Symptoms of COPD - a dangerous disease that masquerades as ordinary fatigue. Chronic obstructive pulmonary disease (COPD): causes, symptoms, treatment Clinical manifestations of COPD

Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive pulmonary disease (COPD) and chronic obstructive airway disease (COPD), among others, is an obstructive pulmonary disease characterized by chronic shortness of breath. Usually worsens over time. The main symptoms include shortness of breath, cough and sputum production. Most people with chronic bronchitis have COPD. Tobacco smoking is the most common cause of COPD, with other factors such as air pollution and genetics playing a lesser role. In developing countries, one of the common sources of air pollution is poor ventilation in the preparation and heating of food. Long-term exposure to these irritants causes an inflammatory response in the lungs leading to narrowing of the small airways and decomposition of lung tissue known as emphysema. Diagnosis is based on difficulty breathing, which is determined by lung function tests. Unlike asthma, difficulty breathing is not significantly relieved by medication. COPD can be prevented by reducing exposure to causative factors. These include measures to reduce smoking intensity and improve indoor and outdoor air quality. Treatment for COPD includes smoking cessation, vaccinations, rehabilitation, and often inhaled bronchodilators and steroids. Some people may benefit from long-term oxygen therapy or a lung transplant. Patients experiencing periods of acute deterioration may require increased drug use and hospitalization. Globally, COPD affects 329 million people or approximately 5% of the population. It caused 2.9 million deaths in 2013, up from 2.4 million deaths in 1990. The number of deaths is on the rise due to increased smoking and aging populations in many countries. It resulted in an estimated economic cost of $2.1 trillion in 2010.

Signs and symptoms

The most common symptoms of COPD are sputum production, shortness of breath, and a wet cough. These symptoms are observed over a long period of time and usually worsen over time. It is not clear if there are different types of COPD. With respect to the previous division into emphysema and chronic bronchitis, emphysema is just a description of a change in the lungs, not the disease itself, and chronic bronchitis is just a description of the symptoms that COPD may or may not have.

Cough

Chronic cough is the first symptom to appear. When present for more than three months a year for more than two years, with sputum production and no other explanation, it is consistent with chronic bronchitis. This condition can be observed until the full development of COPD. The amount of sputum produced can vary from hours to days. In some cases, the cough may be absent or appear from time to time and not be wet. Some people with COPD attribute their symptoms to "smoker's cough". Sputum may be swallowed or spit out, often depending on social and cultural factors. A violent cough can lead to broken ribs or a brief loss of consciousness. People with COPD often have a long history of viral upper respiratory infections.

Lack of air

Shortness of breath is often a symptom that worries most people. Often described as: "My breathing takes effort," "I feel difficulty breathing," or "I can't get enough air." However, different cultures may use different terms. Usually, shortness of breath worsens as the disease progresses and over time. In the later stages, it occurs during rest and can occur all the time. It is a source of anxiety and low quality of life in those suffering from COPD. Many people with more advanced COPD breathe through pursed lips, as this action can relieve shortness of breath in some people.

Other salient features

In COPD, exhaling may take longer than inhaling. There may be tightness in the chest, but this is rare and may be caused by another problem. People with difficulty breathing may have wheezing or low-pitched breathing sounds when examining their chest with a stethoscope. Emphysematous chest is a characteristic feature of COPD, but is relatively rare. A tripod position may occur as the disease worsens. Advanced COPD causes increased pressure in the pulmonary arteries, which puts pressure on the right ventricle of the heart. This situation is referred to as cor pulmonale and causes symptoms of swollen legs and distended jugular veins. COPD is more common than other lung diseases as a cause of cor pulmonale. Cor pulmonale becomes less common when supplemental oxygen is used. COPD often occurs along with several other conditions with which it shares risk factors. These conditions include coronary heart disease, high blood pressure, diabetes mellitus, muscle wasting, osteoporosis, lung cancer, anxiety disorder, and depression. People with severe illness always feel tired. Finger knuckle thickening is not specific to COPD and warrants testing for lung cancer.

Aggravation

An acute COPD attack is defined as increased shortness of breath, increased sputum production, sputum color change from clear to green or yellow, or increased coughing in COPD sufferers. It may manifest through signs of increased work of breathing, such as rapid breathing, rapid heart rate, sweating, active use of the neck muscles, bluish tint to the skin, and confusion or aggressive behavior in the most severe exacerbations. Moist rales may also be heard when examined with a stethoscope.

The reasons

The predominant cause of COPD is tobacco smoking, with occupational exposure and pollution from indoor open flames being significant causes in some countries. Typically, this exposure can last several decades before symptoms develop. A person's genetic makeup also influences risk.

Smoking

Tobacco smoking is the number one risk factor for COPD worldwide. Of those who smoke, about 20% develop COPD, and of those who smoke throughout their lives, about half develop COPD. In the US and UK, of all COPD sufferers, 80-95% are either current smokers or have smoked previously. The likelihood of developing COPD increases with overall exposure to tobacco smoke. In addition, women are more susceptible to the harmful effects of smoke than men. In non-smokers, passive smoking accounts for about 20% of cases. Other types of smoking, such as smoking marijuana, cigars, and hookah, also carry risks. Women who smoke during pregnancy may increase their child's risk of developing COPD.

Air pollution

Poorly ventilated roasting (smoking stage), often done with coal or vegetable fuels such as wood or manure, leads to indoor air pollution and is one of the most common causes of COPD in developing countries. Cooking is the method of cooking and heating food for about 3 billion people, with greater health effects seen in women due to longer exposure times. Such a fire is used as the main source of energy in 80% of the homes of India, China and sub-Saharan Africa. People living in large cities show an increased prevalence of COPD compared to people living in rural areas. While urban air pollution is a contributing factor, its overall role as a cause of COPD is not clear. Areas with poor ambient air quality, including exhaust pollution, tend to have an increased incidence of COPD. Overall exposure compared to smoking, however, is presumably less.

Workplace exposure

Intense and prolonged workplace exposure to dust, chemicals, and fumes increases the risk of developing COPD in both smokers and non-smokers. Occupational exposure is estimated to be responsible for 10–20% of cases. In the US, it is believed to be associated with more than 30% of never-smokers and is likely to be at increased risk in countries without appropriate technical regulations. Exposure spans multiple industries and sources including high levels of dust from coal mining, gold mining and the cotton textile industry, exposures include cadmium and isocyanates, and welding fumes. Working in the agricultural industry is also risky. In some professions, the risks are estimated to be equivalent to those of half to two packs of cigarettes a day. Exposure to quartz dust also leads to COPD, although the risk does not extend to silicosis. The negative effects of dust and tobacco smoke are additive, or perhaps more than additive.

Genetics

Genetics also play a role in the development of COPD. The disease is more common among relatives of COPD sufferers who smoke than among unrelated smokers. To date, the only certain hereditary risk factor is alpha 1-antitrypsin (AAT) deficiency. This risk is definitely higher if someone with alpha 1 antitrypsin deficiency is also a smoker. This covers approximately 1-5% of cases, and the condition occurs in about 3-4 out of 10,000 people. Other genetic factors are being investigated, of which there are supposed to be many.

Other

There are several other factors that are less closely associated with COPD. The risk is higher for those who are poor, although it is not clear whether this is due to poverty itself or to other risk factors associated with poverty, such as air pollution or malnutrition. There is conditional evidence that people with asthma and airway hyperresponsiveness are at increased risk of developing COPD. Birth factors such as low birth weight may also play a role, as can some infectious diseases including HIV/AIDS and tuberculosis. Respiratory infections such as pneumonia do not increase the risk of developing COPD, at least in adults.

Seizures

An acute attack (abrupt worsening of symptoms) is often triggered by infection or environmental contaminants, or, in some cases, by other factors such as misuse of drugs. Infections cause 50 to 75% of cases, with bacteria accounting for 25%, viruses 25%, and both 25%. Environmental pollutants refer to poor air quality in both indoor and outdoor environments. Exposure to smoking and secondhand smoke increases the risk. Cold temperatures may also play a role, as seizures are more common in winter. People with more severe disease show more frequent attacks: mild disease 1.8 per year, moderate disease 2 to 3 per year, and severe disease 3.4 per year. People with more frequent attacks have a higher rate of lung function depletion. Pulmonary embolism (blood clots in the lungs) can worsen symptoms in those who already have COPD.

Pathophysiology

COPD is a type of obstructive lung disease in which there is chronic, incomplete, bilateral failure to breathe (airflow limitation) and an inability to exhale fully (air trapping). Insufficient breathing is the result of the breakdown of lung tissue (known as emphysema) and a minor airway disease known as obstructive bronchiolitis. The relative contribution of these two factors varies from person to person. Severe destruction of the small airways can lead to the formation of large air bubbles—known as bullae—that replace lung tissue. This form of the disease is called bullous emphysema. COPD develops as a severe chronic inflammatory response to inhaled stimuli. A bacterial infection can also be added to this inflammatory condition. The inflammatory cells involved include neutrophil granulocytes and macrophages, two types of white blood cells. Smokers additionally show Tc1 lymphocyte involvement, and some people with COPD have eosinophil involvement similar to those with asthma. Part of this cellular response is triggered by inflammatory mediators such as chemotactic factors. Other processes implicated in lung injury include oxidative stress caused by high concentrations of free radicals in tobacco smoke and released by inflammatory cells, and degradation of lung connective tissue by proteases that are not adequately inhibited by protease inhibitors. The breakdown of the connective tissue of the lungs is what is called emphysema, which then leads to shortness of breath and ultimately poor absorption and release of respiratory gases. The general muscle wasting that is often seen in COPD may be due in part to inflammatory mediators released from the lungs into the blood. Narrowing of the airways occurs due to inflammation and scarring. This leads to an inability to exhale fully. The maximum decrease in air flow occurs during exhalation, as pressure in the chest compresses the airways at this time. This causes more air from the previous breath to remain in the lungs when the next breath begins, causing the total volume of air in the lungs to rise each time, a process called overexpansion or air entrapment. Excessive expansion due to exercise is associated with shortness of breath in COPD, as it becomes less comfortable to breathe when the lungs are already partially full. Some also have some degree of airway hyperresponsiveness to stimuli, similar to those with asthma. There may be low oxygen levels and eventually high blood carbon dioxide levels due to insufficient gas exchange due to reduced saturation due to lung obstruction, over-expansion, and a decreased urge to breathe. During attacks, inflammation of the airways increases, causing over-expansion of the lungs, insufficient gas exchange, and ultimately low oxygen levels in the blood. Low oxygen levels, if present for a long time, can cause narrowing of the arteries in the lungs, while emphysema leads to breakdown of the lung capillaries. Both changes cause an increase in blood pressure in the pulmonary arteries, which can lead to cor pulmonale.

Diagnostics

Diagnosis of COPD should be made for anyone aged 35 to 40 who demonstrates shortness of breath, chronic cough, sputum production, or frequent colds during the winter, as well as a history of exposure to risk factors for the disease. Spirometry is then used to confirm the diagnosis.

Spirometry

Spirometry measures the number of airway obstructions present and is typically performed after using a bronchodilator, a drug used to open the airways. To make a diagnosis, two main components are evaluated: forced expiratory volume in one second (FEV1), which is the largest volume of air that can be exhaled in the first second, and forced vital capacity (FVC), which is the largest volume of air, which can be exhaled in one large exhalation. Typically, 75-80% of FVC is released in the first second, and an FEV1/FVC ratio of less than 70% in a person with symptoms of COPD means that the person has the disease. Based on these findings, spirometry may lead to overdiagnosis of COPD in the elderly. The UK National Institutes of Health and Care Excellence criteria additionally require an FEV1 of at least 80% of expected. Evidence regarding the use of spirometry in asymptomatic people in an attempt to diagnose disease at an early stage is uncertain and, therefore, it is not currently recommended. Maximal expiratory flow rate (maximum expiratory flow rate), widely used in asthma, insufficient for diagnosing COPD.

Severity

There are several methods for determining how much COPD affects a particular individual. The Modified British Medical Research Council (mMRC) or the COPD Assessment Test (CAT) are simple questionnaires that can be used to determine the severity of symptoms. CAT scores are 0–40, with the highest score corresponding to more severe disease. Spirometry can help determine the severity of airflow limitation. It is usually based on FEV1, expressed as a percentage of the expected "normal" value, appropriate for a person's age, sex, height, and weight. US and European guidelines recommend that treatment recommendations be partly based on FEV1. The recommendations of the Global Initiative on Chronic Obstructive Pulmonary Disease divide people into four categories based on the definition of symptoms and airflow limitation. In addition, weight loss and muscle atrophy, as well as the presence of other diseases, should be taken into account.

