Chronic obstructive pulmonary disease (COPD)

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

Deficiency of alpha-antitrypsin and a variety of occupational contaminants are less frequent causes of the development of this pathology in non-smokers. Over the years, symptoms develop - productive cough and shortness of breath; The frequent signs are weakening of breathing and wheezing. Severe cases can be complicated by weight loss, pneumothorax, right ventricular failure and respiratory failure. The diagnosis is based on anamnesis, physical examination, chest X-ray and lung function tests. Treatment with bronchodilators and glucocorticoids, if necessary, oxygen therapy. 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 - chronic bronchitis with airway obstruction. Chronic bronchitis (also called chronically increased sputum 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, partially coinciding condition characterized by chronic productive cough, wheezing and partially reversible airway obstruction in smokers with an anamnesis of bronchial asthma. In some cases, it is difficult to distinguish chronic obstructive bronchitis from asthmatic bronchitis.

Emphysema is the destruction of the lung parenchyma, leading to a loss of elasticity and destruction of the alveolar septa and a radial traction of the airways, which increases the risk of collapse of the airways. Hyperopia of the lungs, limitation of the respiratory flow impede the passage of air. Air spaces increase and can, in the final analysis, turn into bulls.

[1], [2], [3], [4], [5], [6], [7],

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 ranked fourth in a number of causes of death (119,054 cases compared with 52,193 in 1980). In the period 1980 to 2000, mortality from COPD increased by 64% (from 40.7 to 66.9 per 100 000 population).

Prevalence, incidence and mortality rates increase with age. Prevalence is higher among men, but the overall mortality is the same for men and women. Morbidity and mortality are generally higher among people of the white race, blue-collar workers and people with a lower level of education; probably this is due to the large number of smokers in these categories of the population. Apparently, family cases of COPD are not associated with a deficit of alpha-antitrypsin (an alpha-antiprotease inhibitor).

The incidence of COPD is increasing worldwide due to increased smoking in industrially undeveloped countries, a reduction in mortality due to infectious diseases and widespread use of biomass fuels. COPD caused about 2.74 million deaths worldwide in 2000 and is expected to become one of the world's five major diseases by 2020.

[8], [9], [10], [11], [12],

What causes COPD?

Cigarette smoking is a major risk factor in most countries, although only about 15% of smokers develop clinically evident COPD; The history of the use of 40 or more bladder years is particularly prognostic. Smoke from burning biofuel for home cooking is an important etiological factor in underdeveloped countries. Smokers with pre-existing airway reactivity (defined as increased sensitivity to inhaled methacholine chloride), even in the absence of clinical bronchial asthma, have a higher risk of developing COPD than those without this pathology. Low body weight, childhood respiratory diseases, passive smoking, air pollution and occupational pollutants (eg, mineral or cotton dust) or chemicals (eg cadmium) contribute to the risk of COPD, but are of little importance compared to cigarette smoking.

Genetic factors also matter. The most well-studied genetic disorder - the deficit of alpha-antitrypsin - is a significant cause of the development of emphysema in nonsmokers and affects susceptibility to disease in smokers. Polymorphism of the microsomal epoxide hydrolase genes, the vitamin D-binding protein, 11_-1p and the IL-1 receptor antagonist are associated with a rapid decrease in the forced expiratory volume in 1 s (FEV) in selected populations.

In genetically predisposed people inhalation effects cause an inflammatory response in the respiratory tract and alveoli, which leads 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. In the normal process of recovery of lung protease tissue - neutrophil elastase, tissue metalloproteinases and cathepsins, destroy elastin and connective tissue. Their activity is counterbalanced by antiproteases - alpha-antitrypsin, inhibitor of secretory leukoproteinase, produced by the epithelium of the respiratory tract, elaphin and tissue inhibitor of matrix metalloproteinases. In patients with COPD, activated neutrophils and other inflammatory cells release proteases during inflammation; protease activity exceeds antiprotease activity, and as a result, tissue destruction and increased secretion of mucus occur. Activation of neutrophils and macrophages also results in the accumulation of free radicals, superoxide anions and hydrogen peroxide, which inhibit antiproteases and cause bronchospasm, mucosal edema and increased mucus secretion. Like infection, a role in pathogenesis is played by neutrophilinduced oxidative damage, the release of profibroznyh neuropeptides (eg, bombesin) and a decrease in the production of the growth factor of the vascular endothelium.

Bacteria, especially Haemophilus influenzae, normally colonize the sterile lower respiratory tract in approximately 30% of patients with active COPD. In severely ill patients (for example, after previous hospitalizations) Pseudomonas aeruginosa is often excreted. Some experts suggest that smoking and obstruction of the airways lead to a reduced clearance of mucus in the lower respiratory tract, which predisposes to infection. Repeated infections lead to an increase in the inflammatory response, which accelerates the progression of the disease. However, it is not obvious that prolonged use of antibiotics slows the progression of COPD in susceptible smokers.

