lung diseases. Chronic obstructive pulmonary disease (COPD) - symptoms and treatment. Treatment of the moderate form

chronic obstructive pulmonary disease ( COPD) is a slowly progressive chronic disease with damage to the distal respiratory tract caused by an inflammatory reaction and the lung parenchyma, manifested by the development of emphysema, and accompanied by reversible or irreversible bronchial obstruction.

According to WHO, the prevalence of COPD among men is 9.34:1000, among women - 7.33:1000. Persons over 40 years of age predominate. In Russia, according to the official statistics of the Ministry of Health of the Russian Federation, there are about 1 million patients with COPD. However, according to epidemiological studies, their number may exceed 11 million people. There is a pronounced trend towards an increase in this disease, predominantly in women (in men - by 25% and in women - by 69% over the period from 1990 to 1999). At the same time, mortality from COPD is increasing. Among the leading causes of death in the world, this disease is in 6th place, and this figure doubles every 5 years.

Etiology and pathogenesis

COPD is a consequence of chronic obstructive bronchitis, pulmonary emphysema and bronchial asthma, the etiology and pathogenesis of which are described earlier. These diseases are combined into one group - COPD - from the moment when obstruction develops, and FEV 1 becomes less than 40%. The main etiological factors of COPD are smoking, air pollution, occupational hazards, infections, family and hereditary factors.

The pathophysiological essence of COPD is an increase in airway resistance in bronchitis and bronchial asthma due to the primary lesion of the bronchi and in emphysema - due to a decrease in the tensile strength of the bronchi and a decrease in the forced expiratory rate. In COPD, the normal ratio of lung volumes is disturbed: residual volume, FOB, and total lung capacity increase. Increased airway resistance, decreased elastic recoil of the lungs, or a combination of both lead to an increase in the time of full exhalation, which, with the progression of the disease, does not have time to complete. This leads to an increase in FOB and positive pressure in the alveoli before the start of inspiration, which is accompanied by an increase in the work of the respiratory system.

With COPD, gas exchange worsens and the parameters of the HAC change. Alveolar ventilation, as measured by PaCO 2 , may be increased, normal, or decreased depending on the ratio of tidal volumes to dead space volume. If the ventilation of normally perfused areas of the lungs is disturbed, intracellular shunting of blood from right to left develops, and P (A-a) O 2 increases.

COPD is characterized by both a decrease in perfusion of individual sections of the lungs, and pulmonary hypertension at rest of varying severity, and its increase disproportionately to cardiac output during exercise. Pulmonary hypertension is due to a decrease in the total cross-sectional area of ​​the pulmonary vascular bed and hypoxic pulmonary vasoconstriction, which is more important than the cross-section of the vascular bed. Acidosis, which develops in acute and chronic respiratory failure, increases pulmonary vasoconstriction and causes erythrocytosis, which worsens the rheological properties of the blood. Persistent pulmonary hypertension leads to right ventricular overload, hypertrophy, and right ventricular failure.

Classification

According to the international recommendations GOLD 2003 (Global Initiative for Chronic Obstructive Lung Disease - Global Initiative for Chronic Obstructive Lung Disease), the diagnostic criterion for all stages of COPD is a decrease in the ratio of FEV 1 to forced vital capacity, i.e. Tiffno index

There are four stages according to the severity of the disease. There is no stage zero in the classification, which is characterized by clinical symptoms (cough with sputum and the presence of risk factors), but lung function is not changed. This stage is considered as a predisease, not always turning into chronic obstructive pulmonary disease.

Symptoms

The main complaints in chronic obstructive pulmonary disease are cough with sputum and shortness of breath. Cough at first periodic, observed in the morning and afternoon. As the disease progresses, the cough becomes persistent and may develop at night. Sputum is usually mucous, no more than 40 ml is secreted in the morning. An increase in the amount of sputum and its purulent nature are signs of an exacerbation of the disease. Hemoptysis is usually absent. Dyspnea is expiratory in nature, usually appears on average 10 years later than cough and has varying degrees of severity. Initially, shortness of breath occurs during normal physical exertion. With the progression of the disease, shortness of breath develops with less exertion, becomes constant and intensifies with a respiratory infection.

When questioning, it is necessary to study the history of smoking and calculate the smoker's index (SI) (pack/years) using the formula:

CI (pack/years) = Number of cigarettes smoked (days) ∗ Smoking history (years) / 20

IC = 10 pack/year is a significant risk factor for COPD. It is necessary to find out the presence of other risk factors (dust, chemical pollutants, alkali and acid fumes), past infectious diseases (especially SARS) and genetic predisposition (α1-antitrypsin deficiency). Physical examination reveals an emphysematous (“barrel-shaped”) shape of the chest, participation in the act of breathing of auxiliary muscles. The percussion sound is boxy, the borders of the lungs are lowered, the mobility of the lower edge of the lungs is limited. On auscultation, breathing is weakened, vesicular, less often hard, dry buzzing and wheezing, aggravated by forced breathing.

There are two clinical types of chronic obstructive pulmonary disease in patients with moderate and severe course of the disease - emphysematous and bronchitis.

1. emphysematous type. Patients with this type are called "pink puffers", since there is no cyanosis against the background of severe shortness of breath. The physique in this type of chronic obstructive pulmonary disease is asthenic, emaciation often develops, a slight cough with scanty mucous sputum. Physical and functional examination revealed signs of pulmonary emphysema.
2. bronchitis type. In patients with this type, the symptoms of chronic bronchitis predominate. These patients are called "blue puffers" because they are characterized by cyanosis and edema due to right ventricular failure. The leading symptom is a cough with sputum for many years.

The main differences between the types of chronic obstructive pulmonary disease are presented in the table. Emphysematous and bronchitis types of COPD are extreme manifestations of the disease. Most patients have signs that are characteristic of both, with some predominance of any one of them.

Diagnostics

Laboratory research. In a general blood test, changes are usually not detected. Some patients may have polycythemia. With an exacerbation of the disease, neutrophilic leukocytosis, a stab shift and an increase in ESR are observed. The emphysematous type is characterized by a decrease in the content of α1-antitrypsin in the blood serum. In sputum, the cellular composition characterizing chronic inflammation is revealed. Bacteriological examination allows you to identify the pathogen and determine its sensitivity to antibiotics. A double bacterioscopic examination is required to exclude pulmonary tuberculosis. Conduct a study of the gas composition of the blood to detect hypoxia and hypercapnia.

Instrumental research. The study of the function of external respiration (RF) is mandatory for establishing a diagnosis for all patients, even if they do not have shortness of breath. Early diagnostic signs of COPD are FEV 1 / FVC less than 70% and daily fluctuations in PSV less than 20% with peak flow monitoring.