Other tests

A chest x-ray and complete blood count may be helpful in ruling out other conditions at the time of diagnosis. Characteristic findings on x-ray are over-expanded lungs, a flat diaphragm, an enlarged retrosternal lumen, and bullae, and may help rule out other pulmonary disorders such as pneumonia, pulmonary edema, or pneumothorax. A high-resolution chest CT scan can show the distribution of emphysema in the lungs and is also useful in ruling out other diseases. Except for planned surgery, however, the disease is rarely manageable. An arterial blood test is used to determine the need for oxygen; it is recommended for those with FEV1 less than 35% predicted, peripheral oxygen saturation less than 92%, and people with symptoms of congestive heart failure. In regions of the world where alpha-1 antitrypsin deficiency is common, people with COPD should be tested (particularly those under the age of 45 and emphysema affecting the lower lung).

Differential Diagnosis

It may be necessary to separate COPD from other causes of shortness of breath, such as congestive heart failure, pulmonary embolism, pneumonia, or pneumothorax. Many people with COPD mistakenly believe they have asthma. The distinction between asthma and COPD is made based on symptoms, smoking history, and whether airflow restriction with bronchodilators is reversible, as measured by spirometry. Tuberculosis can also present as a chronic cough and should be taken into account in areas where it is common. Less common conditions that may resemble COPD include bronchopulmonary dysplasia and bronchiolitis obliterans. Chronic bronchitis may have normal airflow and is not classified as COPD.

Prevention

Most cases of COPD are potentially reversible through reduced exposure to smoke and improved air quality. Annual influenza vaccination in people with COPD reduces the incidence of seizures, hospitalization, and death. The pneumococcal vaccine may also be helpful.

To give up smoking

Keeping people from starting to smoke is a key aspect of COPD prevention. Government, public health, and anti-smoking policies can reduce smoking intensity by preventing people from starting to smoke and encouraging people to stop smoking. Smoking bans in public places and the workplace are important measures to reduce the impact of secondhand smoke, and smoking bans in more places are recommended. For smokers, smoking cessation is the only measure to slow the deterioration of COPD. Even at an advanced stage of the disease, it can reduce the degree of deterioration in lung function and slow the onset of disability and death. Smoking cessation begins with a decision to stop smoking, followed by an attempt to quit. It often takes several attempts before long-term abstinence is achieved. Attempts over 5 years lead to success in approximately 40% of people. Some smokers can achieve long-term smoking cessation with willpower alone. Smoking, however, is highly addictive and many smokers require further support. The chance of quitting smoking is increased through social support, participation in smoking cessation programs, and the use of drugs such as nicotine replacement therapy, bupropion, or varenicline.

Occupational health

There are several measures to reduce the likelihood that workers in high-risk industries—such as coal mining, construction, and quarrying—will develop COPD. Examples of such activities include: developing community interventions, educating workers and management about the risks, promoting smoking cessation, screening workers for early signs of COPD, use of respirators, and dust control. Effective dust control can be achieved through improved ventilation, the use of water sprinklers, and the use of mining technologies that minimize dust generation. If a worker develops COPD, further lung damage can be reduced by avoiding dust exposure, for example by changing job duties.

Air pollution

Indoor and outdoor air quality can be improved, which can prevent the development of COPD and slow down the worsening of an existing disease. This can be achieved through community events, cultural change and caring. Several developed countries have been able to successfully improve outdoor and indoor air quality through regulations. This has led to an improvement in the lung function of the populations of these countries. People with COPD may experience fewer symptoms if they stay indoors on days when air quality is poor. A key measure is to reduce exposure to smoke from raw materials for cooking and reheating by improving home ventilation and using better stoves and chimneys. Using the right stoves can improve indoor air quality by up to 85%. The use of alternative energy sources such as solar cooking and electric heating is efficient, as is the use of fuels such as kerosene and coal rather than vegetable.

Control

There is no cure for COPD, but symptoms can be treated and disease progression slowed down. The main goals of management are to reduce risk factors, maintain sustainable COPD, prevent and treat acute attacks, and manage comorbidities. Mortality-reducing interventions include smoking cessation and supplemental oxygen. Stopping smoking reduces the risk of death by 18%. Other recommendations include influenza vaccination once a year, pneumococcal vaccine once every 5 years, and reducing exposure to ambient air pollution. In people with advanced disease, symptomatic treatment can relieve symptoms, with morphine alleviating the sensation of shortness of breath. Non-invasive ventilation may be used to support breathing.

Pulmonary rehabilitation is a program of exercise, disease management, and psychological counseling used to benefit the individual. For those who have experienced a recent episode of illness, pulmonary rehabilitation improves overall quality of life and exercise capacity, and reduces mortality. It also improves a person's sense of the ability to manage their disease and emotional state. Breathing exercises in the complex and in themselves have a limited role. Being underweight or overweight can affect symptoms, disability, and prognosis for COPD. People with COPD who are underweight can increase respiratory muscle strength by increasing calorie intake. When combined with regular exercise or a pulmonary rehabilitation program, this may result in relief of COPD symptoms. Supplementation with nutrients can be helpful for those who are malnourished.

Bronchodilators

Inhaled bronchodilators are predominantly used drugs that have little overall benefit. There are two main types, β2 agonists and anticholinergics; both types are long-acting and short-acting. They alleviate shortness of breath, wheezing and limitation of physical activity, thereby causing an improvement in the quality of life. It is not clear whether they are able to change the course of the disease. For people with mild disease, short-acting agents are recommended as needed. For people with more severe symptoms, long-acting agents are recommended. If long-acting bronchodilators are ineffective, inhaled corticosteroids are usually used. As far as long acting agents are concerned, it is not clear which is more effective, tiotropium (a long acting anticholinergic agent) or long acting beta agonists (LABAs), it is advisable to try each and continue with whichever works best. Both types of agents reduce the risk of acute attacks by 15–25%. While both can be used at the same time, the benefit is of dubious value. There are several short-acting β2 agonists available, including salbutamol (ventaline) and terbutaline. They provide some degree of symptomatic relief for four to six hours. Long-acting β2 agonists such as salmeterol and formoterol are often used as maintenance therapy. Some feel that the useful action is limited, while others consider the useful action obvious. Long-term use in COPD is safe, with side effects including shakiness and palpitations. When used with inhaled steroids, they increase the risk of pneumonia. While steroids and long-acting β2 agonists may work better together, it is not clear whether these modest benefits outweigh the increased risks. There are two main anticholinergics used in COPD, ipratropium and tiotropium. Ipratropium is a short acting agent while tiotropium is long acting. Tiotropium has been associated with reduced exacerbations and improved quality of life, and tiotropium provides this benefit more than ipratropium. It has no effect on mortality or overall hospitalization rate. Anticholinergics can cause dry mouth and urinary tract symptoms. They are also associated with an increased risk of cardiovascular disease and stroke. Aclidinium, another long-acting agent that entered the market in 2012, has been used as an alternative to tiotropium.

Corticosteroids

Corticosteroids are usually taken in inhaled form, but can also be taken as tablets to treat and prevent acute attacks. While inhaled corticosteroids (ICS) do not show benefit in people with mild COPD, they relieve acute attacks in people with moderate to severe disease. When used in combination with long-acting β2 agonists, they reduce mortality more than inhaled corticosteroids or long-acting β2 agonists alone. By themselves, they have no effect on total annual mortality and are associated with an increased incidence of pneumonia. It is not clear whether they affect the progression of the disease. Long-term treatment with steroid tablets is associated with significant side effects.

Other medicines

Long-acting antibiotics, especially those belonging to the macrolide class, such as erythromycin, reduce the frequency of exacerbations in patients who experience two or more attacks per year. This practice may be cost-effective in some regions of the world. There are concerns about antibiotic resistance and hearing problems associated with azithromycin. Methylxanthines such as theophylline are generally more harmful than helpful and thus not recommended, but may be used as a second line agent in those who are not controlled by other measures. Mucolytics may be useful for those people who have very thin mucous membranes, but are generally not required. Cough suppressants are not recommended.

Oxygen

Supplemental oxygen is recommended for people with low resting oxygen levels (oxygen partial pressure less than 50–55 mmHg or oxygen saturation less than 88%). In this group of people, it reduces the risk of heart failure and death if taken 15 hours a day, and may increase a person's ability to exercise. In people with normally or moderately low oxygen levels, supplemental oxygen can relieve the shortness of breath. There is a risk of fires and little benefit if oxygen patients continue to smoke. In this case, some recommend to abandon the use of oxygen supply. During acute attacks, many require oxygen therapy; the use of high concentrations of oxygen without taking into account human oxygen saturation can lead to an increase in carbon dioxide levels and poor results. For people at high risk for high carbon dioxide levels, an oxygen saturation of 88–92% is recommended, while for people outside this risk group, the recommended level is 94–98%.

Surgical intervention

For people with severe enough disease, surgery may be helpful in some cases, which may include a lung transplant or lung volume reduction surgery. Lung reduction surgery involves removing the parts of the lungs most affected by emphysema, allowing the remaining relatively healthy lung to expand and function better. Lung transplantation is sometimes performed for very severe disease, particularly in young individuals.

Seizures

Acute attacks are usually treated with increased use of short-acting bronchodilators. It usually includes a combination of a short-acting inhaled beta-agonist and an anticholinergic agent. These drugs must be taken either via a metered dose inhaler with a spacer or an individual aerodynamic inhaler, both of which are equally effective. Spraying may be more convenient for those who are more unwell. Oral corticosteroids increase the chance of recovery and reduce the overall duration of symptoms. They act equivalent to intravenous steroids, but have fewer side effects. It has the effect of taking steroids for five days, as well as taking for ten and fourteen days. In people with a severe exacerbation, antibiotics improve outcomes. Several different antibiotics may be used, including amoxicillin, doxycycline, and azithromycin; it is not clear whether any of them works better than the others. There is no definitive evidence for people with less severe symptoms. In people with type 2 respiratory failure (drastically elevated CO2 levels), non-invasive supply and exhaust ventilation reduces the likelihood of death or the need for intensive care. In addition, theophylline may be helpful for those who do not respond to other measures. Less than 20% of seizures require hospitalization. In people without acidosis due to respiratory failure, home care ("hospital at home") helps avoid hospitalization.

Forecast

COPD tends to get progressively worse over time and may eventually lead to death. It is estimated that 3% of all disability cases are due to COPD. The proportion of disability due to COPD worldwide declined from 1990 to 2010 due to improved indoor air quality, mainly in Asia. The total number of years of resignation to disability due to COPD, however, has increased. The rate at which COPD worsens varies due to the presence of factors that predispose to poor outcomes, including severe respiratory failure, poor exercise capacity, shortness of breath, severely underweight or overweight, congestive heart failure, long-term smoking, and frequent flare-ups . Long-term outcomes in COPD can be calculated using the BODE index, which is assigned a score of one to ten based on FEV1, body mass index, distance walked in six minutes, and the Medical Research Council's Modified Dyspnea Scale. Significant weight loss is a bad sign. Spirometry results are also good predictors of future disease progression, but not as good as the BODE index.

Epidemiology

Globally, as of 2010, approximately 329 million people (4.8% of the population) suffered from COPD. Both women and men are almost equally susceptible to the disease, as there has been an increase in tobacco smoking among women in developed countries. Growth in developing countries from the 1970s to the 2000s is thought to be due to increased smoking in the region, population growth and an aging population due to fewer deaths from other causes such as infectious diseases. Some countries show increased prevalence, some remain stable, and some show a decline in COPD. Global numbers are expected to continue rising as risk factors remain prevalent and populations continue to age. From 1990 to 2010, COPD deaths dropped slightly from 3.1 million to 2.9 million, and the disease became the fourth leading cause of death. It became the third leading cause of death in 2012 as the number of deaths rose again to 3.1 million. In some countries, mortality has decreased among men but increased among women. This is most likely due to the fact that the intensity of smoking among women and men is becoming the same. COPD is most common among the elderly; it affects 34-200 out of 1,000 people over 65, depending on the population considered. In the UK, it is estimated that 0.84 million people (out of 50 million) are diagnosed with COPD; this translates to about one in 59 people receiving a diagnosis of COPD at some point in their lives. In the most socioeconomically disadvantaged parts of the country, one in 32 people are diagnosed with COPD compared to one in 98 in wealthier areas. In the United States, approximately 6.3% of the adult population, totaling approximately 15 million people, is diagnosed with COPD. COPD could affect 25 million people if undiagnosed causes are considered. In 2011, approximately 730,000 US hospital admissions were due to COPD.