The cardinal pathophysiological feature of COPD is the restriction of airflow caused by emphysema and / or airway obstruction due to increased secretion of mucus, sputum and / or bronchospasm. Increased resistance of the respiratory tract increases the work of breathing, as does hyperinflation of the lungs. Increased respiratory work can lead to alveolar hypoventilation with hypoxia and hypercapnia, although hypoxia is also caused by a ventilation / perfusion (W / P) mismatch. Some patients with advanced disease develop chronic hypoxemia and hypercapnia. Chronic hypoxemia increases pulmonary vascular tone, which, if it has a diffuse character, causes pulmonary hypertension and a pulmonary heart. The purpose of 02 in this case may worsen hypercapnia in some patients by reducing the hypoxic respiratory response, which leads to alveolar hypoventilation.

Histological changes include peribronioolar inflammatory infiltrates, hypertrophy of bronchial smooth muscle and air space disruption due to loss of alveolar structures and septal destruction. The enlarged alveolar spaces are sometimes combined into a bull, defined as an airspace of more than 1 cm in diameter. Bulla can be completely empty or include sections of lung tissue, crossing them in areas of highly developed emphysema; Bullas sometimes occupy the entire half of the thorax.

Symptoms of COPD

It takes years to develop and progress COPD. A productive cough is usually the first sign in patients aged 40-50 years who have smoked more than 20 cigarettes a day for more than 20 years. Shortness of breath, which is progressive, persistent, expiratory or worsens during respiratory infections, eventually appears by the time patients reach the age of over 50 years. Symptoms of COPD usually progress rapidly in patients who continue to smoke and are exposed during the life of a higher exposure to tobacco. At later stages of the disease, there is a headache in the morning, which indicates night hypercapnia or hypoxemia.

In COPD, acute worsening of the condition occurs periodically, manifested by increased symptoms. A particular cause of any exacerbation is almost always impossible to detect, but exacerbations are often attributed to viral ARI or acute bacterial bronchitis. As COPD progresses, exacerbations tend to increase (an average of three episodes a year). Patients who have experienced an exacerbation are likely to have repeated episodes of exacerbations.

Symptoms of COPD include wheezing, increased airiness of the lungs is manifested by a weakening of the heart and respiratory sounds, an increase in the anteroposterior size of the thorax (barrel chest). Patients with early emphysema lose weight and experience muscle weakness due to immobility; hypoxia; release of systemic inflammatory mediators such as tumor necrosis factor (TNF) -a; the intensity of metabolism increases. Symptoms of a neglected disease include breathing with retracted lips, attaching auxiliary muscles with a paradoxical retraction of the lower intercostal spaces (Hoover's symptom) and cyanosis. Symptoms of pulmonary heart include swelling of the veins of the neck; splitting of the second heart tone with an underlined pulmonary component; noise of tricuspid insufficiency and peripheral edema. Right ventricular swelling is rare in COPD due to hyperventilated lungs.

Spontaneous pneumothorax is also common as a result of rupture of bulla and is suspected in any patient with COPD, whose pulmonary status deteriorates sharply.

Systemic diseases that may have a component of emphysema and / or bronchial obstruction that mimic the presence of COPD include HIV infection, sarcoidosis, Sjogren's syndrome, bronchiolitis obliterans, lymphangiomyomiomatosis and eosinophilic granuloma.

Diagnosis of COPD

The diagnosis is based on anamnesis, physical examination and survey data using visualization methods and is confirmed by lung function tests. Differential diagnosis is performed with bronchial asthma, heart failure and bronchiectasis. COPD and bronchial asthma are sometimes easily confused. Bronchial asthma differs from COPD history and reversibility of airway obstruction in the study of lung function.

[13], [14],

Lung function tests

Patients with suspected COPD should undergo lung function tests to confirm airway obstruction and quantify their severity and reversibility. Lung function testing is also necessary to diagnose the subsequent progression of the disease and monitor the response to treatment. The main diagnostic tests are FEV, which is the volume of air exhaled for the first second after a full inspiration; The forced vital capacity of the lungs (FVC), which is the total volume of air exhaled with maximum force; and a volume-flow loop, which is a simultaneous spirometric recording of the airflow and volume during the forced maximum expiration and inspiration.

