Pulmonary disease COPD. Chronic obstructive pulmonary disease: symptoms, treatment of COPD

Chronic obstructive pulmonary disease, or COPD, is one of the most common health problems in humans today. This is due to the deplorable state of our environment.

The quality of the air that a person inhales has noticeably deteriorated, which cannot but affect the health of the organs responsible for the process of air exchange.

What is COPD?

COPD - is a general term for many respiratory diseases, such as, and. May also include other diseases respiratory tract.

The most common causative factor is smoking.

Inflammatory processes in the lungs, provoked by the influence of exhaust, various impurities of atmospheric air, cigarette smoke (passive smoking is not excluded) are fundamental processes for the development of COPD.

According to the statistics of the World Health Organization (WHO) - Chronic obstructive pulmonary disease in adults, occupies the fourth position in the mortality rate.

People suffering from this disease die from developing complications such as:

• respiratory failure;
• cardiovascular disorders (which COPD provokes).

This disease, if properly diagnosed, early stages development is treated in full, applying a number of actions to prevent this disease, it is possible to prevent its development.

According to µb 10 are coded asJ44.0 - if COPD develops in conjunction with affecting the lower respiratory tract. Code for the International Classification of Diseases 10 helps to systematize and track statistics for each disease.

COPD microbial 10 with code J44.9 is reflected in case of undetermined genesis.

Signs of COPD

Symptoms and signs may include:

• fatigue;
• shortness of breath
• paroxysmal nocturnal dyspnea (PND);
• wheezing when breathing;
• cough with sputum (mucous and / or purulent);
• fever
• chest pain.

Risk factors

• For the most part, the most harmful and frequently encountered factor is smoking. Tobacco smoke and cigarette tar adversely affect all respiratory organs. Passive smoking is absolutely no less harmful, but on the contrary, even more dangerous. A person who is close to a smoker consumes a much higher amount of smoke than himself. The category of people who smoke endangers not only themselves, but also the people around them. Among the group of heavy smokers, approximately 15-20% are diagnosed clinical manifestations COPD
• genetic predisposition. An example of disorders leading to this disease is a condition such as:
  • alpha-antitrypsin deficiency (in people who have never smoked and increases the risk for the disease in smokers);
• bacteria. The exacerbation of the disease in question can be influenced by bacteria of such groups as Haemophilus influenza, Moraxella catarrhalis. Another type of bacteria that affects the development of the disease are streptococcus pneumoniae;
• Occupational hazard (dust, fumes of various acids and alkalis, harmful masses released from chemical substances);
• Bronchial hyperreactivity.

Pathogenesis

With prolonged exposure to any risk factor on the human body, inflammation of the walls of the bronchi of a chronic nature develops. The most likely damage to the distal (located in maximum proximity to the alveoli and lung parenchyma).

The production and excretion of mucus is impaired. Small bronchi get clogged and various infections develop against this background. Muscle cells die and are replaced by connective tissue. As a result, emphysema develops - the lung tissue overflows with air because of this, their elasticity decreases markedly.

From bronchi damaged by emphysema, air is released with great difficulty. The volume of air is reduced as gas exchange is not in proper quality. As a result, one of the main symptoms manifests itself - shortness of breath. With exertion or just walking, shortness of breath creates an increasing effect.

As a result of respiratory failure, hypoxia develops. With prolonged exposure to hypoxia on the human body, the lumens of the pulmonary vessels decrease, which leads to (during the course of this disease, an increase and expansion of the right sections of the heart develops).

Classification

This disease is classified according to the severity of the course and the clinical picture.

• Latent, almost impossible to recognize, has no pronounced symptoms.
• Medium, manifested cough in the morning (with phlegm or dry). Shortness of breath more often with minor physical exertion.
• Severe course, occurs in a chronic course and is accompanied by bouts of severe coughing with sputum production, frequent shortness of breath.
• The fourth stage can be fatal, characterized by persistent cough, shortness of breath even at rest, a rapid decrease in body weight.

Aggravation

Let's take a look at what a COPD exacerbation is.

This is a condition in which the course of the disease is aggravated. The clinical picture worsens, shortness of breath increases, coughing attacks become more frequent and intensify. There is a general depression of the body. The treatment that was used earlier does not bring a positive effect. In most cases, the patient needs hospitalization, revision and adjustment of the previously prescribed treatment.

A state of exacerbation can develop against the background of a previous disease (ARI, bacterial infections). A common upper respiratory tract infection for a person with COPD is a condition in which the functionality of the lungs is greatly reduced. The normalization period is delayed for a longer time.

A condition such as an exacerbation of COPD is diagnosed based on symptomatic manifestations, patient complaints, hardware and laboratory studies).

How COPD affects the body

Any disease of a chronic nature has a negative impact on the body in general. So COPD leads to disorders that seem to have nothing to do with the physiological structure of the lungs.

• Violation of the functions of the intercostal muscles (participate in the act of breathing), muscle atrophy may occur;
• Decreased glomerular filtration of the kidneys;
• The risk rises;
• Decreased memory;
• Tendency to depression;
• Decreased protective functions of the body.

Diagnostics

• Blood analysis. This analysis is mandatory for diagnosing COPD. In the acute stage, an increased, neutrophilic leukocytosis can be traced. In patients with developing hypoxia, there is an increase in the number of red blood cells, a low ESR and increased hemoglobin.
• Sputum analysis, what it is - this is the most important procedure for patients who produce sputum. The results of such an analysis can provide answers to many questions. The nature of inflammation, the degree of its severity. You can also trace the presence of atypical cells, in such diseases it is necessary to make sure that there is no oncological disease.

Sputum in patients with COPD is mucous, and in the acute stage it can be purulent. The viscosity of sputum increases, as does its quantity, the color becomes greenish with streaks of yellow.

Sputum analysis is still necessary for such patients, because thanks to it it becomes possible to find out the causative agents of the infection and their resistance to a particular antibacterial drug.

• X-ray diagnostic method, is mandatory for the correct diagnosis and exclusion of other lung diseases (many diseases of the respiratory system can have a similar clinical picture). An x-ray is taken in two positions, frontal and lateral.

During periods of exacerbations, it allows you to exclude or.

• An ECG is used to exclude or confirm such a diagnosis of cor pulmonale (hypertrophy of the muscles of the right heart).

A step test, at the initial stage of the disease, is usually not pronounced and for diagnosis it is necessary to check whether it is present with a small physical activity.

Symptoms to look out for

Consider a number of symptoms that you should pay attention to and, if necessary, consult a doctor for a correct diagnosis.

• Often recurrent acute;
• Attacks of excruciating cough, their number gradually increases;
• Cough with constant expectoration;
• Increase in body temperature;
• Attacks of shortness of breath, which increases with the course of the disease.

Is it possible to be active with a disease such as COPD

The disease in question certainly reduces the quality of life, but it must be remembered that it is important not to forget - an active lifestyle will help in the treatment of the disease and improve the psycho-emotional state.

You need to start physical activity very carefully and gradually!

With particular caution, a group of people who, before the illness, did not lead a very active lifestyle, should start training.

Start with classes lasting no more than ten minutes, it is worth increasing the load slowly with several workouts per week.

Do your daily household chores, this way of physical impact on the body will be gentle options for patients with this disease. Walk up the stairs, take a walk in the fresh air, do household chores (wash the floor, windows, dishes), take on part of the duties of the yard (sweep, plant and care for plants).

Before performing the planned actions, do not forget about the warm-up.

Warming up promotes safe exercise, it slowly and gradually prepares the body for a more serious load. An important point will be considered that the warm-up will help increase the frequency respiratory movements, moderate heart contractions, normalize body temperature.

Treatment

There are several basic principles for the treatment this disease.

• Complete rejection of addiction - smoking;
• Medicamentous method of treatment, with the help of drugs of various groups of orientation;
• Vaccination against infections caused by pneumococcus and;
• Moderate physical activity has a significant effect;
• Oxygen inhalation is used in severe respiratory failure as a way to prolong life.

Groups of drugs used in the treatment

• Bronchodilators (atrovent, salbutamol, aminofillin);
• Hormonal preparations from the group of corticosteroids (symbicort, seretide);
• Drugs that promote sputum discharge (ambrobene, codelac);
• Immunomodulating agents (immunal, Derinat);
• Phosphodiesterase 4 inhibitors (Daxas, Dalisp).