Story

The word "emphysema" is derived from the Greek ἐμφυσᾶν emphysanus meaning "inflate" (to inflate), consisting of ἐν en meaning "in" and φυσᾶν physanus meaning "breathing, flow of air". The term chronic bronchitis came into use in 1808, while the term COPD is believed to have first been used in 1965. It was previously known by several different terms, including chronic obstructive bronchopulmonary disease, chronic obstructive respiratory disease, and chronic difficulty breathing. , chronic airflow limitation, chronic obstructive pulmonary disease, non-specific chronic lung disease, and diffuse obstructive pulmonary syndrome. The terms chronic bronchitis and emphysema were formally used in 1959 at a CIBA guest symposium and in 1962 and at a committee meeting of the American Thoracic Society regarding diagnostic standards. Early descriptions of supposed emphysema include: T. Bonet of a condition of "voluminous lungs" in 1679 and Giovanni Morgagni of lungs that were "swollen, in part due to air" in 1769. The first description of emphysema was made in 1721. Ruish. This was followed by drawings by Matthew Bailey in 1789 and a description of the destructive nature of the disease. In 1814 Charles Badham used "catarrh" to describe the cough and excess mucus in chronic bronchitis. René Laennec, the physician who invented the stethoscope, used the term "emphysema" in his Monograph on Diseases of the Chest and Indirect Auscultation (1837) to describe lungs that did not collapse when he opened the chest during an autopsy. He noted that they did not fall down as usual, as they were full of air, and the airways were filled with mucus. In 1842, John Hutchinson invented the spirometer, which made it possible to measure the vital capacity of the lungs. However, his spirometer was only capable of measuring volume, not airflow. Tiffno and Pinelli in 1947 described the principles of measuring airflow. In 1953, Dr. George L. Waldbott, an American allergist, first described a new disease, which he called "smoker's respiratory syndrome", in the 1953 Journal of the American Medical Association. This was the first mention of an association between tobacco smoking and chronic respiratory disease. Previous treatments have included garlic, cinnamon, and ipecac, among others. Modern methods of treatment were developed in the second half of the 20th century. Evidence supporting the use of steroids in COPD was published in the late 1950s. Bronchodilators came into use in the 1960s as a result of promising research on isoprenaline. Late bronchodilators such as salbutamol were developed in the 1970s, and the use of long-acting β2 agonists began in the mid-1990s.

Society and culture

COPD has been referred to as "smoker's lungs". People with emphysema were known as "pink puffers" or "type A" due to frequent pink complexion, rapid breathing, and pursed lips, while people with chronic bronchitis were referred to as "blue puffers" or "type B" due to frequent bluish discoloration of the skin and lips as a result of low oxygen levels and swelling of the lower legs. This terminology is no longer considered useful because most people with COPD have a combination of both types. Many systems face challenges in providing adequate definition, diagnosis and care for people with COPD; The UK Department of Health has identified this as a major problem for the NHS and has developed a specific strategy to address these issues.

Economy

Globally, as of 2010, COPD is estimated to have resulted in an economic cost of $2.1 trillion, half of which is in developing countries. Of the total costs, $1.9 trillion are direct costs such as medical care, while $0.2 trillion are indirect costs such as lost jobs. Costs are expected to more than double by 2030. In Europe, COPD accounts for 3% of healthcare costs. In the US, the cost of the disease is estimated to be $50 billion, most of which is related to exacerbations. COPD is among the most costly diseases seen in US hospitals in 2011, with a total cost of approximately US$5.7 billion.

Research

Infliximab, an immunosuppressive antibody, has been tested for COPD but found no evidence of benefit, with potential for harm. Roflumilast showed promise in reducing the intensity of seizures, but did not change the quality of life. Several new long acting agents are in development. Stem cell therapy is in the process of being researched, with generally safe and promising animal data, but insufficient human data as of 2014.

Other animals

Chronic obstructive pulmonary disease can occur in several other animals and can be caused by exposure to tobacco smoke. Most cases, however, are relatively mild. In horses, the disease is known as recurrent airway obstruction and is usually associated with an allergic reaction to fungi found in straw. COPD is also common in older dogs.

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MD, prof. S.I. Ovcharenko, Department of Faculty Therapy No. 1, State Educational Institution of Higher Professional Education MMA named after. THEM. Sechenov

Chronic obstructive pulmonary disease (COPD) is one of the most widespread diseases, which is largely due to the increasing impact of adverse factors (risk factors): environmental pollution, tobacco smoking and recurrent respiratory infections.

COPD is characterized by airflow limitation that is not completely reversible and is steadily progressive.

The diagnosis of COPD should be considered in every person who coughs, produces sputum, and has risk factors. In all these cases, spirometry should be performed. A decrease in the ratio of forced expiratory volume in 1 second to forced vital capacity (FEV 1 / FVC) of less than 70% is an early and reliable sign of airflow limitation, even if FEV 1 > 80% of the proper value is maintained. Moreover, obstruction is considered chronic (and the patient must be considered suffering from COPD) if it is recorded three times within one year. The stage of the disease (its severity) reflects the value of FEV 1 in the post-bronchodilator test. Chronic cough and excessive sputum production long precede ventilation disorders leading to dyspnoea.

The main goals of treating patients with COPD are clearly formulated in the International Program "Global Strategy: Diagnosis, Treatment and Prevention of COPD", created on the basis of the principles of evidence-based medicine (2003) and in the federal program of the Russian Federation for the diagnosis and treatment of COPD (2004). They are aimed at:

Prevention of disease progression;

Increasing tolerance to physical activity;

Reducing symptoms;

Improving the quality of life;

Prevention and treatment of exacerbations and complications;

Decrease in mortality.

The implementation of these provisions is carried out in the following areas:

Reducing the influence of risk factors;

Implementation of educational programs;

Treatment of COPD in stable condition;

Treatment of an exacerbation of the disease.

Smoking cessation is the first major step in a COPD treatment program to prevent progression of the disease and by far the most effective intervention to reduce the risk of developing COPD. Special programs for the treatment of tobacco dependence have been developed:

Long-term treatment program with the goal of complete smoking cessation;

A short treatment program to reduce the amount of tobacco smoked and increase motivation to quit smoking completely;

Smoking reduction program.

The long-term treatment program is designed for patients with a strong desire to quit smoking. The program lasts from 6 months to 1 year and consists of periodic conversations between the doctor and the patient (more frequent in the first 2 months of quitting smoking), and the patient nicotine-containing preparations(NSP). The duration of taking the drugs is determined individually and depends on the degree of nicotine dependence of the patient.

The short treatment program is intended for patients who do not want to quit smoking, but do not reject this possibility in the future. In addition, this program can be offered to patients who wish to reduce the intensity of smoking. The duration of the short program is from 1 to 3 months. Treatment within 1 month allows to reduce the intensity of smoking by an average of 1.5 times, within 3 months - by 2-3 times. A short treatment program is built on the same principles as a long one: doctor's conversations, development of a patient behavior strategy, nicotine replacement therapy, detection and treatment of chronic bronchitis and prevention of its exacerbation as a result of smoking cessation. For this purpose, acetylcysteine ​​is prescribed - 600 mg 1 time per day in a blister. The difference with this program is that a complete cessation of smoking is not achieved.

The smoking reduction program is designed for patients who do not want to quit smoking, but are willing to reduce the intensity of smoking. The essence of the program is that the patient continues to receive nicotine at the usual level for him, combining cigarette smoking with taking NSP, but at the same time reduces the number of cigarettes smoked per day. Within a month, the intensity of smoking can be reduced by an average of 1.5-2 times, i.e. the patient reduces the intake of harmful substances contained in cigarette smoke, which is undoubtedly a positive result of treatment. This program also uses the doctor's conversations and the development of a strategy for the patient's behavior.

The effectiveness of a combination of two methods has been confirmed - nicotine replacement therapy and conversations between doctors and medical staff with the patient. Even short three-minute smoking cessation consultations are effective and should be used at every medical appointment. Smoking cessation does not lead to the normalization of lung function, but it can slow down the progressive deterioration of FEV 1 (further, the decrease in FEV 1 occurs at the same rate as in non-smoking patients.)

An important role in inducing smoking cessation, in improving the skills of inhalation therapy in patients with COPD and their ability to cope with the disease, is played by educational programs.

For people with COPD, education should cover all aspects of managing the disease and can take many forms: consultations with a doctor or other healthcare professional, home or out-of-home programs, and full-fledged pulmonary rehabilitation programs. For patients with COPD, it is necessary to understand the nature of the disease, risk factors leading to the progression of the disease, clarify their own role and the role of the doctor in order to achieve the optimal result of treatment. Education should be tailored to the needs and environment of the individual patient, be interactive, improve the quality of life, be easy to implement, practical, and appropriate to the intellectual and social level of the patient and those caring for them.

To give up smoking;

Basic information about COPD;

Basic approaches to therapy;

Specific treatment issues (in particular the correct use of inhaled medicines);

Self-management skills (peak flowmetry) and decision-making during an exacerbation. Patient education programs should include the distribution of printed materials and the conduct of educational sessions and workshops aimed at providing information about the disease and teaching patients special skills.

It has been established that training is most effective when it is carried out in small groups.

The choice of drug therapy depends on the severity (stage) of the disease and its phase: a stable state or an exacerbation of the disease.

According to modern ideas about the nature of COPD, the main and universal source of pathological manifestations that develop with the progression of the disease is bronchial obstruction. Hence it follows that bronchodilators should occupy and currently occupy a leading place in the complex therapy of patients with COPD. All other means and methods of treatment should be used only in combination with bronchodilators.

Treatment of COPD in a stable condition of the patient

Treatment of stable COPD patients is necessary to prevent and control symptoms of the disease, reduce the frequency and severity of exacerbations, improve general condition and increase exercise tolerance.

The management of patients with COPD in a stable state is characterized by a stepwise increase in the amount of therapy, depending on the severity of the disease.

It should be emphasized once again that at present the leading place in the complex therapy of patients with COPD is occupied by bronchodilators. All categories of bronchodilators have been shown to increase exercise tolerance even in the absence of an increase in FEV 1 values. Inhalation therapy is preferred (Evidence level A). The inhalation route of administration of drugs provides direct penetration of the drug into the respiratory tract and, thus, contributes to a more effective drug effect. In addition, the inhalation route of administration reduces the potential risk of systemic side effects.

Particular attention should be paid to teaching patients the correct technique of inhalation in order to increase the effectiveness of inhalation therapy. m-Cholinolytics and beta 2-agonists are used mainly with the help of metered-dose inhalers. To increase the efficiency of drug delivery to the site of pathological reactions (i.e., to the lower respiratory tract), spacers can be used - devices that increase the flow of the drug into the airways by 20%.

In patients with severe and extremely severe COPD, bronchodilatory therapy is carried out with special solutions through a nebulizer. Nebulizer therapy is also preferred, as is the use of a metered-dose aerosol with a spacer, in the elderly and patients with cognitive impairment.

To reduce bronchial obstruction in patients with COPD, short-acting and long-acting anticholinergics, short- and long-acting beta2-agonists, methylxanthines, and their combinations are used. Bronchodilators are given "on demand" or on a regular basis to prevent or reduce symptoms of COPD. The sequence of application and the combination of these drugs depends on the severity of the disease and individual tolerance.

For mild COPD, short-acting bronchodilators are used, “on demand”. In moderate, severe and extremely severe disease, long-term and regular treatment with bronchodilators is a priority, which reduces the rate of progression of bronchial obstruction (Evidence A). The most effective combination of bronchodilators with a different mechanism of action, because. the bronchodilator effect is enhanced and the risk of side effects is reduced compared with an increase in the dose of one of the drugs (level of evidence A).

m-Cholinolytics occupy a special place among bronchodilators due to the role of the parasympathetic (cholinergic) autonomic nervous system in the development of the reversible component of bronchial obstruction. The appointment of anticholinergic drugs (ACP) is advisable for any severity of the disease. The best known short-acting AChP is ipratropium bromide, which is usually given at 40 mcg (2 doses) 4 times a day (Evidence B). Due to insignificant absorption through the bronchial mucosa, ipratropium bromide practically does not cause systemic side effects, which allows it to be widely used in patients with cardiovascular diseases. ACPs do not have a negative effect on the secretion of bronchial mucus and the processes of mucociliary transport. Short-acting m-anticholinergics have a longer bronchodilator effect than short-acting beta2-agonists (Evidence A).

