Complications of COPD and their treatment. All about COPD (chronic obstructive pulmonary disease): symptoms, stages, treatment methods

On early stages disease, he is episodic, but later he constantly worries, even in a dream. Cough accompanied by phlegm. Usually it is not much, but in the acute stage, the amount of discharge increases. Possible purulent sputum.

Another symptom of COPD is shortness of breath. It appears late, in some cases even 10 years after the onset of the disease.

COPD sufferers are divided into two groups - "pink puffers" and "bluish puffers". "Pink puffers" (emphysematous type) are often thin, their main symptom is shortness of breath. Even after a little physical exertion, they puff, puffing out their cheeks.

"Bluish edema" (bronchitis type) are overweight. COPD is manifested in them mainly by a strong cough with sputum. Their skin is cyanotic, their legs swell. This is due to cor pulmonale and stagnation of blood in the systemic circulation.

Description

According to the World Health Organization (WHO), COPD affects 9 men out of 1000 and about 7 women out of 1000. In Russia, about 1 million people suffer from this disease. Although there is reason to believe that there are many more.

In severe COPD, the gas composition of the blood is determined.

If therapy is ineffective, sputum is taken for bacteriological analysis.

Treatment

Chronic obstructive pulmonary disease is an incurable disease. However, adequate therapy can reduce the frequency of exacerbations and significantly prolong the life of the patient. For COPD treatment drugs are used that expand the lumen of the bronchi and mucolytic agents that thin the sputum and contribute to its removal from the body.

To relieve inflammation, glucocorticoids are prescribed. However, their long-term use is not recommended due to serious side effects.

During the period of exacerbation of the disease, if its infectious nature is proved, antibiotics are prescribed or antibacterial agents depending on the sensitivity of the microorganism.

Patients with respiratory failure prescribed oxygen therapy.

Those suffering from pulmonary hypertension and COPD in the presence of edema are prescribed diuretics, with arrhythmias - cardiac glycosides.

A person suffering from COPD is referred to a hospital if he has:

It is also important to treat infectious diseases respiratory tract.

Those working in hazardous industries must strictly observe safety precautions and wear respirators.

Unfortunately, in large cities it is not possible to exclude one of the risk factors - polluted atmosphere.

COPD is best treated early. For timely diagnosis of this disease, it is necessary to undergo medical examination in time.

This is a progressive disease characterized by an inflammatory component, impaired bronchial patency at the level of the distal bronchi, and structural changes in lung tissue and vessels. Main Clinical signs- cough with the release of mucopurulent sputum, shortness of breath, discoloration of the skin (cyanosis or pinkish color). Diagnosis is based on data from spirometry, bronchoscopy, and blood gases. Treatment includes inhalation therapy, bronchodilators

General information

Chronic obstructive disease (COPD) is now isolated as an independent lung disease and delimited from a number of chronic processes. respiratory system occurring with obstructive syndrome (obstructive bronchitis, secondary pulmonary emphysema, bronchial asthma and etc.). According to epidemiological data, COPD more often affects men over 40 years of age, occupies a leading position among the causes of disability and 4th among the causes of mortality in the active and able-bodied part of the population.

Causes of COPD

Among the causes that cause the development of chronic obstructive pulmonary disease, 90-95% is given to smoking. Among other factors (about 5%), there are occupational hazards (inhalation of harmful gases and particles), childhood respiratory infections, concomitant bronchopulmonary pathology, and the state of the environment. In less than 1% of patients, COPD is based on a genetic predisposition, expressed in a deficiency of alpha1-antitrypsin, which is formed in the liver tissues and protects the lungs from damage by the elastase enzyme.

COPD is an occupational disease of miners, railroad workers, construction workers in contact with cement, workers in the pulp and paper and metallurgical industries, and agricultural workers involved in the processing of cotton and grain. Among the occupational hazards, the leading causes of COPD development are:

• contacts with cadmium and silicon
• metalworking
• the harmful role of products formed during the combustion of fuel.

Pathogenesis

Environmental factors and genetic predisposition cause a chronic inflammatory lesion of the inner lining of the bronchi, leading to impaired local bronchial immunity. At the same time, the production of bronchial mucus increases, its viscosity increases, thereby creating favorable conditions for the reproduction of bacteria, impaired bronchial patency, changes in lung tissue and alveoli. The progression of COPD leads to the loss of a reversible component (edema of the bronchial mucosa, spasm of smooth muscles, mucus secretion) and an increase in irreversible changes leading to the development of peribronchial fibrosis and emphysema. Progressive respiratory failure in COPD may be accompanied by bacterial complications leading to recurrent lung infections.