Bronchodilatory test is carried out:

1. with short-acting β2-agonists (inhalation of 400 µg salbutamol or 400 µg fenoterol), evaluation is carried out after 30 minutes;
2. with M-anticholinergics (inhalation of ipratropium bromide 80 mcg or a combination of fenoterol 50 mcg and ipratropium bromide 20 mcg (4 doses)), evaluation is carried out after 30-45 minutes.

The increase in FEV 1 is calculated by the formula:

((FEV 1 dilat (ml) − FEV ref (ml)) / FEV 1 ref) ∗ 100%

The increase in FEV 1 > 15% (or 200 ml) of due is a positive test, indicating the reversibility of bronchial obstruction. In the absence of an increase in FEV 1, but a decrease in shortness of breath, the appointment of bronchodilator drugs is indicated.

Primary x-ray examination reveals changes in the lungs and basal areas corresponding to emphysema and chronic bronchitis, and other lung diseases that have clinical symptoms similar to COPD (lung cancer, tuberculosis). During an exacerbation of COPD, pneumonia, spontaneous pneumothorax, pleural effusion, and others are excluded.

ECG is used to exclude possible pathology of the heart, leading to stagnation in the pulmonary circulation with a clinical picture of left ventricular failure, and to identify right ventricular hypertrophy - a sign of cor pulmonale. EchoCG is used to determine the morphometric parameters of the left and right ventricles and calculate the pressure in the pulmonary artery.

Bronchoscopic examination is performed for the differential diagnosis of COPD with diseases of the bronchi and lungs, which have similar symptoms. Bronchoscopy is performed with frequently recurring exacerbations of COPD to obtain a secret and its bacteriological examination and lavage of the bronchial tree. Bronchographic examination is indicated for suspected bronchiectasis, obliteration of small bronchi and bronchioles, cicatricial stenosis of the bronchi.

Differential diagnosis. The differential diagnosis is carried out with lung cancer, in which there may be cough with blood, chest pain, weight loss and lack of appetite, hoarseness, pleural effusion. The diagnosis of lung cancer is confirmed by sputum cytology, bronchoscopy, computed tomography, and transthoracic needle biopsy. In some cases, differential diagnosis is carried out with chronic heart failure, bronchiectasis, pneumonia, tuberculosis, bronchiolitis obliterans.

Treatment

General recommendations. The goal of treatment is to slow the progression of the disease. One of the main interventions in the treatment of COPD is smoking cessation, which gives a more pronounced and persistent slowdown in the decline in FEV 1 Smokers should be helped to quit this bad habit: a date for quitting smoking should be set, the patient should be supported and helped to implement this decision. For some patients, nicotine patches or nicotine gum can be recommended to combat nicotine addiction, which significantly increase the number of quitters. But only 25-30% of patients refrain from smoking for 6-12 months.

If there are harmful environmental factors that cause COPD, a change of profession or place of residence can be recommended. But these recommendations can cause great difficulties for the patient and his family. Recommend the fight against dust and gas pollution in the workplace and at home, the rejection of the use of aerosols and household insecticides.

Vaccination against influenza and pneumococcal infection is mandatory. Exercise therapy is useful for increasing exercise tolerance and training the respiratory muscles.

Medical treatment. Treatment of patients with chronic obstructive pulmonary disease with a stable course is carried out with bronchodilator drugs. Short-acting inhaled bronchodilators are usually used: β2-agonists (salbutamol and fenoterol) or M-anticholinergics (ipratropium bromide, tiotropium bromide), after 4-6 hours. Long-term monotherapy with short-acting β2-agonists is not recommended. Long-acting theophyllines are recommended for some patients with insufficiency of inhaled orondilators.

Treatment of exacerbations on an outpatient basis. Exacerbation of COPD is manifested by increased cough with purulent sputum, fever, increased shortness of breath, and weakness. With a mild exacerbation of COPD, increase the dose and / or frequency of taking bronchodilators. Patients who have not used these drugs are prescribed combinations of bronchodilators (M-anticholinergics with short-acting β2-agonists), and if they are not effective enough, theophylline is prescribed.

With an increase in the separation of purulent sputum and increased shortness of breath, antibiotic therapy is carried out. Amoxicillin, new generation macrolides (azithromycin, clarithromycin), second generation cephalosporins (cefuroxime), or respiratory fluoroquinolones (levofloxacin, moxifloxacin) are prescribed for 10 to 12 days.

With the development of bronchial obstruction for the first time, anamnestic indications of the effectiveness of glucocorticoid treatment of previous exacerbations and a decrease in FEV 1

Treatment of exacerbation in a hospital setting. Indications for hospitalization are the following criteria:

1. deterioration in the condition of patients against the background of ongoing treatment (pronounced increased dyspnea, deterioration in general condition, a sharp decrease in activity);
2. lack of positive dynamics from long-term outpatient treatment, including glucocorticoids, in patients with severe COPD;
3. the appearance of symptoms that characterize the strengthening of respiratory and right ventricular failure (cyanosis, swelling of the jugular veins, peripheral edema, liver enlargement), and the occurrence of rhythm disturbances;
4. elderly age;
5. severe comorbidities;
6. poor social status.

Therapy should begin with oxygen treatment using nasal catheters or face masks 4 - 6 l / min with a fractional concentration of oxygen in the inhaled mixture of 30 - 60% and humidification. Blood gas monitoring should be carried out every 30 minutes. PaO 2 should be maintained at 55 - 60 mm Hg. Art.

bronchodilator therapy. Assign inhalation of a combination of β2-adrenergic agonists and M-anticholinergics. Solutions of ipratropium bromide 2 ml should be used: 40 drops (0.5 mg) through an oxygen nebulizer in combination with solutions of salbutamol 2.5 - 5.0 mg glylifenoterol 0.5 - 1 mg (0.5 - 1 ml 10 - 20 drops) every 4-6 hours. With insufficient effectiveness of inhaled drugs, aminophylline 240 mg / h up to 960 mg / day is administered intravenously at a rate of 0.5 mg / kg / h under the control of ECG and the concentration of theophylline in the blood, which should be 10-15 mcg / ml.

If bronchodilators are not effective enough, or if the patient is already taking systemic glucocorticoids, it is necessary to increase the oral dose. Inside, prednisolone is prescribed at 0.5 mg / kg / day (~ 40 mg / day). It is possible to replace prednisolone with another glucocorticoid in an equivalent dose. With contraindications to taking the drug orally, prednisolone is prescribed intravenously at a dose of 3 mg / kg / day. The course of treatment is 10-14 days. The daily dose is reduced by 5 mg / day after 3-4 days until the reception is completely stopped.

