addition to congenital deficiency of α1-antitrypsin, hereditary defects in α1-antichymotrypsin, α2-macroglobulin, vitamin D-binding protein, and cytochrome P4501A1 may be involved in the development and progression of COPD.

Pathogenesis.

If we talk about chronic obstructive bronchitis, then the main consequence of the impact of etiological factors is the development of chronic inflammation. The localization of inflammation and the features of triggering factors determine the specifics of the pathological process in COB. Biomarkers of inflammation in COB are neutrophils. They are mainly involved in the formation of local deficiency of antiproteases, the development of "oxidative stress", play a key role in the chain of processes characteristic of inflammation, ultimately leading to irreversible morphological changes.

An important role in the pathogenesis of the disease is played by impaired mucociliary clearance. The efficiency of mucociliary transport, the most important component of the normal functioning of the airways, depends on the coordination of the action of the ciliated apparatus of the ciliated epithelium, as well as the qualitative and quantitative characteristics of bronchial secretions. Under the influence of risk factors, the movement of cilia is disrupted up to a complete stop, metaplasia of the epithelium develops with the loss of cells of the ciliated epithelium and an increase in the number of goblet cells. The composition of the bronchial secretion changes, which disrupts the movement of significantly thinned cilia. This contributes to the occurrence of mucostasis, causing blockade of the small airways.

The change in the viscoelastic properties of bronchial secretions is also accompanied by significant qualitative changes in the composition of the latter: the content of nonspecific components of local immunity in the secretion, which have antiviral and antimicrobial activity, is reduced - interferon, lactoferin and lysozyme. Along with this, the content of secretory IgA decreases. Violations of mucociliary clearance and the phenomenon of local immunodeficiency create optimal conditions for the colonization of microorganisms. Thick and viscous bronchial mucus with reduced bactericidal potential is a good breeding ground for various microorganisms (viruses, bacteria, fungi).

The whole complex of the listed pathogenetic mechanisms leads to the formation of two main processes characteristic of COB: impaired bronchial patency and the development of centrilobular emphysema.

Bronchial obstruction in COB consists of irreversible and reversible components. The irreversible component is determined by the destruction of the elastic collagen base of the lungs and fibrosis, changes in the shape and obliteration of the bronchioles. The reversible component is formed due to inflammation, contraction of bronchial smooth muscles and mucus hypersecretion. Ventilation disorders in COB are mainly obstructive, which is manifested by expiratory dyspnea and a decrease in FEV1, an indicator that reflects the severity of bronchial obstruction. The progression of the disease as a mandatory sign of COB is manifested by an annual decrease in FEV1 by 50 ml or more.

Classification.

Experts of the international program "Global Initiative for Chronic Obstructive Lung Disease" (GOLD - Global Strategy for Chronic Obstructive Lung Disease) distinguish the following stages of COPD (see table).

Note. Stage zero COPD, which is listed in the GOLD classification, is considered as a group.

The course of the disease.

When assessing the nature of the course of the disease, it is important not only to change the clinical picture, but also to determine the dynamics of the fall in bronchial patency. Wherein special meaning has a definition of the FEV1 parameter - forced expiratory volume in the first second. Normally, with age, non-smokers experience a drop in FEV1 by 30 ml per year. In smokers, the decrease in this parameter reaches 45 ml per year. A prognostically unfavorable sign is an annual decrease in FEV1 by 50 ml, which indicates a progressive course of the disease.

Clinic.

The main complaint in the relatively early stages of the development of chronic obstructive bronchitis is a productive cough, mainly in the morning. With the progression of the disease and the addition of an obstructive syndrome, more or less constant shortness of breath appears, the cough becomes less productive, paroxysmal, hacking.

Auscultation reveals a wide variety of phenomena: weakened or hard breathing, dry whistling and wet rales of various sizes, in the presence of pleural adhesions, persistent pleural “crackling” is heard. Patients with severe disease usually present with clinical symptoms of emphysema; dry rales, especially on forced exhalation; in the later stages of the disease, weight loss is possible; cyanosis (in its absence, there may be a slight hypoxemia); there is a presence of peripheral edema; swelling of the cervical veins, an increase in the right heart.