The course of COPD is aggravated by a gas exchange disorder, manifested by a decrease in O2 and CO2 retention in arterial blood, an increase in pressure in the pulmonary artery and leading to the formation of cor pulmonale. Chronic cor pulmonale causes circulatory failure and death in 30% of patients with COPD.

Classification

International experts distinguish 4 stages in the development of chronic obstructive pulmonary disease. The criterion underlying COPD classification, is a decrease in the ratio of FEV (forced expiratory volume) to FVC (forced vital capacity)

• Stage 0(predisease). It is characterized by an increased risk of developing COPD, but does not always transform into it. Manifested by persistent cough and sputum secretion with unchanged lung function.
• Stage I(mild COPD). Minor obstructive disorders (forced expiratory volume in 1 second - FEV1> 80% of normal), chronic cough and sputum production are detected.
• Stage II(moderate course of COPD). Progressive obstructive disorders (50%
• Stage III(severe course of COPD). Increased airflow limitation during exhalation (30%
• Stage IV(extremely severe COPD). It is manifested by a severe form of life-threatening bronchial obstruction (FEV, respiratory failure, development of cor pulmonale.

Symptoms of COPD

In the early stages, chronic obstructive pulmonary disease proceeds secretly and is not always detected on time. A characteristic clinic unfolds, starting with the moderate stage of COPD.

The course of COPD is characterized by cough with sputum and shortness of breath. In the early stages, there is an episodic cough with mucus sputum (up to 60 ml per day) and shortness of breath during intense exertion; as the severity of the disease progresses, the cough becomes constant, shortness of breath is felt at rest. With the addition of infection, the course of COPD worsens, the nature of sputum becomes purulent, and its amount increases. The course of COPD can develop in two types of clinical forms:

• Bronchitis type. In patients with the bronchitis type of COPD, the predominant manifestations are purulent inflammatory processes in the bronchi, accompanied by intoxication, cough, and copious sputum. Bronchial obstruction is pronounced significantly, pulmonary emphysema is weak. This group of patients is conditionally referred to as "blue puffers" due to diffuse blue cyanosis of the skin. The development of complications and the terminal stage occur at a young age.
• emphysematous type. With the development of COPD according to the emphysematous type, expiratory dyspnea (with difficult exhalation) comes to the fore in the symptoms. Emphysema prevails over bronchial obstruction. By characteristic appearance patients (pink-gray skin color, barrel chest, cachexia), they are called "pink puffers." It has a more benign course, patients tend to live to old age.

Complications

The progressive course of chronic obstructive pulmonary disease can be complicated by pneumonia, acute or chronic respiratory failure, spontaneous pneumothorax, pneumosclerosis, secondary polycythemia (erythrocytosis), congestive heart failure, etc. In severe and extremely severe COPD, patients develop pulmonary hypertension and cor pulmonale . The progressive course of COPD leads to changes in the daily activity of patients and a decrease in their quality of life.

Diagnostics

The slow and progressive course of chronic obstructive pulmonary disease raises the question of timely diagnosis of the disease, which helps to improve the quality and increase life expectancy. When collecting anamnestic data, attention should be paid to the presence of bad habits(smoking) and production factors.

• FVD research. The most important method functional diagnostics is spirometry, which reveals the first signs of COPD. It is obligatory to measure the speed and volume indicators: vital capacity (VC), forced vital capacity (FVC), forced expiratory volume in 1 second. (FEV1) and others in the post-bronchodilator test. The summation and ratio of these indicators makes it possible to diagnose COPD.
• Sputum analysis. Cytological examination of sputum in patients with COPD makes it possible to assess the nature and severity of bronchial inflammation, to exclude cancer alertness. Outside of exacerbation, the nature of sputum is mucous with a predominance of macrophages. In the acute phase of COPD, sputum becomes viscous, purulent.
• Blood analysis. A clinical blood test for COPD reveals polycythemia (an increase in the number of red blood cells, hematocrit, hemoglobin, blood viscosity) as a result of the development of hypoxemia in the bronchitis type of the disease. In patients with severe symptoms of respiratory failure, the gas composition of the blood is examined.
• Radiography chest. X-ray of the lungs excludes other diseases with similar clinical manifestations. In patients with COPD, the x-ray shows compaction and deformation of the bronchial walls, emphysematous changes in the lung tissue.