COPD treatment with folk remedies

Treatment of some symptoms of this disease can be carried out using traditional medicine recipes.

It is important to remember the need to consult with a specialist! Treatment with alternative medicine is an addition to the treatment that the doctor must prescribe.

Steam inhalation

This procedure is carried out at home with ease. You will need a container for the solution, a towel and a little time.

• For one liter of hot water (90-100 degrees), 5-6 drops of pine essential oil, eucalyptus oil and chamomile.
• Inhalations with the addition of sea salt (a liter of boiling water, 2-3 tablespoons of sea salt).
• Inhalations of the collection of mint, calendula and oregano herbs (2 tablespoons of the collection per liter of boiling water).

Also, when treating chronic pulmonary obstruction, you can do.

Breathing exercises

Breathing exercises, activities aimed at strengthening the muscles of the lungs and intercostal muscles have a very beneficial effect.

Gymnastics option. On inspiration, raise your hands up, and on exhalation, tilt the body and arms to the left, on the next breath, raise your hands up, and tilt the body and arms to the right.

Chronic obstructive pulmonary disease is a chronic non-allergic inflammatory disease respiratory system, resulting from irritation of the lungs by toxic substances. The abbreviated name of the disease - COPD, is an abbreviation made up of the first letters of the full name. The disease affects the final sections of the respiratory tract - the bronchi, as well as the respiratory tissue - the lung parenchyma.

COPD is the result of exposure to harmful dust and gases on the human respiratory system. The main symptoms of COPD are cough and shortness of breath during exercise. Over time, the disease progresses steadily, and the severity of its symptoms increases.

The main mechanisms of painful changes in the lungs in COPD:

• development of emphysema - swelling of the lungs with rupture of the walls of the respiratory vesicles-alveoli;
• the formation of irreversible bronchial obstruction - difficulties for the passage of air through the bronchi due to the thickening of their walls;
• a steady increase in chronic respiratory failure.

About the causes of COPD and its dangers

Inhalation of tobacco smoke, toxic gases and dust causes inflammation in the airways. it chronic inflammation destroys the respiratory tissue of the lungs, forms emphysema, violates the natural protective and regenerative mechanisms, causes fibrous degeneration of the small bronchi. As a result, the correct functioning of the respiratory system is disrupted, air is retained in the lungs, and the airflow rate in the bronchi progressively decreases. These internal disturbances cause the patient to experience shortness of breath on exertion and other symptoms of COPD.

Smoking is the main causative factor in COPD. According to statistics, every 3rd resident smokes in Russia. Thus, the total number of smoking Russians is about 55 million people. In absolute numbers by the number of smokers Russian Federation ranks 4th in the world.

Smoking is both a risk factor for COPD and cardiovascular disease.

Experts predict that by 2020 smoking will kill 20 people per minute. WHO estimates that smoking is responsible for 25% of deaths in patients with ischemic disease heart and 75% of deaths in patients with chronic bronchitis and COPD.

The combined effect on the lungs of tobacco smoking and harmful industrial aerosols is a particularly deadly combination. People with this combination of risk factors develop the most severe form of the disease, rapidly leading to permanent lung damage and death from respiratory failure.

COPD is one of the leading causes of morbidity and mortality worldwide, which leads to significant, ever-increasing economic and social damage to society.

What signs will help to suspect COPD?

The presence of COPD should be suspected in people with persistent cough, shortness of breath, sputum production, with past or present exposure to risk factors. These symptoms alone are not diagnostic, but the combination of them greatly increases the likelihood of a diagnosis of COPD being made.

Chronic cough is often the 1st symptom of COPD and is underestimated by the patient himself. People consider these coughs to be a natural consequence of smoking or exposure to other harmful air pollutants. At first, the cough may be intermittent, but over time it becomes daily, constant. In COPD, chronic cough may be without sputum (unproductive).

Shortness of breath on exertion is the main COPD symptom. Patients describe shortness of breath as a feeling of heaviness in the chest, suffocation, lack of air, the need to make efforts to breathe.

Typically, people with COPD cough up a small amount of sticky sputum after a coughing episode. The purulent nature of sputum indicates an exacerbation of inflammation in the airways. A persistent cough with phlegm can bother a person for several years before the onset of shortness of breath (before the start of airflow limitation). However, a decrease in airflow rate in COPD can develop without chronic cough and sputum production.

As the disease progresses, complaints of general weakness, constant malaise, bad mood, increased irritability, and weight loss may appear.

What does an examination reveal in a COPD patient?

In the initial period of the disease, the examination does not reveal any abnormalities characteristic of COPD. Over time, with an increase in bloating and an irreversible violation of bronchial patency, a barrel-shaped deformation of the chest appears - a characteristic expansion of it in the anterior-posterior size. The appearance and severity of deformity depend on the degree of swelling of the lungs.

Widely known are 2 types of COPD patients - "pink puffers" and "blue puffers". In a number of patients, symptoms of pulmonary distention come to the fore, and in others, airway obstruction. But those and others have both signs.

At severe forms disease, there may be a loss of muscle mass, which leads to a lack of weight. In obese patients, despite the increased weight, one can also notice a decrease in muscle mass.

Prolonged intense work of the respiratory muscles leads to its fatigue, which is further aggravated by malnutrition. A sign of fatigue of the main respiratory muscle (diaphragm) is the paradoxical movement of the anterior wall of the abdominal cavity - its retraction during inspiration.

Cyanosis (cyanosis) of the skin of a gray-ashy shade indicates a pronounced lack of oxygen in the blood and a severe degree of respiratory failure. It is important to determine the level of consciousness. Lethargy, drowsiness, despite severe shortness of breath, or, conversely, the excitement accompanying it, indicate oxygen starvation, life threatening which requires urgent care.

Symptoms of COPD on external examination

An external examination of the lungs in the initial period of the disease carries scarce information. When percussion of the chest, a box sound may appear. When listening to the patient's lungs during an exacerbation, dry whistling or buzzing rales appear.

In the clinically significant stage of COPD, external examination data reflect severe pulmonary emphysema and severe bronchial obstruction. The doctor finds during the study: boxed sound when percussion, limitation of diaphragm mobility, chest rigidity, weakening of breathing, wheezing or buzzing scattered wheezing. The predominance of one or another sound phenomenon depends on the type of disease.

Instrumental and laboratory diagnostics

The diagnosis of COPD must be confirmed with spirometry, a lung function test. Spirometry in COPD detects bronchial airflow limitation. A characteristic feature of the disease is the irreversibility of bronchial obstruction, that is, the bronchi practically do not expand when inhaled with a standard dose of a bronchodilator drug (400 μg of salbutamol).

Radiation diagnostic methods (X-ray, CT) are used to exclude other severe lung diseases that have similar symptoms.

At clinical signs severe respiratory failure requires an assessment of the levels of oxygen and carbon dioxide in the arterial blood. If this analysis is not possible, a pulse oximeter that measures saturation can help assess the lack of oxygen. When blood saturation is less than 90%, immediate administration of oxygen inhalation is indicated.

Principles of COPD treatment

Key points in the treatment of patients with COPD:

• smoking patients need to stop smoking, otherwise taking medication loses its meaning;
• smoking cessation is facilitated by nicotine replacement drugs (chewing gum, inhaler, nasal spray, skin patch, sublingual tablets, lozenges);
• to reduce shortness of breath and swelling of the lungs, drugs are used that expand the bronchi for 12-24 hours (long-acting bronchodilators) in inhalations;
• to reduce the severity of inflammation with frequent exacerbations, roflumilast is prescribed - new drug for the treatment of COPD;
• patients with decreased oxygen saturation in the blood<90%, показана длительная кислородотерапия >15 hours a day;
• for patients with a low inhalation rate, inhalation of drugs can be carried out using a nebulizer - a special compressor inhaler;
• exacerbation of the disease with expectoration of purulent sputum is treated with antibiotics and expectorants;
• all patients with COPD are shown classes in the pulmonary rehabilitation program, including smoking cessation, education, feasible physical training, nutritional counseling and social support;
• to prevent infectious exacerbations, COPD patients are recommended annual influenza vaccination, as well as vaccination against pneumococcus.