Auscultation determines the splitting of the first tone in the pulmonary artery. The appearance of noise in the projection area of ​​the tricuspid valve indicates pulmonary hypertension, although auscultatory symptoms may be masked by severe emphysema.

Signs of an exacerbation of the disease: the appearance of purulent sputum; increase in the amount of sputum; increased shortness of breath; increased wheezing in the lungs; the appearance of heaviness in the chest; fluid retention.

Acute phase reactions of blood are weakly expressed. Erythrocytosis and an associated decrease in ESR may develop. In sputum, causative agents of exacerbation of COB are detected. Chest radiographs may show increased and deformed bronchovascular pattern and signs of pulmonary emphysema. The function of external respiration is disturbed according to the obstructive type or mixed with a predominance of obstructive.

Diagnostics.

The diagnosis of COPD should be considered in every person who has a cough, excessive sputum production, and/or shortness of breath. It is necessary to take into account the risk factors for the development of the disease in each patient. In the presence of any of these symptoms, it is necessary to conduct a study of the function of external respiration. These signs are not diagnostically significant in isolation, but the presence of several of them increases the likelihood of the disease. Chronic cough and excessive sputum production often long precede ventilation problems leading to dyspnoea.

It is necessary to talk about chronic obstructive bronchitis with the exclusion of other causes of the development of bronchial obstruction syndrome. Diagnosis criteria - risk factors + productive cough + + bronchial obstruction. Establishing a formal diagnosis of COB entails the next step - determining the degree of obstruction, its reversibility, as well as the severity of respiratory failure.

COB should be suspected in chronic productive cough or exertional dyspnoea, the origin of which is unclear, as well as signs of forced expiratory slowing. The basis for the final diagnosis are:

detection of functional signs of airway obstruction that persists despite intensive treatment using all possible means;

exclusion of specific pathology (for example, silicosis, tuberculosis, or tumors of the upper respiratory tract) as the cause of these functional disorders.

So, the key symptoms for staging diagnosis of COPD.

Chronic cough: disturbs the patient constantly or periodically; more often observed during the day, less often at night. Cough is one of the leading symptoms of the disease; its disappearance in COPD may indicate a decrease in the cough reflex, which should be considered as an unfavorable sign.

Chronic sputum production: at the beginning of the disease, the amount of sputum is small. The sputum is mucous in nature and is excreted mainly in the morning. However, with an exacerbation of the disease, its amount may increase, it becomes more viscous, the color of sputum changes.

Shortness of breath: progressive (increases with time), persistent (daily). Increases with exercise and during respiratory infections.

The action of risk factors in history: smoking and tobacco smoke; industrial dust and chemicals; smoke from household heating appliances and fumes from cooking.

During a clinical examination, an elongated expiratory phase in the respiratory cycle is determined, over the lungs - with percussion a pulmonary sound with a box shade, with auscultation of the lungs - weakened vesicular breathing, scattered dry rales.

The diagnosis is confirmed by a study of the function of external respiration.

Determination of forced vital capacity (FVC), forced expiratory volume in the first second (FEV) and calculation of the FEV/FVC index.

Spirometry shows a characteristic decrease in expiratory respiratory flow with a slowdown in forced expiratory flow (decrease in FEV1). Forced expiratory slowing is also clearly seen in the flow-volume curves. VC and FVC are somewhat reduced in patients with severe COB, but closer to normal than the exhalation parameters. FEV1 is much lower than normal; the FEV1/VC ratio in clinically severe COPD is usually below 70%. The diagnosis can be considered confirmed only if these disorders persist, despite long-term, maximally intensive treatment.

An increase in FEV1 of more than 12% after inhaled bronchodilators indicates a significant reversibility of airway obstruction. It is often noted in patients with COB, but is not pathognomonic for the latter. The absence of such reversibility, when judged by single testing data, does not always indicate fixed obstruction. Quite often reversibility of obstruction comes to light only after long, most intensive medical treatment.