ECG changes are characterized by hypertrophy of the right heart, indicating the development of pulmonary hypertension. Diagnostic bronchoscopy in COPD is indicated for differential diagnosis, examination of the bronchial mucosa and assessment of its condition, sampling of bronchial secretions for analysis.

COPD treatment

The goals of chronic obstructive pulmonary disease therapy are to slow down the progression of bronchial obstruction and respiratory failure, reduce the frequency and severity of exacerbations, improve the quality and increase the life expectancy of patients. A necessary element of complex therapy is the elimination of the cause of the disease (primarily smoking).

COPD treatment is carried out by a pulmonologist and consists of the following components:

• patient education in the use of inhalers, spacers, nebulizers, criteria for assessing their condition and self-care skills;
• the appointment of bronchodilators (drugs that expand the lumen of the bronchi);
• the appointment of mucolytics (drugs that thin sputum and facilitate its discharge);
• appointment of inhaled glucocorticosteroids;
• antibiotic therapy during exacerbations;
• oxygenation of the body and pulmonary rehabilitation.

In the case of a comprehensive, methodical and adequately selected treatment of COPD, it is possible to reduce the rate of development of respiratory failure, reduce the number of exacerbations and prolong life.

Forecast and prevention

Regarding complete recovery, the prognosis is unfavorable. The steady progression of COPD leads to disability. The prognostic criteria for COPD include: the possibility of excluding the provoking factor, the patient's compliance with recommendations and therapeutic measures, the patient's social and economic status. An unfavorable course of COPD is observed in severe concomitant diseases, heart and respiratory failure, elderly patients, bronchitis type of the disease. A quarter of patients with severe exacerbations die within a year. Measures to prevent COPD are the exclusion of harmful factors (cessation of smoking, compliance with labor protection requirements in the presence of occupational hazards), prevention of exacerbations and other bronchopulmonary infections.

COPD can develop as an independent disease, it is characterized by airflow limitation caused by an abnormal inflammatory process, which, in turn, occurs as a result of constant irritating factors (smoking, hazardous industries). Often the diagnosis of COPD combines two diseases at once, for example, chronic bronchitis and emphysema. This combination is often observed in long-term smokers.

One of the main causes of disability in the population is COPD. Disability, reduced quality of life and, unfortunately, mortality - all this accompanies this disease. According to statistics, about 11 million people suffer from this disease in Russia, and the incidence is increasing every year.

Risk factors

The following factors contribute to the development of COPD:

• smoking, including passive;
• frequent pneumonia;
• unfavorable ecology;
• hazardous industries (work in a mine, exposure to cement dust from builders, metal processing);
• heredity (lack of alpha1-antitrypsin can contribute to the development of bronchiectasis and emphysema);
• prematurity in children;
• low social status, unfavorable living conditions.

COPD: symptoms and treatment

At the initial stage of development, COPD does not manifest itself in any way. The clinical picture of the disease occurs with prolonged exposure to adverse factors, such as smoking for more than 10 years or working in hazardous industries. The main symptoms of this disease are chronic cough, especially in the morning, a large amount of sputum when coughing and shortness of breath. At first, it appears during physical exertion, and with the development of the disease - even with slight exertion. It becomes difficult for patients to eat, and breathing requires high energy costs, shortness of breath appears even at rest.

Patients lose weight and become physically weak. Symptoms of COPD periodically increase and exacerbate. The disease proceeds with periods of remission and exacerbation. Deterioration of the physical condition of patients during periods of exacerbation can be from minor to life-threatening. Chronic obstructive pulmonary disease lasts for years. The further the disease develops, the more severe the exacerbation.

Four stages of the disease

There are only 4 degrees of severity of this disease. Symptoms do not appear immediately. Often, patients seek medical help late, when an irreversible process develops in the lungs and they are diagnosed with COPD. Disease stages:

1. Mild - usually not manifested by clinical symptoms.
2. Moderate - there may be a cough in the morning with or without sputum, shortness of breath with physical activity.
3. Severe - cough with a large discharge of sputum, shortness of breath even with slight exertion.
4. Extremely severe - threatens the life of the patient, the patient loses weight, shortness of breath even at rest, cough.