A distinctive feature of short-acting beta 2-agonists (salbutamol, fenoterol) is the speed of action on bronchial obstruction. Moreover, the bronchodilating effect is higher, the more pronounced the lesion of the distal bronchi. Patients within a few minutes feel an improvement in breathing and in therapy "on demand" (for mild COPD - stage I) they often prefer them. However, the regular use of short-acting beta2-agonists as monotherapy for COPD is not recommended (Evidence A). In addition, short-acting beta 2-agonists should be used with caution in elderly patients with concomitant heart disease (with coronary artery disease and hypertension), because. these drugs, especially in combination with diuretics, can cause transient hypokalemia, and, as a result, cardiac arrhythmias.

Many studies have shown that long-term use of ipratropium bromide is more effective for the treatment of COPD than long-term monotherapy with short-acting beta2-agonists (Evidence A). However, the use of ipratropium bromide in combination with short-acting beta2-agonists has a number of advantages, including a reduction in the frequency of exacerbations, and thereby a reduction in the cost of treatment.

Regular treatment with long-acting bronchodilators (tiotropium bromide, salmeterol, formoterol) is recommended for moderate, severe and very severe COPD (Evidence A). They are more effective and convenient to use than short-acting bronchodilators, but they are more expensive to treat (Evidence A). In this regard, patients with severe COPD may be prescribed short-acting bronchodilator drugs in various combinations (see Table 1).

Table 1

The choice of bronchodilators depending on the severity of COPD

Ipratropium bromide is prescribed 40 mcg (2 doses) 4 times a day, tiotropium bromide - 1 time per day at a dose of 18 mcg through "HandiHaler", salbutamol - 100-200 mcg up to 4 times a day, fenoterol - 100-200 mcg up to 4 times a day, salmeterol - 25-50 mcg 2 times a day, formoterol 4.5-12 mcg 2 times a day. When using inhaled short-acting bronchodilators, preference is given to CFC-free dosage forms.

Tiotropium bromide is a representative of a new generation of ACPs, a long-acting drug whose bronchodilating effect persists for 24 hours (Evidence level A), which makes it possible to use this drug once a day. The low frequency of side effects (dry mouth, etc.) indicates a sufficient safety of using this drug in COPD. Early studies have shown that tiotropium bromide not only significantly improves lung volume and peak expiratory flow in patients with COPD, but also reduces the frequency of exacerbations with long-term use.

According to the anticholinergic effect of tiotropium bromide, inhaled by patients with COPD using a metered-dose powder inhaler "HandiHaler", is approximately 10 times greater than ipratropium bromide.

The results of controlled 12-month studies showed a significant superiority of tiotropium bromide over ipratropium bromide in terms of the effect of:

On indicators of bronchial patency;

The severity of shortness of breath;

Need for short-acting bronchodilators;

frequency and severity of exacerbations.

Long-acting beta2-agonists (salmeterol, formoterol) are also recommended for regular use in the treatment of COPD. They, regardless of changes in bronchial patency, can improve clinical symptoms and quality of life of patients, reduce the number of exacerbations (level of evidence B). Salmeterol improves the condition of patients when used at a dose of 50 mcg twice a day (level of evidence B). Formoterol, like salmeterol, acts for 12 hours without loss of effectiveness (level of evidence A), but the effect of formoterol develops faster (after 5-7 minutes) than that of salmeterol (after 30-45 minutes).

Long-acting beta 2-agonists, in addition to the bronchodilator effect, also show other positive qualities in the treatment of patients with COPD:

Reduce hyperinflation of the lungs;

Activate mucociliary transport;

Protect the cells of the mucous membrane of the respiratory tract;

Show antineutrophil activity.

Treatment with a combination of an inhaled beta2-agonist (rapid or long-acting) and an ACP improves airflow better than either agent alone (Evidence A).

Methylxanthines (theophylline) with insufficient efficacy of AHP and beta 2-agonists can be added to regular inhaled bronchodilator therapy for more severe COPD (Evidence level B). All studies that have shown the effectiveness of theophylline in COPD concern long-acting drugs. The use of prolonged forms of theophylline may be indicated for nocturnal symptoms of the disease. The bronchodilating effect of theophylline is inferior to that of beta 2-agonists and ACP, but its oral administration (prolonged forms) or parenteral administration (methylxanthines are not prescribed by inhalation) causes a number of additional effects: reduction of pulmonary hypertension, increased diuresis, stimulation of the central nervous system, improvement of respiratory muscle tone which may be useful in some patients.

Theophylline may be beneficial in the treatment of COPD, but inhaled bronchodilators are preferred due to its potential side effects. Currently, theophylline belongs to the second-line drugs, i.e. is prescribed after ACP and beta 2-agonists or their combinations, or for those patients who cannot use inhaled delivery vehicles.

In real life, the choice between ACPs, beta 2-agonists, theophylline, or a combination of them depends largely on the availability of drugs and the individual response to treatment in terms of symptom relief and the absence of side effects.

Inhaled glucocorticoids (IGCs) are prescribed in addition to bronchodilator therapy in patients with clinical symptoms of the disease, FEV 1<50% от должного (тяжелое теение ХОБЛ — стадия III и крайне тяжелое течение ХОБЛ — стадия IV) и повторяющимися обострениями (3 раза и более за последние три года) (уровень доказательности А). Предпочтительно применение ИГК длительного действия — флутиказона или будесонида. Эффективность лечения оценивается через 6-12 недель применения ИГК.

The combination with long-acting beta 2-agonists increases the effectiveness of corticosteroid therapy (the effect is superior to the results of separate use). This combination demonstrates the synergism of the action of drugs when exposed to various links in the pathogenesis of COPD: bronchial obstruction, inflammation and structural changes in the airways, mucociliary dysfunction. The combination of long-acting beta2-agonists and ICS (salmeterol/fluticasone and formoterol/budesonide) results in a better risk/benefit ratio than the individual components.

Long-term treatment with systemic glucocorticoids is not recommended due to an unfavorable balance of efficacy and risk of adverse events (Evidence A).

Mucolytic (mucoregulators, mucokinetics) and expectorants shown to a very limited cohort of COPD patients with a stable course in the presence of viscous sputum and do not significantly affect the course of the disease.

For the prevention of exacerbation of COPD, long-term use of the mucolytic acetylcysteine ​​(preferably 600 mg in a blister), which simultaneously has antioxidant activity, seems promising. Taking acetylcysteine ​​for 3-6 months at a dose of 600 mg/day is accompanied by a significant decrease in the frequency and duration of COPD exacerbations.

Application antibacterial agents for prophylactic purposes in patients with COPD should not be a daily practice, tk. According to the results of modern studies, antibiotic prophylaxis of exacerbations of COPD has a low, but statistically significant efficiency, manifested in a decrease in the duration of exacerbations of the disease. However, there is a risk of adverse drug events in patients and the development of pathogen resistance.

In order to prevent exacerbation of COPD during epidemic outbreaks of influenza, it is recommended vaccines, containing killed or inactivated viruses. Vaccines are prescribed to patients once, in October - the first half of November, or twice (in autumn and winter) annually (level of evidence A). Influenza vaccine can reduce the severity and mortality in patients with COPD by 50%. A pneumococcal vaccine containing 23 virulent serotypes is also used, but data on its effectiveness in COPD are insufficient (Evidence level B).

Non-drug treatment with a stable course of COPD includes oxygen therapy. Correction of hypoxemia with oxygen is the most pathophysiologically sound method for the treatment of respiratory failure. Patients with chronic respiratory failure are shown constant many hours of low-flow (more than 15 hours a day) oxygen therapy. Long-term oxygen therapy is currently the only therapy that can reduce mortality in patients with extremely severe COPD (Evidence A).

For patients with COPD at all stages of the course of the process are effective physical training programs increase exercise tolerance and reduce shortness of breath and fatigue. Physical training necessarily includes exercises for the development of strength and endurance of the lower extremities (metered walking, bicycle ergometer). In addition, they may include exercises that increase the strength of the muscles of the upper shoulder girdle (manual ergometer, dumbbells).

Physical exercise is the main component pulmonary rehabilitation. In addition to physical training, rehabilitation activities include: psychosocial support, educational programs, nutritional support. One of the tasks of rehabilitation is to identify and correct the causes of nutritional status disorders in patients with COPD. The most rational diet is the frequent intake of small portions of protein-rich foods. The best way to correct a deficiency in body mass index is to combine supplementary nutrition with physical training, which has a non-specific anabolic effect. The positive effect of rehabilitation programs is also achieved through psychosocial interventions.

There are no absolute contraindications to pulmonary rehabilitation. Ideal candidates for inclusion in rehabilitation programs are patients with moderate to severe COPD, i.e. patients in whom the disease imposes serious restrictions on the usual level of functional activity.

In recent years, there have been reports of the use of methods surgical treatment in patients with severe COPD. Operative correction of lung volumes by the method bullectomy, resulting in reduced dyspnea and improved lung function. However, this method is a palliative surgical procedure with unproven efficacy. The most radical surgical method is lung transplant in carefully selected patients with very severe COPD. The selection criterion is FEV 1<35% от должной величины, pО 2 <55-60 мм рт. ст., pСО 2 >50 mmHg and evidence of secondary pulmonary hypertension.

Treatment of COPD during an exacerbation

The primary causes of exacerbation of COPD include tracheobronchial infections (often viral etiology) and exposure to aerosolants.

Among the so-called. secondary causes of exacerbation of COPD include: thromboembolism of the branches of the pulmonary artery, pneumothorax, pneumonia, chest trauma, the appointment of beta-blockers and other drugs, heart failure, heart rhythm disturbances, etc.

All exacerbations should be considered as a factor in the progression of COPD, and therefore more intensive therapy is recommended. First of all, this applies to bronchodilator therapy: the doses of drugs are increased and the methods of their delivery are modified (preference is given to nebulizer therapy). For this purpose, special solutions of bronchodilators are used - ipratropium bromide, fenoterol, salbutamol, or a combination of ipratropium bromide with fenoterol.

Depending on the severity of the course and the degree of exacerbation of COPD, treatment can be carried out both on an outpatient basis (mild exacerbation or moderate exacerbation in patients with mild COPD) and on an inpatient basis.

As a bronchodilator in severe COPD exacerbation, it is recommended to prescribe nebulized solutions short-acting beta 2-agonists (level of evidence A). The regimen of high doses of bronchodilators can bring a significant positive effect in acute respiratory failure.

In the treatment of severe patients with the presence of multiple organ pathology, tachycardia, hypoxemia, the role of ACP drugs increases. Ipratropium bromide is prescribed both as monotherapy and in combination with beta 2 agonists.

The generally accepted dosing regimen for inhaled bronchodilators in COPD exacerbations is shown in Table 2.

table 2

Dosing regimens for inhaled bronchodilators in exacerbations of COPD

The appointment of any other bronchodilators or their dosage forms (xanthines, bronchodilators for intravenous administration) should be preceded by the use of the maximum doses of these drugs, administered through a nebulizer or spacer.

The advantages of inhalation through a nebulizer are:

No need to coordinate inspiration with inhalation;

Ease of performing the inhalation technique for the elderly and severely ill;

The possibility of introducing a high dose of a medicinal substance;

The possibility of including a nebulizer in the oxygen supply circuit or the ventilation circuit;

Lack of freon and other propellants;

Ease of use.

Due to the variety of adverse effects of theophylline, its use requires caution. At the same time, if it is impossible, for various reasons, to use inhaled forms of drugs, as well as if other bronchodilators and glucocorticoids are not sufficiently effective, it is possible to prescribe theophylline preparations. The use of theophylline in exacerbations of COPD is debated, since in controlled studies the effectiveness of theophylline in patients with exacerbations of COPD was not high enough, and in some cases, treatment was accompanied by such adverse reactions as hypoxemia. The high risk of unwanted side reactions makes it necessary to measure the concentration of the drug in the blood, which in the practice of a doctor seems to be very difficult.

To stop the exacerbation, along with bronchodilator therapy, antibiotics, glucocorticoids are used, and in a hospital setting - controlled oxygen therapy and non-invasive ventilation of the lungs.

Glucocorticoids. With exacerbation of COPD, accompanied by a decrease in FEV 1<50% от должного, используют глюкокортикоиды параллельно с бронхолитической терапией. Предпочтение отдают системным глюкокортикоидам: например, назначают по 30-40 мг преднизолонав течение 10-14 дней с последующим переводом на ингаляционный путь введения.

