Hoble signs of treatment. Chronic obstructive pulmonary disease (COPD) - symptoms and treatment

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

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

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

COPD - the definition of the disease

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

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

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

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

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

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

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

Causes and treatment during an exacerbation

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

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

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

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

Symptoms and methods of diagnosis

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

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

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

Patients with COPD are divided into two groups:

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

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

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

Complications

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

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

Complications of chronic obstructive pulmonary disease include:

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

Prevention

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

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

Don't forget about timely treatment any infectious diseases respiratory tract.

Those whose work involves exposure to hazardous substances should be aware of safety precautions and the use of individual funds protection.

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

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

Video

conclusions

It is a progressive disease. It cannot be completely cured in the later stages, so patients should lead a proper lifestyle, control symptoms, which can slow down the development of chronic obstruction.

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

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

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

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

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

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

ICD-10 code

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

J44.9 Chronic obstructive pulmonary disease, unspecified

Epidemiology of COPD

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

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

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

What causes COPD?

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

Genetic factors also play a role. The most well-studied genetic disorder, alpha-antitrypsin deficiency, is a significant cause of emphysema in non-smokers and affects susceptibility to the disease in smokers. Polymorphisms in the microsomal epoxy hydrolase, vitamin D-binding protein, 11_-1p, and IL-1 receptor antagonist genes are associated with 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, a secretory leukoproteinase inhibitor produced by the epithelium of the respiratory tract, elafin, and a tissue inhibitor of matrix metalloproteinases. In COPD patients, activated neutrophils and other inflammatory cells secrete proteases during inflammation; protease activity exceeds antiprotease activity, resulting in tissue destruction and increased secretion of mucus. Activation of neutrophils and macrophages also leads to the accumulation of free radicals, superoxide anions and hydrogen peroxide, which inhibit antiproteases and cause bronchospasm, mucosal edema, and increased mucus secretion. Like infection, neutrophil-induced oxidative damage, release of profibrous neuropeptides (eg, bombesin), and reduced production of vascular endothelial growth factor play a role in pathogenesis.

Lung function studies

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

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

Additional lung function tests are needed only in certain circumstances, such as surgical lung volume reduction. Other investigational tests 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 flattening of the diaphragm, 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 alpha antitrypsin must 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 right leg bundle of His. Multifocal atrial tachycardia, an arrhythmia that can 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 gases. arterial blood to quantify hypoxemia and hypercapnia. Hypercapnia can coexist with hypoxemia. In such 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 ensuring long-term normal condition and lung function through pharmacotherapy and oxygen therapy, smoking cessation, exercise, improved nutrition and pulmonary rehabilitation. Surgery COPD is indicated for selected patients. Controlling COPD involves treating both chronic stable disease and exacerbations.

Drug treatment for COPD

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

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

Beta-agonists relax the smooth muscles of the bronchi and increase the clearance of the ciliated epithelium. Salbutamol aerosol, 2 puffs (100 mcg/dose), inhaled from a metered dose inhaler 4-6 times a day, is usually the drug of choice because of its low cost; regular use has no advantage over use on demand and causes more undesirable effects. Long-acting beta-agonists are preferred for patients with nocturnal symptoms or for those who find frequent inhaler use uncomfortable; salmeterol powder, 1 breath (50 mcg) 2 times a day or formoterol powder (Turbohaler 4.5 mcg, 9.0 mcg or Aerolizer 12 mcg) 2 times a day or formoterol 12 mcg ppm 2 times a day can be used. Powder forms may be more effective for patients who have coordination problems when using a metered dose inhaler. Patients should be made aware of the difference between short-acting and long-acting drugs because long-acting drugs used on an as-needed basis or more than twice a day increase the risk of developing cardiac arrhythmias. Side effects 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; the maximum effect is achieved after 1-2 hours), so a beta-agonist is often prescribed with it in one combined inhaler or separately as necessary remedy emergency assistance. Tiotropium, a long-acting quaternary anticholinergic, is M1- and M2-selective and may therefore be superior to ipratropium bromide because blockade of the M receptor (as with ipratropium bromide) may limit bronchodilation. Dose - 18 mcg 1 time per day. Tiotropium is not available in all countries of the world. The effectiveness of tiotropium in COPD has been proven in large-scale studies as a drug that significantly slows down the fall in FEV in patients with 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 increase in the incidence of pneumonia in patients with COPD, in contrast to long-term treatment COPD combination budesonide + formoterol, the use of which does not increase the risk of developing pneumonia.