COPD prevention

most effective prevention COPD would be a worldwide ban on the production, sale and smoking of tobacco and tobacco products. But while the world is ruled by capital and greed, this can only be dreamed of.

The drowning will have to take their salvation into their own hands:

• to prevent the development of COPD in a smoker, you need to part with cigarettes (cigarettes, tobacco, etc.);
• to prevent the development of COPD in a non-smoker, he does not need to start smoking;
• to prevent the development of COPD in workers in hazardous industries, it is necessary to strictly observe safety precautions and the maximum allowable periods of continuous work in this industry.

To prevent COPD in your children and grandchildren, set an example of a healthy lifestyle and zero tolerance for smoking.

Individuals with COPD have different life expectancies, depending on a number of factors. The most important of these are the presence of concomitant complications in the form of heart disease and the level of pressure in the pulmonary artery. COPD has the following decoding: chronic obstructive pulmonary disease. This pathology occurs mainly in smokers with experience. In addition, it is caused by exposure to harmful chemicals and dust. Genetic predisposition also plays a role. The disease is characterized by constant progression, and its exacerbation often occurs. Therefore, the question of how long such patients live is very relevant.

The disease has chronic course and is characterized by a decrease in the volume of air entering the lungs. This is caused by narrowing of the bronchial tubes. According to statistics, men over 40 years of age, smokers with experience, are more affected by this disease. But since the number of women who actively smoke has recently increased sharply, their proportion among the sick has also increased. Chronic obstructive pulmonary disease is not cured completely, you can only stop its progression and thus prolong the life of the patient. The first symptom of the disease is shortness of breath.

Stages and symptoms of the disease that affect the life of the patient

AT clinical picture COPD symptoms include increased sputum production, severe coughing, and shortness of breath. This symptomatology is caused by inflammatory processes in the lungs and obstruction. These symptoms are present in the initial stages of the disease, in the later stages they are joined by problems in the work of the heart and pain in the bones. Often COPD combines the symptoms and signs of emphysema and obstructive bronchitis.

At the beginning of the disease, the patient's cough disturbs mainly after a night's sleep, later it becomes permanent. The cough is not dry, accompanied by profuse sputum. Shortness of breath is associated with difficulty exhaling.

Depending on the severity of symptoms, 4 stages of the disease are distinguished:

1. The first stage of the disease is mild, manifested in episodic bouts of dry cough. Shortness of breath appears only with significant physical exertion. There is no marked deterioration in well-being. Identification of COPD at this stage and treatment will help maintain normal duration and quality of life of the patient. Reliable diagnosis during this period of the disease is carried out only by 25%.
2. The stage of moderate severity is characterized by certain restrictions that the disease imposes on the patient. So, there is a pronounced violation of the functioning of the lungs and shortness of breath even with minor loads. Cough bothers more often, especially in the morning. The patient is prescribed medication. The prognosis for life at this stage is less favorable.
3. Severe stage - the patient complains of symptoms such as constant shortness of breath and shortness of breath. Cyanosis of the skin and complications in the work of the heart appear, exacerbation often occurs. On average, patients with similar manifestations live no more than 8 years. In the case of the addition of additional diseases or if an exacerbation of COPD occurs, the mortality rate reaches 30%.
4. The latter is a very severe stage of the disease: most patients at this stage live no more than a year. They need a constant intake medicines to sustain life. Often there is a need for artificial ventilation of the lungs. All symptoms of the disease, especially cough and shortness of breath, are maximally pronounced. In addition, all sorts of complications join.

There are also such forms of the disease as emphysematous, bronchitis and mixed.

The life expectancy of patients

What is the life expectancy of people with COPD? A timely diagnosis has a direct impact on the life expectancy of patients with such a diagnosis. Quite often, a reduction in the life expectancy of people with this disease occurs due to delayed diagnosis.

Most patients do not apply in time for a qualified medical care, and therefore there is late treatment and high premature mortality. In the absence of proper treatment, the prognosis is always unfavorable, since the disease is steadily progressing. But if you consult a doctor in time and start adequate treatment, then the life expectancy of such patients increases significantly. COPD can be diagnosed by spirometry, X-ray, ultrasound of the heart, ECG, fibrobronchoscopy. In addition, the doctor conducts a physical examination and prescribes a laboratory blood test.

Chronic obstructive pulmonary disease significantly impairs the patient's daily life, depriving him of the opportunity to fully perform elementary household skills.

Nevertheless, the life of such patients is different, some live longer, others less. The prognosis depends on certain factors that directly affect the duration of their life. Among them:

• the presence of cardiac hypertrophy;
• the pressure of the pulmonary trunk is higher than normal;
• heart rate level;
• reduced oxygen content in the blood.

Since the methods and effectiveness of the treatment directly affect the quality and life expectancy of patients, they must strictly comply with all the instructions of the attending physician. In particular, they strictly show:

• to give up smoking;
• a special diet that includes food enriched with proteins and vitamins;
• sports;
• special breathing exercises;
• weight loss in the presence of excess;
• medical treatment.

How to increase life expectancy?

Morbidity and mortality from chronic obstructive pulmonary disease worldwide remains high. Measures therapeutic effect are aimed at achieving the following goals:

• reduction in mortality;
• reduction in the severity of symptoms;
• improving the quality of life of patients;
• facilitating exercise tolerance;
• prevention of exacerbations and complications.

As part of drug treatment drugs are used that act to improve sputum discharge and bronchial patency (bronchodilators and mucolytics). Corticosteroids are also given to reduce pulmonary edema (prednisone) and antibacterial drugs especially if there is an exacerbation.

Video about COPD and how to detect it:

In the absence of positive dynamics under the influence of such treatment, surgical methods. They are aimed at reducing the volume of the lungs, due to which they will be relieved acute symptoms or a lung transplant.

Treatment of this disease is a long process that requires an integrated approach. In the mild stages of COPD, drug therapy can be dispensed with, in more advanced conditions, oxygen therapy is required, and in the absence of the desired effect and the patient's condition worsens, surgical methods are resorted to.

However, the most important point in the treatment of COPD is the correction of lifestyle. The patient needs to stop bad habits, monitor your diet, regularly perform breathing techniques, and also play sports.

Diagnostic methods - differential diagnostics

To identify this pathology, the following diagnostic measures are used:

• Seeing an appropriate specialist. Using a phonendoscope, the doctor will be able to detect wheezing in the lungs, as well as trace the nature of the respiratory process. At this stage, the doctor finds out the conditions in which the patient works, whether he has bad habits.
• Spirometry. The most common method for diagnosing the disease in question, which is distinguished by its simplicity and low cost. With its help, the doctor evaluates the quality of the passage of air masses through the respiratory tract, vital capacity, forced expiratory volume and other indicators. In some cases, before and after this procedure, inhalation is carried out with drugs that promote bronchial expansion.
• Bodyplethysmography. It makes it possible to determine those lung volumes that cannot be measured by spirometry. During breathing, the mechanical vibrations of the chest are measured, which are then compared with the results of spirography.
• Sputum analysis. Needed to study the nature of the inflammatory process in the bronchi. In the presence of exacerbations, sputum changes its consistency and color. In addition, this procedure favors the detection of oncological alertness.
• General blood testing. At advanced stages, chronic obstructive pulmonary disease manifests itself as an increase in the number of red blood cells and hemoglobin. ESR increase indicates the development of exacerbations.
• The study of the gas composition of the blood. Relevant for suspected respiratory failure.
• Radiography of the lungs. It makes it possible to exclude other diseases that are similar in their manifestations to COPD. Structural changes in the bronchial walls and lung tissue will be clearly visible on the radiograph. In some cases, computed tomography may be required for an accurate diagnosis.
• Electrocardiography. Pulmonary hypertension adversely affects the functioning of the right ventricle, which can provoke the death of the patient. ECG makes it possible to detect changes in the structures of the heart and respond to them in a timely manner.

Video: COPD treatment - from tradition to the future

Fibrobronchoscopy prescribed in order to exclude pathologies, which in their symptomatic picture are similar to chronic obstructive pulmonary disease. This technique allows you to study the bronchial mucosa, assess its condition, collect bronchial secretions for laboratory study.