Reduction of FEV, FVC and FEV1 / FVC ratio is a sign of airway obstruction. The volume-flow loop shows the deflection in the expiratory segment. FEV is reduced to 60 ml / year in smokers, compared to a less steep decline of 25-30 ml / year for nonsmokers, the change in rates begins at about the age of 30. Smokers of middle age who already have low FEV, the decline develops more quickly. When FEV falls below about 1 L, patients develop shortness of breath when they are at household level; When FEV falls below approximately 0.8 liters, patients have the risk of hypoxemia, hypercapnia and pulmonary heart disease. FEV and FVC are easily measured by stationary spirometers and determine the severity of the disease, because they correlate with symptoms and lethality. Normal levels are determined depending on the age, sex and growth of the patient.

Additional indicators of the study of pulmonary function are needed only under certain circumstances, such as surgical lung volume reduction. Other test tests may include increased total lung capacity, functional residual capacity and residual volume, which can help distinguish COPD from restrictive lung diseases, in which these indicators decrease; The vital capacity decreases and the diffusivity of carbon monoxide in unit breath (DS) decreases. Reduced DS is not specific and decreases with other disorders that damage the pulmonary vascular bed, such as interstitial lung diseases, but can help distinguish COPD from bronchial asthma, in which DSS0 is normal or elevated.

Methods of visualization of COPD

Radiography of the chest has a 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, a rapid constriction of the vessels of the lung root (in the anterior-posterior projection), and the expansion of the augmented airspace. Compaction of the diaphragm due to hyperinflation causes an increase in the angle between the breastbone and the front of the diaphragm on the roentgenogram in the lateral projection to more than 90 ° in comparison with the normal index of 45 °. X-ray negative bullets more than 1 cm in diameter, surrounded by arcade fuzzy dimming, indicate locally pronounced changes. The predominant emphysema changes in the bases of the lungs indicate a deficiency of alpha1-antitrypsin. Lungs can look normal or have increased transparency due to loss of parenchyma. Chest X-ray images of patients with chronic obstructive bronchitis may be normal or demonstrate bilateral bilateral basilar reinforcement of the bronchoconstrictor component.

The enlarged lung root indicates an increase in central pulmonary arteries observed with pulmonary hypertension. The dilatation of the right ventricle observed with the pulmonary heart can be masked by increased lightness of the lung or may manifest as an enlargement of the shadow of the heart into the retina or widening of the transverse cardiac shade in comparison with the previous chest radiographs.

CT data will help to clarify the changes detected on chest radiography, suspicious for concomitant or complicating diseases, such as pneumonia, pneumoconiosis or lung cancer. CT helps evaluate the distribution and distribution of emphysema by visual assessment or analysis of lung density distribution. These parameters can be useful in preparing for surgical reduction of lung volume.

Advanced Studies in COPD

Alpha antitrypsin levels should be determined in patients under 50 years of age with symptoms of COPD and in non-smokers of any age with COPD to detect a deficiency of alpha-antitrypsin. Other facts in favor of antitrypsin deficiency include a family history of early COPD or liver disease in early childhood, the distribution of emphysema in the lower lobes and COPD on the background of ANCA-positive vasculitis (antineutrophil cytoplasmic antibodies). Low levels of alpha-antitrypsin should be confirmed phenotypically.

To exclude cardiac causes, dyspnea often causes an ECG, usually a diffuse low QRS voltage with a vertical cardiac axis caused by increased lightness of the lungs, and an increased tooth amplitude or a deviation of the right tooth vector caused by dilated right atrium 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. Multifocal atrial tachycardia, arrhythmia, which can accompany COPD, manifests as tachyarrhythmia with polymorphic denticles P and variable intervals PR.

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

A clinical blood test has little diagnostic value in the diagnosis of COPD, but can reveal erythrocythemia (Hct> 48%) reflecting chronic hypoxemia.

[15], [16], [17], [18]

Diagnosis of exacerbations of COPD

Patients with exacerbations accompanied by increased work of breathing, drowsiness and low O2 saturation with oximetry should be examined for arterial blood gases in order to quantify hypoxemia and hypercapnia. Hypercapnia can coexist with hypoxemia. In such patients, hypoxaemia often provides more respiratory excitement than hypercapnia (which is normal), and oxygen therapy can enhance hypercapnia, reducing hypoxic respiratory response and increasing hypoventilation.

The partial pressure of arterial oxygen (PaO2) is less than 50 mm Hg. Art. Or the partial pressure of arterial carbon dioxide (Ra-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 prolonged periods of time.

Radiography of the chest is often prescribed to exclude pneumonia or pneumothorax. Rarely infiltrate in patients permanently receiving systemic glucocorticoids, may be a consequence of aspergillus pneumonia.