Often, patients in the initial stages do not seek help from a doctor, precious time for treatment has already been lost, this is the insidiousness of COPD. The first and second degrees of severity usually occur without pronounced symptoms. Worries only cough. Severe shortness of breath appears in the patient, as a rule, only at the 3rd stage of COPD. The degrees from the first to the last in patients can proceed with minimal symptoms in the remission phase, but it is worth a little hypothermia or a cold, the condition worsens sharply, an exacerbation of the disease occurs.

Diagnosis of the disease

Diagnosis of COPD is carried out on the basis of spirometry - this is the main study for making a diagnosis.

Spirometry is a measurement of respiratory function. The patient is invited to take a deep breath and the same maximum exhalation into the tube of a special device. After these steps, the computer connected to the device will evaluate the indicators, and if they differ from the norm, the study is repeated 30 minutes after inhaling the medicine through the inhaler.

This test will help the pulmonologist determine if coughing and shortness of breath are symptoms of COPD or some other disease, such as bronchial asthma.

To clarify the diagnosis, the doctor may prescribe additional methods of examination:

• general blood analysis;
• measurement of blood gases;
• general sputum analysis;
• bronchoscopy;
• bronchography;
• CT (X-ray computed tomography);
• ECG (electrocardiogram);
• X-ray of the lungs or fluorography.

How to stop the progression of the disease?

Smoking cessation is an effective and proven method that can stop the progression of COPD and the decline in lung function. Other methods can alleviate the course of the disease or delay the exacerbation, the progression of the disease is not able to stop. In addition, the ongoing treatment in patients who quit smoking is much more effective than in those who could not give up this habit.

Prevention of influenza and pneumonia will help prevent aggravation of the disease and further development illness. It is necessary to get vaccinated against influenza annually before the winter season, preferably in October.

Revaccination against pneumonia is required every 5 years.

COPD treatment

There are several treatments for COPD. These include:

• drug therapy;
• oxygen therapy;
• pulmonary rehabilitation;
• surgery.

Drug therapy

If drug therapy for COPD is chosen, treatment consists of continuous (lifelong) use of inhalers. An effective drug that helps relieve shortness of breath and improve the patient's condition is selected by a pulmonologist or therapist.

Short-acting beta-agonists (rescue inhalers) can quickly relieve shortness of breath, they are used only in emergency cases.

Short-acting anticholinergics can improve lung function, relieve severe symptoms of the disease and improve the general condition of the patient. With mild symptoms, they can not be used constantly, but only as needed.

For patients with severe symptoms, long-acting bronchodilators are prescribed in the last stages of COPD treatment. Preparations:

• Long-acting beta2-agonists (Formoterol, Salmeterol, Arformoterol) can reduce the number of exacerbations, improve the quality of life of the patient and alleviate the symptoms of the course of the disease.
• Long-acting M-anticholinergics (Tiotropium) will help improve lung function, reduce shortness of breath and relieve symptoms of the disease.
• For treatment, a combination of beta 2-agonists and anticholinergics is often used - this is much more effective than using them separately.
• Theophylline (Teo-Dur, Slo-bid) reduces the frequency of exacerbations of COPD, treatment with this drug complements the action of bronchodilators.
• Glucocorticoids, which have powerful anti-inflammatory effects, are widely used to treat COPD in the form of tablets, injections or inhalations. Inhaled drugs such as Fluticasone and Budisonin may reduce the number of exacerbations, increase the period of remission, but will not improve respiratory function. They are often given in combination with long-acting bronchodilators. Systemic glucocorticoids in the form of tablets or injections are prescribed only during periods of exacerbation of the disease and for a short time, because. have a number of adverse side effects.
• Mucolytic drugs, such as Carbocestein and Ambroxol, significantly improve sputum discharge in patients and have a positive effect on their general condition.
• Antioxidants are also used to treat this disease. The drug "Acetylcestein" is able to increase periods of remission and reduce the number of exacerbations. This drug is used in combination with glucocorticoids and bronchodilators.

Treatment of COPD with non-pharmacological methods

In combination with drugs for the treatment of the disease, non-drug methods are also widely used. These are oxygen therapy and rehabilitation programs. In addition, patients with COPD should understand that it is necessary to completely stop smoking, because. without this condition, not only recovery is impossible, but the disease will also progress at a faster pace.