Conservative treatment of COPD - effective therapeutic methods, drugs

The primary tasks in choosing the tactics of treating this disease are to improve the patient's quality of life, minimize the risk of exacerbations, and limit the development of bronchial obstruction.

1. Minimize exposure to rooms/areas with high concentrations of harmful substances.
2. Maintaining a sports lifestyle for patients diagnosed with mild COPD. The emphasis should be on walking, swimming, gymnastics.
3. Regular flu vaccination and pneumococcal infections. The most suitable time for injections is from October to mid-November.
4. Rejection of bad habits. First of all, this concerns smoking.
5. Adequate nutrition enriched with proteins. Patients should also monitor their body weight to avoid obesity.

To study all the subtleties of behavior in this pathology, it is recommended to visit "Schools for patients with COPD".

The specialists working here will carry out explanatory work on the selection of adequate physical activity, familiarize them with the available medicines in the fight against the disease, teach,.

In the event that the patient has COPD grade 2 and above, he is prescribed one of the following procedures:

• Oxygen therapy. Oxygen supply (at least 1-2 liters per minute) is carried out for 15 hours.
• Application of oxygen respirators, the ventilation mode of which is selected for each patient within the hospital. Said respirator must function while the patient is asleep, and they are also called upon for several hours during the daytime.
• percussion drainage bronchial contents.
• Breathing exercises.

The procedures described above are relevant to carry out when 3 important conditions are met:

1. The patient receives the necessary medication.
2. The patient completely gave up smoking.
3. The patient has a desire to carry out oxygen therapy.

Drug therapy involves taking the following drugs:

• Bronchodilator drugs. Such drugs eliminate spasm in the bronchi, contribute to their expansion, and ensure the maintenance of their normal shape. In the initial stages of the disease, short-acting medications are prescribed, the effect of which lasts a maximum of 6 hours. In more neglected conditions, they turn to long-acting agents - they last for 12-24 hours.
• Mucolytics. Liquefies mucus and makes it easier to expel.
• Anti-inflammatory therapy. It is used in cases where the drugs described above do not stop inflammatory processes in the bronchi. Includes the following drugs:
  - Glucocorticosteroids. They are often used by inhalation. It takes several months to improve. Discontinuation of these drugs leads to a worsening of the course of the disease. The main side effect of this treatment is candidiasis. oral cavity. This complication can be avoided by rinsing the mouth after each inhalation.
  - Vitamin therapy.
  - Phosphodiesterase-4 inhibitors. Help to minimize the risk of exacerbations in bronchitis type of pathology.
• Antibiotic therapy. It is indicated only for infectious exacerbations.

Video: Chronic obstructive pulmonary disease

Surgical treatment of COPD - types of operations and indications for their implementation

Surgical manipulations with the disease in question are carried out in the following cases:

• The age of the patient does not exceed 75 years.
• The patient refrains from smoking for at least 3 months.
• Medical treatment and pulmonary rehabilitation are not able to cope with severe shortness of breath. At the same time, an appropriate intensive care of COPD for a long period of time is an obligatory moment. If the patient's health worsens after all the measures taken, he is referred for a consultation with a thoracic surgeon in order to decide whether the surgical intervention is appropriate.
• CT confirms severe emphysema in the upper lobe.
• There are signs of hyperinflation.
• Forced expiratory volume after taking bronchodilators in the first second is not more than 45% of the predicted value.

Before the operation, a thorough examination and an intensive two-week drug therapy, the purpose of which is to reduce inflammation and reduce bronchial obstruction.

Algorithm for lung volume reduction surgery:

1. Anesthesia. resort to general anesthesia with artificial lung ventilation. The operated person is laid on his side.
2. Implementation of resection in the 5th or 6th intercostal space. The surgeon performs a lateral thoracotomy.
3. Revision of the pleural cavity.
4. Maximum elimination (about 30%) of the transformed lung tissue. This manipulation is called reduction pneumoplasty.
5. Layered suturing of the wound.
6. Transfer to spontaneous breathing.

In the event that, against the background of active destruction of the walls of the alveoli in the lungs, extensive bullae (air spaces) have formed, the doctor may prescribe bullectomy. This procedure can solve the problem associated with respiratory failure.

With advanced forms of COPD, lung transplant. The essence of the operation is to replace the damaged lung with a healthy one, which is taken from a deceased donor.

Such an operation is fraught postoperative complications in the form of infection - or rejection - of the transplanted organ.

In general, if everything goes well, the patient's standard of living in the future improves significantly.

How to prevent complications after COPD treatment - recovery after treatment and surgery, recommendations for patients

To restore working capacity after an operation for the treatment of the disease in question, on average, it takes a year.

During the first 4-5 days the patient stays with drainage tubes in the treated area. During this period, he is worried about headaches, shortness of breath, fatigue. These phenomena are explained by oxygen deficiency in the body. To replenish it, within a few hours after surgery, the patient is prescribed a set of breathing exercises, exercise therapy, as well as oxygen therapy.

To minimize the risk of infection, prescribe antibiotic therapy, and for cupping pain The first time you should take painkillers.

• Very important throughout rehabilitation period watch your weight. Extra pounds will put pressure on the diaphragm. You need to eat often, but in small portions, with an emphasis on healthy foods.
• Physical activity should be limited at first hiking outdoors.
• Bad habits should be abandoned forever.
• Also need avoid hypothermia and protect yourself from colds as much as possible.

Video: What can not be done with obstructive bronchitis? — Doctor Komarovsky

Folk remedies for the treatment of COPD

In the treatment of the pathology in question, traditional medicine recipes are used only as an auxiliary method to alleviate the symptoms of the disease.

Similar treatment not able to completely replace drug therapy!

Used to improve sputum discharge inhalations with decoctions medicinal herbs . As the main ingredient, you can choose mint, oregano, marshmallow, coltsfoot. At it is forbidden to add any essential oil : It can lead to pneumonia.

In general, there are a lot of recipes for traditional medicine to combat the manifestations of COPD.

The most accessible to the general public are the following:

1. 1 tsp flaxseed oil is taken 3 times a day 30 minutes before meals for a month. After a 2-week break, the reception of the specified oil is resumed.
2. Badger / pork fat (0.5 l.), honey (1 l.), chocolate (0.5 kg), aloe leaves are mixed. These components are placed in a container and heated on a steam bath. At the same time, the temperature should not rise above 37.5 C, otherwise the honey will lose its healing properties. The prepared mixture should be taken before meals three times a day, 1 tbsp.

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Chronic obstructive pulmonary disease (COPD) is characterized by the presence of partially reversible airway obstruction caused by an abnormal inflammatory response to exposure to toxins, often cigarette smoke.

Alpha-antitrypsin deficiency and various occupational pollutants - less common causes development of this pathology in non-smokers. Over the years, symptoms develop - a productive cough and shortness of breath; shortness of breath and wheezing are common signs. Severe cases may be complicated by weight loss, pneumothorax, right ventricular failure, and respiratory failure. Diagnosis is based on history, physical examination, chest x-ray, and lung function tests. Treatment with bronchodilators and glucocorticoids, if necessary, oxygen therapy is carried out. Approximately 50% of patients die within 10 years of diagnosis.

Chronic obstructive pulmonary disease (COPD) includes chronic obstructive bronchitis and emphysema. Many patients have signs and symptoms of both conditions.

Chronic obstructive bronchitis is chronic bronchitis with airway obstruction. Chronic bronchitis (also called chronic mucus secretion syndrome) is defined as a productive cough lasting at least 3 months for 2 consecutive years. Chronic bronchitis becomes chronic obstructive bronchitis if spirometric signs of airway obstruction develop. Chronic asthmatic bronchitis is a similar, overlapping condition characterized by chronic productive cough, wheezing, and partially reversible airway obstruction in a history of smokers bronchial asthma. In some cases, it is difficult to distinguish chronic obstructive bronchitis from asthmatic bronchitis.

Emphysema is a destruction of the lung parenchyma, resulting in loss of elasticity and destruction of the alveolar septa and radial airway extension, which increases the risk of airway collapse. Hyperairiness of the lungs, restriction of the respiratory flow makes it difficult for air to pass through. The air spaces enlarge and may eventually turn into bullae.