If signs of a bacterial infection appear (an increase in the volume of purulent sputum and increased shortness of breath), antibiotic therapy is carried out. The causative agents of a bacterial infection are most often Haemophilus influenzae, Streptococcus pncumoniae, Moraxella catarrhalis, Enterococcus spp, Mycoplasma pneumoniae. The drugs of choice are amoxicillin/clavulant 625 mg orally 3 times a day for 7 to 14 days, clarithromycin 500 mg orally 2 times a day, or azithromycin 500 mg once a day or 500 mg on the first day, then 250 mg / day for 5 days. Perhaps the appointment of pneumotropic fluoroquinolones (levofloxacin inside 250-500 mg 1-2 times a day or ciprofloxacin inside 500 mg 2-3 times a day).

With complicated exacerbation of COPD in elderly patients and FEV 1

Excretion of sputum. In COPD, treatment is carried out aimed at improving sputum discharge. With a debilitating unproductive cough, postural drainage is effective. To liquefy sputum, expectorants and mucolytic agents are used orally and in aerosols. But the same effect can be obtained by simply drinking heavily.

Surgery. There are surgical treatments for COPD. Bullectomy is performed to relieve symptoms in patients with large bullae. But its effectiveness has been established only among those who quit smoking in the near future. Thoroscopic laser bullectomy and reduction pneumoplasty (removal of the overinflated part of the lung) have been developed. But these operations are still used only in clinical trials. There is an opinion that in the absence of the effect of all the measures taken, one should contact a specialized center to resolve the issue of lung transplantation.

Forecast

Chronic obstructive pulmonary disease has a progressive course. The prognosis depends on the age of the patient, elimination of provoking factors, complications (acute or chronic respiratory failure, pulmonary hypertension, chronic cor pulmonale), a decrease in FEV 1 and the effectiveness of the treatment. In severe and extremely severe course of the disease, the prognosis is unfavorable.

Prevention

Of greatest importance for prevention is the exclusion of risk factors that contribute to the progression of the disease. The main components of prevention are smoking cessation and prevention of infectious diseases of the respiratory tract. Patients must strictly follow the recommendations of doctors, they must be informed about the disease itself, methods of treatment, trained in the correct use of inhalers, self-monitoring skills using a peak fluorometer and decision-making in case of exacerbation.

All iLive content is reviewed by medical experts to ensure it is as accurate and factual as possible.

We have strict sourcing guidelines and only cite reputable websites, academic research institutes and, where possible, proven medical research. Note that the numbers in brackets (, etc.) are clickable links to such studies.

If you believe any of our content is inaccurate, outdated, or otherwise questionable, please select it and press Ctrl + Enter.

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

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

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

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

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

ICD-10 code

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

J44.9 Chronic obstructive pulmonary disease, unspecified

Epidemiology of COPD

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

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

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

What causes COPD?

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

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

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

Lung function studies

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

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

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

COPD Imaging Methods

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

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

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

Additional Research in COPD

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

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

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

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

Diagnosis of COPD exacerbations

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

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

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

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

COPD treatment

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

Drug treatment for COPD

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

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

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

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

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

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

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

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

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

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

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

Oxygen therapy for COPD

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

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

Patients who are recovering from acute respiratory illness and who meet the listed criteria should be given O2 and re-examined for breathing room air after 30 days.

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

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

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

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

Smoking cessation

Quitting smoking is both extremely difficult and extremely important; this slows, 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 dyspnea. Patients with very severe COPD can usually achieve walking for 30 minutes at a speed of 1-2 miles per hour. To maintain physical fitness, exercises should be performed 3-4 times a week. O2 saturation is monitored and, if necessary, additional O2 is administered. Upper limb endurance training is useful for daily activities such as bathing, dressing, and cleaning. Patients with COPD should be taught energy-saving ways of doing daily work and distributing activities. It is also necessary to discuss problems in the sexual area and consult on energy-saving ways of sexual intercourse.

Food

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

Pulmonary rehabilitation in COPD

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

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

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

Surgical treatment of COPD

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

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

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

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

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

Treatment of acute exacerbation of COPD

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

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

Oxygen

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

Respiratory support

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

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

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

Drug treatment for COPD

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

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

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

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

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

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

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

COPD prognosis

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

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

Pulmonary obstruction is a disease that results in inflammation and narrowing of the bronchi and severe damage to the structure and function of the lungs. The disease has a tendency to progression and chronic course.

Is there any problem? Enter in the form "Symptom" or "Name of the disease" press Enter and you will find out all the treatment of this problem or disease.

The site provides background information. Adequate diagnosis and treatment of the disease is possible under the supervision of a conscientious physician. All drugs have contraindications. You need to consult a specialist, as well as a detailed study of the instructions! .

Pathology is called COPD - chronic obstructive pulmonary disease.

What happens with lung obstruction

The mucous membrane of the airways has villi that trap viruses and harmful substances that enter the body. As a result of a long negative impact on the bronchi, provoked by various factors (tobacco smoke, dust, toxic substances), the protective functions of the bronchi are reduced, and inflammation develops in them.

The consequences of inflammation in the bronchi are swelling of the mucous membrane, as a result of which the bronchial passage narrows. On examination, the doctor hears hoarse, whistling sounds from the chest, characteristic of obstruction.

Normally, when you inhale, the lungs expand, and when you exhale, they completely narrow. With obstruction, air enters them when you inhale, but does not completely leave them when you exhale. Over time, as a result of improper functioning of the lungs, patients may develop emphysema.

The reverse side of the disease is insufficient supply of oxygen to the lungs, as a result of which necrosis of the lung tissue occurs, the organ decreases in volume, which will inevitably lead to human disability and death.

Symptoms of the disease

In the first and second stages of the disease, the disease manifests itself only with a cough, to which rarely any of the patients pays due attention. More often, people go to the hospital at the third and fourth stages of the disease, when serious changes develop in the lungs and bronchi, accompanied by pronounced negative symptoms.

Typical symptoms of pulmonary obstruction:

• Dyspnea,
• Isolation of purulent sputum,
• bubbling breath,
• Hoarse voice,
• Swelling of the limbs.

Causes of pulmonary obstruction

The most important cause of pulmonary obstruction is long-term smoking, against which there is a gradual decrease in the protective function of the bronchi, they narrow and provoke changes in the lungs. The characteristic cough of this disease is called "smoker's cough" - hoarse, frequent, disturbing a person in the morning or after physical exertion.

Every year it will become more and more difficult for a smoker, shortness of breath, weakness, earthiness of the skin will be added to a prolonged cough. Habitual physical activity will be difficult, and during expectoration, purulent greenish sputum may appear, sometimes with blood impurities.

More than 80% of patients with chronic obstructive pulmonary disease are long-term smokers.

Obstruction can occur against the background of diseases:

• bronchiolitis. A severe disease accompanied by chronic inflammation of the bronchioles.
• Pneumonia.
• Poisoning with toxic substances.
• Heart disease.
• Various formations that occur in the trachea and bronchi.
• Bronchitis.