Therapy with systemic glucocorticoids (orally or parenterally) contributes to a more rapid increase in FEV 1, a decrease in dyspnea, an improvement in arterial blood oxygenation, and a shortening of hospital stays (Evidence A). They should be prescribed as early as possible, even upon admission to the emergency department. Oral or intravenous administration of glucocorticoids for exacerbations of COPD at the hospital stage is carried out in parallel with bronchodilator therapy (if indicated, in combination with antibiotics and oxygen therapy). The recommended dosage has not been definitively determined, but given the serious risk of adverse events with high-dose steroid therapy, prednisolone 30–40 mg for 10–14 days should be considered an acceptable compromise between efficacy and safety (Evidence D). Further continuation of oral administration does not lead to an increase in efficacy, but increases the risk of adverse events.

Antibacterial agents are indicated with increased shortness of breath, an increase in sputum volume and its purulent character. In most cases of exacerbations of COPD, antibiotics can be given by mouth. The duration of antibiotic therapy is from 7 to 14 days (see Table 3).

Table 3

Antibacterial therapy for exacerbations of COPD

For uncomplicated exacerbations, the drug of choice is amoxicillin (alternatively, respiratory fluoroquinolones or amoxicillin / clavulanate, as well as the "new" macrolides - azithromycin, clarithromycin, can be used). In complicated exacerbations, the drugs of choice are respiratory fluoroquinolones (levofloxacin, moxifloxacin) or II-III generation cephalosporins, including those with antipseudomonal activity.

Indications for parenteral use of antibiotics are:

Lack of an oral form of the drug;

Gastrointestinal disorders;

Severe exacerbation of the disease;

Low compliance with the patient.

oxygen therapy is one of the key areas of complex treatment of patients with exacerbation of COPD in a hospital setting. An adequate level of oxygenation, namely pO 2 >8.0 kPa (more than 60 mm Hg. Art.) or pCO 2 >90%, as a rule, is quickly achieved with uncomplicated exacerbations of COPD. After the start of oxygen therapy through nasal catheters (flow rate - 1-2 l / min) or a Venturi mask (oxygen content in the inhaled oxygen-air mixture 24-28%), blood gases should be monitored after 30-45 minutes (adequacy of oxygenation, exclusion of acidosis , hypercapnia).

Auxiliary IVL. If, after a 30-45-minute inhalation of oxygen in a patient with acute respiratory failure, the effectiveness of oxygen therapy is minimal or absent, a decision should be made on assisted ventilation. Recently, special attention has been paid to non-invasive positive pressure ventilation. The effectiveness of this method of treating respiratory failure reaches 80-85% and is accompanied by the normalization of arterial blood gases, a decrease in shortness of breath, and, more importantly, a decrease in the mortality of patients, a decrease in the number of invasive procedures and associated infectious complications, as well as a decrease in the duration of the hospital treatment period. (Evidence level A).

In cases where non-invasive ventilation is ineffective (or unavailable) in a patient suffering from a severe exacerbation of COPD, invasive ventilation is indicated.

A schematic diagram of the treatment of COPD exacerbation is shown in the figure below.

Picture. Schematic diagram of the treatment of exacerbations of COPD

Unfortunately, COPD patients seek medical help, usually in the later stages of the disease, when they already have respiratory failure or develop cor pulmonale. At this stage of the disease, treatment is extremely difficult and does not give the expected effect. In connection with the above, the early diagnosis of COPD and the timely implementation of the developed treatment program remain extremely relevant.

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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 a variety of occupational pollutants are less common causes 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 worldwide 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 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 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 based 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 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 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.

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 ​​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. 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 total lung capacity is reached, and hold the 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 commonly 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 the middle stage of COPD, as well as in patients who continue to smoke and have stopped smoking and in people 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 trials have established an increased 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 patients with COPD 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 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 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. 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; 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. 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 normalizes hematocrit, modestly improves neurological status and psychological state, 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 severe COPD who do not meet criteria 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 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 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; this slows, but does not completely stop, the progression of airway inflammation The best effect is obtained by the simultaneous use of different methods of quitting smoking: setting a date for quitting smoking, behavior modification methods, group classes, nicotine replacement therapy (chewing gum, transdermal therapeutic system, inhaler, pills or nasal spray solution), bupropion and medical support. Smoking cessation rates are approximately 30% per year, even with the most effective method, the combination 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 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. Upper limb endurance training is 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. Smaller improvements are seen in lower limb strength, endurance, and maximum O2 consumption. 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, 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. 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. Patients with life-threatening exacerbations with uncorrectable hypoxemia, acute respiratory acidosis, new arrhythmias, or deterioration of respiratory function despite inpatient treatment, as well as patients who require sedation for treatment, are subject to mandatory admission to the intensive care unit with constant monitoring of the 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 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 first-line drugs. 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 per 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.

DEFINITION.

Chronic obstructive pulmonary disease(COPD) is a disease characterized by partially irreversible, steadily progressive airflow limitation caused by an abnormal inflammatory response of lung tissue to damaging environmental factors - smoking, inhalation of particles or gases. The term "COPD" refers to a combination of chronic bronchitis and emphysema.

Important provisions on COPD are set out in an international document compiled by experts from 48 countries - "Global Initiative for the Treatment of Chronic Obstructive Pulmonary Disease - GOLD, 2003". The key points about COPD should be noted.

COPD has ceased to be a collective concept (chronic obstructive bronchitis, severe forms of bronchial asthma, bronchitis obliterans, cystic fibrosis, etc.);

The concept of COPD does not apply only to patients with end-stage respiratory failure;

The concept of "chronic obstructive bronchitis" is absorbed by the concept of "chronic obstructive pulmonary disease".

RELEVANCE.

COPD is currently the fourth leading cause of death in the world, with a predicted increase in prevalence and mortality in the coming decades. According to the Global Burden of Disease Study, the prevalence of COPD in 1990 was 9.34 per 1000 men and 7.33 per 1000 women (GOLD, 2003). Data on prevalence, morbidity, and mortality from COPD significantly underestimate the overall cost of the disease, as usually COPD is not recognized and diagnosed until it becomes clinically significant. The significant increase in the overall burden of COPD over the past 20 years reflects the increase in tobacco smoking as well as the changing age structure of the population.

risk factors for hobl. Internal factors:

Genetic factors (deficiency of alpha-1 antitrypsin);

Airway hypersensitivity;

Lung growth.

External factors:

tobacco smoking;

Professional dust and chemicals;

Domestic and outdoor air pollutants;

infections;

Socio-economic status.

ETIOLOGY AND PATHOGENESIS.

The development of COPD can be hereditarily determined with congenital deficiency of alpha-1-antitrypsin, but more often it is due to active or passive smoking, air pollution, prolonged exposure to occupational factors (dust, fumes, chemical irritants), unfavorable home atmosphere (kitchen fumes, household chemicals). ). The pathogenetic basis of COPD is a chronic inflammatory process of the tracheobronchial tree, lung parenchyma and blood vessels, in which increased numbers of macrophages, T-lymphocytes and neutrophils are detected. Inflammatory cells secrete a large number of mediators: leukotriene B4, interleukin 8, tumor necrosis factor and others that can damage the structure of the lungs and maintain neutrophilic inflammation. In addition, the imbalance of proteolytic enzymes, antiproteinases and oxidative stress play a role in the pathogenesis of COPD.

Morphologically, in the tracheobronchial tree, inflammatory cells infiltrate the surface epithelium. The mucous glands expand and the number of goblet cells increases, which leads to hypersecretion of mucus. In small bronchi and bronchioles, the inflammatory process occurs cyclically with structural remodeling of the bronchial wall, characterized by an increase in collagen content and the formation of scar tissue, leading to persistent airway obstruction.

In the development of COPD, there is a sequential phasing: the disease begins with mucus hypersecretion followed by dysfunction of the ciliated epithelium, bronchial obstruction develops, which leads to the formation of pulmonary emphysema, impaired gas exchange, respiratory failure, pulmonary hypertension and the development of cor pulmonale. The given data on causes, pathogenesis, morphology show that COPD is the result of chronic bronchitis, prolonged bronchospastic syndrome and/or pulmonary emphysema and other parenchymal destructions (including congenital) associated with a decrease in the elastic properties of the lungs.

Chronic hypoxia leads to compensatory erythrocytosis - secondary polycythemia with a corresponding increase in blood viscosity and microcirculation disorders, which exacerbate ventilation-perfusion mismatches.

An exacerbation of the infectious process in the respiratory system leads to an increase in all signs of the disease. In conditions of mucostasis, local and sometimes systemic immunodeficiency, the colonization of microorganisms can take on an uncontrolled character and go into a qualitatively different form of relationship with the macroorganism - an infectious process. Another way is also possible - the usual infection by airborne droplets with a highly virulent flora, which is easily realized under conditions of impaired defense mechanisms. It should be emphasized that bronchopulmonary infection, although frequent, is not the only cause of exacerbation. Along with this, exacerbations of the disease are possible, associated with an increased effect of exogenous damaging factors, or due to inadequate physical activity. In these cases, signs of infection of the respiratory system are minimal. As COPD progresses, the intervals between exacerbations become shorter.

COPD CLASSIFICATION(GOLD, 2003)

0 - risk of developing the disease:

Normal spirometry;

Chronic symptoms (cough, sputum production);

I - easy course:

FEV 1 / FVC<70% от должного;

Presence or absence of chronic symptoms (cough, sputum);

II - moderate course:

FEV 1 / FVC<70% от должного;

50%≤FEV 1<80% от должных значений;

III - severe course:

FEV 1 / FVC<70% от должного;

30%≤FEV 1<50% от должных значений;

Presence or absence of chronic symptoms;

IV - extremely severe course:

FEV 1 / FVC<70% от должного;

FEV 1 ≤30% predicted or FEV 1<50% от должного в сочетании с хронической дыхательной недостаточностью (PaO2≤60% мм рт. ст. и/или PaCO 2 ≥ 50 мм рт. ст.);

The presence of cough, sputum, shortness of breath, clinical signs of right ventricular failure.

CLINIC.

The clinical picture of COPD is characterized by the same type of clinical manifestations - cough and shortness of breath, despite the heterogeneity of the diseases that make it up. The degree of their severity depends on the stage of the disease, the rate of progression of the disease and the predominant level of damage to the bronchial tree.

The rate of progression and severity of symptoms of COPD depends on the intensity of exposure to etiological factors and their summation. Thus, the standards of the American Thoracic Society emphasize that the appearance of the first clinical symptoms in patients with COPD is usually preceded by smoking at least 20 cigarettes a day for 20 years or more.

The first symptoms that patients usually seek medical attention for are cough and shortness of breath, sometimes accompanied by wheezing with sputum production. These symptoms are more pronounced in the morning.

The earliest symptom, appearing by 40-50 years of age, is a cough. By the same time, in the cold seasons, episodes of a respiratory infection begin to occur, which are not initially associated with one disease. Dyspnea felt on exertion occurs on average 10 years after the onset of cough. However, in some cases, the onset of the disease with shortness of breath is possible.

Sputum is secreted in a small (rarely > 60 ml / day) amount in the morning, has a mucous character. Exacerbations of an infectious nature are manifested by the aggravation of all signs of the disease, the appearance of purulent sputum and an increase in its amount.

Shortness of breath can vary over a very wide range: from feeling short of breath during standard physical exertion to severe respiratory failure.

A number of COPD patients have obstructive sleep apnea syndrome. The combination of bronchial obstruction, characteristic of COPD, with sleep apnea is called overlap syndrome, in which gas exchange disorders are most pronounced. There is an opinion that in most patients chronic hypercapnia is formed mainly at night.

There are two clinical forms of the disease - emphysematous and bronchitis.

The emphysematous form (type) of COPD is associated mainly with panacinar emphysema. Such patients are figuratively called "pink puffers", because in order to overcome the prematurely occurring expiratory collapse of the bronchi, exhalation is made through lips folded into a tube and is accompanied by a kind of puffing. The clinical picture is dominated by dyspnea at rest due to a decrease in the diffusion surface of the lungs. Such patients are usually thin, their cough is often dry or with a small amount of thick and viscous sputum. The complexion is pink, because. sufficient oxygenation of the blood is maintained by increasing ventilation as much as possible. The limit of ventilation is reached at rest, and patients tolerate physical activity very poorly. Pulmonary hypertension is moderately pronounced, because. the reduction of the arterial bed, caused by atrophy of the interalveolar septa, does not reach significant values. Cor pulmonale is compensated for a long time. Thus, the emphysematous type of COPD is characterized by the predominant development of respiratory failure.