ICD-10 code

J44.0 Chronic obstructive pulmonary disease with acute respiratory infection lower respiratory tract

J44.9 Chronic obstructive pulmonary disease, unspecified

Epidemiology of COPD

In 2000, about 24 million people in the US had COPD, of which only 10 million were diagnosed. In the same year, COPD was the fourth leading cause of death (119,054 cases compared to 52,193 in 1980). Between 1980 and 2000, COPD mortality increased by 64% (from 40.7 to 66.9 per 100,000 population).

Prevalence, incidence, and mortality rates increase with age. The prevalence is higher among males, but overall mortality is the same for males and females. Morbidity and mortality are generally higher among whites, blue-collar workers, and those with lower levels of education; this is probably due to the large number of smokers in these categories of the population. Familial cases of COPD do not appear to be associated with alpha-antitrypsin (an alpha-antiprotease inhibitor) deficiency.

The incidence of COPD is increasing worldwide due to an increase in smoking in non-industrialized countries, a decrease in mortality due to infectious diseases, and the widespread use of biomass fuels. COPD caused approximately 2.74 million deaths in the world in 2000 and is expected to become one of the five major diseases in the world by 2020.

What causes COPD?

Smoking cigarettes - main factor risk in most countries, although only about 15% of smokers develop clinically apparent COPD; a history of use of 40 or more pack-years is especially predictive. Smoke from biofuel combustion for home cooking is an important aetiological factor in underdeveloped countries. Smokers with pre-existing airway reactivity (defined as increased sensitivity to inhaled methacholine chloride), even in the absence of clinical asthma, have a higher risk of developing COPD than individuals without this pathology. Low body weight, childhood respiratory disease, secondhand smoke, air pollution, and occupational pollutants (eg, mineral or cotton dust) or chemicals (eg, cadmium) contribute to the risk of COPD but are of little significance compared to cigarette smoking.

Genetic factors also play a role. The most well-studied genetic disorder, alpha-antitrypsin deficiency, is a significant cause of emphysema in non-smokers and affects susceptibility to the disease in smokers. Polymorphisms in the microsomal epoxy hydrolase, vitamin D-binding protein, 11_-1p, and IL-1 receptor antagonist genes are associated with rapid decline forced expiratory volume in 1 s (FEV) in selected populations.

In genetically predisposed individuals, inhalation exposure induces an inflammatory response in the airways and alveoli, leading to the development of the disease. It is assumed that the process is due to an increase in protease activity and a decrease in antiprotease activity. In the normal process of tissue repair, lung proteases - neutrophil elastase, tissue metalloproteinases and cathepsins - destroy elastin and connective tissue. Their activity is balanced by antiproteases - alpha-antitrypsin, a secretory leukoproteinase inhibitor produced by the epithelium of the respiratory tract, elafin, and a tissue inhibitor of matrix metalloproteinases. In COPD patients, activated neutrophils and other inflammatory cells secrete proteases during inflammation; protease activity exceeds antiprotease activity, resulting in tissue destruction and increased secretion of mucus. Activation of neutrophils and macrophages also leads to the accumulation of free radicals, superoxide anions and hydrogen peroxide, which inhibit antiproteases and cause bronchospasm, mucosal edema, and increased mucus secretion. Like infection, neutrophil-induced oxidative damage, release of profibrous neuropeptides (eg, bombesin), and reduced production of vascular endothelial growth factor play a role in pathogenesis.

Lung function studies

Patients with suspected COPD should undergo a pulmonary function test to confirm airway obstruction and quantify its severity and reversibility. Pulmonary function testing is also needed to diagnose subsequent disease progression and monitor response to treatment. The main diagnostic tests are FEV, which is the volume of air exhaled in the first second after a full breath; forced vital capacity (FVC), which is the total volume of air exhaled with maximum force; and volume-flow loop, which is a simultaneous spirometric recording of airflow and volume during forced maximum exhalation and inhale.

A decrease in FEV, FVC, and the FEV1/FVC ratio is a sign of airway obstruction. The volume-flow loop shows deflection in the expiratory segment. FEV decreases to 60 ml/yr in smokers, compared to a less steep decline of 25-30 ml/yr in non-smokers, beginning around age 30. In middle-aged smokers who already have a low FEV, the decline develops more rapidly. When the FEV falls below approximately 1 L, patients develop dyspnea with everyday exercise; when the FEV falls below about 0.8 L, patients are at risk of hypoxemia, hypercapnia, and cor pulmonale. FEV and FVC are easily measured with stationary spirometers and determine disease severity because they correlate with symptoms and mortality. Normal levels are determined depending on the age, sex and height of the patient.

Additional lung function tests are needed only under certain circumstances, such as surgical lung volume reduction. Other tests under investigation may include increased total lung capacity, functional residual capacity, and residual volume, which may help distinguish COPD from restrictive lung diseases, in which these are reduced; the vital capacity decreases and the diffusion capacity of carbon monoxide in a single breath (DR) decreases. Decreased VR is not specific and is reduced in other disorders that damage the pulmonary vasculature, such as interstitial lung disease, but may help distinguish COPD from asthma, in which VR is normal or elevated.

COPD Imaging Methods

Chest x-ray has characteristic, though not diagnostic, changes. Changes associated with emphysema include hyperinflation of the lung, manifested by a flattening of the diaphragm, a narrow cardiac shadow, rapid vasoconstriction of the lung root (anterior-posterior view), and expansion of the retrosternal air space. Flattening of the diaphragm due to hyperinflation causes an increase in the angle between the sternum and anterior diaphragm on a lateral radiograph to more than 90° compared to the normal 45°. X-ray negative bullae more than 1 cm in diameter, surrounded by arcade blurred shading, indicate locally pronounced changes. Predominant emphysematous changes in the bases of the lungs indicate alpha1-antitrypsin deficiency. The lungs may appear normal or may be translucent due to loss of parenchyma. Chest radiographs of patients with chronic obstructive bronchitis may be normal or show bilateral basilar enhancement of the bronchovascular component.

An enlarged lung root indicates an increase in central pulmonary arteries observed in pulmonary hypertension. Right ventricular dilatation seen in cor pulmonale may be masked by increased airiness of the lung or may appear as expansion of the heart shadow into the retrosternal space or widening of the transverse cardiac shadow compared to previous chest radiographs.

CT findings can help clarify changes seen on a chest x-ray that are suspicious of concomitant or complicating diseases such as pneumonia, pneumoconiosis, or lung cancer. CT helps evaluate the spread and distribution of emphysema by visually evaluating or analyzing the density distribution of the lung. These parameters may be useful in preparation for lung volume reduction surgery.

Additional Research in COPD

Alpha-antitrypsin levels should be measured in symptomatic COPD patients < 50 years of age and non-smokers of any age with COPD to detect alpha-antitrypsin deficiency. Other evidence for antitrypsin deficiency includes a family history of early COPD or early liver disease. childhood, the distribution of emphysema in the lower lobes and COPD against the background of ANCA-positive vasculitis (anti-neutrophil cytoplasmic antibodies). Low levels of alpha-antitrypsin should be confirmed phenotypically.

An ECG is often done to rule out cardiac causes of dyspnea, usually showing a diffusely low QRS voltage with a vertical cardiac axis caused by increased lung airiness, and increased waveform amplitude or right waveform vector deviation caused by right atrial dilatation in patients with severe emphysema. Manifestations of right ventricular hypertrophy, deviation of the electrical axis to the right> 110 without blockade of the right leg of the bundle of His. Multifocal atrial tachycardia, an arrhythmia that may accompany COPD, presents as a tachyarrhythmia with polymorphic P waves and variable PR intervals.

Echocardiography is sometimes useful for assessing right ventricular function and pulmonary hypertension, although it is technically difficult in patients with COPD. Investigation is most often ordered when concomitant lesions of the left ventricle or heart valves are suspected.

CBC is of little diagnostic value in diagnosing COPD, but may reveal erythrocythemia (Hct > 48%) reflecting chronic hypoxemia.