Against the background of the development of inflammation of the lungs, the symptoms are not very pronounced, but the most serious destruction occurs. In order to avoid the consequences of the disease, it is necessary to undergo a thorough examination during the period of illness and after it.

The reason for the development of COPD is a long stay with harmful and toxic substances.

The disease is diagnosed in people who, by the nature of their profession, are forced to work in "harmful" industries.

If a disease is detected, it will be necessary to abandon such work, and then undergo a comprehensive recommended treatment.
Most obstructive pulmonary disease affects adults, but the relentless trend of early tobacco smoking may soon change the statistics.

It is not necessary to exclude a genetic predisposition to the disease, which is often traced within the family.

Video

Emphysema due to obstruction

As a result of partial blockage of the lumen in the bronchi, formed against the background of inflammatory processes in the mucous membrane, obstructive changes occur in the lungs. With pathology, air does not leave the lungs during exhalation, but accumulates, stretching the lung tissue, as a result, a disease occurs - emphysema.

In terms of symptoms, the disease is similar to other respiratory diseases - obstructive bronchitis or bronchial asthma. A common cause of emphysema is long-term, chronic bronchitis, which is more common in older men and women.

Various lung diseases - and tuberculosis - can provoke the disease.

The cause of emphysema will be:

• Smoking,
• Contaminated air,
• Work in "harmful" production, associated with the inhalation of parts of silicon, asbestos

Sometimes emphysema can develop as a primary disease, causing severe lung failure.

Common symptoms of emphysema include:

• severe shortness of breath,
• Blueness of the skin, lips, tongue and nose,
• Noticeable swelling in the area of ​​the ribs,
• Extension above the clavicle.

In emphysema or COPD, the first symptom is shortness of breath, which first manifests itself with small physical exertion. If the disease is not treated at this stage, the disease will progress rapidly.

The patient will begin to experience difficulty in breathing with little physical exertion, at rest. The disease should be treated at the first appearance of bronchitis, subsequently irreversible changes in the organs may develop, which will lead to the patient's disability.

Diagnosis of obstructive syndrome

The examination of the patient begins with a questioning and examination of the patient. Signs of obstructive disease are already detected at these stages.

Held:

• Listening with a phonendoscope
• Tapping (percussion) in the chest area (in case of bronchial and pulmonary diseases there will be an “empty” sound),
• X-ray of the lungs, with which you can find out about pathological changes in the lung tissue, find out about the state of the diaphragm,
• Computed tomography helps to determine whether there are formations in the lungs, what shape they have,
• Lung function tests that help determine how much air a person inhales and exhales.

After identifying the degree of the obstructive process, they begin therapeutic measures.

Complex therapy of the disease

If violations in the lungs occurred as a result of long-term smoking, it is necessary to get rid of the bad habit. Quit smoking should not be gradual, but completely, as quickly as possible. Due to constant smoking, there is even more injury to the lungs, which already function poorly as a result of pathological changes. Initially, nicotine patches or e-cigarettes can be used.

If the cause of the obstruction is bronchitis or asthma, then these diseases should be treated to prevent the development of pathological changes in the lungs.

If the obstruction was provoked by an infectious disease, then antibiotics are used as a treatment to destroy bacteria in the body.

Treatment can be carried out instrumentally, using a special device that is used for alveolar massage. With the help of this device, it is possible to influence all the lungs, which is impossible when using drugs that are received in full by the healthy part of the organ, and not by the diseased one.

As a result of the use of such acupressure, oxygen is evenly distributed throughout the bronchial tree, which nourishes the damaged lung tissue. The procedure is painless, occurs with the help of inhalation of air through a special tube, which is supplied with the help of pulses.




In the treatment of pulmonary obstruction, oxygen therapy is used, which can be carried out in the hospital and at home. At the initial stage of the disease, therapeutic exercises are used as a treatment.

At the last stage of the disease, the use of conservative methods will not bring results, therefore, surgical removal of the overgrown lung tissue is used as a treatment.

The operation can be carried out in two ways. The first method consists in the complete opening of the chest, and the second method is characterized by the use of the endoscopic method, in which several punctures are made in the chest area.

As a preventive measure of the disease, it is necessary to lead a healthy lifestyle, give up bad habits, treat the diseases that have arisen in time and, at the first unpleasant symptoms, go to the doctor for an examination.

Surgical treatment of pathology

The issues of surgical treatment of this disease are still being discussed. One of the methods of such treatment is to reduce the volume of the lungs and transplant new organs. Bullectomy for pulmonary obstruction is indicated only for patients who have bullous emphysema with enlarged bullae, which is manifested by hemoptysis, shortness of breath, chest pain, and infection in the lungs.

Scientists have conducted a number of studies on the effect of reducing lung volume in the treatment of obstruction, which have shown that such a surgical intervention has a positive effect on the patient's condition. It is much more effective than drug treatment of the disease.

After such an operation, you can observe the following changes:

• Restoration of physical activity;
• Improving the quality of life;
• Decreased chance of death.

Such surgical treatment is in the experimental phase and is not yet available for widespread use.

Another type of surgical treatment is lung transplantation. With it, you can:

• Restore normal lung function;
• Improve physical performance;
• Improve the patient's quality of life.

We are treated at home with the help of folk remedies

It is better to combine the treatment of such a disease with folk remedies with the medication prescribed by the attending physician. This gives much more effectiveness than using only home treatments.

Before using any herbs or infusions, you should consult a doctor so as not to aggravate the condition.

With pulmonary obstruction, the following folk recipes are used:

1. Grind and mix 2 parts nettle and one part sage. Add a glass of boiling water and leave for one hour. After strain and drink every day for several months.
2. To remove phlegm from the lungs, you need to use an infusion of flax seeds 300 g, chamomile officinalis 100 g, the same amount of marshmallow, anise and licorice root. Pour boiling water over the mixture for one hour, strain and drink half a glass every day.
3. An excellent result is given by a decoction of a spring primrose horse. To prepare, pour boiling water over a tablespoon of chopped root and put in a water bath for 20-30 minutes. Take 1 teaspoon before meals several times a day.
4. If a strong cough is annoying, then adding 10-15 drops of propolis to a glass of warm milk will help to quickly remove it.
5. Pass half a kilogram of aloe leaves through a meat grinder, add a half-liter jar of honey and 300 ml of Cahors to the resulting slurry, mix everything thoroughly and put it in a jar with a tight lid. You need to insist 8-10 days in a cool place. Take a spoon every day several times.
6. A decoction of elecampane will make the patient feel better, help to remove sputum. Pour boiling water over a spoonful of herbs and drink like tea every day.
7. It is effective to take yarrow juice. Consume 2 tablespoons several times a day.
8. Black radish with honey is an ancient way to treat all respiratory diseases. It helps to expel phlegm and helps with expectoration. For cooking, you need to cut a small depression in the radish and pour honey. Wait a little until the juice stands out, which you can drink a teaspoon several times a day. Do not drink water or tea.
9. Mix in equal proportions coltsfoot, nettle, St. John's wort, motherwort and eucalyptus. pour a spoonful of the resulting mixture with a glass of boiling water and let it brew. Then strain and drink as a tea every day for several months.
10. Onions with honey work well. First, boil whole onions until softened, then pass them through a meat grinder, add a few tablespoons of honey, 2 tablespoons of sugar, 2 tablespoons of vinegar. Mix everything thoroughly and press down a little. Use a spoon every day.
11. To remove a strong cough, you need to use viburnum with honey. Pour 200 g of berries with a glass of water, add 3-4 tablespoons of honey, and simmer until all the water has evaporated. The resulting mixture should be taken in a teaspoon per hour for the first 2 days, then several tablespoons a day.
12. Mix half a teaspoon of such herbs: marshmallow, sage, coltsfoot, fennel, dill, and pour boiling water into a container with a tight lid. Insist 1-2 hours. Drink 100 ml every day 3 times.

Possible consequences and complications

The disease has sad consequences if treatment is not started in time. Among the possible complications, the most dangerous are:

• Pulmonary hypertension;
• respiratory failure;
• Deterioration of blood circulation.

Frequent consequences of a neglected initial form of the disease are:

• Dyspnea;
• Hacking cough;
• Increased fatigue;
• Chronic weakness;
• Strong sweating;
• Decreased performance.

Complications are dangerous for a child's body. They can appear if you do not pay attention to the first symptoms of the disease in time. Among them is a regular cough.

Prevention of pathology and prognosis

Pulmonary obstruction responds well to treatment. The process goes unnoticed and without complications, if you notice the first symptoms in time, do not start the disease and get rid of the causes of its occurrence. Timely and steamy treatment helps to remove all unpleasant symptoms and delay the progression of the pathology.

There are several factors that can adversely affect the prognosis:

• Bad habits, mainly smoking;
• Frequent exacerbations;
• Formation of cor pulmonale;
• Elderly age;
• Negative response to therapy.

In order not to get sick with lung obstruction, it is necessary to carry out prevention:

1. To refuse from bad habits. From smoking, this is one of the main causes of this disease.
2. Increase the level of immunity. Eat vitamins and minerals in sufficient quantities regularly.
3. Refuse junk and fatty foods, eat a lot of vegetables and fruits.
4. To maintain the protective function, do not forget about garlic and onions, which help protect the body from viruses.
5. Avoid all foods and items that cause an allergic reaction.
6. Fight against occupational factors that cause this disease. This includes providing personal respiratory protection, and reducing the concentration of harmful substances in the air.
7. Avoid infectious diseases, vaccinate on time.
8. Lead a healthy lifestyle and regularly harden the body, increasing its endurance.
9. Take regular walks outdoors.
10. Do physical exercises.

5 / 5 ( 8 votes)

COPD, the symptoms of which significantly impair the quality and duration of life of patients, is a serious pathology of the human respiratory system. At the heart of the disease is a partial restriction of air supply to the human respiratory tract. The changes are irreversible and tend to progress.

Development of chronic obstructive pulmonary disease

The main reason for the development of pathology in adults is nicotine addiction. The disease can occur against the background of:

1. Hazards in production (constant inhalation of gases). Obstructive pulmonary pathology is a standard disease for miners, agricultural workers, and railway workers. The disease occurs during prolonged work with silicon, cotton, grain, elements of the pulp and paper and metallurgical industries.
2. Frequent and prolonged respiratory disorders in childhood.
3. Environmental pollution. Dirt, exhaust gases increase the secretion of viscous mucus, disrupting the airway.
4. genetic predisposition. A sign is the insufficiency of alpha-1-antitrypsin, which is responsible for protecting the lung mucosa from the negative effects of the environment. Its insufficiency is fraught with susceptibility of the lungs to all kinds of pathologies.

Over time, COPD irreversibly changes the airways: peribronchial fibrosis develops, emphysema is possible. Respiratory failure is increasing, bacterial complications are added. Against the background of obstruction, gas exchange is disturbed (the O2 index decreases, CO2 in the arterial blood increases), cor pulmonale occurs (the cause of poor blood circulation, mortality of patients).

Stages of lung obstruction

Experts distinguish 4 stages of COPD. The distribution by stages is based on a decrease in the ratio of FEV1 (forced expiratory volume in the first second) to FVC (forced vital capacity) - the so-called Tiffno test. Pathology is evidenced by a decrease in this indicator of less than 70% against the background of taking bronchodilator drugs. Each stage of COPD is characterized by certain symptoms:

1. Stage 0 - premorbid condition. This is a period of increased risk of developing pathology. It begins with a cough, which is transformed into a permanent one, while the secretion of sputum increases. Lung function does not change. Timely treatment at this stage prevents the further development of the disease.
2. Stage 1 - mild COPD. Chronic cough and sputum production remain, minor obstructive disorders appear (FEV1 is more than 80%).
3. Stage 2 - moderate pathology. Significantly increased obstructive disorders (FEV1 less than 80%, but more than 50%). Shortness of breath, palpitations, weakness, dizziness develop.
4. Stage 3 - a severe form of pathology. Significant obstructive disorders (FEV1 less than 50%, but more than 30%). Shortness of breath and exacerbations intensify. These symptoms are observed even at rest.
5. Stage 4 is a very severe form of COPD. The extreme degree of bronchial obstruction, which is life threatening (FEV1 less than 30%) of the patient. There are signs of significant respiratory failure, possibly cor pulmonale.

Clinical forms of the disease

Symptoms of COPD develop in stage 2 of the disease. Deciphering the disease in the early stages is almost impossible, since it often proceeds secretly. Main symptoms: cough with sputum, shortness of breath. Initially, episodic cough, mucous sputum. Shortness of breath appears against the background of strong physical exertion. Then the cough becomes constant, the amount of sputum increases (it becomes viscous, purulent). Shortness of breath worries patients constantly.