Establishment of a reversible component of bronchial obstruction and its more detailed characterization are carried out during inhalation tests with bronchodilators (anticholinergics and β2-agonists). The test with berodual allows you to objectively assess both the adrenergic and cholinergic components of the reversibility of bronchial obstruction. In most patients, there is an increase in FEV1 after inhalation of anticholinergic drugs or sympathomimetics. Bronchial obstruction is considered reversible with an increase in FEV1 by 12% or more after inhalation of pharmaceuticals. It is recommended to conduct a pharmacological test before prescribing bronchodilatory therapy. At home, for monitoring lung function, it is recommended to determine the peak expiratory flow rate (PEF) using peak flow meters.

The steady progression of the disease is the most important sign of COPD. The severity of clinical signs in patients with COPD is constantly increasing. To determine the progression of the disease, a repeated determination of FEV1 is used. A decrease in FEV1 by more than 50 ml per year indicates the progression of the disease.

In COPD, disturbances in the distribution of ventilation and perfusion occur and manifest themselves in various ways. Excessive ventilation of the physiological dead space indicates the presence in the lungs of areas where it is very high in comparison with the blood flow, i.e., it goes “idle”. Physiological shunting, in contrast, indicates the presence of poorly ventilated but well-perfused alveoli. In this case, part of the blood coming from the arteries of the small circle in left heart not fully oxygenated, leading to hypoxemia. In the later stages, general alveolar hypoventilation occurs with hypercapnia exacerbating the hypoxemia caused by physiological shunting. Chronic hypercapnia is usually well compensated and blood pH is close to normal, except for periods of sharp exacerbation of the disease.

X-ray of the chest organs. Examination of the patient should begin with the production of images in two mutually perpendicular projections, preferably on a film measuring 35 x 43 cm with an X-ray image intensifier. Polyprojection radiography allows you to judge the localization and extent of the inflammatory process in the lungs, the condition of the lungs as a whole, the roots of the lungs, pleura, mediastinum and diaphragm. A picture only in a direct projection is allowed for patients who are in a very serious condition.

CT scan. Structural changes in the lung tissue are significantly ahead of irreversible airway obstruction, detected in the study of the function of external respiration and estimated by average indicators of less than 80% of the proper values. In the zero stage of COPD, using CT, gross changes in the lung tissue are detected. This raises the question of starting the treatment of the disease as early as possible. In addition, CT makes it possible to exclude the presence of lung tumors, the likelihood of which in chronic smokers is much higher than in healthy people. CT can detect widespread congenital malformations in adults: cystic lung, pulmonary hypoplasia, congenital lobar emphysema, bronchogenic cysts, bronchiectasis, as well as structural changes in the lung tissue associated with other past lung diseases that can significantly affect the course of COPD.

In COPD, CT allows examining the anatomical characteristics of the affected bronchi, determining the extent of these lesions in the proximal or distal part of the bronchus; using these methods, bronchiectasis is better diagnosed, their localization is clearly established.

Via electrocardiography evaluate the state of the myocardium and the presence of signs of hypertrophy and overload of the right ventricle and atrium.

At laboratory research erythrocyte count may reveal erythrocytosis in patients with chronic hypoxemia. When determining the leukocyte formula, eosinophilia is sometimes detected, which, as a rule, indicates COB of the asthmatic type.

Sputum examination useful for determining the cellular composition of bronchial secretions, although the value of this method is relative. Bacteriological examination of sputum is necessary to identify the pathogen with signs of a purulent process in the bronchial tree, as well as its sensitivity to antibiotics.

Assessment of symptoms.

The rate of progression and the severity of COPD symptoms depend on the intensity of exposure to etiological factors and their combined effect. In typical cases, the disease makes itself felt over the age of 40 years.

Cough is the earliest symptom, appearing by 40-50 years of age. By the same time, in the cold seasons, episodes of a respiratory infection begin to occur, which are not initially associated with one disease. Subsequently, the cough takes on a daily character, rarely aggravated at night. Cough is usually unproductive; can be paroxysmal in nature and provoked by inhalation of tobacco smoke, weather changes, inhalation of dry cold air and a number of other environmental factors.