Diagnosis of COPD exacerbations

Patients with exacerbations associated with increased work of breathing, drowsiness, and low O2 saturation on oximetry should be screened for arterial blood gases to quantify hypoxemia and hypercapnia. Hypercapnia can coexist with hypoxemia. In these patients, hypoxemia often provides more respiratory excitation than hypercapnia (which is normal), and oxygen therapy may exacerbate hypercapnia by decreasing the hypoxic respiratory response and increasing hypoventilation.

Values partial pressure arterial oxygen (PaO2) less than 50 mm Hg. Art. or partial pressure of arterial carbon dioxide (Pa-CO2) more than 50 mm Hg. Art. in conditions of respiratory acidemia, acute respiratory failure is determined. However, some patients with chronic COPD live with such indicators for long periods of time.

A chest x-ray is often done to rule out pneumonia or pneumothorax. Rarely, infiltrate in patients receiving chronic systemic glucocorticoids may be due to Aspergillus pneumonia.

Yellow or green sputum is a reliable indicator of the presence of neutrophils in the sputum, indicating bacterial colonization or infection. Gram stain usually reveals neutrophils and a mixture of organisms, often Gram-positive diplococci (Streptococcus pneumoniae) and/or Gram-negative rods (H. influenzae). Sometimes exacerbations are caused by other oropharyngeal flora, such as Moraxella (Branhamella) catarrhalis. In hospitalized patients, Gram stains and cultures may reveal resistant gram-negative organisms (eg, Pseudomonas) or, rarely, gram-positive staphylococcal infection.

COPD treatment

Treatment of chronic stable COPD is aimed at preventing exacerbations and maintaining long-term normal health and lung function through pharmacotherapy and oxygen therapy, smoking cessation, exercise, improved nutrition, and pulmonary rehabilitation. Surgical treatment of COPD is indicated for selected patients. Controlling COPD involves treating both chronic stable disease and exacerbations.

Drug treatment for COPD

Bronchodilators are the backbone of COPD control; drugs include inhaled beta-agonists and anticholinergics. Any patient with symptomatic COPD should use one or both classes of drugs that are equally effective. For initial therapy, the choice between short-acting beta-agonists, long-acting beta-agonists, anticholinergics (which have a greater bronchodilating effect), or a combination of beta-agonists and anticholinergics is often decided based on the cost of treatment, patient preference, and symptoms. Currently, there is evidence that the regular use of bronchodilators slows the deterioration of lung function, drugs quickly reduce symptoms, improve lung function and performance.

In the treatment of chronic stable disease, metered dose inhalers or dry powder inhalers are preferred over nebulized home therapy; home nebulizers quickly become dirty due to incomplete cleaning and drying. Patients should be taught to exhale as much as possible, inhale the aerosol slowly until reaching total capacity lungs and hold your breath for 3-4 seconds before exhaling. Spacers ensure optimal distribution of the drug to the distal airways, so coordinating inhaler activation with inhalation is not as important. Some spacers prevent the patient from inhaling if they inhale too quickly.

Beta-agonists relax the smooth muscles of the bronchi and increase the clearance of the ciliated epithelium. Salbutamol aerosol, 2 puffs (100 mcg/dose), inhaled from a metered dose inhaler 4-6 times a day, is usually the drug of choice because of its low cost; regular use has no advantage over use on demand and causes more undesirable effects. Long-acting beta-agonists are preferred for patients with nocturnal symptoms or for those who find frequent inhaler use uncomfortable; salmeterol powder, 1 breath (50 mcg) 2 times a day or formoterol powder (Turbohaler 4.5 mcg, 9.0 mcg or Aerolizer 12 mcg) 2 times a day or formoterol 12 mcg ppm 2 times a day can be used. Powder forms may be more effective for patients who have coordination problems when using a metered dose inhaler. Patients should be made aware of the difference between short-acting and long-acting drugs because long-acting drugs used on an as-needed basis or more than twice a day increase the risk of developing cardiac arrhythmias. Side effects usually occur with any beta-agonist and include tremor, restlessness, tachycardia, and mild hypokalemia.

Anticholinergics relax bronchial smooth muscle through competitive inhibition of muscarinic receptors. Ipratropium bromide is commonly used due to its low price and availability; the drug is taken in 2-4 breaths every 4-6 hours. Ipratropium bromide has a slower onset of action (within 30 minutes; reaching the maximum effect after 1-2 hours), so a beta-agonist is often prescribed with it in one combined inhaler or separately as necessary remedy emergency assistance. Tiotropium, a long-acting quaternary anticholinergic, is M1- and M2-selective and may therefore be superior to ipratropium bromide because blockade of the M receptor (as with ipratropium bromide) may limit bronchodilation. Dose - 18 mcg 1 time per day. Tiotropium is not available in all countries of the world. The effectiveness of tiotropium in COPD has been proven in large-scale studies as a drug that significantly slows down the fall in FEV in patients with moderate COPD stage, as well as in patients who continue to smoke and have stopped smoking and in persons over 50 years of age. In patients with COPD, regardless of the severity of the disease, long-term use of tiotropium improves quality of life indicators, reduces the frequency of exacerbations and the frequency of hospitalizations in patients with COPD, and reduces the risk of mortality in COPD. Side effects of all anticholinergics are dilated pupils, blurred vision, and xerostomia.

Inhaled glucocorticoids inhibit airway inflammation, reverse the downregulation of beta receptors, and inhibit the production of cytokines and leukotrienes. They do not change the pattern of lung function decline in COPD patients who continue to smoke, but they do improve short-term lung function in some patients, increase the effect of bronchodilators, and may reduce the incidence of COPD exacerbations. The dose depends on the drug; for example, fluticasone at a dose of 500-1000 mcg per day and beclomethasone 400-2000 mcg per day. Long-term risks of long-term use of inhaled glucocorticoids (fluticasone + salmeterol) in randomized controlled clinical research found an increase in the incidence of pneumonia in patients with COPD, in contrast to long-term treatment of COPD with a combination of budesonide + formoterol, the use of which does not increase the risk of developing pneumonia.

Differences in the development of pneumonia as a complication in COPD patients receiving long-term inhaled glucocorticoids as part of fixed combinations is associated with different pharmacokinetic properties of glucocorticoids, which can lead to different clinical effects. For example, budesonide is cleared from the airways faster than fluticasone. These differences in clearance may increase in individuals with significant obstruction, leading to increased accumulation of drug particles in the central respiratory tract, reduced absorption by peripheral tissues. Thus, budesonide can be cleared from the lungs before it leads to a significant reduction in local immunity and to bacterial proliferation, which provides an advantage, since in 30-50% of patients with moderate and severe COPD, bacteria are constantly present in the respiratory tract. Possible complications of steroid therapy include cataract formation and osteoporosis. Patients on long-term use of these drugs should be monitored periodically by an ophthalmologist and have bone densitometry performed, and should also take supplemental calcium, vitamin D, and bisphosphonates.

Combinations of a long-acting beta-agonist (eg, salmeterol) and an inhaled glucocorticoid (eg, fluticasone) are more effective than either of these drugs alone in the treatment of chronic stable disease.

Oral or systemic glucocorticoids can be used to treat chronic stable COPD, but they are likely to be effective in only 10-20% of patients and the long-term risks may outweigh the benefits. No formal comparisons have been made between oral and inhaled glucocorticoids. Initial doses of oral drugs should be for prednisolone 30 mg once a day, the response to treatment should be checked by spirometry. If FEV improves by more than 20%, then the dose should be reduced by 5 mg prednisolone per week to the lowest dose that maintains improvement. If an exacerbation develops following a decrease, inhaled glucocorticoids may be useful, but a return to a higher dose is likely to provide faster resolution of symptoms and recovery of FEV. In contrast, if the increase in FEV is less than 20%, the dose of glucocorticoids should be rapidly reduced and discontinued. An alternating drug regimen may be an option if it reduces the number of adverse effects while maintaining the day-to-day effect of the drug itself.