Particular attention should be paid to the quality and good nutrition patients with COPD. Treatment and improvement of the quality of life for patients with a similar diagnosis largely depends on themselves.

Oxygen therapy

Patients with a similar diagnosis often suffer from hypoxia - this is a decrease in oxygen in the blood. Therefore, not only the respiratory system suffers, but also all organs, because. they don't get enough oxygen. Patients may develop a range of side effects.

To improve the condition of patients and eliminate hypoxia and the consequences of respiratory failure in COPD, treatment is carried out with oxygen therapy. Preliminary, the level of oxygen in the blood is measured in patients. To do this, use such a study as the measurement of blood gases in arterial blood. Blood sampling is carried out only by a doctor, because. blood for research should be taken exclusively arterial, venous will not work. It is also possible to measure the level of oxygen using a pulse oximeter device. It is put on the finger and the measurement is taken.

Patients should receive oxygen therapy not only in a hospital, but also at home.

Nutrition

About 30% of patients with COPD experience difficulty in eating, this is due to severe shortness of breath. Often they simply refuse to eat, and significant weight loss occurs. Patients weaken, immunity decreases, and in this state, infection can be added. You cannot refuse to eat. For such patients, fractional nutrition is recommended.

Patients with COPD should eat often and in small portions. Eat foods rich in proteins and carbohydrates. Before eating, it is advisable to rest a little. The diet must include multivitamins and nutritional supplements (they are an additional source of calories and nutrients).

Rehabilitation

Patients with this disease are recommended annual spa treatment and special lung programs. In the rooms of physiotherapy exercises, they can be trained in a special breathing exercises to be carried out at home. Such interventions can significantly improve the quality of life and reduce the need for hospitalization in patients diagnosed with COPD. Symptoms and traditional treatment are discussed. Once again, we emphasize that much depends on the patients themselves, effective treatment possible only with a complete cessation of smoking.

COPD treatment folk remedies can also bring positive results. This disease existed before, only its name changed over time and traditional medicine coped with it quite successfully. Now, when there are scientifically based methods of treatment, folk experience can complement the action of medications.

IN traditional medicine for the treatment of COPD, the following herbs are successfully used: sage, mallow, chamomile, eucalyptus, linden flowers, sweet clover, licorice root, marshmallow root, flax seeds, anise berries, etc. Decoctions, infusions are prepared from this medicinal raw material or used for inhalation.

COPD - medical history

Let's turn to the history of this disease. The concept itself - chronic obstructive pulmonary disease - appeared only at the end of the 20th century, and such terms as "bronchitis" and "pneumonia" were first heard only in 1826. Further, 12 years later (1838), the well-known clinician Grigory Ivanovich Sokolsky described another disease - pneumosclerosis. At that time, most medical scientists assumed that pneumosclerosis was the cause of most diseases of the lower respiratory tract. Such damage to the lung tissue is called "chronic interstitial pneumonia".

In the next few decades, scientists around the world studied the course and proposed treatments for COPD. The history of the disease includes dozens of scientific works of physicians. So, for example, the great Soviet scientist, the organizer of the pathological and anatomical service in the USSR, Ippolit Vasilyevich Davydovsky, made invaluable contributions to the study of this disease. He described diseases such as chronic bronchitis, lung abscess, bronchiectasis, and called chronic pneumonia "chronic non-specific pulmonary consumption."

In 2002 candidate medical sciences Alexey Nikolaevich Kokosov published his work on the history of COPD. In it, he pointed out that in the pre-war period and during the Second World War, the lack of proper and timely treatment, coupled with enormous physical exertion, hypothermia, stress and malnutrition, led to an increase in cardiopulmonary insufficiency among front-line veterans. Many symposiums and works of physicians have been devoted to this issue. At the same time, Professor Vladimir Nikitich Vinogradov proposed the term COPD (chronic nonspecific lung disease), but this name did not take root.

A little later, the concept of COPD appeared and was interpreted as a collective concept that includes several diseases of the respiratory system. Scientists around the world continue to study the problems associated with COPD and offer new methods of diagnosis and treatment. But regardless of them, doctors agree on one thing: quitting smoking is the main condition for successful treatment.

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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 smokers with a history of 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 of the 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?