Accession of infection is fraught with aggravation of the patient's condition: the body temperature rises, the amount of sputum increases, a wet cough appears. Obstruction can develop in two clinical forms:

1. bronchitis type. Symptoms are associated with purulent inflammation of the bronchi. The patient has the following symptoms: significant intoxication, cough, copious purulent sputum. In the first place - a significant bronchial obstruction, and pulmonary emphysema is weakly expressed. Symptoms and treatment of the disease depend on the age of the patient. Bronchitis type COPD can lead to the development of serious complications. At the terminal stage of obstruction, patients have "blue edema".
2. With the development of the emphysematous type of COPD, patients complain of expiratory shortness of breath (expiration is difficult). Emphysematous changes in the lungs come to the fore, and not obstructive manifestations. Patients acquire a pinkish-gray color of the skin, cachectic exhaustion is observed. When diagnosing, the doctor notes the barrel-shaped chest, so patients with this diagnosis are called "pink puffers." This form of the disease is much more favorable than the previous one. It has a slow progression. She has a favorable prognosis.

COPD can be made worse by:

• pneumonia;
• respiratory failure (acute and chronic);
• erythrocytosis (secondary polycythemia);
• congestive heart failure;
• pulmonary hypertension and cor pulmonale.

Diagnostic methods

Pathology slowly but surely progresses, damaging the human airways. This requires timely and accurate diagnosis of the body. To make a diagnosis of COPD, a doctor will:

1. Collecting an anamnesis with the obligatory specification of the presence of bad habits and production risk factors.
2. Spirometry is the "gold standard" for diagnosing COPD. Evaluate speed and volume indicators. Among them: vital capacity (VC), forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1). Indicators are analyzed before and after taking bronchodilators to assess the degree of reversibility of obstruction.
3. Sputum cytology. This study is carried out in order to determine the nature, severity of bronchial inflammation, to exclude oncopathology. Viscous, purulent sputum with a large number of bronchial epithelial cells and leukocytes indicates an exacerbation of the pathology, and the presence of a large number of macrophages of a mucous nature indicates remission of obstruction.
4. Clinical and biochemical blood tests. Deciphering a blood test with obstruction indicates polycythemia (an increase in all blood cells), and increased viscosity is the result of the development of oxygen deficiency. To confirm hypoxemia, the gas composition of the blood is studied.
5. X-ray examination. It is carried out for differential diagnosis with other pathologies, but with a similar clinic. In COPD, radiographs show seals, deformations of the walls of the bronchi, changes in the lungs of an emphysematous nature.
6. ECG. Hypertrophic changes are revealed in the right parts of the heart, blockade of the legs of His is possible, an increase in the T wave.
7. Bronchoscopy. It is carried out for the differential diagnosis of pathology. The doctor examines and evaluates the condition of the mucosa in an adult patient, takes the secret of the bronchi for analysis. By bronchoscopy, you can inject the drug into the lesion.

The purpose of a comprehensive and methodical examination of the patient is to establish a correct and timely diagnosis.

This will slow down the development of respiratory failure, reduce the frequency of exacerbations, and significantly improve the duration and quality of life.

Video about the diagnosis and treatment of COPD:

Forecast and prevention

The prognosis of pathology is unfavorable. With the progression of obstruction, the patient's performance decreases, disability may occur. To reduce the frequency and severity of exacerbations, it is recommended:

• eliminate the provoking factor;
• strictly follow all the recommendations of the doctor;
• saturate the body with vitamins, minerals and healthy food.

Video about symptoms and treatment of COPD:

To prevent the development of obstructive pathologies, it is necessary to stop smoking, follow the rules of labor protection in production, treat respiratory pathologies in a timely manner, and prevent exacerbations of COPD.

Smoking is the leading cause of COPD, and most people with this disease either still smoke or have smoked in the past. Long-term exposure to other lung irritants, such as air pollution, chemical fumes, or dust, can also contribute to the development of COPD.

What is chronic obstructive pulmonary disease (COPD)

The air you inhale travels down through the windpipe into branches of the windpipe called the bronchi.

In your lungs, your bronchi branch into thousands of small, thin tubes called bronchioles. These tubes end in clusters of tiny round air sacs called alveoli.

Small blood vessels called capillaries run through the walls of the alveoli. When air reaches the alveoli, oxygen enters through their walls into the blood in the capillaries. At the same time, carbon dioxide (carbon dioxide) moves from the capillaries to the alveoli. This process is called gas exchange.

The airways and alveoli are elastic, and when you inhale, each alveolus fills with air like a small balloon, and when you exhale, the alveoli shrink.

In chronic obstructive pulmonary disease, less air enters the lungs and therefore less air leaves them. This happens for one or more of these reasons:

• The airways and alveoli lose their elasticity.
• The walls between many alveoli are destroyed.
• The walls of the airways are swollen and inflamed.
• The airways produce more mucus than usual, which can clog them.

The term COPD includes two main diseases - emphysema and chronic bronchitis. In emphysema, the walls between many of the alveoli are damaged or even destroyed. As a result, the alveoli lose their shape, resulting in fewer shapeless large alveoli instead of many smaller ones. If this happens, then gas exchange in the lungs worsens.

In chronic bronchitis, the lining of the airways is constantly irritated and inflamed. This leads to swelling of the mucous membrane and narrowing of the airways. During chronic bronchitis, thick mucus is present in the respiratory system, which also makes breathing difficult.

Most people with COPD also have emphysema and chronic bronchitis. Thus, the general term "COPD" is more accurate.

Forecast

COPD is one of the leading causes of disability and is the third leading cause of death in developed countries. Currently, chronic obstructive pulmonary disease is diagnosed in millions of people. And many more people can have this condition and not even know it.

COPD develops slowly. Symptoms often get worse over time and can limit your ability to do daily activities. Severe COPD can almost completely disable you, preventing even basic activities like walking, cooking, or taking care of yourself.

Most cases of COPD are diagnosed in middle-aged or older people. The disease is not transmitted from person to person, so you cannot catch it from someone else.

There is currently no cure for COPD because doctors do not know how to reverse damage to the airways and lungs. However, existing treatments and lifestyle changes can help you feel better, stay more active, and slow the progression of the disease.

Causes of COPD

Long-term exposure to irritants that damage the lungs and airways is usually the cause of COPD.

The most common irritant that causes COPD is tobacco smoke. Tobacco smoke from pipes, cigars, cigarettes, etc. can also cause chronic obstructive pulmonary disease, especially if the smoke is inhaled directly into the lungs.

Passive smoking, air pollution, chemical fumes or dust from the environment or workplace can also contribute to the development of COPD. (Passive smoking is the inhalation of tobacco smoke when other people smoke near you).

In rare cases, a genetic disorder called alpha-1 antitrypsin deficiency may play a role in causing COPD. People with this disease have low levels of alpha-1 antitrypsin (AAT), a protein synthesized in the liver.

If a person has low levels of the AAT protein, this can lead to lung damage and COPD if you are exposed to smoke or other lung irritants. If you have this condition and you smoke, COPD can get worse very quickly.

Although rare, some people with asthma can develop COPD. Asthma is a chronic lung disease that causes inflammation and swelling of the airways. Treatment can usually reverse inflammation and relieve swelling. However, if asthma is left untreated, COPD can develop.