Theophylline plays a minor role in the treatment of chronic stable COPD and exacerbations of COPD at present, when safer and more effective drugs are available. effective drugs. Theophylline reduces spasm of smooth muscle fibers, increases the clearance of the ciliated epithelium, improves right ventricular function and reduces pulmonary vascular resistance and blood pressure. Its mode of action is poorly understood but likely different from that of beta-agonists and anticholinergics. Its role in improving diaphragmatic function and reducing dyspnea during exercise is debatable. Theophylline at low doses (300-400 mg per day) has anti-inflammatory properties and may enhance the effects of inhaled glucocorticoids.

Theophylline may be used in patients who do not respond adequately to inhalers and if the drug is symptomatic. Serum drug concentrations do not require monitoring as long as the patient is responding to the drug, has no symptoms of toxicity, or is available for contact; oral forms theophylline with slow release, which require less frequent use, increase compliance. Toxicity is common and includes insomnia and gastrointestinal disturbances, even at low blood concentrations. More serious adverse effects, such as supraventricular and ventricular arrhythmias and seizures, tend to occur at blood concentrations greater than 20 mg/l. Hepatic metabolism of theophylline varies markedly with genetic factors, age, cigarette smoking, hepatic dysfunction, and concomitant use of small amounts of drugs such as macrolide and fluoroquinolone antibiotics and non-sedating H2-histamine receptor blockers.

The anti-inflammatory effects of phosphodiesterase-4 antagonists (roflumipast) and antioxidants (N-acetylcysteine) in the treatment of COPD are being investigated.

Oxygen therapy for COPD

Long-term oxygen therapy prolongs life in patients with COPD whose PaO2 is consistently less than 55 mmHg. Art. Continuous 24-hour oxygen therapy is more effective than 12-hour night regimen. Oxygen therapy brings hematocrit to normal, moderately improves neurological status and psychological status, apparently by improving sleep, and reducing pulmonary hemodynamic disturbances. Oxygen therapy also increases exercise tolerance in many patients.

A sleep study should be performed in patients with severe COPD who are not eligible for long-term oxygen therapy, but clinical findings suggest pulmonary hypertension in the absence of daytime hypoxemia. Nocturnal oxygen therapy may be considered if a sleep study shows an occasional decrease in oxygen saturation.

Patients who are recovering from an acute respiratory disease and meeting the listed criteria, you need to assign O2 and re-examine the indicators when breathing room air after 30 days.

O is administered through a nasal catheter at a flow rate sufficient to achieve a PaO2 > 60 mmHg. Art. (SaO > 90%), usually 3 L/min at rest. O2 comes from electric oxygen concentrators, LPG systems or compressed gas cylinders. Hubs, which restrict mobility but are the least expensive, are preferred by patients who spend most of their time at home. Such patients may have small O2 reservoirs for backup in case of a power outage or for portable use.

Fluid systems are preferred for patients who spend a lot of time away from home. Portable liquid O2 canisters are easier to carry and have a larger capacity than portable compressed gas cylinders. Large cylinders of compressed air are the most expensive way to provide oxygen therapy and should only be used if other sources are not available. All patients should be advised of the dangers of smoking while using O.

Various devices make it possible to conserve the oxygen used by the patient, for example by using a reservoir system or by providing O only at the moment of inhalation. These devices control hypoxemia as effectively as continuous delivery systems.

Some patients require supplemental O2 while traveling by air because the cabin pressure of civil airliners is low. Eucapnic patients with COPD who have a PaO2 greater than 68 mm Hg at sea level. Art., in flight, on average, have a PaO2 of more than 50 mm Hg. Art. and do not require additional oxygen therapy. All COPD patients with hypercapnia, significant anemia (Hct

Smoking cessation

Quitting smoking is both extremely difficult and extremely important; it slows but does not completely stop the progression of airway inflammation Best effect gives simultaneous use of different ways to quit smoking: setting a date for quitting, behavior modification methods, group sessions, nicotine replacement therapy (chewing gum, transdermal therapeutic system, inhaler, tablets or nasal spray), bupropion and medical support. The smoking cessation rate is approximately 30% per year, even with the most effective method- combinations of bupropion with nicotine replacement therapy.

Vaccine therapy

All patients with COPD should receive annual flu shots. Influenza vaccine can reduce the severity and mortality in patients with COPD by 30-80%. If a patient cannot be vaccinated, or if the predominant strain of influenza virus is not included in a given year's vaccine form, treatment is appropriate for influenza outbreaks prophylactic(amantadine, rimantadine, oseltamivir, or zanamivir) for the treatment of influenza outbreaks. The pneumococcal polysaccharide vaccine produces minimal adverse effects. Vaccination with polyvalent pneumococcal vaccine should be given to all patients with COPD aged 65 years and older and patients with COPD with FEV1

Physical activity

Skeletal muscle fitness deteriorated due to inactivity or prolonged hospitalization for respiratory failure can be improved by a program of metered exercise. Specific respiratory muscle training is less beneficial than general aerobic training. A typical training program starts with a slow treadmill walk or an ergometer bike ride with no load for a few minutes. The duration and intensity of exercise is progressively increased over 4-6 weeks until the patient is able to exercise for 20-30 minutes non-stop with controlled dyspnoea. Patients with very severe COPD can usually achieve walking for 30 minutes at a speed of 1-2 miles per hour. To maintain physical fitness, exercises should be performed 3-4 times a week. O2 saturation is monitored and, if necessary, additional O2 is administered. endurance training upper limbs Useful for daily activities such as bathing, dressing and cleaning. Patients with COPD should be taught energy-saving ways of doing daily work and distributing activities. It is also necessary to discuss problems in the sexual area and consult on energy-saving ways of sexual intercourse.

Food

Patients with COPD have an increased risk of weight loss and reduced nutritional status due to a 15-25% increase in respiratory energy expenditure, higher postprandial metabolism, and higher levels of heat production (i.e., the thermal effect of nutrition), possibly because a distended stomach prevents sinking already flattened diaphragm and increased work of breathing, higher energy expenditure for daily activities, mismatch between energy intake and energy requirements, and catabolic effects of inflammatory cytokines such as TNF-a. Overall muscle strength and O use efficiency deteriorate. Patients with lower nutritional status have a poorer prognosis, so it is prudent to recommend a balanced diet with adequate calories combined with exercise to prevent or reverse muscle wasting and malnutrition. However, excessive weight gain should be avoided and obese patients should aim for a more normal body mass index. Studies examining the contribution of diet to patient rehabilitation have not shown improvement in lung function or exercise tolerance. The role of anabolic steroids (eg, megestrol acetate, oxandrolone), growth hormone therapy, and TNF antagonists in correcting nutritional status and improving functional status and prognosis in COPD has not been adequately studied.

Pulmonary rehabilitation in COPD

Pulmonary rehabilitation programs complement pharmacotherapy to improve physical function; many hospitals and healthcare facilities offer formal multidisciplinary rehabilitation programs. Pulmonary rehabilitation includes exercise, education, and behavior modification. Treatment must be individualized; patients and family members are educated about COPD and treatment, and the patient is encouraged to take full responsibility for personal health. A carefully integrated rehabilitation program helps patients with severe COPD adjust to physiological limitations and gives them real insight into how their condition can improve.

The effectiveness of rehabilitation is manifested in greater independence and improvement in the quality of life and tolerance to stress. Small improvements are seen in increased strength lower extremities, endurance and maximum consumption of O2. However, pulmonary rehabilitation does not usually improve lung function or increase life expectancy. To achieve a positive effect, patients with a severe form of the disease require at least a three-month rehabilitation, after which they must continue to engage in support programs.

Specialized programs are available for patients who remain on a ventilator after acute respiratory failure. Some patients may be completely off the ventilator, while others may only be off the ventilator for a day. If there are adequate conditions at home and if the family members are sufficiently well trained, it is possible to discharge the patient from the hospital with a ventilator.

Surgical treatment of COPD

Surgical approaches in the treatment of severe COPD include lung reduction and transplantation.

Lung volume reduction by resection of functionally inactive emphysematous areas improves exercise tolerance and two-year mortality in patients with severe emphysema, predominantly in the upper lung regions, with initially low exercise tolerance after pulmonary rehabilitation.