Yellow or green sputum is a reliable indicator of the presence of neutrophils in sputum, indicating bacterial colonization or infection. Gram stain usually allows the detection of neutrophils and a mixture of microorganisms, often Gram-positive diplococci (Streptococcus pneumoniae) and / or gram-negative rods (H. Influenzae). Sometimes an exacerbation is caused by another oropharyngeal flora, for example Moraxella (Branhamella) catarrhalis. In hospitalized patients, Gram staining and culture can reveal resistant Gram-negative microorganisms (for example, Pseudomonas) or, rarely, Gram-positive infection caused by staphylococcus.

[19], [20], [21], [22],

Treatment of COPD

Treatment of chronic stable COPD is aimed at preventing exacerbations and ensuring long-term normal and pulmonary function through pharmacotherapy and oxygen therapy, quitting smoking, exercise, improving nutrition and pulmonary rehabilitation. Surgical treatment of COPD is shown to individual patients. Control of COPD involves treatment of both chronic stable disease, and exacerbations.

Medicinal treatment of COPD

Bronchodilators are the basis for controlling COPD; drugs include inhaled beta-agonists and anticholinergics. Any patient with symptomatic COPD should use drugs of one or both classes that are equally effective. For initial therapy, the choice between short-acting beta-agonists, long-acting beta-agonists, anticholinergics (which have a greater effect of bronchodilation), or a combination of beta-agonists and anticholinergic drugs is often decided based on the cost of treatment, patient preferences and symptoms. Currently, data have been obtained that the regular use of bronchodilators slows down the deterioration of pulmonary function, the drugs rapidly reduce symptoms, improve pulmonary function and performance.

In the treatment of chronic stable disease, the administration of metered-dose inhalers or powder inhalers is preferred over nebulized home therapy; Home nebulizers are quickly contaminated due to incomplete cleaning and drying. Patients should be trained to breathe as much as possible, inhale the aerosol slowly until reaching the total lung capacity and hold their breath for 3-4 seconds before exhaling. Spacers guarantee the optimal distribution of the drug to the distal airways, so coordinating the activation of the inhaler with inhalation is not so important. Some spacers do not allow the patient to inhale, if he takes too much breath.

Beta-agonists relax the smooth muscles of the bronchi and increase the clearance of the ciliated epithelium. Salbutamol aerosol, 2 breaths (100 μg / dose), inhaled from the metered-dose inhaler 4-6 times a day, is usually the drug of choice because of its low price; regular application has no advantages over use as required and causes more undesirable effects. Long-acting beta-agonists are preferred for patients with nocturnal symptoms or for those who find the frequent use of an inhaler inconvenient; you can use salmeterol powder, 1 inhale (50 mcg) 2 times a day or powder formoterol (Turbohaler 4.5 mcg, 9.0 mcg or Aerolaser 12 mcg) 2 times a day or formoterol DAI 12 mcg 2 times a day. Powder forms can be more effective for patients who have coordination problems when using a metered-dose inhaler. Patients need to clarify the difference between short-term and long-acting drugs, because long-acting drugs that are used as needed or more than 2 times a day increase the risk of arrhythmias. Side effects usually occur when using any beta-agonist and include tremor, anxiety, tachycardia and mild hypokalemia.

Anticholinergic drugs relax the smooth muscles of the bronchi through competitive inhibition of muscarinic receptors. Ipratropium bromide is usually used because of low price and availability; the drug is taken 2-4 times every 4-6 hours. Ipratropium bromide has a slower onset of action (within 30 minutes, achieving a maximum effect in 1-2 hours), so a beta-agonist is often given with it in a single combined inhaler or separately as a necessary emergency aid. Tiotropium, a quaternary anticholinergic long-acting agent, is M1- and M2-selective and may therefore have an advantage over ipratropium bromide, since M receptor blockade (as in the case of ipratropium bromide) can limit bronchodilation. Dose - 18 mcg 1 time in the bluish. Tiotropium is not available in all countries of the world. The effectiveness of tiotropium in COPD has been demonstrated in large-scale studies, as a drug significantly slowing the fall in FEV in patients with moderate COPD, as well as in patients who continue to smoke and quit smoking and in people over 50 years of age. In patients with COPD, regardless of the severity of the disease, prolonged use of tiotropium improves the quality of life, reduces the frequency of exacerbations and the frequency of hospitalization of patients with COPD, reduce the risk of mortality in COPD. Side effects of all anticholinergic drugs - dilated pupils, blurred vision and xerostomia.