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

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

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

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

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

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

Oxygen therapy for COPD

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

A sleep study should be performed in patients with 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 an acute respiratory disease and meeting the listed criteria, you need to assign O2 and re-examine the indicators when breathing room air after 30 days.

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

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

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

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

Smoking cessation

Quitting smoking is both extremely difficult and extremely important; 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. For supporting physical form exercises should be performed 3-4 times a week. O2 saturation is monitored and, if necessary, additional O2 is administered. endurance training upper limbs Useful for daily activities such as bathing, dressing and cleaning. Patients with COPD should be taught energy-saving ways of doing daily work and distributing activities. It is also necessary to discuss problems in the sexual area and consult on energy-saving ways of sexual intercourse.

Food

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

Pulmonary rehabilitation in COPD

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

The effectiveness of rehabilitation is manifested in greater independence and improvement in the quality of life and tolerance to stress. 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 regions, with initially low exercise tolerance after pulmonary rehabilitation.

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

Rarely, patients have bullae so large that they compress the functional lung. These patients can be helped by surgical resection of the bullae, which leads to the disappearance of manifestations and improvement in pulmonary function. In general, resection is most effective for bullae that occupy more than a third of half of the chest and FEV about half of the proper normal volume. 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 worsening respiratory function despite inpatient treatment, as well as patients who require sedation for treatment.

Oxygen

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

Respiratory support

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

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

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

Drug treatment for COPD

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

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

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

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

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

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

If Pseudomonas spp. is suspected. and / or other Enterobactereaces spp., parenteral ciprofloxacin 400 mg 2-3 times a day, then orally 750 mg 2 times a day, or parenteral levofloxacin 750 mg 1 time a day, then 750 mg 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 old age, high PaCO2 values ​​and continuous use of oral glucocorticoids.

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

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

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

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

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

About the causes of COPD and its dangers

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

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

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

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

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

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

What signs will help to suspect COPD?

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

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

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

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

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

What does an examination reveal in a COPD patient?

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

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

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

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

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

Symptoms of COPD on external examination

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

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

Instrumental and laboratory diagnostics

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

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

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

Principles of COPD treatment

Key points in the treatment of patients with COPD:

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

COPD prevention

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

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

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

Lead by example to prevent COPD in your children and grandchildren healthy lifestyle life and intolerance to smoking.

Long inflammatory diseases bronchi, flowing from frequent relapses, cough, sputum and shortness of breath are collectively referred to as chronic obstructive pulmonary disease, or COPD for short. 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 all his life medical care. 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, but 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 air supply in Airways Therefore, shortness of breath is formed not only during physical exertion, but also at rest.
4. The fourth stage is an extremely difficult course. 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 disease lungs 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 their quality of life. 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 research blood. 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.

Particularly noteworthy differential diagnosis 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:

• home therapy 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

Target drug treatment reduce the frequency of exacerbations and the severity of symptoms, 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 during this exercise you experience discomfort, you shouldn't 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, it is added intravenous administration eufillina.
• 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%.
• Connecting an intravenous or oral administration 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

Exist surgical methods COPD treatment. 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 exercise are undesirable and everyday 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 compliance with safety regulations at work can you protect yourself from extreme 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.

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

General information

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

Causes of COPD

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

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

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

Pathogenesis

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

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

Classification

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

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

Symptoms of COPD

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

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

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

Complications

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

Diagnostics

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

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

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

COPD treatment

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

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

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

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

Forecast and prevention

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