Cigarette smoking is a major risk factor 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 food is an important etiological factor in underdeveloped countries. Smokers with preexisting 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, respiratory diseases in childhood, 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 importance 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 a rapid decrease in 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, an inhibitor of secretory leukoproteinase 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. The 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 pulmonary function testing 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 a volume-flow loop, which is a simultaneous spirometric recording of airflow and volume during a forced maximum exhalation and inhalation.

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 is indicative of the enlargement of the central pulmonary arteries seen in pulmonary hypertension. Right ventricular dilatation seen with 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 liver disease in early childhood, distribution of emphysema in the lower lobes, and COPD with ANCA-positive vasculitis (anti-neutrophil cytoplasmic antibodies). Low levels of alpha-antitrypsin should be confirmed phenotypically.

ECG is often done to rule out cardiac causes of dyspnoea, 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 right leg 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 quantification 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 ​​of partial pressure of 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. Surgery 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 total lung capacity is reached, and hold the breath for 3-4 seconds before exhaling. Spacers guarantee optimal distribution medicinal product 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 a necessary means of 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 middle stage COPD, 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. Remote risks long-term use 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 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 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 periodically monitored 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 medicines in monotherapy mode, 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 arterial 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 in 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; slow-release oral formulations of theophylline that 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. The 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 leads to normal hematocrit, moderately improves neurological status and psychological condition, apparently by improving sleep, and reduces pulmonary hemodynamic disturbances. Oxygen therapy also increases exercise tolerance in many patients.

A sleep study should be performed in patients with advanced COPD who are not eligible for long-term oxygen therapy, but data clinical examination indicate 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 acute respiratory illness and who meet the listed criteria should be given O2 and re-examined for 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 oxygen used by the patient, for example by using a reservoir system or by providing O only at the time of inspiration. 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; this slows down, but does not completely stop the progression of airway inflammation. The best effect is obtained by simultaneous use different ways smoking cessation: quit date setting, 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 the patient cannot be vaccinated, or if the predominant strain of influenza virus is not included in that year's vaccine form, influenza outbreaks should be treated with prophylactic agents (amantadine, rimantadine, oseltamivir, or zanamivir) intended 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 dyspnea. 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.

Nutrition

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. For achievement positive effect patients with a severe form of the disease require at least three months of rehabilitation, after which they must continue to engage in supportive 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, a heterogeneous pattern of lung damage on CT with a predominant lesion 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. 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, should be subject to continuous monitoring of respiratory status.

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 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 in complicated exacerbation of COPD with risk factors with FEV 35-50% of the due value 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 the result of intercurrent disease rather than progression of the underlying disease. Death is usually caused by acute respiratory failure, pneumonia, lung cancer, heart disease, or pulmonary embolism.

Chronic obstructive pulmonary disease (COPD diagnosis formulation) is a pathological process characterized by partial restriction of airflow in the airways. The disease causes irreversible changes in the human body, so there is a great threat to life if the treatment was not prescribed on time.

Causes

The pathogenesis of COPD is not yet fully understood. But experts identify the main factors that cause the pathological process. Typically, the pathogenesis of the disease involves progressive bronchial obstruction. The main factors influencing the formation of the disease are:

1. Smoking.
2. Unfavorable working conditions.
3. Damp and cold climate.
4. Mixed infection.
5. Acute lingering bronchitis.
6. Diseases of the lungs.
7. genetic predisposition.

What are the manifestations of the disease?

Chronic obstructive pulmonary disease is a pathology that is most often diagnosed in patients aged 40 years. The first symptoms of the disease that the patient begins to notice are cough and shortness of breath. Often this condition occurs in combination with wheezing when breathing and sputum secretions. At first, it comes out in a small volume. Symptoms become more pronounced in the morning.

Cough is the very first symptom that worries patients. In the cold season, respiratory diseases are exacerbated, which play an important role in the formation of COPD. Obstructive pulmonary disease has the following symptoms:

1. Shortness of breath, which bothers when performing physical exertion, and then can affect a person during rest.
2. Under the influence of dust, cold air shortness of breath increases.
3. Symptoms are complemented by an unproductive cough with sputum that is difficult to secrete.
4. Dry wheezing at a high rate during exhalation.
5. Symptoms of emphysema.

stages

The classification of COPD is based on the severity of the course of the disease. In addition, it implies the presence of a clinical picture and functional indicators.