Inhaled glucocorticoids inhibit the inflammation of the respiratory tract, alter the reduced regulation of beta receptors and inhibit the production of cytokines and leukotrienes. They do not alter the nature of the decline in pulmonary function in patients with COPD who continue to smoke, but they do improve the short-term lung function in some patients, enhance the effect of bronchodilators and can reduce the frequency of exacerbations of COPD. The dose depends on the drug; for example, fluticasone in a dose of 500-1000 mcg per day and beclomethasone 400-2000 mcg per day. The long-term risks of prolonged use of inhaled glucocorticoids (fluticasone + salmeterol) in randomized controlled clinical trials have established an increase in the incidence of pneumonia in COPD patients, unlike long-term COPD treatment 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 complications in COPD patients who receive long-term inhaled glucocorticoids in fixed combinations, are associated with different pharmacokinetic properties of glucocorticoids, which can lead to various clinical effects. For example, budesonide is more rapidly removed from the respiratory tract than fluticasone. These differences in clearance may increase in persons with significant obstruction, resulting in increased accumulation of drug particles in the central airway, reduced absorption of peripheral tissues. Thus, budesonide can be removed from the lungs before it leads to a significant decrease in local immunity and to the proliferation of bacteria, which provides an advantage, since in 30-50% of patients with moderate and severe COPD, bacteria are constantly present in the respiratory tract. Probably complications of steroid therapy include the formation of cataracts and osteoporosis. Patients who use these drugs for a long time should periodically be observed by an ophthalmologist and perform bone densitometry, 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 any of these drugs in the monotherapy regimen in the treatment of chronic stable disease.

Oral or systemic glucocorticoids can be used to treat chronic stable COPD, but they probably can only be effective in 10-20% of patients, and long-term risks may exceed positive effects. Formal comparisons between oral and inhaled glucocorticoids have not been carried out. Initial doses of oral preparations should be 30 mg once daily for prednisolone, the response to treatment should be checked by spirometry. If FEV improves by more than 20%, the dose should decrease by 5 mg of prednisolone per week to the lowest dose that supports improvement. If the aggravation develops against the background of the decrease, inhalation glucocorticoids may be useful, but a return to a higher dose is likely to provide a faster disappearance of symptoms and recovery of FEV. In contrast, if the increase in FEV is less than 20%, the dose of glucocorticoids should be reduced quickly and their intake is terminated. The purpose of the drug according to the alternating scheme can be a choice, if it reduces the number of undesirable effects, providing an everyday effect of the drug itself.

Theophylline plays an insignificant role in the treatment of chronic stable COPD and exacerbations of COPD now, when safer and more effective drugs are available. Theophylline reduces spasm of smooth muscle fibers, increases the clearance of ciliated epithelium, improves right ventricular function and reduces pulmonary vascular resistance and blood pressure. His mode of action is poorly understood, but probably different from the mechanism of action of beta-agonists and anticholinergics. His role in improving diaphragmatic function and reducing shortness of breath during exercise is controversial. Theophylline in low doses (300-400 mg per day) has anti-inflammatory properties and can enhance the effects of inhaled glucocorticoids.

Theophylline can be used in patients who do not adequately respond to inhalers, and if symptomatic efficacy is observed with the drug. Concentrations of the drug in the serum do not require monitoring until the patient responds to the drug, has no symptoms of toxicity, or is available to the contact; Oral forms of theophylline with slow release, which require less frequent use, increase compliance. Toxicity is observed frequently and includes insomnia and gastrointestinal disorders, even at low concentrations in the blood. More serious adverse effects, such as supraventricular and ventricular arrhythmias and seizures, tend to occur at concentrations in the blood of more than 20 mg / L. The hepatic metabolism of theophylline changes markedly depending on genetic factors, age, cigarette smoking, hepatic dysfunction, and concomitant administration of a small amount of drugs, such as macrolide and fluoroquinolone antibiotics and H2-histamine receptor blockers that do not have sedative effects.

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

Oxygen therapy in COPD

Long-term oxygen therapy prolongs life for patients with COPD, whose PaO2 is constantly less than 55 mm Hg. Art. Continuous 24-hour oxygen therapy is more effective than a 12-hour night regimen. Oxygen therapy leads the hematocrit to the norm, moderately improves the neurological status and psychological state, most likely, by improving sleep, and reduces pulmonary hemodynamic disorders. Oxygen therapy also increases exercise tolerance in many patients.

A sleep study should be performed in patients with severe COPD who do not meet the criteria for prolonged oxygen therapy, but clinical examination data indicate pulmonary hypertension in the absence of diurnal hypoxemia. Nocturnal oxygen therapy can be prescribed if the study during sleep shows an episodic decrease in carbonation <88%. Such treatment prevents the progression of pulmonary hypertension, but its effect on survival is unknown.

Patients who recover after an acute respiratory illness and the corresponding listed criteria need to be assigned O2 and re-examined the parameters when breathing room air after 30 days.

O is applied through the nasal catheter with a flow rate sufficient to achieve PaO2> 60 mmHg. Art. (SaO> 90%), usually 3 l / min at rest. O2 comes from electric oxygen concentrators, liquefied O2 systems or compressed gas cylinders. Concentrators that limit mobility but are least expensive are preferred for patients who spend most of their time at home. Such patients may have small O2 reservoirs for backup cases in the absence of electricity or for portable use.