Who is at risk for developing COPD

The main risk factor for developing COPD is smoking. Most people with COPD currently smoke or have smoked in the past. People with a family history of chronic obstructive pulmonary disease are generally more likely to develop the disease if they smoke.

Long-term exposure to other lung irritants is also a risk factor for developing COPD. These irritants include:

• second hand smoke
• air pollution
• chemical fumes
• dust in the environment
• house dust

Symptoms of chronic obstructive pulmonary disease usually begin to develop in people aged 40 or older. Rarely, people under 40 can develop COPD. This can happen if a person has an alpha-1 antitrypsin deficiency (a hereditary disease).

What are the signs and symptoms of COPD

First, COPD may cause no symptoms or cause only mild symptoms. As the disease progresses, the symptoms usually become more severe. Common signs and symptoms of chronic obstructive pulmonary disease are:

• Persistent cough or cough that produces a lot of mucus (often called "smoker's bronchitis").
• Difficulty breathing, especially during physical activity.
• Shortness of breath (whistling or wheezing during breathing).
• Chest tightness.

If you have COPD, you may also have frequent colds or the flu.

Not everyone who has the above symptoms has COPD. Also, not every person with COPD experiences these symptoms. Some of the symptoms of chronic obstructive pulmonary disease are similar to those of other diseases and conditions. For an accurate diagnosis, you need to see a doctor.

If your symptoms are mild, you may not even notice them, or you can make some lifestyle changes to make breathing easier. For example, you can use the elevator instead of the stairs.

Over time, the symptoms of COPD can become severe enough to require medical attention. For example, you may develop shortness of breath during physical activity.

The severity of your symptoms will depend on how badly your lungs are damaged. If you continue to smoke, the destruction of lung tissue will occur faster than if you stop smoking.

Severe COPD can cause other symptoms, such as swelling in the ankles, feet, or legs, weight loss, and decreased muscle endurance.

Some severe symptoms may require hospital treatment. You or someone close to you (if you are unable to do so) should seek emergency medical attention if:

• You have severe difficulty breathing (you are short of breath and have difficulty speaking).
• Your lips or nails turn blue or grey. (This is a sign of low oxygen levels in the blood.)
• Your brain function has deteriorated (disturbances in thinking, poor thinking).
• Your heartbeat is very fast.
• The recommended treatment for symptoms that are getting worse is not working.

Diagnosis of COPD

Your doctor will diagnose COPD based on your symptoms, your medical and family history, and the results of tests and diagnostic procedures.

Your doctor may ask if you smoke or if you come into contact with lung irritants such as secondhand smoke (secondhand smoke), air pollution, chemical fumes, or dust.

If you have a chronic cough, you need to let your doctor know (how long you have had a persistent cough, how much mucus you cough up). Also, if you have a history of COPD in your family, you should also tell your doctor.

The doctor will examine you and listen to your lungs with a stethoscope to check your breathing for wheezing or other unusual sounds in your chest. He may also recommend one or more diagnostic procedures to diagnose COPD.

Pulmonary function test

A lung function test measures how much air you can breathe in and out, how fast you can breathe out, and how well your lungs deliver oxygen to your blood.

The main diagnostic procedure for diagnosing COPD is spirometry. Other lung function tests, such as a lung diffusivity test, may also be used.

Spirometry

During this painless procedure, the diagnostician will ask you to take a deep breath. Then, you will blow into a tube attached to a small appliance as hard as you can. This device is called a spirometer.

This device measures the amount of air you exhale. It also measures maximum expiratory flow.

Your doctor may give you medicine to help open your airways and then ask you to blow into the tube again. He can then compare the test results before and after taking the medicine.

Spirometry can detect COPD before symptoms appear. Your doctor may also use the test results to find out how severe your COPD is and to help set treatment goals.

The test results can also help identify another medical condition, such as asthma or heart failure, as these may also be causing your symptoms.

Other diagnostic procedures

• Chest x-ray (Computed tomography or CT). Diagnosis using CT allows you to take pictures of the internal organs of the chest, such as the heart, lungs and blood vessels. The images may show signs of COPD. They may also show another medical condition, such as heart failure, which may also be causing your symptoms.
• Analysis of arterial blood gases. This blood test measures the level of oxygen in the blood using a blood sample taken from an artery. The results of this test can tell you how serious your COPD is and whether you need oxygen therapy.

COPD treatment

Chronic obstructive pulmonary disease cannot be cured. However, lifestyle changes and treatment can help you feel better, stay more active, and slow the progression of the disease.

Goals of COPD treatment:

• Relief of your symptoms.
• Slowing down the progression of the disease.
• Improving well-being during physical activity (increasing your ability to stay active).
• Prevention and treatment of complications.
• Improvement in general health.

In order to start treatment for your illness, you need to see a pulmonologist (a doctor who specializes in diseases of the respiratory tract).

Lifestyle changes

Quit smoking and avoid exposure to lung irritants

Quitting smoking is the most important step you can take to treat COPD. Talk to your doctor about programs and tools that can help you quit smoking.

Also, try to avoid secondhand smoke, stay away from smoking areas, dusty places, and avoid breathing in chemical fumes or other toxic substances that you may inhale.

Other lifestyle changes

If you suffer from chronic obstructive pulmonary disease, you may have trouble eating enough food due to symptoms such as shortness of breath and fatigue. (This problem is more common in severe disease.)

As a result, you may not be getting enough calories and nutrients, which can worsen your condition and increase your risk of infections.

Talk to your doctor about a nutrition plan that will suit your body's needs. Your doctor may suggest eating smaller amounts but more often; rest before eating; and take vitamins or nutritional supplements.

Also, talk to your doctor about what activities are safe for you. You may find it difficult to be active with COPD symptoms. However, physical activity can strengthen the muscles that help you breathe and improve your overall health.

Medicines

Bronchodilators (bronchodilators)

Bronchodilators relax the muscles in the airways. This helps open the airways and makes breathing easier.

Depending on the severity of your COPD symptoms, your doctor may prescribe short-acting or long-acting bronchodilators. Short-acting bronchodilators are drugs that last about 4-6 hours and should only be used when needed. Long-acting bronchodilators work for approximately 12 hours or more and are used daily.

Most bronchodilators are taken with a device called an inhaler. This device allows the medication to be delivered directly to the lungs. Not all inhalers are used in the same way. Ask your doctor to show you the correct way to use your inhaler.

If COPD symptoms are mild, your doctor may only prescribe short-acting bronchodilators. In this case, you can only use medications when symptoms appear.

If you have moderate to severe COPD, your doctor may prescribe short-acting and long-acting bronchodilators on a regular basis.