The classification of COPD involves 4 stages:

1. The first stage - the patient does not notice any pathological abnormalities. He may be visited by a chronic cough. Organic changes are uncertain, so it is not possible to make a diagnosis of COPD at this stage.
2. The second stage - the disease is not severe. Patients go to the doctor for advice on shortness of breath during exercise. Another chronic obstructive pulmonary disease is accompanied by an intense cough.
3. The third stage of COPD is accompanied by a severe course. It is characterized by the presence of a limited air supply in Airways Therefore, shortness of breath is formed not only during physical exertion, but also at rest.
4. The fourth stage is an extremely difficult course. Emerging COPD symptoms are life threatening. Obstruction of the bronchi is observed and is formed cor pulmonale. Patients who are diagnosed with stage 4 COPD receive a disability.

Diagnostic methods

Diagnosis of the presented disease includes the following methods:

1. Spirometry is a method of research, thanks to which it is possible to determine the first manifestations of COPD.
2. Measurement of lung capacity.
3. Cytological examination of sputum. This diagnosis allows you to determine the nature and severity of the inflammatory process in the bronchi.
4. A blood test can detect an increased concentration of red blood cells, hemoglobin and hematocrit in COPD.
5. X-ray of the lungs allows you to determine the presence of compaction and changes in the bronchial walls.
6. ECG provides data on the development pulmonary hypertension.
7. Bronchoscopy is a method that allows you to establish the diagnosis of COPD, as well as view the bronchi and determine their condition.

Treatment

Chronic obstructive pulmonary disease is a pathological process that cannot be cured. However, the doctor prescribes a certain therapy to his patient, thanks to which it is possible to reduce the frequency of exacerbations and prolong the life of a person. The course of prescribed therapy is greatly influenced by the pathogenesis of the disease, because it is very important to eliminate the cause that contributes to the occurrence of pathology. In this case, the doctor prescribes the following measures:

1. COPD treatment involves the use of medications, the action of which is aimed at increasing the lumen of the bronchi.
2. To liquefy sputum and remove it, mucolytic agents are used in the therapy process.
3. Help to stop inflammatory process with glucocorticoids. But their long-term use is not recommended, as serious side effects begin to occur.
4. If there is an exacerbation, then this indicates the presence of its infectious origin. In this case, the doctor prescribes antibiotics and antibacterial drugs. Their dosage is prescribed taking into account the sensitivity of the microorganism.
5. For those suffering from heart failure, oxygen therapy is necessary. In case of exacerbation, the patient is prescribed sanitary-resort treatment.
6. If the diagnosis confirms the presence of pulmonary hypertension and COPD, accompanied by reporting, then treatment includes diuretics. Glycosides help to eliminate the manifestations of arrhythmia.

COPD is a disease that cannot be treated without a properly formulated diet. The reason is that the loss muscle mass can lead to death.

A patient may be admitted to hospital if he/she has:

• greater intensity of the increase in the severity of manifestations;
• treatment does not give the desired result;
• new symptoms appear
• the rhythm of the heart is disturbed;
• diagnosis defines diseases such as diabetes, pneumonia, insufficient performance of the kidneys and liver;
• unable to provide medical care on an outpatient basis;
• difficulties in diagnosis.

Preventive actions

Prevention of COPD includes a set of measures, thanks to which each person will be able to warn his body against this. pathological process. It consists of the following recommendations:

1. Pneumonia and influenza are the most common causes of COPD. Therefore, it is essential to get flu shots every year.
2. Once every 5 years, vaccinate against pneumococcal infection, thanks to which it is possible to protect your body from pneumonia. Only the attending physician will be able to prescribe vaccination after an appropriate examination.
3. Taboo on smoking.

Complications of COPD can be very diverse, but, as a rule, they all lead to disability. Therefore, it is important to carry out treatment on time and be under the supervision of a specialist all the time. And it is best to conduct quality preventive actions to prevent the formation of a pathological process in the lungs and warn yourself against this disease.

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Diseases with similar symptoms:

Asthma - chronic illness, which is characterized by short-term attacks of suffocation, caused by spasms in the bronchi and swelling of the mucous membrane. This disease does not have a certain risk group and age restrictions. But, as medical practice shows, women suffer from asthma 2 times more often. According to official figures, there are more than 300 million people with asthma in the world today. The first symptoms of the disease appear most often in childhood. Older people suffer the disease much more difficult.