Bronchitis form (type) is observed with centriacinar emphysema. Constant hypersecretion causes an increase in inspiratory and expiratory resistance, which contributes to a significant violation of ventilation. In turn, a sharp decrease in ventilation leads to a significant decrease in the content of O 2 in the alveoli, followed by a violation of the perfusion-diffusion ratios and blood shunting. This determines the characteristic blue tint of diffuse cyanosis in patients of this category. Such patients are obese, the clinical picture is dominated by cough with copious sputum. Diffuse pneumosclerosis and obliteration of the lumen of blood vessels lead to the rapid development of cor pulmonale and its decompensation. This is facilitated by persistent pulmonary hypertension, significant hypoxemia, erythrocytosis and constant intoxication due to a pronounced inflammatory process in the bronchi.

The selection of two forms has prognostic value. Thus, in the later stages of the emphysematous type, decompensation of the cor pulmonale occurs in comparison with the bronchitis variant of COPD. In clinical conditions, patients with a mixed type of disease are more common.

The classification of COPD according to severity distinguishes a number of stages in the course of the disease. Stage 0 means an increased risk of developing COPD. It is characterized by the onset of symptoms (cough, sputum production) with normal ventilatory function and actually corresponds to chronic bronchitis. For mild COPD ( stage I) and minimal clinical signs (cough, sputum) obstructive disorders are recorded. For moderate COPD ( stage II) more pronounced obstructive disorders of pulmonary ventilation are recorded, and in addition to coughing and sputum, shortness of breath appears, which indicates the development of respiratory failure. In severe and extremely severe COPD ( stage III–IV) there is chronic respiratory failure and signs of cor pulmonale (right ventricular failure). Obstructive disorders detected in the study of the ventilation function of the lungs can reach critical values.

THE MAIN SIGNS THAT ALLOW TO SUSPECT COBL.

chronic cough

Intermittent or daily. Often happens throughout the day.

Chronic expectoration of sputum

Any episode of chronic sputum production may indicate COPD.

Dyspnea

Progressive, persistent. Increases with physical activity and respiratory infections.

History of exposure to risk factors

Tobacco smoking, occupational pollutants and chemicals. Smoke from the kitchen and heating at home.

If any of these signs are present, COPD should be suspected and a respiratory function test should be performed.

History of smoking

A prerequisite for the diagnosis of COPD, according to WHO recommendations, is the calculation of the index of a smoking person. The calculation of the index of a smoking person is carried out as follows: the number of cigarettes smoked per day is multiplied by the number of months in a year, i.e. at 12; if this value exceeds 160, then smoking in this patient poses a risk for the development of COPD; if the values ​​of this index exceed more than 200, the patient should be classified as "malicious smokers".

The history of smoking is recommended to be calculated in units of "packs / years". The history of smoking should include counting the number of cigarettes smoked per day multiplied by the number of years and thus the total number of packs/years of smoking is calculated. At the same time, one pack contains 20 cigarettes and the number of cigarettes smoked per day for one year is equal to one pack/year.

Total packs/years = number of cigarettes smoked per day x number of years / 20

It is believed that if this value exceeds 25 packs / years, then the patient can be classified as a "malicious smoker". In the event that this indicator reaches the value of 10 packs / years, then the patient is considered an "unconditional smoker". A patient is considered an "ex-smoker" if they have stopped smoking for 6 months or more. This must be taken into account when diagnosing COPD.

Objective research.

The results of an objective study of COPD patients depend on the severity of bronchial obstruction and emphysema.

Inspection. In the later stages of COPD, there are clinical signs of pulmonary emphysema (increased anteroposterior chest size, enlarged intercostal spaces). With severe emphysema, the appearance of the patient changes, a barrel-shaped chest appears. In connection with the expansion of the chest and the upward displacement of the clavicles, the neck seems short and thickened, the supraclavicular fossae protrude (filled with expanded tops of the lungs). With the development of chronic respiratory failure and pulmonary hypertension, "warm" acrocyanosis, swollen jugular veins are noted.

Percussion. In the presence of emphysema - percussion box sound, expansion of the boundaries of the lungs. In cases of severe emphysema, absolute dullness of the heart may not be completely determined. The edges of the lungs are displaced downward, their mobility during breathing is limited. As a result, a soft, painless edge of the liver may protrude from under the edge of the costal arch with its normal size.

Auscultation. In the lungs, scattered dry rales of various timbres are heard. As the disease progresses, wheezing is added to the cough, most noticeable with accelerated exhalation. Sometimes auscultatory phenomena in the lungs are not detected, and in order to detect them, it is necessary to offer the patient to make a forced exhalation. The mobility of the diaphragm is limited with severe emphysema, which leads to a change in the auscultatory picture: weakened breathing appears, the severity of wheezing decreases, expiration lengthens.

The sensitivity of objective methods to determine the severity of COPD is low. Among the classic signs are wheezing and prolonged expiratory time (more than 5 s), which indicate bronchial obstruction.

DIAGNOSTICS.

Diagnostic methods can be divided into a mandatory minimum, used in all patients, and additional methods used for special indications.

Mandatory methods, in addition to physical ones, include determining the function of external respiration (RF), a blood test, a cytological examination of sputum, an X-ray examination, a blood test and an ECG.

Laboratory research methods.

Sputum examination.

Cytological examination of sputum provides information about the nature of the inflammatory process and its severity. It is a required method.

Microbiological (cultural) examination of sputum is advisable to carry out with uncontrolled progression of the infectious process and the selection of rational antibiotic therapy. It is an additional method of examination.

Blood study.

clinical analysis. With a stable course of COPD, there are no significant changes in the content of peripheral blood leukocytes. During exacerbation, neutrophilic leukocytosis with a stab shift and an increase in ESR are most often observed. However, these changes are not always observed.

With the development of hypoxemia in patients with COPD, a polycythemic syndrome is formed, which is characterized by a change in hematocrit (hematocrit > 47% in women and > 52% in men), an increase in the number of erythrocytes, a high level of hemoglobin, low ESR and increased blood viscosity.

X-ray examination chest organs is a mandatory method of examination. X-ray of the lungs in direct and lateral projections in COPD reveals an increase in the transparency of the lung tissue, low standing of the dome of the diaphragm, limitation of its mobility, and an increase in the retrosternal space, which is typical for emphysema.

In mild COPD, significant x-ray changes may not be detected. In patients with moderate and severe COPD, it is possible to detect a low position of the dome of the diaphragm, flattening and limitation of its mobility, hyperair lung fields, bullae and an increase in the retrosternal space; narrowing and elongation of the heart shadow; against the background of depletion of vascular shadows, a high density of the walls of the bronchi is determined, infiltration along their course, i.e. a number of signs are revealed that characterize the inflammatory process in the bronchial tree and the presence of emphysema.

CT scan lungs is an additional method and is carried out according to special indications. It allows you to quantify the morphological changes in the lungs, primarily emphysema, more clearly identify the bullae, their location and size.

Electrocardiography allows a number of patients to identify signs of hypertrophy of the right heart, but its ECG criteria change dramatically due to emphysema. ECG data in most cases allow us to exclude the cardiac genesis of respiratory symptoms.

Bronchological examination(fibrobronchoscopy) is optional for patients with COPD. It is carried out to assess the condition of the bronchial mucosa and differential diagnosis with other lung diseases. In some cases, diseases that cause chronic bronchial obstruction can be identified.

The study should include:

Inspection of the bronchial mucosa;

Cultural examination of bronchial contents;

Bronchoalveolar lavage with the determination of the cellular composition to clarify the nature of inflammation;

Biopsy of the bronchial mucosa.

Examination of the function of external respiration(spirography) is of leading importance in the diagnosis of COPD and an objective assessment of the severity of the disease. It is mandatory to determine the following volume and speed indicators: vital capacity (VC), forced vital capacity (FVC), forced expiratory volume in 1 second (FEV 1), maximum expiratory rate at the level of 75, 50 and 25% (MSV 75- 25). The study of these indicators forms functional diagnosis of COPD.

Functional disorders in COPD are manifested not only by a violation of bronchial patency, but also by a change in the structure of static volumes, a violation of the elastic properties, diffusion capacity of the lungs, and a decrease in physical performance. The definition of these groups of disorders is optional.

Violation of bronchial patency. Most important for the diagnosis of COPD is the determination of chronic airflow limitation, i.e. bronchial obstruction. The main criterion for determining chronic airflow limitation, or chronic obstruction, is a drop in FEV 1 to a level that is less than 80% of the proper values. Bronchial obstruction is considered chronic if it is recorded during repeated spirometry studies at least 3 times within one year, despite ongoing therapy.

Inhaled bronchodilator tests are used to study the reversibility of obstruction and their effect on the flow-volume curve, mainly on the forced expiratory volume in 1 second (FEV 1) is assessed. When examining a specific patient with COPD, it must be remembered that the reversibility of obstruction is a variable and in the same patient it may be different during periods of exacerbation and remission.

Bronchodilation tests. As bronchodilator drugs when testing in adults, it is recommended to prescribe:

Beta 2 - short-acting agonists (starting from the minimum dose to the maximum allowable: fenoterol - from 100 to 800 mcg; salbutamol - from 200 to 800 mcg, terbutaline - from 250 to 1000 mcg) with measurement of bronchodilatory response after 15 minutes;

Anticholinergics - Ipratropium bromide is recommended as the standard drug, starting with the lowest possible doses of 40 mcg to the maximum possible doses of 80 mcg, with the bronchodilatory response measured after 30-45 minutes.

It is possible to conduct bronchodilation tests by prescribing higher doses of drugs that are inhaled through nebulizers.

In order to avoid distorting the results and for the correct performance of the bronchodilation test, it is necessary to cancel the ongoing therapy in accordance with the pharmacokinetic properties of the drug being taken (beta-2 - short-acting agonists - 6 hours before the start of the test, long-acting beta-2 - agonists - for 12 hours, prolonged theophyllines - for 24 hours).

An increase in FEV 1 by more than 15% of the baseline is conditionally characterized as a reversible obstruction.

FEV monitoring 1 . An important method to confirm the diagnosis of COPD is the monitoring of FEV 1 - a long-term repeated measurement of this spirometric indicator. In adulthood, an annual fall in FEV 1 is normally noted within 30 ml per year. Conducted in different countries, large epidemiological studies have established that patients with COPD are characterized by an annual drop in FEV 1 of more than 50 ml per year.

The gas composition of the blood. COPD is accompanied by a violation of ventilation-perfusion ratios, which can lead to arterial hypoxemia - a decrease in oxygen tension in arterial blood (PaO2). In addition, ventilatory respiratory failure leads to an increase in the tension of carbon dioxide in arterial blood (PaCO2). In COPD patients with chronic respiratory failure, the onset of acidosis is metabolically compensated by increased bicarbonate production, which allows maintaining a relatively normal pH level.

Pulse oximetry It is used to measure and monitor blood oxygen saturation (SaO2), however, it allows you to register only the level of oxygenation and does not allow you to monitor changes in PaCO2. If the SaO2 is less than 94%, then a blood gas test is indicated.

With the progression of COPD, an increase in pressure in the pulmonary artery is often observed.

The severity of pulmonary hypertension has prognostic value. Among the non-invasive methods for controlling pulmonary hypertension, the best results are obtained using doppler echocardiography. In the normal practice of managing patients with COPD, the use of direct methods for measuring pressure in the pulmonary artery is not recommended.

differential diagnosis.

In the early stages of COPD development, one should distinguish between chronic obstructive bronchitis (COB) and bronchial asthma (BA), since fundamentally different approaches to the treatment of each of these diseases are required at this time.

Clinical examination reveals paroxysmal symptoms in asthma, often with a combination of extrapulmonary signs of allergy (rhinitis, conjunctivitis, skin manifestations, food allergy). Patients with COB are characterized by constant, little-changing symptoms.

An important element of differential diagnosis is a decrease in FEV 1 per 50 ml in patients with COB, which is not observed in BA. COB is characterized by reduced diurnal variability in peak flow measurements< 15%. При БА разность между утренними и вечерними показателями пикфлоуметрии повышена и превышает 20%. При БА чаще наблюдается бронхиальная гиперреактивность. Из лабораторных признаков при БА чаще встречается увеличение содержания IgЕ. При появлении у больных БА необратимого компонента бронхиальной обструкции, дифференциальный диагноз этих заболеваний теряет смысл, так как можно констатировать присоединение второй болезни – ХОБ и приближение конечной фазы заболевания – ХОБЛ.

TREATMENT.

The goal of treatment is to reduce the rate of progression of the disease, leading to an increase in bronchial obstruction and respiratory failure, reduce the frequency and duration of exacerbations, increase exercise tolerance and improve the quality of life.