Liquid systems are preferable for patients who spend a lot of time outside the home. Portable canisters of liquid O2 are easier to carry, and they have a greater capacity than portable cylinders of compressed gas. Large cylinders of compressed air are the most expensive way to provide oxygen therapy, so it should only be used if other sources are not available. All patients need to explain the danger of smoking during use.

Different devices allow saving the oxygen used by the patient, for example by using a reservoir system or supplying O only at the time of inspiration. These devices control hypoxemia as effectively as continuous feed systems.

Some patients need an additional O2 while traveling by air, as the pressure in the cockpit of civil airliners is low. Eucaphnic patients with COPD, at which at sea level, PaO2 is greater than 68 mm Hg. In flight, on the average, PaO2 is greater than 50 mm Hg. Art. And do not require additional oxygen therapy. All patients with COPD with hypercapnia, significant anemia (Hct <30) or concomitant cardiac or cerebrovascular diseases should use supplemental O2 for long flights and must warn the airline when booking tickets. Patients are not allowed to transport or use their own O2. The airline provides O2 through its own system, and most require notification minimum of 24 hours, medical confirmation of necessity and discharge of O before the flight. Patients should have their own nasal catheters, because some airlines provide only masks. Provision of equipment in the city of destination, if required, must be prepared in advance so that the supplier can meet the traveler at the airport.

Smoking cessation

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

Vaccinotherapy

All patients with COPD need to do annual flu shots. Influenza vaccine for 30-80% is able to reduce the severity of the course and mortality in patients with COPD. If the patient can not be vaccinated or if the predominant strain of the influenza virus is not included in the vaccine form of the year, influenza outbreaks should be treated with prophylactic drugs (amantadine, rimantadine, oseltamivir or zanamivir) for the treatment of influenza outbreaks. Pneumococcal polysaccharide vaccine gives minimal undesirable effects. Vaccination with a polyvalent pneumococcal vaccine should be given to all COPD patients aged 65 years and older and to patients with COPD with FEV1 <40% of the expected.

Physical activity

The physical condition of skeletal muscles, worsened by lack of mobility or prolonged hospitalization with respiratory failure, can be improved by a program of metered exercise. Specific training of the respiratory muscles is less useful than general aerobic training. A typical training program begins with a slow walk on the treadmill or riding a bicycle ergometer without load for several minutes. The duration and intensity of exercise progressively increases for more than 4-6 weeks, until the patient can train for 20-30 minutes without stopping with controlled dyspnea. Patients with very severe COPD can usually achieve a walking regimen for 30 minutes at a rate of 1 -2 miles per hour. To maintain the physical form of the exercise should be done 3-4 times a week. Saturation 02 is monitored and, if necessary, an additional O2 is assigned. Endurance training for upper extremities is useful for performing everyday activities such as bathing, dressing and cleaning. Patients with COPD should be trained in energy-saving ways of doing daily work and distributing activity. It is also necessary to discuss problems in the sexual sphere and to consult on energy saving methods of sexual contacts.

Food

In patients with COPD, the risk of losing body weight and reducing nutrition status is increased due to an increase of 15-25% in energy expenditure on respiration, higher postprandial metabolism and heat production (that is, the heat effect of nutrition), possibly because the stretchy stomach prevents the lowering already a smoothed diaphragm and increases the work of breathing, higher energy costs for daily activity, inconsistencies in energy intake and energy needs, and the catabolic effects of inflammatory cytokines inov, such as TNF-a. The overall muscle strength and effectiveness of use of O are deteriorating. Patients with a lower nutritional status have a worse prognosis, so it is advisable to recommend a balanced diet with an adequate amount of calories in conjunction with physical exercises to prevent or restore muscle atrophy and malnutrition. However, excessive weight gain should be avoided, and obese patients should seek a more normal body mass index. Studies that examined the contribution of diet to patient rehabilitation did not demonstrate an improvement in pulmonary function or tolerance to exercise. The role of anabolic steroids (eg, megestrol acetate, oxandrolone), growth hormone therapy and TNF antagonists in correcting the nutritional status and improving the functional status and prognosis in COPD has not been studied sufficiently.

[23], [24], [25], [26], [27], [28]

Pulmonary rehabilitation in COPD

Pulmonary rehabilitation programs complement pharmacotherapy to improve physical function; Many hospitals and health facilities offer formal multidisciplinary rehabilitation programs. Pulmonary rehabilitation includes physical exercises, education and behavior correction. Treatment should be individualized; patients and family members are told about COPD and treatment, the patient is encouraged to take maximum responsibility for personal health. A carefully integrated rehabilitation program helps patients with severe COPD adjust to physiological limitations and gives them realistic ideas about the possibility of improving their condition.