Sputum is secreted in a small amount, more often in the morning, and has a mucous character. Exacerbations of an infectious nature are manifested by the aggravation of all signs of the disease, the appearance of purulent sputum and an increase in its amount, and sometimes a delay in its release. Sputum has a viscous consistency, often "lumps" of secretion are found in it. With an exacerbation of the disease, sputum becomes greenish in color, an unpleasant odor may appear.

The diagnostic value of an objective examination in COPD is negligible. Physical changes depend on the degree of airway obstruction, the severity of emphysema. The classic signs of COPD are wheezing with a single breath or with forced expiration, indicating a narrowing of the airways. However, these signs do not reflect the severity of the disease, and their absence does not exclude the presence of COPD in a patient. Other signs, such as weakening of breathing, restriction of chest expansion, participation of additional muscles in the act of breathing, central cyanosis, also do not indicate the degree of airway obstruction.

Bronchopulmonary infection - although frequent, but not the only cause of exacerbation. Along with this, it is possible to develop an exacerbation of the disease due to the increased action of exogenous damaging factors or with inadequate physical activity. In these cases, signs of damage to the respiratory system are less pronounced. As the disease progresses, the intervals between exacerbations become shorter.

Shortness of breath as the disease progresses can vary from a feeling of lack of air during habitual physical exertion to pronounced manifestations at rest.

Dyspnea felt on exertion occurs on average 10 years after the onset of cough. It is the reason for most patients to see a doctor and the main cause of disability and anxiety associated with the disease. As lung function decreases, shortness of breath becomes more pronounced. With emphysema, the onset of the disease is possible from it. This occurs in situations where a person comes into contact with finely dispersed (less than 5 microns) pollutants at work, as well as in hereditary a1-antitrypsin deficiency, leading to the early development of panlobular emphysema.

At wording diagnosis COPD is indicated

severity of the course of the disease: mild course (stage I), moderate course (stage II), severe course (III stage) and extremely severe (stage IV),

exacerbation or remission of the disease, exacerbation of purulent bronchitis (if any);

the presence of complications (cor pulmonale, respiratory failure, circulatory failure),

indicate risk factors, the index of a smoking person.

Chronic obstructive pulmonary disease (COPD) is a combination of two lung conditions: chronic bronchitis and emphysema (chest enlargement). COPD severely restricts the flow of oxygen to the lungs as well as the removal of carbon dioxide from the lungs. Bronchitis inflames and constricts the airways, while emphysema damages the alveoli (tiny air sacs) in the lungs, making them less effective at transporting oxygen from the lungs to the bloodstream.

Tobacco smoking is the root cause of chronic obstructive pulmonary disease (COPD), and a huge number of people suffer from this disease. Since there are many people who use tobacco products, as well as ex-smokers. Breathing in other substances that irritate the lungs, such as dirt, dust, or chemicals, over a long period of time can also cause or contribute to COPD.

Development of COPD

The air ducts branch out like an inverted tree, and at the end of each branch there are many small air sacs with balloons - alveoli. At healthy people every airway is clear and open. The alveoli are small and delicate, and the airways with air sacs are resilient.

The difference between healthy bronchi and sputum

When a person takes a breath, each alveolus is filled with oxygen, like a small balloon. When you exhale, the balloon contracts and gases are released. With COPD, the airways and alveoli become less elastic and flexible. Less oxygen gets in and less oxygen gets out because:

• air ducts and alveoli lose elasticity (for example, an old rubber band);
• the walls between the many alveoli fall into disrepair;
• the walls of the airways become thick and inflamed (swollen);
• cells in the airways secrete more body fluid (phlegm), which leads to clogging of the airways.

COPD progresses slowly and it can take many years before a person notices symptoms, such as feeling short of breath. Most of the time, COPD is diagnosed in people aged 30 or older. The older you are, the more likely you are to get COPD.

COPD is in fourth place in the world in terms of the percentage of deaths from the disease. There is no cure for COPD. There are medications that can slow down the progression of COPD, but the damage to the lungs will still be done. COPD is not contagious - you can't catch it from another person.

What causes COPD?