Patient education- a crucial stage of individual work with the patient. The patient should be well aware of the essence of the disease, the features of its course, be an active, conscious participant in the treatment process. Educational programs for patients must include training in the proper use of drugs (individual inhalers, spacers, nebulizers). Patients should be taught the basic rules of self-control, including using a peak flow meter, should be able to objectively assess their condition and, if necessary, take emergency self-help measures. An important step in the education of patients is their professional orientation, especially in cases where environmental aggression is associated with the professional activities of the patient.

Smoking cessation is the first mandatory step. The patient must be clearly aware of the harmful effects of tobacco smoke on his respiratory system. A specific smoking restriction and cessation program is being drawn up. In cases of nicotine dependence, it is advisable to use nicotine replacement drugs. Perhaps the involvement of psychotherapists, acupuncturists. The positive effect of smoking cessation is expressed in any stage of COPD.

Bronchodilator therapy.

According to modern ideas about the nature of COPD, bronchial obstruction is the main and universal source of all pathological events that develop with the constant progression of the disease and lead to respiratory failure.

The use of bronchodilator drugs is the basic therapy that is mandatory in the treatment of patients with COPD. All other means and methods should be used only in combination with basic therapy.

Preference is given to the use of inhaled forms of bronchodilators. The inhalation route of administration of drugs contributes to a faster penetration of the drug into the affected organ, therefore, a more effective drug effect. At the same time, the potential risk of developing systemic side effects is significantly reduced. The use of a spacer allows you to: facilitate inhalation, increase its effectiveness, further reduce the potential risk of systemic and local side effects.

Optimal today is the use of powder inhalers or bronchodilators in solutions for nebulizer therapy.

Of the existing bronchodilators in the treatment of COPD, m-anticholinergics, beta-2-agonists and methylxanthines are used; the sequence of application and the combination of these drugs depends on the severity of the disease, the individual characteristics of its progression.

Traditionally, basic bronchodilators for the treatment of COPD are considered m-cholinolytics. They are represented by ipratropium bromide (duration of action 6-8 hours) and a combined bronchodilator - berodual (ipratropium bromide + fenoterol). Currently, a new long-acting anticholinergic, tiotropium bromide (spiriva), has appeared, which is used once a day.

Are used selective sympathomimetics (beta-2-agonists) short (4-6 hours) action: fenoterol, salbutamol, terbutaline. The action of sympathomimetics comes quickly, but they are characterized by a number of systemic side effects due to the effect on the cardiovascular system. With age, the sensitivity of receptors to sympathomimetics decreases. In recent years, for the relief of bronchial obstruction and basic therapy for COPD, a new drug from the group of beta-2-agonists, oxys turbuhaler, has become widely used, the active substance of which is formoterol, which has not only a rapid onset of action (after 1-3 minutes), but also effect (for 12 hours or more).

Theophyllines prolonged action (teotard, teopek) are effective in the treatment of COPD and are currently used quite widely both as monotherapy and in addition to sympathomimetics. But due to their narrow margin between therapeutic and toxic doses, preference is given to inhaled bronchodilators.

In stage I COPD, short-acting bronchodilators are used as needed. In stage II-IV, the systematic use of one bronchodilator (or a combination of drugs) of short or long action with a rapidly onset effect is prescribed. Inhaled corticosteroids are used if their use significantly improves clinical and ventilatory parameters.

Mucoregulatory agents. The improvement of mucociliary clearance is largely achieved with a targeted effect on bronchial secretions using mucoregulatory drugs.

The use of proteolytic enzymes as mucolytic agents is unacceptable due to the high risk of developing serious side effects - hemoptysis, allergies, bronchoconstriction. Ambroxol(ambrosan, lazolvan) stimulates the formation of low viscosity tracheobronchial secretion due to the depolymerization of acid mucopolysaccharides of bronchial mucus and the production of neutral mucopolysaccharides by goblet cells.

A distinctive feature of the drug is its ability to increase the synthesis, secretion of surfactant and block the breakdown of the latter under the influence of adverse factors.

When combined with antibiotics, Ambroxol enhances their penetration into the bronchial secretion and bronchial mucosa, increasing the effectiveness of antibiotic therapy and reducing its duration. The drug is used inside and in inhalation.

Acetylcysteine free from damaging action of proteolytic enzymes. The sulfhydryl groups of its molecule break the disulfide bonds of sputum mucopolysaccharides. The stimulation of mucosal cells also leads to liquefaction of sputum. Acetylcysteine ​​increases the synthesis of glutathione, which is involved in detoxification processes. It is used orally and in inhalation.

Carbocysteine normalizes the quantitative ratio of acidic and neutral sialomucins of bronchial secretion. Under the influence of the drug, regeneration of the mucous membrane occurs, a decrease in the number of goblet cells, especially in the terminal bronchi, i.e. the drug has mucoregulatory and mucolytic effects. This restores the secretion of IgA and the number of sulfhydryl groups. Applied inside.

Glucocorticosteroid therapy. The indication for the use of corticosteroids in COPD is the ineffectiveness of the maximum doses of basic therapy - bronchodilators. GCS, which are so effective in the treatment of bronchial asthma, are used in the treatment of COPD only with a proven clinical or spirometric effect. A reversibility test was formulated to predict the appropriateness of prescribing corticosteroids: after the initial determination of FEV 1, corticosteroids are prescribed orally (for 1–2 weeks) or inhaled (for a period of 6–12 weeks). An increase in FEV 1 of 15% (or 200 ml) after a trial of steroids is considered positive and warrants continued therapy with inhaled corticosteroids. This test can also be performed using peak flowmetry (an increase in expiratory power by 20% is considered positive).

The use of corticosteroids in tablets for more than 2 weeks is undesirable. It is optimal to use inhaled corticosteroids or solutions (suspensions) for nebulizers (for example, pulmicort suspension). In severe and extremely severe COPD ( stage III–IV) as a basic therapy, it is recommended to use the combination drug Symbicort, which includes GCS budesonide and long-acting beta-2-agonist formoterol.

In the treatment of exacerbations of moderate to severe COPD, the use of nebulizer therapy is necessary. The nebulizer allows the inhalation of bronchodilators and glucocorticosteroid hormones in high doses.

Correction of respiratory failure achieved through the use of oxygen therapy, training of the respiratory muscles. It should be emphasized that the intensity, volume and nature of drug treatment depend on the severity of the condition and the ratio of reversible and irreversible components of bronchial obstruction. With the depletion of the reversible component, the nature of the therapy changes. Methods aimed at correcting respiratory failure come first. At the same time, the volume and intensity of basic therapy are preserved.

Indication for systematic oxygen therapy is a decrease in the partial tension of oxygen in the blood - PaO2 to 60 mm Hg. Art., decrease in oxygen saturation - SaO2< 85% при стандартной пробе с 6-минутной ходьбой и < 88% в покое. Предпочтение отдается длительной (18 часов в сутки) малопоточной (2-5 л в мин) кислородотерапии как в стационарных условиях, так и на дому. При тяжелой дыхательной недостаточности применяются гелиево-кислородные смеси. Для домашней оксигенотерапии используются концентраторы кислорода, а также приборы для проведения неинвазивной вентиляции с отрицательным и положительным давлением на вдохе и выдохе.

Respiratory muscle training achieved with the help of individually selected breathing exercises. Perhaps the use of transcutaneous electrical stimulation of the diaphragm.

In severe polycythemic syndrome (Hb > 155 g/l), it is recommended to erythrocyte phoresis with the removal of 500-600 ml of deplasmated erythrocyte mass. If it is technically impossible to carry out erythrocytaphoresis, it is possible to carry out bloodletting in a volume of 800 ml of blood with adequate replacement with isotonic sodium chloride solution or herudotherapy(treatment with leeches).

Antibacterial therapy. During the stable course of COPD, antibiotic therapy is not carried out.

In the cold season, patients with COPD often experience exacerbations of infectious origin. The most common causes are Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarralis, and viruses. Antibiotics are prescribed in the presence of clinical signs of intoxication, an increase in the amount of sputum and the appearance of purulent elements in it. Usually, treatment is prescribed empirically with drugs inside and lasts 7-14 days, with severe exacerbation, parenteral administration is used.

Taking into account the specified spectrum of microorganisms, the following are used:

oral aminopenicillins (amoxicillin),

cephalosporins II-III generations (cefuroxime orally, ceftriaxone - enterally),

new oral macrolides (spiramycin, clarithromycin, azithromycin, midecamycin),

respiratory (pneumotropic) fluoroquinolones III-IV generations (levofloxacin).

The selection of an antibiotic according to the sensitivity of the flora in vitro is carried out only if empirical antibiotic therapy is ineffective.

Do not prescribe antibiotics in inhalation.

Vaccination against influenza (vaxigrip, grippol, influvac, begrivak, etc.), against pneumococcus (pneumococcus 23) reduces the number of exacerbations of the disease and the severity of their course, thereby reducing the number of days of disability and improving bronchial patency. Annual prophylactic influenza vaccination is recommended for COPD patients with mild to moderate severity of the disease with a frequency of infectious relapses of more than 2 times a year. A single vaccination with pneumo 23 is effective for 5 years, then revaccination is carried out every 5 years.

rehabilitation therapy.

Rehabilitation therapy is prescribed for COPD of any severity. The doctor determines an individual rehabilitation program for each patient. Depending on the severity, phase of the disease and the degree of compensation of the respiratory and cardiovascular systems, the program includes a regimen, exercise therapy, physiotherapy, spa treatment.

Long-term inflammatory disease of the bronchi, occurring with frequent relapses, cough, sputum and shortness of breath is called by the general term - chronic obstructive pulmonary disease, abbreviated as COPD. The development of pathology is facilitated by poor environmental conditions, work in rooms with polluted air and other factors that provoke diseases of the pulmonary system.

The term COPD appeared relatively recently, about 30 years ago. Basically, the disease worries smokers. The disease is constantly current, with periods of short or long remission, a disease, a sick person needs medical care all his life. Chronic obstructive pulmonary disease is a pathology that is accompanied by a restriction of airflow in the respiratory tract.

Over time, the disease progresses, the condition worsens.

What it is?

Chronic obstructive pulmonary disease (COPD) is an independent disease characterized by partially irreversible restriction of airflow in the respiratory tract, which, as a rule, is steadily progressive and provoked by an abnormal inflammatory response of lung tissue to irritation by various pathogenic particles and gases.

Causes

The main cause of COPD is smoking, active and passive. Tobacco smoke damages the bronchi and lung tissue itself, causing inflammation. Only 10% of cases of the disease are associated with the influence of occupational hazards, constant air pollution. Genetic factors may also be involved in the development of the disease, causing a deficiency of certain lung-protecting substances.

Main risk factors for COPD:

Symptoms of COPD

The course of COPD is usually progressive, however, most patients develop advanced clinical symptoms over several years and even decades.

The first specific symptom of the development of COPD in a patient is the appearance of a cough. At the onset of the disease, the patient’s cough only bothers him in the morning and is of a short duration, however, over time, the patient’s condition worsens and an excruciating cough with a copious amount of mucus sputum is observed. Isolation of yellow viscous sputum indicates the purulent nature of the secret of an inflammatory nature.

A long period of COPD is inevitably accompanied by the development of emphysema of the lungs of bilateral localization, as evidenced by the appearance of expiratory dyspnea, that is, difficulty in breathing in the "exhalation" phase. A characteristic feature of dyspnea in COPD is its permanent nature with a tendency to progression in the absence of therapeutic measures. The appearance in a patient of persistent headaches without a clear localization, dizziness, decreased ability to work and drowsiness testify in favor of the development of hypoxic and hypercapnic lesions of brain structures.

The intensity of these manifestations varies from stability to exacerbation, in which the severity of shortness of breath increases, the volume of sputum and the intensity of cough increase, the viscosity and nature of the sputum discharge changes. The progression of the pathology is uneven, but gradually the patient's condition worsens, extrapulmonary symptoms and complications join.

Stages of the course of the disease

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 intake of air into the respiratory tract, so shortness of breath is formed not only during physical exertion, but also at rest.
4. The fourth stage is an extremely difficult course. The resulting symptoms of COPD are life-threatening. Obstruction of the bronchi is observed and cor pulmonale is formed. Patients who are diagnosed with stage 4 COPD receive a disability.

What else should you know?

As the severity of COPD increases, choking attacks become more frequent and more severe, with symptoms escalating rapidly and staying longer. It is important to know what to do when an asthma attack occurs. Your doctor will help you find medications that will help with such attacks. But in cases of a very severe attack, you may need to call an ambulance team. Hospitalization in a specialized pulmonology department is optimal, however, if it is absent or full, the patient can be hospitalized in a therapeutic hospital in order to stop the exacerbation and prevent complications of the disease.