The effectiveness of rehabilitation is manifested in greater independence and better quality of life and tolerance to stress. Small improvements are noticeable in increasing the strength of the lower extremities, endurance and maximum consumption of O2. However, pulmonary rehabilitation usually does not improve pulmonary function and does not increase life expectancy. To achieve a positive effect, patients with a severe form of illness require at least a three-month rehabilitation, after which they must continue to work on supporting programs.

Specialized programs are available for patients who remain on ventilation after acute respiratory failure. Some patients may be completely withdrawn from the ventilator, while others may remain without ventilation only during the day. If there are adequate conditions at home and if the family members are sufficiently well-trained, the patient can be discharged from the hospital with mechanical ventilation.

Surgical treatment of COPD

Surgical approaches to the treatment of severe COPD include reducing lung volume and transplantation.

Reducing lung volume by resection of functionally inactive emphysematous areas improves exercise tolerance and a two-year mortality in patients with severe emphysema, predominantly in the upper lungs, with initially low tolerance to post pulmonary rehabilitation.

Other patients may experience a decrease in symptoms and an increase in performance after surgery, but the level of lethality does not change or worsen compared to drug therapy. Long-term results of treatment are unknown. Improvement of the condition is observed less often than with lung transplantation. It is believed that the improvement is a consequence of an increase in lung function and an improvement in the diaphragmatic function and the W / P ratio. The operational mortality rate is approximately 5%. The best candidates for lung volume reduction are patients with FEV 20-40% of the predicted, DSrd more than 20% of the due, with significant decrease in tolerance to physical activity, heterogeneous character of lung lesion according to CT with predominant lesion of upper lobes, RACO less than 50 mm Hg. Art. And in the absence of severe pulmonary arterial hypertension and coronary artery disease.

In rare cases, patients have such large bullae that they compress the functional lung. These patients can be assisted by surgical resection of the bull, which leads to the disappearance of manifestations and improvement of pulmonary function. In general, resection is most effective at bullae, occupying more than a third of the thorax and FEV about half of the normal volume. The improvement in pulmonary function depends on the amount of normal or minimally altered lung tissue that has been compressed by the resected bulb. Sequential chest radiographs and CT scans are the most informative studies to determine whether a patient's functional status is the result of a viable lung bulb compression or a general emphysema. A markedly decreased DSS0 (<40% of due) indicates a common emphysema and suggests a more modest outcome from surgical resection.

Since 1989, transplantation of one lung has largely replaced the transplantation of two lungs in patients with COPD. Candidates for transplantation - patients younger than 60 years with FEV less than 25% of due or with severe pulmonary arterial hypertension. The purpose of lung transplantation is to improve the quality of life, because life expectancy increases rarely. Five-year survival after transplantation with emphysema is 45-60%. Patients require lifelong immunosuppression, which is associated with a risk of opportunistic infections.

Treatment of acute exacerbation of COPD

The immediate task 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 arise from bacterial or viral infections. Exacerbations are facilitated by factors such as smoking, inhalation of irritating pollutants and high levels of air pollution. Moderate exacerbations can often be treated out-patient, if home conditions permit. Older attenuated patients and patients with concomitant pathology, anamnesis of respiratory failure or acute changes in the parameters of the gas composition of arterial blood are hospitalized for observation and treatment. Obligatory hospitalization in the intensive care unit with constant monitoring of the respiratory status is subject to patients with life-threatening exacerbations with unresponsive hypoxemia, acute respiratory acidosis, new arrhythmias or impairment of respiratory function, despite inpatient treatment, and patients who need sedation for treatment.

Oxygen

Most patients need an additional O2, even if they do not need it all the time. The administration of O2 can worsen hypercapnia, reducing the hypoxic respiratory response. After 30 days, the PaO2 value for room air breathing should be checked again to assess the patient's need for additional O2.

Respiratory support

Non-invasive positive pressure ventilation [eg, pressure support or two-level ventilation with positive airway pressure through the face mask] is an alternative to full artificial ventilation. Noninvasive ventilation probably reduces the need for intubation, reduces the duration of inpatient treatment, and reduces mortality in patients with severe exacerbations (determined at pH <7.30 in hemodynamically stable patients without a direct threat of respiratory arrest). Non-invasive ventilation, apparently, does not have any effect in patients with less severe exacerbation. However, it can be administered to patients in this group if the arterial blood gas composition deteriorates despite initial drug therapy, or if the patient is a potential candidate for complete mechanical ventilation, but does not require intubation for airway control or sedation for treatment. If the condition worsens on non-invasive ventilation, it is necessary to switch to invasive artificial ventilation.