Other patients may experience relief of symptoms and improved performance after surgery, but the mortality rate does not change or worsens compared to drug therapy. Long-term results of treatment are unknown. Improvement of the condition is observed less frequently than with lung transplantation. The improvement is believed to be due to an increase in lung function and an improvement in diaphragmatic function and V/R ratio. Operational mortality is approximately 5%. The best candidates for lung volume reduction are patients with FEV 20-40% of predicted, APRD greater than 20% of predicted, with a significant decrease in exercise tolerance, heterogeneous lung disease on CT with predominant involvement of the upper lobes, PaCO less than 50 mmHg Art. and in the absence of severe pulmonary arterial hypertension and coronary artery disease.

Rarely, patients have bullae so large that they compress the functional lung. These patients can be helped by surgical resection of the bullae, which leads to the disappearance of manifestations and improvement in pulmonary function. In general, resection is most effective for bullae that occupy more than a third of half of the chest and FEV about half of the proper normal volume. The improvement in lung function depends on the amount of normal or minimally altered lung tissue that has been compressed by the resected bulla. Serial chest x-rays and CT are the most informative studies for determining whether a patient's functional status is the result of bulla compression of the viable lung or generalized emphysema. A markedly reduced DSS0 (

Since 1989, single lung transplantation has largely replaced double lung transplantation in patients with COPD. Transplant candidates are patients younger than 60 years of age with an FEV less than 25% predicted or with severe pulmonary arterial hypertension. The goal of a lung transplant is to improve the quality of life because life expectancy rarely increases. The five-year survival rate after transplantation for emphysema is 45-60%. Patients require lifelong immunosuppression, which carries the risk of opportunistic infections.

Treatment of acute exacerbation of COPD

The immediate goal is to provide adequate oxygenation, slow the progression of airway obstruction, and treat the underlying cause of the exacerbation.

The cause is usually unknown, although some acute exacerbations occur due to bacterial or viral infections. Exacerbations are facilitated by factors such as smoking, inhalation of irritating pollutants, and high levels of air pollution. Mild flare-ups can often be treated on an outpatient basis if home conditions permit. Elderly debilitated patients and patients with comorbidities, a history of respiratory failure, or acute changes in arterial blood gases are hospitalized for observation and treatment. Mandatory hospitalization in the department intensive care patients with life-threatening exacerbations with uncorrectable hypoxemia, acute respiratory acidosis, new arrhythmias, or worsening respiratory function despite inpatient treatment, as well as patients who require sedation for treatment.

Oxygen

Most patients need supplemental O2, even if they don't need it all the time. Administration of O2 may worsen hypercapnia by decreasing the hypoxic respiratory response. After 30 days, the PaO2 value when breathing room air should be rechecked to assess the patient's need for additional O2.

Respiratory support

Non-invasive positive pressure ventilation [eg, pressure support or bi-level positive airway pressure ventilation through a facemask] is an alternative to full mechanical ventilation. Non-invasive ventilation likely reduces the need for intubation, shortens hospital stay, and reduces mortality in patients with severe exacerbations (determined by pH

Deterioration of blood gases and mental status and progressive respiratory muscle fatigue are indications for endotracheal intubation and mechanical ventilation. Ventilation options, treatment strategies, and complications are discussed in Chap. 65 on page 544. Risk factors for ventilator dependence include FEV 60 mmHg. Art.), a significant limitation in the ability to perform physical exercises and poor nutritional status. Therefore, the patient's wishes regarding intubation and mechanical ventilation should be discussed and documented.

If the patient requires prolonged intubation (eg, more than 2 weeks), a tracheostomy is indicated to ensure comfort, communication, and nutrition. With a good multidisciplinary recovery program, including nutritional and psychological support, many patients requiring long-term mechanical ventilation can be successfully removed from the ventilator and returned to their previous level of functioning.

Drug treatment for COPD

Beta-agonists, anticholinergics, and/or corticosteroids should be given concomitantly with oxygen therapy (regardless of how oxygen is administered) to reduce airway obstruction.

Beta-agonists are the basis of drug therapy for exacerbations. The most commonly used salbutamol is 2.5 mg via nebulizer or 2-4 inhalations (100 mcg/breath) via metered dose inhaler every 2-6 hours. Inhalation using a metered dose inhaler results in rapid bronchodilation; there is no evidence that nebulizers are more effective than metered dose inhalers.

The effectiveness of ipratropium bromide, an anticholinergic agent used most often, has been proven in exacerbation of COPD; it must be administered simultaneously or alternately with beta-agonists via a metered dose inhaler. Dosage - 0.25-0.5 mg via nebulizer or 2-4 inhalations (21 mcg / breath) with a metered dose inhaler every 4-6 hours. Ipratropium bromide usually provides a bronchodilator effect similar to that of beta-agonists. The therapeutic value of tiotropium, a long-acting anticholinergic drug, has not been established.

The use of glucocorticoids should be started immediately for all, even moderate, exacerbations. Choices include prednisolone 60 mg once daily orally, tapered for more than 7-14 days, and methyl prednisolone 60 mg once daily IV, tapered for more than 7-14 days. These drugs are equivalent in acute effects. From inhaled glucocorticoids in the treatment of exacerbations of COPD, a suspension of budesonide is used, which is recommended as nebulizer therapy at a dose of 2 mg 2-3 times a day in combination with solutions of short-acting, preferably combined bronchodilators.

Methylxanthines, once considered the mainstay of treatment for COPD exacerbations, are no longer used. Their toxicity outweighs their effectiveness.

Antibiotics are recommended for exacerbations in patients with purulent sputum. Some doctors prescribe antibiotics empirically for changes in sputum color or for nonspecific chest x-ray changes. Before prescribing treatment, there is no need to conduct a bacteriological and bacterioscopic examination, if there is no suspicion of an unusual or resistant microorganism. Antibacterial therapy for uncomplicated exacerbation of COPD in persons 50% of the due includes amoxicillin 500-100 mg 3 times a day or macrolides of the II generation (azithromycin 500 mg 3 days or clarithromycin 500 mg 2 times a day), cephalosporins II-III generation (cefuroxime axetil 500 mg twice daily, cefixime 400 mg once daily) given for 7-14 days are effective and inexpensive drugs first line. The choice of drug should be dictated by the local pattern of bacterial susceptibility and the patient's history. In most cases, treatment should be started with oral medications. Antibacterial therapy for complicated exacerbation of COPD with risk factors for FEV 35-50% of due includes amoxicillin-clavulanate potassium 625 mg 3 times a day or 1000 mg 2 times a day; fluoroquinolones (levofloxacin 500 mg once a day, moxifloxacin 400 mg once a day, or gatifloxacin 320 mg once a day These drugs are prescribed orally, or, if necessary, following the principle of "step therapy" for the first 3-5 days parenterally (amoxicillin- clavulanate 1200 mg three times a day or fluoroquinolones (levofloxacin 500 mg once a day, moxifloxacin 400 mg once a day).These drugs are effective against beta-lactamase-producing strains of H. influene and M. catarrhalis, but did not outperform first-line drugs in most patients Patients should be taught to recognize signs of an exacerbation by normal to purulent sputum and begin a 10–14-day course of antibiotic therapy Long-term antibiotic prophylaxis is recommended only in patients with structural changes in the lungs such as bronchiectasis or an infected bulla.

If Pseudomonas spp. is suspected. and / or other Enterobactereaces spp., parenteral ciprofloxacin 400 mg 2-3 times a day, then orally 750 mg 2 times a day, or parenteral levofloxacin 750 mg 1 time a day, then 750 mg a day orally, ceftazidime 2.0 g 2-3 times a day.

COPD prognosis

The severity of airway obstruction predicts survival in patients with COPD. Mortality in patients with an FEV greater than or equal to 50% is expected to be slightly higher than in the general population. With an FEV of 0.75-1.25 liters, the five-year survival rate is approximately 40-60%; if less than 0.75 l, then approximately 30-40%. Cardiac disease, low body weight, resting tachycardia, hypercapnia, and hypoxemia reduce survival, while a significant response to bronchodilators is associated with improved survival. Risk factors for death in patients in the acute phase requiring hospitalization are advanced age, high PaCO2 values, and continuous use of oral glucocorticoids.

Mortality in COPD in quit smokers is often due to intercurrent disease rather than progression of the underlying disease. Death is usually caused by acute respiratory failure, pneumonia, lung cancer, heart failure, or pulmonary embolism.