Such patients often develop depression and anxiety over time due to the awareness of the disease, which becomes worse. Shortness of breath and difficulty breathing also contribute to feelings of anxiety. In such cases, it is worth talking with your doctor about what types of treatment can be selected to relieve breathing problems during attacks of shortness of breath.

The quality of life

To assess this parameter, the SGRQ and HRQol Questionnaires, Pearson χ2 and Fisher tests are used. The age of onset of smoking, the number of packs smoked, the duration of symptoms, the stage of the disease, the degree of shortness of breath, the level of blood gases, the number of exacerbations and hospitalizations per year, the presence of concomitant chronic pathologies, the effectiveness of basic treatment, and participation in rehabilitation programs are taken into account.

1. One of the factors that must be taken into account when assessing the quality of life of patients with COPD is the length of smoking and the number of cigarettes smoked. Research confirms. That with an increase in the smoking experience in COPD patients, social activity significantly decreases, and depressive manifestations increase, responsible for the decrease not only in working capacity, but also in the social adaptation and status of patients.
2. The presence of concomitant chronic pathologies of other systems reduces the quality of life due to the syndrome of mutual burdening and increases the risk of death.
3. Older patients have worse functional performance and ability to compensate.

Complications

Like any other inflammatory process, obstructive pulmonary disease sometimes leads to a number of complications, such as:

• pneumonia ();
• respiratory failure;
• pulmonary hypertension (high pressure in the pulmonary artery);
• irreversible;
• thromboembolism (blockage of blood vessels by blood clots);
• bronchiectasis (development of functional inferiority of the bronchi);
• cor pulmonale syndrome (increased pressure in the pulmonary artery, leading to thickening of the right heart sections);
• (heart rhythm disorder).

Diagnosis of COPD

Timely diagnosis of chronic obstructive pulmonary disease can increase the life expectancy of patients and significantly improve the quality of their existence. When collecting anamnestic data, modern specialists always pay attention to production factors and the presence of bad habits. Spirometry is considered the main method of functional diagnostics. It reveals the initial signs of the disease.

Comprehensive diagnosis of COPD includes the following steps:

1. X-ray of the sternum. Should be done annually (at least).
2. Sputum analysis. Determination of its macro- and microscopic properties. If necessary, conduct a study on bacteriology.
3. Clinical and biochemical blood tests. It is recommended to do 2 times a year, as well as during periods of exacerbations.
4. Electrocardiogram. Since chronic obstructive pulmonary disease often gives complications to the heart, it is advisable to repeat this procedure 2 times a year.
5. Analysis of the gas composition and pH of the blood. Do at 3 and 4 degrees.
6. Oxygemometry. Assessment of the degree of blood oxygen saturation by a non-invasive method. It is used in the exacerbation phase.
7. Monitoring the ratio of fluid and salt in the body. The presence of a pathological shortage of individual microelements is determined. It is important during an exacerbation.
8. Spirometry. Allows you to determine how severe the condition of the pathologies of the respiratory system. It is necessary to take place once a year and more often in order to adjust the course of treatment in time.
9. Differential diagnosis. Most often diff. diagnosed with lung cancer. In some cases, it is also required to exclude heart failure, tuberculosis, pneumonia.

Especially noteworthy is the differential diagnosis of bronchial asthma and COPD. Although these are two separate diseases, they often occur in one person (the so-called cross syndrome).

How is COPD treated?

With the help of drugs of modern medicine, it is still impossible to cure chronic obstructive pulmonary disease completely. Its main function is to improve the quality of life of patients and prevent severe complications of the disease.

COPD can be treated at home. The following cases are an exception:

• therapy at home does not give any visible results or the patient's condition worsens;
• respiratory failure intensifies, developing into an asthma attack, the heart rhythm is disturbed;
• 3 and 4 degrees in the elderly;
• severe complications.

Quitting smoking is very difficult and at the same time very important; it slows down, but does not completely stop the decline in FEV1. Multiple strategies are most effective at the same time: quit date setting, behavior change techniques, group denial, nicotine replacement therapy, varenicline or bupropion, and physician support.

Smoking cessation rates of over 50% per year, however, have not been demonstrated even with the most effective interventions such as bupropion plus nicotine replacement therapy or varenicline alone.

Medical treatment

The goal of drug treatment is to reduce the frequency of exacerbations and the severity of symptoms, to prevent the development of complications. As the disease progresses, the amount of treatment only increases. The main drugs in the treatment of COPD:

1. Bronchodilators are the main drugs that stimulate the expansion of the bronchi (atrovent, salmeterol, salbutamol, formoterol). It is preferably administered by inhalation. Short-acting drugs are used as needed, long-acting drugs are used constantly.
2. Glucocorticoids in the form of inhalations - used for severe degrees of the disease, with exacerbations (prednisolone). With severe respiratory failure, attacks are stopped by glucocorticoids in the form of tablets and injections.
3. Antibiotics - are used only during an exacerbation of the disease (penicillins, cephalosporins, it is possible to use fluoroquinolones). Tablets, injections, inhalations are used.
4. Mucolytics - thin the mucus and facilitate its excretion (carbocysteine, bromhexine, ambroxol, trypsin, chymotrypsin). Used only in patients with viscous sputum.
5. Antioxidants - able to reduce the frequency and duration of exacerbations, are used in courses of up to six months (N-acetylcysteine).
6. Vaccines - Influenza vaccination reduces mortality in half of cases. It is held once in October - early November.

Breathing exercises for COPD

Experts identify 4 most effective exercises, which should be paid attention to in the fight against COPD.

1. Sitting on a chair and leaning, not stooping, against its back, the patient should take a short and strong breath through the nose and, counting to ten, exhale forcefully through pursed lips. It is important to ensure that the duration of the exhalation is longer than the inhalation. Repeat this exercise 10 times.
2. The second exercise is performed from the same position as the first. In this case, you should slowly raise your hands alternately up, while inhaling, and on lowering, exhale. The exercise is repeated 6 times.
3. The next exercise is carried out sitting on the edge of a chair. Hands should be on your knees. It is necessary to simultaneously bend the arms in the hands and legs in the ankle joint 12 times in a row. When bending, take a deep breath, and when unbending, exhale. This exercise allows you to saturate the blood with oxygen and successfully cope with its deficiency.
4. The fourth exercise is also carried out without getting up from the chair. The patient should take the deepest possible breath and, counting to 5, exhale slowly. This exercise is carried out for 3 minutes. If discomfort occurs during this exercise, you should not do it.

Gymnastics is an excellent tool to stop the progression of the disease and prevent its recurrence. However, it is very important to consult with your doctor before starting breathing exercises. The fact is that this treatment for a number of chronic diseases cannot be carried out.

Features of nutrition and lifestyle

The most important component of treatment is the exclusion of provoking factors, for example, smoking or leaving a harmful enterprise. If this is not done, the whole treatment as a whole will be practically useless.

In order to quit smoking, you can use acupuncture, nicotine replacement drugs (patches, chewing gum), etc. Due to the tendency of patients to lose weight, adequate protein nutrition is necessary. That is, meat products and / or fish dishes, sour-milk products and cottage cheese must be present in the daily diet. Due to developing shortness of breath, many patients try to avoid physical exertion. This is fundamentally wrong. Daily physical activity is required. For example, daily walks at a pace that your condition allows. Breathing exercises have a very good effect, for example, according to the Strelnikova method.

Every day, 5-6 times a day, you need to do exercises that stimulate diaphragmatic breathing. To do this, you need to sit down, put your hand on your stomach to control the process and breathe with your stomach. Spend 5-6 minutes on this procedure at a time. This method of breathing helps to use the entire volume of the lungs and strengthen the respiratory muscles. Diaphragmatic breathing can also help reduce shortness of breath on exertion.

Oxygen therapy

Most patients require oxygen supplementation, even those who have not previously used it for a long time. Hypercapnia may worsen with oxygen therapy. The deterioration occurs, as is commonly believed, due to the weakening of the hypoxic stimulation of respiration. However, increasing the V/Q ratio is probably the more important factor. Prior to the appointment of oxygen therapy, the V / Q ratio is minimized with a decrease in perfusion of poorly ventilated areas of the lungs due to vasoconstriction of the pulmonary vessels. The increase in the V / Q ratio against the background of oxygen therapy is due.

Decreased hypoxic pulmonary vasoconstriction. Hypercapnia may be aggravated by the Haldane effect, but this version is questionable. The Haldane effect is to reduce the affinity of hemoglobin for CO2, which leads to an excessive accumulation of CO2 dissolved in blood plasma. Many patients with COPD may have both chronic and acute hypercapnia, and therefore severe CNS involvement is unlikely unless PaCO2 is greater than 85 mmHg. The target level for PaO2 is about 60 mmHg; higher levels have little effect but increase the risk of hypercapnia. Oxygen is delivered through a venturi mask and must therefore be closely monitored and the patient closely monitored. Patients whose condition worsens on oxygen therapy (eg, in association with severe acidosis or CVD disease) require ventilatory support.

Many patients who require oxygen therapy at home for the first time after being discharged from the hospital due to a COPD exacerbation get better after 50 days and no longer require further oxygen. Therefore, the need for home oxygen therapy should be reassessed 60–90 days after discharge.

Treatment of exacerbation of COPD

The goal of exacerbation treatment is to manage the current exacerbation as much as possible and prevent future exacerbations. Depending on the severity, exacerbations can be treated on an outpatient basis or in a hospital.

Basic principles of treatment of exacerbations:

• With an exacerbation of the disease, the use of short-acting bronchodilators is preferable to long-acting ones. Doses and frequency of administration, as a rule, increase compared to usual. It is advisable to use spacers or nebulizers, especially in critically ill patients.
• It is necessary to correctly assess the severity of the patient's condition, exclude complications that can be disguised as exacerbations of COPD, and promptly send for hospitalization in life-threatening situations.
• With insufficient effect of bronchodilators, intravenous administration of aminophylline is added.
• If monotherapy was previously used, a combination of beta-stimulants with anticholinergics (also short-acting) is used.
• Dosed oxygen therapy in the treatment of patients in a hospital through nasal catheters or a Venturi mask. The oxygen content in the inhaled mixture is 24-28%.
• Connection of intravenous or oral administration of glucocorticosteroids. An alternative to the systemic use of corticosteroids is the inhalation of pulmicort through a nebulizer 2 mg twice a day after berodual inhalations.
• In the presence of symptoms of bacterial inflammation (the first sign of which is the appearance of purulent sputum), broad-spectrum antibiotics are prescribed.
• Other activities - maintaining water balance, anticoagulants, treatment of concomitant diseases.

Surgery

There are surgical treatments for COPD. Bullectomy is performed to relieve symptoms in patients with large bullae. But its effectiveness has been established only among those who quit smoking in the near future. Thoroscopic laser bullectomy and reduction pneumoplasty (removal of the overinflated part of the lung) have been developed.

But these operations are still used only in clinical trials. There is an opinion that in the absence of the effect of all the measures taken, one should contact a specialized center to resolve the issue of lung transplantation

Care of the terminally ill

In severe stages of the disease, when death is already inevitable, physical activity is undesirable and daily activity is aimed at minimizing energy costs. For example, patients may limit their living space to one floor of the house, eat more often and in small portions rather than infrequently and in large quantities, and avoid tight shoes.

The care of the terminally ill should be discussed, including the inevitability of mechanical ventilation, the use of temporary pain relief sedatives, the appointment of a medical decision maker in the event of a patient's disability.

Prevention

Prevention is very important to prevent the occurrence of various respiratory problems, and in particular chronic obstructive pulmonary disease. First of all, of course, you should give up tobacco. In addition, as a preventive measure for the disease, doctors advise:

• conduct a full treatment of viral infections;
• observe safety precautions when working in hazardous industries;
• take daily walks in the fresh air for at least an hour;
• timely treat defects of the upper respiratory tract.

Only with a careful attitude to your health and safety at work can you protect yourself from an extremely dangerous disease called COPD.

Forecast for life

COPD has a conditionally poor prognosis. The disease slowly but constantly progresses, leading to disability. Treatment, even the most active, can only slow down this process, but not eliminate the pathology. In most cases, treatment is lifelong, with ever-increasing doses of medication.

With continued smoking, obstruction progresses much faster, significantly reducing life expectancy.

The incurable and deadly COPD simply urges people to stop smoking forever. And for people at risk, there is only one advice - if you find signs of a disease, immediately contact a pulmonologist. After all, the earlier the disease is detected, the less likely it is to die prematurely.