Tobacco use is the main cause of COPD. A huge number of cases of COPD develop after repeated use of fumes and other substances that irritate and damage the lungs and airways. Tobacco smoking is the main irritant that causes COPD. Pipe, cigarette, hookah and other types can also cause COPD.

Breathing other fumes and dust over a long period of time can also contribute to the development of COPD. The lungs and airways are very sensitive to these irritants. They cause inflammation and constriction of the airways, destroy the elastic fibers that allow the lung to expand, and then return to its resting form. This makes it difficult to breathe air in and out of the lungs.

Other things that can irritate the lungs and contribute to COPD include:

• working around certain types of chemicals and breathing in gases for years;
• work in a dusty area for many years;
• severe exposure to air pollution;
• passive smoking (smoke in the air from other people, smoking cigarettes) also plays a role in the individual development of COPD.

Genes - tiny bits of information in your body's cells passed down by your parents - may play a role in the development of COPD. Rarely, COPD is caused by a genomic disorder called alpha-1 antitrypsin. Alpha-1 antitrypsin is a protein in human blood that inactivates damaging proteins. People with antitrypsin deficiency have low levels of alpha-1 antitrypsin; protein imbalance leads to lung destruction and COPD. If people with this disease smoke, the disease progresses more quickly.

Who is at risk for COPD?

Most people with COPD are smokers or have been smokers in the past. People with family history COPD is more likely to get sick if you smoke. The chance of developing COPD is also higher in people who have been in contact with mild irritants for many years, such as:

1. Air pollution. Chemical fumes, fumes and dust are commonly associated with certain workplaces.
2. A person with frequent and severe lung infections, especially during childhood, may be more likely to develop lung damage that leads to COPD. Fortunately, this is much less common today with antibiotic treatment.
3. Most people with COPD are at least 40 years old or around middle age when symptoms begin. This is unusual, but possible, for people under 40 who have COPD.

Signs and symptoms of COPD

COPD produces symptoms, disability, and a deterioration in quality of life that may respond to medication and other treatments that affect the obstruction. Symptoms of COPD include:

• shortness of breath or shortness of breath during exertion or at rest (in the later stages);
• tightness in the chest during exercise or at rest;
• chronic cough with sputum production, a feature of chronic bronchitis;
• wheezing, especially on exhalation;
• weight loss and loss of appetite;
• ankle swelling.

Persistent cough and sputum are common feature COPD They often occur several years before airflow in and out of the lungs decreases. However, not all symptoms appear when COPD develops.

The severity of the symptoms depends on which part of the lung was affected by the "collapse". If the patient continues to smoke, then the destruction of the lungs occurs faster.

How is COPD diagnosed?

Doctors consider a diagnosis of COPD if a person has typical symptoms and a history of exposure to lung irritants, especially cigarette smoking. medical history, physical examination, and breath tests are the most important tests to determine if a patient has COPD.

The attending physician conducts an examination, “listens” to the lungs. The specialist will also ask questions about relatives and medical history and If the patient worked in a hazardous industry or was exposed to other negative environmental influences, then this should be told to the doctor.

Treatment and prevention

COPD treatment is divided into medical and conservative approaches. The basis of conservative therapy is absolute abstinence from nicotine and the elimination of other inhaled harmful substances. Teaching the patient breathing exercises in combination with training.

Vaccination against pneumococcal and influenza viruses is prescribed to prevent infection. Prevention of osteoporosis Calcium and vitamin D3 are beneficial as it produces glucocorticoid-induced osteoporosis. Existing sources of infection must be excluded comorbidities and need treatment.

Most effective way prevention is the avoidance of risk factors. It has been shown that middle-aged smokers who were able to quit smoking experienced a significant improvement in well-being, slowing down the progression of the disease.

Complications

Acute and chronic respiratory failure are complications of COPD. Viral or bacterial infections can cause more severe deterioration that will last for a long time. In addition, comorbidities such as cardiovascular diseases and metabolic syndrome, lung cancer, muscle weakness and osteoporosis, and depression are complications of COPD.

Typical weight loss. Pulmonary hypertension can lead to right ventricular failure with hepatomegaly and ascites.

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