Combination of bronchodilators with inhaled glucocorticosteroids (IGCS)

If COPD symptoms are more severe, or if your symptoms occur frequently, your doctor may prescribe a combination of medications, such as bronchodilators and inhaled steroids. Steroids help reduce airway inflammation.

In general, the use of inhaled steroids alone is not the preferred treatment.

Your doctor may recommend that you try using inhaled steroids with a bronchodilator for 6 weeks to 3 months to see if adding a steroid helps relieve your breathing problems.

Vaccines

flu shot

The flu can cause serious problems for people with COPD. Flu shots may reduce the risk of contracting the flu (not proven - can be life-threatening). Talk to your doctor about getting your yearly flu shot.

Vaccination against pneumococcal infection

This vaccine reduces the risk of developing pneumococcal pneumonia and its complications. People with COPD are at a higher risk of developing pneumonia than people without COPD. Talk to your doctor about whether you should get this vaccine.

Pulmonary rehabilitation

The Pulmonary Rehabilitation (Rehabilitation) Program helps improve the condition of people suffering from chronic breathing problems.

Rehabilitation may include an exercise program, disease management training, nutritional counseling, and psychological support. The goal of the program is to help you stay active and carry out your daily activities.

Doctors, nurses, physiotherapists, pulmonologists, rehabilitation specialists and nutritionists will help you with this. These health professionals will help you create a program that meets your needs.

oxygen therapy

If you have severe COPD and low blood oxygen levels, oxygen therapy can help you breathe better. In this type of treatment, oxygen is given to your lungs through nasal prongs or an oxygen mask.

You may need supplemental oxygen all the time or only at certain times. For some people with severe COPD, using oxygen therapy for most of the day can help:

• Perform tasks or activities while experiencing fewer symptoms.
• Protect your heart and other organs from damage.
• Sleep more during the night and improve alertness during the day.
• Live longer.

Surgery

Surgery may benefit some people with COPD. Surgery is usually the last resort for people experiencing severe symptoms that do not improve with medication.

People with chronic obstructive pulmonary disease, which is mainly associated with emphysema, usually have bullectomy or lung volume reduction surgery. A lung transplant may be an option for people with very severe COPD.

Bullectomy

When the walls of the alveoli collapse, large air spaces called bullae begin to form in the lungs. These air spaces can become so large that they interfere with breathing. During a bullectomy, doctors remove one or more very large bullae from the lungs.

Lung volume reduction surgery

During lung volume reduction surgery (LULA), surgeons remove damaged tissue from the lungs. This helps the lungs function better. This surgery is only done in some people with COPD, and if done successfully, it can help improve a person's breathing and quality of life.

lung transplant

During a lung transplant, your damaged lung is removed and replaced with a healthy lung from a deceased donor.

A lung transplant can improve your lung function and quality of life. However, there are many risks associated with lung transplantation, such as infections. The operation can lead to death if the body rejects the transplanted lungs.

If you have very severe COPD, talk to your doctor about whether you need a lung transplant. Ask your doctor about the benefits and risks of this type of surgery.

Complications of COPD

Symptoms of COPD usually worsen slowly over time. However, they can also get worse suddenly. For example, a cold, flu, or lung infection can cause your condition to worsen quickly, making it difficult for you to breathe. You may also experience increased chest tightness and coughing, a change in the color or amount of sputum coming out of your lungs, and a rise in body temperature.

Call your doctor right away if your symptoms suddenly get worse. To help you breathe, he may prescribe antibiotics to treat the infection, as well as other medications such as bronchodilators and inhaled steroids. Some severe symptoms may require hospitalization.

COPD prevention

There are some steps you can take to help prevent COPD from developing even before it starts. If you already suffer from this condition, you can take steps to prevent complications and slow the progression of the disease.

Preventing COPD before the onset of this disease

If you do not smoke, never try to start smoking, as smoking is the main cause of chronic obstructive pulmonary disease. If you already smoke, you need to completely get rid of this bad habit. If you smoke and want to quit but can't do it on your own, talk to your doctor about programs and tools that can help you quit.

Also, try to avoid inhaling harmful substances that irritate the lungs, as exposure to them can contribute to the development of COPD. Passive smoking, air pollution, chemical fumes and dust can all cause this disease.

Preventing Complications and Slowing the Development of COPD

If you already have the first signs of COPD, the most important step you can take is to quit smoking completely. This can help you prevent complications and slow the progression of the disease. You should also avoid exposure to the lung irritants mentioned above.

Follow the COPD treatment plan your doctor has given you. It can help you breathe easier, stay more active, avoid developing severe symptoms, and keep them under control.

Talk to your doctor about whether you should get flu and pneumonia shots. These vaccines can reduce the risk of these diseases (not enough evidence - vaccines can be life-threatening), which are major health risks for people with COPD.

Living with COPD

Chronic obstructive pulmonary disease is currently not cured. However, you can take steps to control your symptoms and slow the progression of the disease. You need:

• Get ongoing care
• Keep disease and symptoms under control
• Prepare for emergencies

Avoid lung irritants

If you smoke, you need to quit smoking. Smoking is the main cause of COPD development. Talk to your doctor about programs and tools that can help you quit smoking.

Also, try to avoid inhaling substances that irritate the lungs, as they can contribute to the development of COPD. The main irritants of the lungs are:

• second hand smoke
• air pollution
• chemical fumes

Try to make sure that these irritants are not present in your home. If your home has been painted or has been treated with bug sprays, you should be out of the house for as long as possible.

If the air is very polluted and dusty, keep your windows closed and stay at home (if possible).

Get ongoing care

If you suffer from chronic obstructive pulmonary disease, it is very important to receive ongoing medical care. Take all the medicines your doctor has prescribed for you. Bring a list of all the medications you take to your regular health check-ups.

Talk to your doctor about whether you should get flu and pneumonia shots. Also, ask him about other diseases that COPD can increase your risk of developing. These can include heart disease, lung cancer, and pneumonia.

COPD symptom control

There are some things you can do to help control your COPD symptoms. For example:

• Perform physical activities slowly.
• Put the items you use often in one place so they are easy to reach.
• Find very easy ways to cook, clean, and do other chores around the house.
• Wear clothes and shoes that are easy to put on and take off.

Depending on how severe your illness is, you may want to ask your family and friends for help with daily tasks.

Prepare for emergencies

If you have COPD, you need to know when and where to seek help in an emergency. You should seek emergency medical attention if you have severe symptoms such as shortness of breath or an inability to speak normally.

Call your doctor if you notice that your symptoms are getting worse or if you have signs of an infection, such as fever. Your doctor may change or adjust your treatments to relieve and treat the symptoms of chronic obstructive pulmonary disease.

Keep on hand the phone numbers of your doctor, hospital, or someone who can help you. You should also have a referral to your doctor and a list of all medications you are taking handy.