Deterioration of gas composition of blood and mental status and progressive fatigue of respiratory muscles are indications for endotracheal intubation and artificial ventilation of the lungs. Variants of ventilation, treatment strategies and complications are discussed in Ch. 65 on page 544. Risk factors for dependence on mechanical ventilation include FEV <0.5 L, stable blood gas composition (PaO2 <50 mmHg and / or PaCO2> 60 mmHg), a significant limitation of the ability to exercise and poor nutrition status. Therefore, the patient's wishes for intubation and mechanical ventilation should be discussed and documented.

If the patient needs a prolonged intubation (for example, more than 2 weeks), tracheostomy is prescribed to ensure comfort, communication and nutrition. When performing a good multidisciplinary recovery program, including nutritional and psychological support, many patients requiring sustained mechanical ventilation can be successfully removed from the device and returned to their previous level of functioning.

Medicinal treatment of COPD

Beta-agonists, anticholinergics and / or corticosteroids should be given concomitantly with oxygen therapy (no matter how oxygen is used), in order to reduce airway obstruction.

Beta-agonists are the basis of drug therapy for exacerbations. The most widely used is salbutamol 2.5 mg through a nebulizer or 2-4 inhalations (100 μg / inh) through a metered-dose inhaler every 2-6 hours. Inhalation using a metered-dose inhaler leads to rapid bronchodilation; there is no data indicating a higher effectiveness of nebulizers compared to metered-dose inhalers.

The efficacy of ipratropium bromide, an anticholinergic agent, is most often used, with exacerbation of COPD; it should be administered simultaneously or alternately with beta-agonists via a metered-dose inhaler. Dosage - 0.25-0.5 mg through a nebulizer or 2-4 inhalations (21 mcg / inhalation) with a metered-dose inhaler every 4-6 h. Ipratropium bromide usually provides a bronchodilating effect similar to the effect of beta-agonists. The therapeutic value of tiotropium, a prolonged anticholinergic drug, has not been established.

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

Methylxanthines, which were once considered as the basis for treating exacerbations of COPD, are no longer used. Their toxicity exceeds efficiency.

Antibiotics are recommended for exacerbations in patients with purulent sputum. Some doctors prescribe antibiotics empirically when the color of the sputum changes or when nonspecific changes in chest radiography are made. Before the appointment of treatment, there is no need for 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 <65 years of age, FEV> 50% of due includes amoxicillin 500-100 mg 3 times per day or macrolides of the second generation (azithromycin 500 mg 3 days or clarithromycin 500 mg twice a day), cephalosporins II- III generation (cefuroxime axetil 500 mg 2 times a day, cefixime 400 mg 1 time per day), prescribed for 7-14 days, are effective and inexpensive first-line drugs. The choice of medication should be dictated by the local structure of bacterial sensitivity and the patient's history. In most cases, treatment should be initiated with oral medications. Antibiotic therapy for a complicated exacerbation of COPD with risk factors for FEV 35-50% of the 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 administered orally, or if necessary, following the principle of "stepwise therapy" for the first 3-5 days parenterally (amoxicillin- clavulanate 1200 mg 3 times a day or fluoroquinolones (levofloxacin 500 mg once a day, moxifloxacin 400 mg once a day) These drugs are effective against strains of H. Influene and M. Catarrhalis producing beta-lactamases but did not exceed in effectiveness first-line drugs in most patients Patients should be trained to recognize signs of exacerbation from sputum change from normal to purulent and begin a 10-14-day course of antibiotic therapy, and prolonged antibiotic prophylaxis is recommended only for patients with structural changes in lungs such as bronchiectasis or infected bull.

If suspected Pseudomonas spp. And / or other Enterobactereaces spp., parenterally ciprofloxacin 400 mg 2-3 times a day, then 750 mg orally 2 times a day, or parenterally, levofloxacin 750 mg once a day, then 750 mg daily, ceftazidime 2.0 g 2-3 times a day.

Prognosis of COPD

Severity of airway obstruction predicts survival in COPD patients. Mortality in patients with FEV, equal to or greater than 50%, is presumably slightly larger than in the general population. With FEV 0.75-1.25 liters, the five-year survival rate is approximately 40-60%; if less than 0.75 liters, then about 30-40%. Heart disease, low body weight, tachycardia at rest, hypercapnia and hypoxemia reduce survival, whereas a significant response to bronchodilator drugs is associated with improved survival. The risk factors for death in patients in the acute phase requiring hospitalization are advanced age, high values of RaCO2 and the continued use of oral glucocorticoids.

Mortality in COPD in quitting patients is often the result of intercurrent diseases, rather than the progression of the underlying disease. Death is usually caused by acute respiratory failure, pneumonia, lung cancer, heart disease or pulmonary embolism.